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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

View in Context

eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

View in Context

eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 35–29. 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 2023 > Noninvasive Cestode Infections

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eFigure 10–8. The timing of the principal cardiac murmurs. Heart murmurs can be either systolic or diastolic. During systole, while the LV is contracting, the aortic valve is open and the mitral valve is closed. Turbulent flow can occur either because of an incompetent mitral valve, leading to regurgitation of blood back into the atrium, or from a narrowed aortic valve. In diastole, the situation is reversed, with filling of the LV through an open mitral valve while the aortic valve is closed. Turbulent flow occurs when there is narrowing of the mitral valve or incompetence of the aortic valve. Stenosis of valves usually develops slowly over time; lesions that cause valvular regurgitation can be either chronic or acute. (Reproduced, with permission, from Hammer GD, McPhee SJ. Pathophysiology of Disease, 8th ed. McGraw-Hill, 2019.) Several examples depict the timing patterns of different cardiac murmurs.

Current Medical Diagnosis & Treatment 2023 > Heart Disease: Symptoms & Signs

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eFigure 10–18. Atrial septal anatomy. A: Embryologically, the septum primum (first septum) divides the atrium by migrating to the ventricles. The gap preceding the septal migration is the ostium primum. B: Once the septum primum completes its journey, fenestrations (holes) appear and generally coalesce into a single ostium secundum. C: A second septum (septum secundum) grows down on the right atrial side of the septum primum and covers the entire septal area except for a large oval hole that forms in its distal portion (the foramen ovale). D: I f there is redundancy of either the septum primum (as shown) or both septae, then that defines a septal aneurysm. Four illustrations, A through D, show atrial septal anatomy.

Current Medical Diagnosis & Treatment 2023 > Atrial Septal Defect & Patent Foramen Ovale

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eFigure 10–23. Simultaneous left and right atrial and differential pressure across an atrial septal defect. The pressure difference across the defect is greatest before the v wave. The right atrial pressure tracing is inverted because it is recorded by a differential manometer. (Reproduced with permission from Cheitlin MD et al; Clinical Cardiology, 6th ed. Appleton & Lange: The McGraw-Hill LLC Companies Inc, 1993.) Examples of the atrial and differential pressure and the E C G pattern across an A S D.

Current Medical Diagnosis & Treatment 2023 > Atrial Septal Defect & Patent Foramen Ovale

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eFigure 10–31. ECG showing atrial fibrillation. Note the absence of distinct P wave, chaotic activity of atria, irregular R-R intervals with narrow QRS complex. (Reproduced with permission from Gutierrez C, Blanchard DG. Diagnosis and treatment of atrial fibrillation. Am Fam Physician, 2016;94 (6):442–52.) A 12 lead electrocardiograph shows the rhythmic tracing indicative of atrial fibrillation.

Current Medical Diagnosis & Treatment 2023 > Mitral Stenosis

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eFigure 10–34. First-degree atrioventricular (AV) block. The PR interval is prolonged to 0.28 s. The laddergram beneath the ECG illustrates the three levels of AV conduction: the atrium, the AV node, and the ventricles, with the delay in AV conduction represented as occurring in the AV node. Reproduced with permission from Jason E. Roediger, CCT, CRAT. ECG Guru Instructor Resources. https://www.ecgguru.com/blog-ecg-challenge-week-june-24-%E2%80%93-july-1-2012-pinpoint-primary-disturbance. A 12 lead electrocardiograph shows the rhythmic tracing observed in a case of first degree A V block.

Current Medical Diagnosis & Treatment 2023 > Chronic Stable Angina Pectoris (Chronic Coronary Syndromes)

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eFigure 10–60. Atrial fibrillation in Wolff-Parkinson-White (WPW) syndrome. A, B, and D: Rapid, wide, irregular QRS complex tachycardia with varying QRS complex morphologies. C: The direction of cardiac impulse conduction in a WPW syndrome patient during atrial fibrillation. The two arrows indicate the direction of the impulse movement, both anterograde from atrial (A) tissues to ventricular (V) tissues through both the accessory pathway (AP) and the atrioventricular node (AVN). The larger of the two arrows indicates that the majority of impulses travel to the ventricular via the AP. E: A 12-lead ECG demonstrating a rapid, wide, irregular QRS complex tachycardia with varying QRS complex morphologies. LBB, left bundle branch; RBB, right bundle branch; SAN, sinoatrial node. (Reproduced, with permission, from Tintinalli JE, Ma OJ, Yealy DM, et al. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill, 2020.) A multi-part illustration depicts E C G tracings indicative of atrial fibrillation in W P W syndrome.

Current Medical Diagnosis & Treatment 2023 > PSVT Due to Accessory AV Pathways (Preexcitation Syndromes)

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eFigure 10–65. Multifocal atrial tachycardia with varying P-wave morphologies and P-P intervals; right atrial overload with peaked P waves in II, III, and aVF (with vertical P-wave axis); superior QRS axis; slow R-wave progression with delayed transition in precordial leads in patient with severe chronic obstructive lung disease. (Reproduced, with permission from Jameson JL, et al. Harrison’s Principles of Internal Medicine, 20th ed. McGraw-Hill, 2018.) A 12 lead electrocardiograph shows the rhythmic tracing indicative of multifocal atrial tachycardia.

Current Medical Diagnosis & Treatment 2023 > Atrial Tachycardia

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eFigure 10–76. Patient who had dilated cardiomyopathy. The ECG shows the morphologic characteristics observed in this situation (sinus tachycardia, low voltage in frontal plane, important alterations of P and QRS-T). (Reproduced with permission from Fuster V, et.al. Hurst's The Heart, 14e, McGraw Hill, 2017.) The electrocardiogram leads 1, 2, 3, V 1 and right atrial leads of a patient with dilated cardiomyopathy.

Current Medical Diagnosis & Treatment 2023 > Dilated Cardiomyopathy

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