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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–21. Schistosoma eggs. A: Eggs of Schistosoma mansoni in an unstained wet mount. B: Egg of Schistosoma haematobium in a wet mount of urine concentrates, showing the characteristic terminal spine. C: Egg of Schistosoma japonicum in an unstained wet mount. Note the small, inconspicuous spines (red arrow). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) Three photomicrographs show Schistosoma eggs.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–21. Schistosoma eggs. A: Eggs of Schistosoma mansoni in an unstained wet mount. B: Egg of Schistosoma haematobium in a wet mount of urine concentrates, showing the characteristic terminal spine. C: Egg of Schistosoma japonicum in an unstained wet mount. Note the small, inconspicuous spines (red arrow). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) Three photomicrographs show Schistosoma eggs.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–21. Schistosoma eggs. A: Eggs of Schistosoma mansoni in an unstained wet mount. B: Egg of Schistosoma haematobium in a wet mount of urine concentrates, showing the characteristic terminal spine. C: Egg of Schistosoma japonicum in an unstained wet mount. Note the small, inconspicuous spines (red arrow). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) Three photomicrographs show Schistosoma eggs.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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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 37–24. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–24. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–24. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–24. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–24. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–24. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–24. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–24. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–24. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–24. Life cycle of Clonorchis sinensis (Chinese liver fluke). Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail intermediate host . Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae . Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes approximately 1 month. The adult flukes (measuring 10–25 mm by 3–5 mm) reside in small- and medium-sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trematode species.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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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 37–27. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal’s intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–27. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal’s intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–27. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal’s intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–27. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal’s intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–27. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal’s intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–27. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal’s intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

Current Medical Diagnosis & Treatment 2024 > Noninvasive Cestode Infections

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eFigure 37–27. Life cycle of cestodes. Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, Taenia solium, or T asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T saginata) and pigs (T solium and T asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal’s intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . Length of adult worms is usually 5 M or less for T saginata (however, it may reach up to 25 M) and 2–7 M for T solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T saginata adults usually have 1000 to 2000 proglottids, while T solium adults have an average of 1000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T saginata may produce up to 100,000, and T solium may produce 50,000 eggs per proglottid respectively. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Taeniasis species.

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 37–28. 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.

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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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 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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eFigure 37–45. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidade Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2024 > Gnathostomiasis

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eFigure 37–45. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidade Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2024 > Gnathostomiasis

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eFigure 37–45. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidade Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2024 > Gnathostomiasis

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eFigure 37–45. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidade Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2024 > Gnathostomiasis

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eFigure 37–45. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidade Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2024 > Gnathostomiasis

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eFigure 37–45. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidade Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2024 > Gnathostomiasis

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eFigure 37–45. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidade Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2024 > Gnathostomiasis

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eFigure 37–45. Life cycle of Gnathostoma spinigerum. In the natural definitive host (pigs, cats, dogs, wild animals), the adult worms reside in a tumor that they induce in the gastric wall. They deposit eggs that are unembryonated when passed in the feces . Eggs become embryonated in water, and eggs release first-stage larvae . If ingested by a small crustacean (Cyclops, first intermediate host), the first-stage larvae develop into second-stage larvae . Following ingestion of the Cyclops by a fish, frog, or snake (second intermediate host), the second-stage larvae migrate into the flesh and develop into third-stage larvae . When the second intermediate host is ingested by a definitive host, the third-stage larvae develop into adult parasites in the stomach wall . Alternatively, the second intermediate host may be ingested by the paratenic host (animals such as birds, snakes, and frogs) in which the third-stage larvae do not develop further but remain infective to the next predator . Humans become infected by eating undercooked fish or poultry containing third-stage larvae, or reportedly by drinking water containing infective second-stage larvae in Cyclops . (Adapted from a drawing provided by Dr. Sylvia Paz Díaz Camacho, Universidade Autónoma de Sinaloa, Mexico. Content source: Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the Gnathostoma species.

Current Medical Diagnosis & Treatment 2024 > Gnathostomiasis

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