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Figure 30–1. Eruptive xanthomas on the arm of a man with untreated hyperlipidemia and diabetes mellitus. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 2nd ed. McGraw-Hill, 2013.) A photo shows red, raised and eruptive papules covering the surface of the skin.

Current Medical Diagnosis & Treatment 2024 > Lipid Disorders: Clinical Presentations

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Figure 34–3. Chickenpox (varicella) with classic “dew drop on rose petal” appearance. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 2nd ed. McGraw-Hill, 2013.) A photo of the close-up view of the pimple shows that it appears like a reddish drop on the skin.

Current Medical Diagnosis & Treatment 2024 > Human Herpesviruses

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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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)

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

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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

Current Medical Diagnosis & Treatment 2024 > Enterobiasis

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eFigure 37–41. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod  and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle.  (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2024 > Dracunculiasis

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eFigure 37–41. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod  and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle.  (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2024 > Dracunculiasis

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eFigure 37–41. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod  and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle.  (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2024 > Dracunculiasis

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eFigure 37–41. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod  and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle.  (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2024 > Dracunculiasis

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eFigure 37–41. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod  and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle.  (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2024 > Dracunculiasis

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eFigure 37–41. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod  and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle.  (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2024 > Dracunculiasis

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eFigure 37–41. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod  and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle.  (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2024 > Dracunculiasis

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eFigure 37–41. Life cycle of Dracunculus medinensis (Guinea worm). Humans become infected by drinking unfiltered water containing copepods (small crustaceans) that are infected with larvae of D medinensis . Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space . After maturation into adults and copulation, the male worms die and the females (length: 70–120 cm) migrate in the subcutaneous tissues toward the skin surface . Approximately 1 year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae . The larvae are ingested by a copepod  and after 2 weeks (and two molts) have developed into infective larvae . Ingestion of the copepods closes the cycle.  (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of the nematode or roundworm Dracunculus medinensis.

Current Medical Diagnosis & Treatment 2024 > Dracunculiasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–47. Filariasis (elephantiasis). Life cycles of Wuchereria bancrofti and Brugia malayi. A: The typical vector for B malayi filariasis are mosquito species in the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly reside in the lymphatics . The adult worms resemble those of W bancrofti but are smaller. Female worms measure 43–55 mm in length by 130–170 mcm in width, and males measure 13–23 mm in length by 70–80 mcm in width. Adults produce microfilariae, measuring 177–230 mcm in length and 5–7 mcm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into lymph and enter the bloodstream reaching the peripheral blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . B: Different species of the following genera of mosquitoes are vectors of W bancrofti filariasis depending on geographic distribution. Among them are Culex (C annulirostris, C bitaeniorhynchus, C quinquefasciatus, and C pipiens); Anopheles (A arabinensis, A bancroftii, A farauti, A funestus, A gambiae, A koliensis, A melas, A merus, A punctulatus and A wellcomei); Aedes (A aegypti, A aquasalis, A bellator, A cooki, A darlingi, A kochi, A polynesiensis, A pseudoscutellaris, A rotumae, A scapularis, and A vigilax); Mansonia (M pseudotitillans, M uniformis); Coquillettidia (C juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics . The female worms measure 80–100 mm in length and 0.24–0.30 mm in diameter, while the males measure about 40 mm by 0.1 mm. Adults produce microfilariae measuring 244–296 mcm by 7.5–10 mcm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the thoracic muscles . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s proboscis  and can infect another human when the mosquito takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Brugia malayi and Wuchereria bancrofti.

Current Medical Diagnosis & Treatment 2024 > Lymphatic Filariasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–48. Life cycle of Onchocerca volvulus (blinding worm). During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . In subcutaneous tissues, the larvae  develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33–50 cm in length and 270–400 mcm in diameter, while males measure 19–42 mm by 130–210 mcm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220–360 mcm by 5–9 mcm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal . After ingestion, the microfilariae migrate from the blackfly’s midgut through the hemocoel to the thoracic muscles . There, the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly’s proboscis  and can infect another human when the fly takes a blood meal . (Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Onchocerca volvulus, that causes onchocerciasis, or river blindness.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–49. Skin thickening from the long-term effects of microfilariae of Onchocerca volvulus–producing elephant skin. (Used, with permission, from W Peters and HM Gilles.) A photo shows thickened and dry skin with multiple folds.

Current Medical Diagnosis & Treatment 2024 > Onchocerciasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 18–1. Jaundice. (Reproduced, with permission, from Sherlock S, Summerfield JA. Color Atlas of Liver Disease. Mosby, 1991.) A photo shows a patient with yellow-colored skin and sclera.

Current Medical Diagnosis & Treatment 2024 > Jaundice & Evaluation of Abnormal Liver Biochemical Tests

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eFigure 18–3. Vascular spider telangiectasia. (Reproduced, with permission, from Sherlock S, Summerfield JA. Color Atlas of Liver Disease. Mosby, 1991.) A photo shows streaks of thin blood vessels originating from a point on the skin.

Current Medical Diagnosis & Treatment 2024 > Jaundice & Evaluation of Abnormal Liver Biochemical Tests

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eFigure 18–21. Spider telangiectasias of the thoracic wall in chronic liver disease. The small dilated blood vessels seen in patients with liver disease are called spider telangiectasias because they tend to radiate outward resembling a spider's web. (Used, with permission, from Neil Mehta, MD.) A photo shows streaks of blood vessels originating from a point on the skin.

Current Medical Diagnosis & Treatment 2024 > Cirrhosis

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eFigure 18–22. Spider telangiectasias of the face in chronic liver disease. When these small dilated blood vessels near the skin surface appear on the face, they are usually around the nose (as seen here) or on the cheeks. (Used, with permission, from Neil Mehta, MD.) A photo shows streaks of blood vessels originating from a point on the nose.

Current Medical Diagnosis & Treatment 2024 > Cirrhosis

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eFigure 18–30. Portal hypertensive gastropathy. Classic endoscopic "snakeskin" appearance of portal hypertensive gastropathy, a common cause of chronic GI bleeding in patients with cirrhosis. (Used, with permission, from Neil Mehta, MD.) An endoscopic image shows that the inner walls of the gastrointestinal region have a snake-skin appearance.

Current Medical Diagnosis & Treatment 2024 > Cirrhosis

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Figure 19–2. Skin dimpling. (Used, with permission, from Armando E. Giuliano, MD.) A photo of a breast with dimpling in the bottom right of the breast. The breast appears dented and misshapen.

Current Medical Diagnosis & Treatment 2024 > Carcinoma of the Female Breast

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eFigure 20–18. Condylomata acuminata of vulvar and perineal skin. (Reproduced, with permission, from DeCherney AH, Nathan L, Laufer N, Roman S. Current Diagnosis & Treatment: Obstetrics & Gynecology, 12th edition. McGraw-Hill, 2019.) A patient exhibits waxy, white plaques on both sides of the vaginal opening and between the vagina and anus.

Current Medical Diagnosis & Treatment 2024 > Condyloma Acuminata

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eFigure 33–4. Molluscum contagiosum. Close-up of a molluscum contagiosum lesion showing a dome-shaped pearly papule with a characteristic umbilicated center. (Reproduced with permission from Richard P. Usatine RP, Smith MA, Mayeaux EJ Jr., Chumley H. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) A close up image of skin infected with Molluscum contagiosum. A small, pink, round swelling on the surface of the skin is seen with an umbilicated white center.

Current Medical Diagnosis & Treatment 2024 > HIV Infection & AIDS: Complications

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Figure 33–6. Molluscum contagiosum. Extensive molluscum contagiosum lesions on the face of a young woman, suggestive she may have HIV. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 3rd ed. McGraw-Hill, 2019.) Numerous fluid filled skin colored eruptions are seen spread out across the chin and sides of a person's mouth.

Current Medical Diagnosis & Treatment 2024 > HIV Infection & AIDS: Complications

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eFigure 33–5. Bacillary angiomatosis. Bacillary angiomatosis is a systemic infection caused by Bartonella species. Its cutaneous lesions appear as scattered papules and nodules (like the one shown here) or as abscesses. In people with HIV, bacillary angiomatosis most often occurs when the CD4 count is below 200/mcL. It can be treated with antibiotics. (Reproduced, with permission, from Usatine RP, Moy RL, Tobinick EL, Siegel DM. Skin Surgery: A Practical Guide. Mosby, 1998. Copyright © Elsevier.) A close-up photo of a red, raised, highly vascular skin lesion. The lesion has a depression at its center.

Current Medical Diagnosis & Treatment 2024 > HIV Infection & AIDS: Complications

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eFigure 39–2. Deep frostbite, with the first and second toes showing an ischemic eschar with well-demarcated borders and clearcut margins, and hemorrhagic bullae on the second toe, the third toe showing a clear bulla and surrounding erythema, and the fourth toe showing complete necrosis. (Used, with permission, from Dean SM, Satiani B, Abraham WT. Color Atlas and Synopsis of Vascular Diseases. McGraw-Hill, 2014.) A photo shows mottled and black skin of the first, second, and fourth toes of a patient.

Current Medical Diagnosis & Treatment 2024 > Frostbite

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eFigure 39–3. Severely burned firefighter prior to initial debridement. Burns proved to be 40% total body surface area. (Used, with permission, from Brent R.W. Moelleken, MD, FACS.) A photo shows that the legs of a firefighter are severly burned and appear black. A photo shows severly burned arms of a patient, with a layer of skin peeling off. A photo shows skin and tissues peeling off the chest of a patient.

Current Medical Diagnosis & Treatment 2024 > Thermal Burns

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eFigure 39–3. Severely burned firefighter prior to initial debridement. Burns proved to be 40% total body surface area. (Used, with permission, from Brent R.W. Moelleken, MD, FACS.) A photo shows that the legs of a firefighter are severly burned and appear black. A photo shows severly burned arms of a patient, with a layer of skin peeling off. A photo shows skin and tissues peeling off the chest of a patient.

Current Medical Diagnosis & Treatment 2024 > Thermal Burns

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eFigure 39–3. Severely burned firefighter prior to initial debridement. Burns proved to be 40% total body surface area. (Used, with permission, from Brent R.W. Moelleken, MD, FACS.) A photo shows that the legs of a firefighter are severly burned and appear black. A photo shows severly burned arms of a patient, with a layer of skin peeling off. A photo shows skin and tissues peeling off the chest of a patient.

Current Medical Diagnosis & Treatment 2024 > Thermal Burns

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eFigure 39–5. Successfully grafted patient with 40% total body surface area burns. (Used, with permission, from Brent R.W. Moelleken, MD, FACS.) A photo shows grafted leg of a patient. The skin appears scaly and dark. A photo shows grafted wrists of a patient. The skin appears scaly and dark. A photo shows grafted forearm of a patient. The skin appears scaly and dark. A photo shows grafted skin of a patient. The skin appears scaly and pink.

Current Medical Diagnosis & Treatment 2024 > Thermal Burns

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eFigure 39–5. Successfully grafted patient with 40% total body surface area burns. (Used, with permission, from Brent R.W. Moelleken, MD, FACS.) A photo shows grafted leg of a patient. The skin appears scaly and dark. A photo shows grafted wrists of a patient. The skin appears scaly and dark. A photo shows grafted forearm of a patient. The skin appears scaly and dark. A photo shows grafted skin of a patient. The skin appears scaly and pink.

Current Medical Diagnosis & Treatment 2024 > Thermal Burns

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eFigure 39–5. Successfully grafted patient with 40% total body surface area burns. (Used, with permission, from Brent R.W. Moelleken, MD, FACS.) A photo shows grafted leg of a patient. The skin appears scaly and dark. A photo shows grafted wrists of a patient. The skin appears scaly and dark. A photo shows grafted forearm of a patient. The skin appears scaly and dark. A photo shows grafted skin of a patient. The skin appears scaly and pink.

Current Medical Diagnosis & Treatment 2024 > Thermal Burns

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eFigure 39–5. Successfully grafted patient with 40% total body surface area burns. (Used, with permission, from Brent R.W. Moelleken, MD, FACS.) A photo shows grafted leg of a patient. The skin appears scaly and dark. A photo shows grafted wrists of a patient. The skin appears scaly and dark. A photo shows grafted forearm of a patient. The skin appears scaly and dark. A photo shows grafted skin of a patient. The skin appears scaly and pink.

Current Medical Diagnosis & Treatment 2024 > Thermal Burns

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eFigure 39–5. Successfully grafted patient with 40% total body surface area burns. (Used, with permission, from Brent R.W. Moelleken, MD, FACS.) A photo shows grafted leg of a patient. The skin appears scaly and dark. A photo shows grafted wrists of a patient. The skin appears scaly and dark. A photo shows grafted forearm of a patient. The skin appears scaly and dark. A photo shows grafted skin of a patient. The skin appears scaly and pink.

Current Medical Diagnosis & Treatment 2024 > Thermal Burns

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Figure 35–2. Methicillin-resistant Staphylococcus aureus (MRSA) abscess on the back of the neck. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) A photo shows an inflamed, swollen lump on the side of the neck, with thin layers of skin peeling off.

Current Medical Diagnosis & Treatment 2024 > Staphylococcus Aureus Infections

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Figure 35–5. Left foot gangrene, with plantar extension. (Used, with permission, from Dean SM, Satiani B, Abraham WT. Color Atlas and Synopsis of Vascular Diseases. McGraw-Hill, 2014.) A photo shows blackened and decayed skin in the toe and the portion under it.

Current Medical Diagnosis & Treatment 2024 > Anaerobic Infections

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eFigure 35–15. Leprosy. Leprosy, caused by Mycobacterium leprae, can cause generalized or diffuse skin involvement, and may result in skin swelling and thickening due to an inflammatory infiltrate. Other organs such as the eyes, nose, and testes may be involved. (Public Health Image Library, CDC) A patient with leprosy exhibits diffuse swelling and thickening of the helix and lobe of the pinna.

Current Medical Diagnosis & Treatment 2024 > Leprosy (Hansen Disease)

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eFigure 6–3. A: Growing 9-mm compound dysplastic nevus on the back of a 44-year-old man. There is asymmetry and variations in color and an irregular border. B: Dermoscopy of this compound dysplastic nevus shows an irregular network with multiple asymmetrically placed dots off the network. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) Two photos of compound dysplastic nevi on the skin.

Current Medical Diagnosis & Treatment 2024 > Atypical Nevi

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eFigure 6–3. A: Growing 9-mm compound dysplastic nevus on the back of a 44-year-old man. There is asymmetry and variations in color and an irregular border. B: Dermoscopy of this compound dysplastic nevus shows an irregular network with multiple asymmetrically placed dots off the network. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) Two photos of compound dysplastic nevi on the skin.

Current Medical Diagnosis & Treatment 2024 > Atypical Nevi

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eFigure 6–4. Lentigo simplex. (Used, with permission, from S Goldstein, MD.) A photo shows a dark, rectangular mole on white skin.

Current Medical Diagnosis & Treatment 2024 > Freckles & Lentigines

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Figure 6–4. Seborrheic keratosis with light pigmentation, with waxy, dry, “stuck-on,” appearance. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 2nd ed. McGraw-Hill, 2013.) A photo of a lightly pigmented, waxy, irregularly shaped growth on skin.

Current Medical Diagnosis & Treatment 2024 > Seborrheic Keratoses

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eFigure 6–15. Stretching of the skin prior to biopsy. (Reproduced with permission from Chesnutt MS et al. Office & Bedside Procedures. Appleton & Lange: The McGraw Hill LLC Companies, Inc; 1992.) An illustration shows the process of stretching the skin prior to biopsy.

Current Medical Diagnosis & Treatment 2024 > Basal Cell Carcinoma

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eFigure 6–16. Typical ellipsoid defect after removal of the biopsy specimen. (Reproduced with permission from Chesnutt MS et al. Office & Bedside Procedures. Appleton & Lange: The McGraw Hill LLC Companies, Inc; 1992.) An illustration shows an elliptical hole after the removal of a portion of the skin.

Current Medical Diagnosis & Treatment 2024 > Basal Cell Carcinoma

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eFigure 6–20. This isolated, scaly patch on a patient's arm turned out to be Bowen disease (intraepidermal squamous cell carcinoma) on biopsy. (Used, with permission, from S Goldstein, MD.) A photo shows a dry, scaly, pink, and circular patch on a patient's skin.

Current Medical Diagnosis & Treatment 2024 > Bowen Disease & Paget Disease

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eFigure 6–23. Tinea corporis. (Used, with permission, from TG Berger, MD, Dept. Dermatology, UCSF.) A photo illustrating tinea corporis shows semi-circular patches of inflammed lesions on a patient's skin.

Current Medical Diagnosis & Treatment 2024 > Tinea Corporis or Tinea Circinata

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eFigure 6–29. Erythrasma presenting in the axillary fold. (Used, with permission, from K Zipperstein, MD.) A photo illustrating erythrasma shows a brown scaly patch on a patient's skin.

Current Medical Diagnosis & Treatment 2024 > Tinea Cruris (Jock Itch)

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eFigure 6–30. A diagnostic feature of erythrasma is the coral-red fluorescence observed here in focal distribution under a Wood light. (Used, with permission, from K Zipperstein, MD.) A photo of a patient's skin observed under Wood light shows coral-red fluorescence in the region affected with erythrasma.

Current Medical Diagnosis & Treatment 2024 > Tinea Cruris (Jock Itch)

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eFigure 6–31. Allergic contact dermatitis due to nickel. A chronic nature is suggested by the scaling and thickened skin. (Used, with permission, from R Odom, MD.) A photo shows that the lower portions of the middle and ring fingers have grey discoloration, scaling, and thickening.

Current Medical Diagnosis & Treatment 2024 > Tinea Manuum & Tinea Pedis (Tinea of Palms & Soles)

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eFigure 6–34. Pityriasis (tinea) versicolor: Multiple, small- to medium-sized, well-demarcated hypopigmented macules on the back of a tanned individual with white skin. (Reproduced, with permission, from Wolff K et al (editors). Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, 7e. McGraw-Hill, 2012.) A photo shows a patches of white colored pigmentation on a patient's back.

Current Medical Diagnosis & Treatment 2024 > Tinea Versicolor (Pityriasis Versicolor)

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eFigure 6–37. A: Vitiligo on the hands of a Hispanic man. B: Vitiligo covering more than 50% of this young Hispanic woman's body. The patient is starting topical monobenzone to attempt to bleach the unaffected skin so that she has one matching skin color. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019) Two photos show the appearance of vitiligo on the hands and legs of an affected patient.

Current Medical Diagnosis & Treatment 2024 > Tinea Versicolor (Pityriasis Versicolor)

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eFigure 6–37. A: Vitiligo on the hands of a Hispanic man. B: Vitiligo covering more than 50% of this young Hispanic woman's body. The patient is starting topical monobenzone to attempt to bleach the unaffected skin so that she has one matching skin color. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019) Two photos show the appearance of vitiligo on the hands and legs of an affected patient.

Current Medical Diagnosis & Treatment 2024 > Tinea Versicolor (Pityriasis Versicolor)

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eFigure 6–38. Angular cheilitis (perleche). (Used, with permission, from Lindy Fox, MD.) A close-up photo of inflamed corner of mouth. The skin is broken and red with pus draining from the side.

Current Medical Diagnosis & Treatment 2024 > Mucocutaneous Candidiasis

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eFigure 6–43. Herpetic whitlow of finger. (Used, with permission, from Lindy Fox, MD.) A photo of a lesion in the fingertip. The patch of skin appears grey with purple-red spots.

Current Medical Diagnosis & Treatment 2024 > Herpes Simplex (Cold or Fever Sore; Genital Herpes)

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eFigure 6–45. Waxy umbilicated papules of molluscum contagiosum are spread by wet skin-to-skin contact. (Used, with permission, from K Zipperstein, MD.) A photo shows small papules on a patient's skin.

Current Medical Diagnosis & Treatment 2024 > Molluscum Contagiosum

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eFigure 6–48. A linear pattern of allergic contact dermatitis from poison ivy. Note the impressive line of vesicles where the leaf brushed the skin. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) A patient with contact dermatitis from poison ivy exhibits red patches with a series of tiny pustules over the skin of the forearm.

Current Medical Diagnosis & Treatment 2024 > Impetigo

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eFigure 6–62. Lupus panniculitis profundum. (Used, with permission, from K Zipperstein, MD.) A photo illustrating lupus panniculitis profundum shows a black discoloration patch on a patient's skin.

Current Medical Diagnosis & Treatment 2024 > Erythema Nodosum

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Figure 6–21. Lichen simplex chronicus on the hand. (Used, with permission, from Lindy Fox, MD.) A photo of a plaque on the back of the hand, appearing as an irregular patch of hardened, dry, greyish, thickened skin.

Current Medical Diagnosis & Treatment 2024 > Lichen Simplex Chronicus (Circumscribed Neurodermatitis)

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eFigure 6–67. Lichen simplex chronicus resulting from repeated itch-scratch cycles. Note the hypertrophic leathery, lichenified plaques. The exaggerated skin lines are characteristic. (Used, with permission, from S Goldstein, MD.) A photo shows a light, wrinkled, and leathery patch of skin on a patient's wrist.

Current Medical Diagnosis & Treatment 2024 > Lichen Simplex Chronicus (Circumscribed Neurodermatitis)

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Figure 6–22. Extensive plaque psoriasis involving trunk of person with dark skin type. (Used, with permission, from Kanade Shinkai, MD.) In a patient with plaque psoriasis, pink, raised, irregular plaques of varying sizes are spread all over the abdomen.

Current Medical Diagnosis & Treatment 2024 > Lichen Simplex Chronicus (Circumscribed Neurodermatitis)

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eFigure 6–69. Koebner phenomenon on skin of the hands. A photo illustrating Koebner phenomenon shows small patches of lesions with white spots on the patient's hands.

Current Medical Diagnosis & Treatment 2024 > Psoriasis

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eFigure 6–70. Scale—scalp psoriasis. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) Photo A is of a dry, scaly, white lower scalp with reddish periphery. Photo B is of white pustules over inflamed patch of skin on the patient's arm.

Current Medical Diagnosis & Treatment 2024 > Psoriasis

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eFigure 6–70. Scale—scalp psoriasis. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) Photo A is of a dry, scaly, white lower scalp with reddish periphery. Photo B is of white pustules over inflamed patch of skin on the patient's arm.

Current Medical Diagnosis & Treatment 2024 > Psoriasis

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eFigure 6–71. Plaque—psoriatic plaque. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) A photo of a psoriatic plaque in the elbow pit, appearing as a reddish, well-defined patch of skin with multiple white, scaly spots.

Current Medical Diagnosis & Treatment 2024 > Psoriasis

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eFigure 6–72. Plaque psoriasis involving arm of patient with darker skin. (Used, with permission, from Lindy Fox, MD.) A patient with plaque psoriasis exhibits irregular red plaques of various sizes overlaid with white scaling along the length of the arm.

Current Medical Diagnosis & Treatment 2024 > Psoriasis

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eFigure 6–73. Psoriasis involving palms of patient with darker skin (Used, with permission, from Kanade Shinkai, MD.) A patient with psoriasis exhibits irregular, dry, red plaques of various sizes overlaid with white scaling on the palms of the hands. The thumb joints are significantly swollen and malformed.

Current Medical Diagnosis & Treatment 2024 > Psoriasis

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Figure 6–23. Nail pitting due to psoriasis in a patient with dark skin. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 2nd ed. McGraw-Hill, 2013.) A photo of a thumb nail is shown with many pin dot pits spread over the surface.

Current Medical Diagnosis & Treatment 2024 > Psoriasis

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eFigure 6–76. Pityriasis rosea. (Used, with permission, from TG Berger, MD, Dept. Dermatology, UCSF.) A photo shows small rashes on the skin surface. One of them is large and has a white, crusty appearance.

Current Medical Diagnosis & Treatment 2024 > Pityriasis Rosea

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Figure 6–24. Pityriasis rosea with scaling lesions following skin lines and resembling a Christmas tree. (Used, with permission, from EJ Mayeaux, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) A photo of a patient's back covered with pale, scaled lesions from neck to hip.

Current Medical Diagnosis & Treatment 2024 > Pityriasis Rosea

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eFigure 6–78. Maculopapular skin eruption of secondary syphilis. (Used, with permission, from S Goldstein, MD.) A photo shows small red rashes on a patient's skin.

Current Medical Diagnosis & Treatment 2024 > Pityriasis Rosea

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Figure 6–25. Close-up of seborrheic dermatitis showing flaking skin and erythema around the beard region. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 2nd ed. McGraw-Hill, 2013.) A patient with seborrheic dermatitis exhibits red patches overlaid with white, dry, scaly skin on the cheeks, and around the mouth, and chin.

Current Medical Diagnosis & Treatment 2024 > Seborrheic Dermatitis

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eFigure 6–80. Lichenification—lichen simplex chronicus. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) A photo of a dry, brownish patch of thickened skin on the lower arm. Peripheral erythema is also visible.

Current Medical Diagnosis & Treatment 2024 > Lichen Planus

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eFigure 6–81. Lichen simplex chronicus (dark raised bumps on a Black female). (Used, with permission, from K Zipperstein, MD.) A photo shows dark raised bumps on the skin of a black female.

Current Medical Diagnosis & Treatment 2024 > Lichen Planus

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Figure 6–27. Allergic contact dermatitis to an adhesive dressing in patient with darker skin. Key features are erythematous papules with impetigo-like honey-colored crusting. (Used, with permission, from Kanade Shinkai, MD.) A patient with allergic contact dermatitis exhibits irregular, dark red, raised lesions with scaly margins, along with smaller honey colored, crusted lesions.

Current Medical Diagnosis & Treatment 2024 > Contact Dermatitis

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eFigure 6–86. Allergic contact dermatitis to Neosporin. (Used, with permission, from Lindy Fox, MD.) A photo of a reddish inflamed patch of skin with honey-colored, crusted pustules, on the inner arm of the patient.

Current Medical Diagnosis & Treatment 2024 > Contact Dermatitis

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Figure 6–29. Porphyria cutanea tarda of hands in patient with darker skin. (Used, with permission, from Kanade Shinkai, MD.) A patient with porphyria cutanea tarda exhibits pale pink blisters of varying sizes over the dorsal surface of both hands.

Current Medical Diagnosis & Treatment 2024 > Porphyria Cutanea Tarda

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Figure 6–31. Acne vulgaris. Extensive comedones and hyperpigmented macules are present in patient with dark skin. (Used, with permission, from Kanade Shinkai, MD.) A patient with acne vulgaris exhibits innumerous raised, macular, hyperpigmented lesions below the nose, and around the mouth and chin.

Current Medical Diagnosis & Treatment 2024 > Acne Vulgaris

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eFigure 6–99. Telangiectasias—rosacea. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) A close-up photo of a cluster of spider veins on the patient's nose. The spider veins appear as thin, thread-like patterns on the skin.

Current Medical Diagnosis & Treatment 2024 > Rosacea

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Figure 6–33. Urticaria. (Used, with permission, from TG Berger, MD, Dept Dermatology, UCSF.) A photo of long thread-like, raised structures on the skin.

Current Medical Diagnosis & Treatment 2024 > Urticaria & Angioedema

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eFigure 6–104. A: Polymorphous light eruption on the arm of a young man. Note the sparing of the skin under his watchband. B: A photoallergic drug reaction characterized by widespread eczema in the photodistribution areas such as the face, upper chest, arms, and back of hands. A punch biopsy showed a spongiotic dermatitis. The exact photoallergen was not found. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) Two photos show the appearance of dermatitis.

Current Medical Diagnosis & Treatment 2024 > Photodermatitis

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eFigure 6–104. A: Polymorphous light eruption on the arm of a young man. Note the sparing of the skin under his watchband. B: A photoallergic drug reaction characterized by widespread eczema in the photodistribution areas such as the face, upper chest, arms, and back of hands. A punch biopsy showed a spongiotic dermatitis. The exact photoallergen was not found. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3rd ed. McGraw-Hill, 2019.) Two photos show the appearance of dermatitis.

Current Medical Diagnosis & Treatment 2024 > Photodermatitis

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eFigure 6–105. Lichen sclerosis et atrophicus: buttocks. (Used, with permission, from K Zipperstein, MD.) A photo shows scaly, white discoloration patch on the skin of a patient.

Current Medical Diagnosis & Treatment 2024 > Anogenital Pruritus

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Figure 6–36. Venous stasis ulcer. (Used, with permission, from Lindy Fox, MD.) A lower leg shows large widespread patches of dry, scaly, reddish skin with white streaks and yellow pruritic spots.

Current Medical Diagnosis & Treatment 2024 > Venous Stasis Ulcers

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Figure 6–37. Ulcer—venous stasis ulcer. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 3rd ed. McGraw-Hill, 2019.) A photo of a severe ulceration in the lower leg, close to the medial malleolus. It appears as a large, bloody red patch of exposed skin with serous fluid oozing from the ulcer.

Current Medical Diagnosis & Treatment 2024 > Venous Stasis Ulcers

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Figure 6–39. Minocycline hyperpigmentation. (Used, with permission, from Lindy Fox, MD.) A photo of dark blue-black hyperpigmented patches of skin in the lower legs of a patient.

Current Medical Diagnosis & Treatment 2024 > Pigmentary Disorders

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eFigure 7–10. Blepharitis showing erythema of the eyelids and flaking in the eyelashes. Note the scale that has accumulated in the eyelashes. (Used, with permission, from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS. The Color Atlas of Family Medicine, 3rd ed. McGraw-Hill, 2019.) A patient with blepharitis exhibits redness and flaky skin over the upper and lower eyelids. The eyelashes are coated with clumps of accumulated scales.

Current Medical Diagnosis & Treatment 2024 > Disorders of the Lids & Lacrimal Apparatus

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eFigure 7–32. Vogt–Koyanagi–Harada (VKH) disease. A: Poliosis of the eyelashes. B: Alopecia, vitiligo, and poliosis of the hair. (Reproduced, with permission, from A: Lueder GT. Pediatric Practice: Ophthalmology. McGraw-Hill, 2011; B: Riordan-Eva P, Augsburger JJ. Vaughan & Asbury's General Ophthalmology, 19th ed. McGraw-Hill, 2018.) An eye with a white section of eyelashes at the medial end of the upper eyelid. A patient with patchy hair loss, as well as white hair patches, just above the ear along the front hairline. Depigmented pale pink patches of skin are found over the forehead, scalp, and below the ear.

Current Medical Diagnosis & Treatment 2024 > Uveitis

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eFigure 7–32. Vogt–Koyanagi–Harada (VKH) disease. A: Poliosis of the eyelashes. B: Alopecia, vitiligo, and poliosis of the hair. (Reproduced, with permission, from A: Lueder GT. Pediatric Practice: Ophthalmology. McGraw-Hill, 2011; B: Riordan-Eva P, Augsburger JJ. Vaughan & Asbury's General Ophthalmology, 19th ed. McGraw-Hill, 2018.) An eye with a white section of eyelashes at the medial end of the upper eyelid. A patient with patchy hair loss, as well as white hair patches, just above the ear along the front hairline. Depigmented pale pink patches of skin are found over the forehead, scalp, and below the ear.

Current Medical Diagnosis & Treatment 2024 > Uveitis

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Figure 22–2. Typical inflammatory changes of gout at first metatarsophalangeal joint (podagra). (Used, with permission, from Richard P. Usatine, MD in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 2nd ed. McGraw-Hill, 2013.) A photo of the foot of a patient with gout in the foot. The first joint of the big toe is swollen and the skin is tight and shiny.

Current Medical Diagnosis & Treatment 2024 > Crystal Deposition Arthritis

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eFigure 22–21. Active discoid lupus skin lesions. (Used, with permission, from Rebecca L. Manno, MD.) A patient with discoid lupus exhibits scaly, flat, plaques on the forearm. The lesions have peeled removed the top layer of skin in several places, revealing the pink, underlying skin.

Current Medical Diagnosis & Treatment 2024 > Systemic Lupus Erythematosus

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eFigure 22–24. Sclerodactyly of the hands in a patient with systemic sclerosis. (Used, with permission, from Nicole Richman, MD.) A patient with systemic sclerosis exhibits dark, thickened skin over the dorsal surface of fingers.

Current Medical Diagnosis & Treatment 2024 > Systemic Sclerosis (Scleroderma)

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eFigure 22–25. Palmar telangiectasia with ulnar deviation in a patient with systemic sclerosis. (Used, with permission, from Rebecca L. Manno, MD.) A patient with systemic sclerosis exhibits numerous, red, hemorrhagic spots of various sizes over the skin of the palm and fingers.

Current Medical Diagnosis & Treatment 2024 > Systemic Sclerosis (Scleroderma)

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eFigure 26–8. Neurofibromatosis. (From Jack Resnick, Sr, MD; reproduced with permission from Usatine RP, Smith MA, Mayeaux EJ, Jr, Chumley H, Tysinger J. The Color Atlas of Family Medicine. McGraw-Hill, 2009.) A photo shows bumps covering a patient's skin entirely.

Current Medical Diagnosis & Treatment 2024 > Selected Neurocutaneous Diseases

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eFigure 26–10. Close-up of neurofibromas on the back of a 44-year-old man. These are soft and round. (Reproduced with permission from Richard P. Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H, Tysinger J. The Color Atlas of Family Medicine. McGraw-Hill, 2009.) A photo shows bumps scattered on the skin of a patient.

Current Medical Diagnosis & Treatment 2024 > Selected Neurocutaneous Diseases

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eFigure 15–18. Nonpalpable purpura. (Reproduced, with permission, from Bondi EE, Jegasothy BV, Lazarus GS [editors]. Dermatology: Diagnosis & Treatment. Originally published by Appleton & Lange. Copyright © 1991 by The McGraw-Hill Companies, Inc.) A photo shows a red lesions on the surface of a patient's skin.

Current Medical Diagnosis & Treatment 2024 > Aplastic Anemia

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Figure 29–1. Acanthosis nigricans of the nape of the neck, with typical dark and velvety appearance. (Used, with permission, from Umesh Masharani, MB, BS, MRCP [UK].) A photo of the nape of a patient's neck. The skin over the neck is darkened, cracked, and has a velvety texture.

Current Medical Diagnosis & Treatment 2024 > Diabetes Mellitus

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eFigure 41–3. In the mid-esophagus is a near circumferential mass with luminal narrowing. Biopsies confirmed squamous cell carcinoma. (Used, with permission, from Yao-Wen Cheng, MD.) An internal view of an esophagus shows a swollen mass of skin on the lower edge, white in color, representing squamous cell carcinoma.

Current Medical Diagnosis & Treatment 2024 > Esophageal Cancer

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eFigure 41–5. Diffusely spreading gastric adenocarcinoma with submucosal spread resulting in disruption of normal gastric folds inferiorly. (Used, with permission, from Yao-Wen Cheng, MD.) An internal view of a stomach shows a thin layer of folded tissue where the skin is filled with blood and fluid, caused by gastric adenocarcinoma.

Current Medical Diagnosis & Treatment 2024 > Gastric Adenocarcinoma

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eFigure 14–12. Venous ulcer on the ankle of an elderly man. The venous ulcer was caused by the restricted oxygen supply to the skin on the leg caused by DVT. (Reproduced with permission from alamy.com.) A patient with D V T exhibits a large red irregular venous ulcer, with thick white margins, on the ankle. The peripheral region shows dark pigmentation.

Current Medical Diagnosis & Treatment 2024 > Chronic Venous Insufficiency

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eFigure 14–13. Chronic lymphatic insufficiency: lymphedema. Lower legs are thickened of woody consistency and three is massive hyperkeratosis and pebbly and papillomatous overgrowths. The 60-year-old patient had innumerable episodes of erysipelas and cellulitis. There is also diabetes and atherosclerosis. (Reproduced with permission from Wolff K, Johnson R, Saavedra AP, Roh EK. Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, 8e; 2017.) A patient with lymphedema exhibits thick woody skin and pebble like appearance with nodular overgrowth, on the lower leg.

Current Medical Diagnosis & Treatment 2024 > Lymphedema

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