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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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > American Trypanosomiasis (Chagas Disease)

View in Context

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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > 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 2024 > Leishmaniasis

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–9. 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 host . 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 2024 > Malaria

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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