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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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