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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector's midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2025 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector's midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2025 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector's midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2025 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector's midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2025 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector's midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2025 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector's midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2025 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector's midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2025 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector's midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2025 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector's midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2025 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–6. Trypanosoma cruzi trypomastigote in a thin blood smear stained with Giemsa. Note the anterior location of the nucleus. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A photomicrograph of trypanosoma cruzi trypomastigote in a thin, Giemsa stained blood smear.

Current Medical Diagnosis & Treatment 2025 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–7. Life cycle of leishmaniasis. Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (ie, promastigotes) from their proboscis during blood meals . Promastigotes that reach the puncture wound are phagocytized by macrophages and other types of mononuclear phagocytic cells. Promastigotes transform in these cells into the tissue stage of the parasite (ie, amastigotes) , which multiply by simple division and proceed to infect other mononuclear phagocytic cells . Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (, ). In sandflies, amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of leishmaniasis parasite.

Current Medical Diagnosis & Treatment 2025 > Leishmaniasis

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eFigure 37–7. Life cycle of leishmaniasis. Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (ie, promastigotes) from their proboscis during blood meals . Promastigotes that reach the puncture wound are phagocytized by macrophages and other types of mononuclear phagocytic cells. Promastigotes transform in these cells into the tissue stage of the parasite (ie, amastigotes) , which multiply by simple division and proceed to infect other mononuclear phagocytic cells . Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (, ). In sandflies, amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of leishmaniasis parasite.

Current Medical Diagnosis & Treatment 2025 > Leishmaniasis

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eFigure 37–7. Life cycle of leishmaniasis. Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (ie, promastigotes) from their proboscis during blood meals . Promastigotes that reach the puncture wound are phagocytized by macrophages and other types of mononuclear phagocytic cells. Promastigotes transform in these cells into the tissue stage of the parasite (ie, amastigotes) , which multiply by simple division and proceed to infect other mononuclear phagocytic cells . Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (, ). In sandflies, amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of leishmaniasis parasite.

Current Medical Diagnosis & Treatment 2025 > Leishmaniasis

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eFigure 37–7. Life cycle of leishmaniasis. Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (ie, promastigotes) from their proboscis during blood meals . Promastigotes that reach the puncture wound are phagocytized by macrophages and other types of mononuclear phagocytic cells. Promastigotes transform in these cells into the tissue stage of the parasite (ie, amastigotes) , which multiply by simple division and proceed to infect other mononuclear phagocytic cells . Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (, ). In sandflies, amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of leishmaniasis parasite.

Current Medical Diagnosis & Treatment 2025 > Leishmaniasis

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eFigure 37–7. Life cycle of leishmaniasis. Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (ie, promastigotes) from their proboscis during blood meals . Promastigotes that reach the puncture wound are phagocytized by macrophages and other types of mononuclear phagocytic cells. Promastigotes transform in these cells into the tissue stage of the parasite (ie, amastigotes) , which multiply by simple division and proceed to infect other mononuclear phagocytic cells . Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (, ). In sandflies, amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of leishmaniasis parasite.

Current Medical Diagnosis & Treatment 2025 > Leishmaniasis

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eFigure 37–7. Life cycle of leishmaniasis. Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (ie, promastigotes) from their proboscis during blood meals . Promastigotes that reach the puncture wound are phagocytized by macrophages and other types of mononuclear phagocytic cells. Promastigotes transform in these cells into the tissue stage of the parasite (ie, amastigotes) , which multiply by simple division and proceed to infect other mononuclear phagocytic cells . Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (, ). In sandflies, amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of leishmaniasis parasite.

Current Medical Diagnosis & Treatment 2025 > Leishmaniasis

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eFigure 37–7. Life cycle of leishmaniasis. Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (ie, promastigotes) from their proboscis during blood meals . Promastigotes that reach the puncture wound are phagocytized by macrophages and other types of mononuclear phagocytic cells. Promastigotes transform in these cells into the tissue stage of the parasite (ie, amastigotes) , which multiply by simple division and proceed to infect other mononuclear phagocytic cells . Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (, ). In sandflies, amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of leishmaniasis parasite.

Current Medical Diagnosis & Treatment 2025 > Leishmaniasis

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eFigure 37–7. Life cycle of leishmaniasis. Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (ie, promastigotes) from their proboscis during blood meals . Promastigotes that reach the puncture wound are phagocytized by macrophages and other types of mononuclear phagocytic cells. Promastigotes transform in these cells into the tissue stage of the parasite (ie, amastigotes) , which multiply by simple division and proceed to infect other mononuclear phagocytic cells . Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (, ). In sandflies, amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of leishmaniasis parasite.

Current Medical Diagnosis & Treatment 2025 > Leishmaniasis

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eFigure 37–7. Life cycle of leishmaniasis. Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies inject the infective stage (ie, promastigotes) from their proboscis during blood meals . Promastigotes that reach the puncture wound are phagocytized by macrophages and other types of mononuclear phagocytic cells. Promastigotes transform in these cells into the tissue stage of the parasite (ie, amastigotes) , which multiply by simple division and proceed to infect other mononuclear phagocytic cells . Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (, ). In sandflies, amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of leishmaniasis parasite.

Current Medical Diagnosis & Treatment 2025 > Leishmaniasis

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–11. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2025 > Malaria

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–16. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat's feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2025 > Toxoplasmosis

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eFigure 37–17. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–17. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–17. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–17. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–17. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–17. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–17. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–17. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–17. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–17. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–18. Trophozoites of Entamoeba histolytica with ingested erythrocytes stained with trichrome. The ingested erythrocytes appear as dark inclusions. Erythrophagocytosis (ingestion of RBCs by the parasite) is the only morphologic characteristic that can be used to differentiate E histolytica from the nonpathogenic Entamoeba dispar. However, erythrophagocytosis is not typically observed on stained smears of E histolytica. The parasites above show nuclei that have the typical small, centrally located karyosome, and thin, uniform peripheral chromatin. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A photomicrograph of Trophozoites of Entamoeba histolytica with ingested erythrocytes stained with trichrome.

Current Medical Diagnosis & Treatment 2025 > Amebiasis

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eFigure 37–20. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2025 > Giardiasis

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eFigure 37–20. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2025 > Giardiasis

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eFigure 37–20. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2025 > Giardiasis

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eFigure 37–20. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2025 > Giardiasis

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eFigure 37–20. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2025 > Giardiasis

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eFigure 37–20. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2025 > Giardiasis

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eFigure 37–21. Giardia lamblia trophozoite: Giardia duodenalis trophozoites in Kohn stain. G duodenalis trophozoites are pear-shaped and measure 10–20 mcM in length. In permanent, stained specimens, two large nuclei are usually visible. The sucking disks (used for attaching to the host's mucosal epithelium), median bodies, and flagella (8) may also be seen. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A photomicrograph of Giardia lamblia trophozoite in a Kohn stain.

Current Medical Diagnosis & Treatment 2025 > Giardiasis

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–22. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–23. Schistosoma eggs. A: Eggs of Schistosoma mansoni in an unstained wet mount. B: Egg of Schistosoma haematobium in a wet mount of urine concentrates, showing the characteristic terminal spine. C: Egg of Schistosoma japonicum in an unstained wet mount. Note the small, inconspicuous spines (red arrow). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) Three photomicrographs show Schistosoma eggs.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–23. Schistosoma eggs. A: Eggs of Schistosoma mansoni in an unstained wet mount. B: Egg of Schistosoma haematobium in a wet mount of urine concentrates, showing the characteristic terminal spine. C: Egg of Schistosoma japonicum in an unstained wet mount. Note the small, inconspicuous spines (red arrow). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) Three photomicrographs show Schistosoma eggs.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–23. Schistosoma eggs. A: Eggs of Schistosoma mansoni in an unstained wet mount. B: Egg of Schistosoma haematobium in a wet mount of urine concentrates, showing the characteristic terminal spine. C: Egg of Schistosoma japonicum in an unstained wet mount. Note the small, inconspicuous spines (red arrow). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) Three photomicrographs show Schistosoma eggs.

Current Medical Diagnosis & Treatment 2025 > Schistosomiasis (Bilharziasis)

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–25. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2025 > Fascioliasis

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eFigure 37–26. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–26. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–26. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–26. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–26. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–26. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–26. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–26. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–26. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–26. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–27. Adult trematodes. Clonorchis sinensis adults are flattened and measure approximately 10–25 mm long by 3–5 mm wide. Like other flukes, they are hermaphroditic, with a single ovary situated anterior to two branches testes. Adults reside in the biliary passages of the liver of the definitive host. A: Adult of C sinensis. B: Adult of C sinensis stained with carmine. Clearly visible in this image are the oral sucker (OS), pharynx (PH), ceca (CE), acetabulum, or ventral sucker (AC), uterus (UT), vitellaria (VT) and testes (TE). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A photo and a diagram of adult trematodes.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–27. Adult trematodes. Clonorchis sinensis adults are flattened and measure approximately 10–25 mm long by 3–5 mm wide. Like other flukes, they are hermaphroditic, with a single ovary situated anterior to two branches testes. Adults reside in the biliary passages of the liver of the definitive host. A: Adult of C sinensis. B: Adult of C sinensis stained with carmine. Clearly visible in this image are the oral sucker (OS), pharynx (PH), ceca (CE), acetabulum, or ventral sucker (AC), uterus (UT), vitellaria (VT) and testes (TE). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A photo and a diagram of adult trematodes.

Current Medical Diagnosis & Treatment 2025 > Clonorchiasis & Opisthorchiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–28. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2025 > Paragonimiasis

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eFigure 37–29. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal's intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal's intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal's intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal's intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal's intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal's intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal's intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–30. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days) and yield oncospheres, which develop into coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–31. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2025 > Noninvasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–32. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2025 > Invasive Cestode Infections

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eFigure 37–36. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2025 > Ascariasis

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eFigure 37–36. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2025 > Ascariasis

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eFigure 37–36. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2025 > Ascariasis

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eFigure 37–36. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2025 > Ascariasis

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eFigure 37–36. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2025 > Ascariasis

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eFigure 37–36. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2025 > Ascariasis

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eFigure 37–36. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2025 > Ascariasis

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eFigure 37–36. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2025 > Ascariasis

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eFigure 37–38. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2025 > Trichuriasis

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eFigure 37–38. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2025 > Trichuriasis

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eFigure 37–38. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2025 > Trichuriasis

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eFigure 37–38. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2025 > Trichuriasis

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eFigure 37–38. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2025 > Trichuriasis

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eFigure 37–38. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2025 > Trichuriasis

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eFigure 37–38. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2025 > Trichuriasis

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eFigure 37–39. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2025 > Hookworm Disease

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eFigure 37–39. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2025 > Hookworm Disease

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eFigure 37–39. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2025 > Hookworm Disease

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eFigure 37–39. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2025 > Hookworm Disease

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eFigure 37–39. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2025 > Hookworm Disease

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eFigure 37–39. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2025 > Hookworm Disease

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–40. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2025 > Strongyloidiasis

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eFigure 37–41. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2025 > Enterobiasis

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eFigure 37–41. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2025 > Enterobiasis

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eFigure 37–41. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2025 > Enterobiasis

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eFigure 37–41. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2025 > Enterobiasis

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eFigure 37–41. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2025 > Enterobiasis

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eFigure 37–41. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2025 > Enterobiasis

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eFigure 37–41. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2025 > Enterobiasis

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eFigure 37–42. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2025 > Dracunculiasis

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eFigure 37–42. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2025 > Dracunculiasis

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eFigure 37–42. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2025 > Dracunculiasis

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eFigure 37–42. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2025 > Dracunculiasis

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eFigure 37–42. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2025 > Dracunculiasis

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eFigure 37–42. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2025 > Dracunculiasis

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eFigure 37–42. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2025 > Dracunculiasis

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eFigure 37–42. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2025 > Dracunculiasis

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eFigure 37–45. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2025 > Trichinosis

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eFigure 37–45. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2025 > Trichinosis

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eFigure 37–45. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2025 > Trichinosis

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eFigure 37–45. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2025 > Trichinosis

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eFigure 37–45. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2025 > Trichinosis

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eFigure 37–45. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2025 > Trichinosis

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eFigure 37–46. Trichinella spiralis. A: Encysted larvae of Trichinella sp. in muscle tissue, stained with hematoxylin and eosin (H&E). The image magnification is 200×. B: Encysted larvae of Trichinella sp. in muscle tissue, stained with H&E. Image was captured at 400× magnification. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) Two photomicrographs depict histopathological features of Trichinella spiralis larvae.

Current Medical Diagnosis & Treatment 2025 > Trichinosis

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eFigure 37–46. Trichinella spiralis. A: Encysted larvae of Trichinella sp. in muscle tissue, stained with hematoxylin and eosin (H&E). The image magnification is 200×. B: Encysted larvae of Trichinella sp. in muscle tissue, stained with H&E. Image was captured at 400× magnification. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) Two photomicrographs depict histopathological features of Trichinella spiralis larvae.

Current Medical Diagnosis & Treatment 2025 > Trichinosis

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eFigure 37–47. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidad Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2025 > Gnathostomiasis

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eFigure 37–47. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidad Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2025 > Gnathostomiasis

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eFigure 37–47. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidad Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2025 > Gnathostomiasis

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eFigure 37–47. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidad Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2025 > Gnathostomiasis

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eFigure 37–47. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidad Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2025 > Gnathostomiasis

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eFigure 37–47. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidad Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2025 > Gnathostomiasis

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eFigure 37–47. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidad Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2025 > Gnathostomiasis

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eFigure 37–47. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidad Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2025 > Gnathostomiasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–50. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito's proboscis and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2025 > Lymphatic Filariasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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eFigure 37–51. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2025 > Onchocerciasis

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