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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

View in Context

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 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

View in Context

eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

View in Context

eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae  that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae  that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae  that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae  that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae  that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae  that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae  that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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