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eFigure 9–15. A: Eosinophilic pneumonitis. This patient with parasite-induced eosinophilic pneumonitis has ill-defined nodular and fluffy, patchy densities scattered throughout both lungs. B: The lateral film from the same patient shows a better-defined infiltrate at the left lung base. An image shows nodular and fluffy patches in both lungs. A lateral view of the left lung shows nodular and fluffy patches in the base of the left lung.

Current Medical Diagnosis & Treatment 2025 > Eosinophilic Pulmonary Syndromes

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eFigure 9–15. A: Eosinophilic pneumonitis. This patient with parasite-induced eosinophilic pneumonitis has ill-defined nodular and fluffy, patchy densities scattered throughout both lungs. B: The lateral film from the same patient shows a better-defined infiltrate at the left lung base. An image shows nodular and fluffy patches in both lungs. A lateral view of the left lung shows nodular and fluffy patches in the base of the left lung.

Current Medical Diagnosis & Treatment 2025 > Eosinophilic Pulmonary Syndromes

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2025 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2025 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2025 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2025 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2025 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2025 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2025 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2025 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2025 > African Trypanosomiasis (Sleeping Sickness)

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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 37–7. 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 37–10. Morphologic characteristics of developmental stages of malarial parasites in the RBC. Note cytoplasmic Schüffner dots and enlarged host cells in Plasmodium vivax and Plasmodium ovale infections; the band-shaped trophozoite often seen in Plasmodium malariae infection; and the small, often multiply infected rings and the banana-shaped gametocytes in Plasmodium falciparum infections. Rings and gametocytes are typically seen in peripheral blood smears from patients with P falciparum infections. (Reproduced with permission from Goldsmith R, Heyneman D: Tropical Medicine and Parasitology. McGraw-Hill, 1989. © The McGraw-Hill Companies, Inc.) A table shows the first three parasitic stages of P vivax, P ovale, P malaria, and P falciparum. A table shows the last three parasitic stages of P vivax, P ovale, P malaria, and P falciparum.

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 37–11. 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 37–18. 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 37–25. 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 37–28. 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 37–31. 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 ing