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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

View in Context

eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

View in Context

eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–29. Life cycle of Hymenolepis diminuta and Hymenolepis nana. A: Eggs of H nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment . When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion  and develop into adults in the small intestine. A morphologically identical variant, H nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae . Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine . An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . The life span of adult worms is 4–6 weeks, but internal autoinfection allows the infection to persist for years. B: Eggs of H diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to adulthood. H diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (eg, oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces  occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length . Eggs are released in the small intestine from gravid proglottids  that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host’s feces .(From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Hymenolepis nana.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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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 37–39. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine  and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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eFigure 37–39. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine  and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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eFigure 37–39. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine  and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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eFigure 37–39. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine  and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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eFigure 37–39. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine  and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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eFigure 37–39. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine  and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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eFigure 37–39. Life cycle of Enterobius vermicularis (pinworm). Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (eg, curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine  and the adults establish themselves in the colon . The time interval from ingestion of infective eggs to oviposition by the adult females is about 1 month. The life span of the adults is about 2 months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside the eggs develop (the eggs become infective) in 4–6 hours under optimal conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Enterobius vermicularis.

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts  and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae  that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts  and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae  that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts  and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae  that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts  and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae  that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts  and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae  that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts  and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae  that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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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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