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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)

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 37–26. 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 37–30. 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 37–45. 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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