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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2024 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2024 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2024 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2024 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2024 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2024 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2024 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2024 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–1. Life cycle of Trypanosoma brucei gambiense. [T b gambiense] [Trypanosoma brucei rhodesiense] During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (eg, lymph, spinal fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are the main reservoir for T b gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T b rhodesiense. A flowchart of the life cycle of the T b gambiense or tsetse fly.

Current Medical Diagnosis & Treatment 2024 > African Trypanosomiasis (Sleeping Sickness)

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–23. Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail  and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress . After ingestion, the metacercariae excyst in the duodenum  and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults . In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Fasciola species.

Current Medical Diagnosis & Treatment 2024 > Fascioliasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–28. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Immature eggs are passed in feces . Under appropriate conditions, the eggs mature (approximately 18–20 days)  and yield oncospheres, which develop into a coracidia . After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) . The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, eg, trout, perch, walleyed pike . In this case, the sparganum can migrate to the musculature of the larger predator fish, and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked . After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms, which will reside in the small intestine. The adults of D latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex . The adults can reach more than 10 M in length, with more than 3000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm)  and are passed in the feces . Eggs appear in the feces 5–6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D latum. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Diphyllobothrium latum.

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.

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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 37–29. 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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