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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 37–2. 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 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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eFigure 37–14. Life cycle of Toxoplasma gondii. The only known definitive hosts for T gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–2 weeks, large numbers may be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water, or plant material contaminated with oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of several routes: eating undercooked meat of animals harboring tissue cysts . consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat) . blood transfusion or organ transplantation . transplacentally from mother to fetus . In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T gondii DNA in amniotic fluid using molecular methods such as PCR . (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Toxoplasma gondii.

Current Medical Diagnosis & Treatment 2024 > Toxoplasmosis

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