Schistosomiasis is infection with blood flukes of the genus Schistosoma, which are acquired transcutaneously by swimming or wading in contaminated freshwater. The organisms infect the vasculature of the GI or GU system. Acute symptoms are dermatitis, followed several weeks later by fever, chills, nausea, abdominal pain, diarrhea, malaise, and myalgia. Chronic symptoms vary with species but include bloody diarrhea (eg, with S. mansoni and S. japonicum) or hematuria (eg, with S. haematobium). Diagnosis is by identifying eggs in stool, urine, or biopsy specimens. Serologic tests may be sensitive and specific but do not provide information about the worm burden or clinical status. Treatment is with praziquantel.
Schistosomiasis is by far the most important trematode infection. Schistosoma is the only trematode that invades through the skin; all other trematodes infect only via ingestion. About 200 million people are infected worldwide.
Five species of schistosomes infect humans; all have similar life cycles involving freshwater snails. S. haematobium causes urinary tract disease; the other Schistosoma sp cause intestinal disease. Geographic distribution differs by species:
Humans are the main reservoir of infection. Dogs, cats, rodents, pigs, horses, and goats are reservoirs for S. japonicum, and dogs are reservoirs for S. mekongi. The disease may be imported in travelers and immigrants from endemic areas, but transmission does not occur within the US and Canada.
Adult worms live and copulate within venules of the mesentery (typically S. japonicum and S. mansoni) or bladder (typically S. haematobium—see Fig. 1: SchistosomaSimplified life cycle.). Some eggs penetrate the intestinal or bladder mucosa and are passed in stool or urine; other eggs remain within the host organ or are transported through the portal system to the liver and occasionally to other sites (eg, lungs, CNS, spinal cord). Excreted eggs hatch in freshwater, releasing miracidia (first larval stage), which enter snails. After multiplication, thousands of free-swimming cercariae are released. Cercariae penetrate human skin within a few minutes after exposure and transform into schistosomula, which travel through the bloodstream to the liver, where they mature into adults. The adults then migrate to their ultimate home in the intestinal veins or the venous plexus of the GU tract.
Eggs appear in stool or urine 1 to 3 mo after cercarial penetration.
Estimates of the adult worm life span range from 3 to 7 yr. The females range in size from 7 to 20 mm; males are slightly smaller.
|Simplified Schistosoma life cycle.
In the human host, eggs containing miracidia are eliminated with feces or urine into water.
In water, the eggs hatch and release miracidia.
The miracidia swim and penetrate a snail (intermediate host).
Within the snail, the miracidia progress through 2 generations of sporocysts to become cercariae.
The free-swimming cercariae are released from the snail and penetrate the skin of the human host.
During penetration, the cercariae lose their forked tail, becoming schistosomula. The schistosomula are transported through the vasculature to the liver. There, they mature into adults.
The paired (male and female) adult worms migrate (depending on their species) to the intestinal veins in the bowel or rectum or to the venous plexus of the GU tract, where they reside and begin to lay eggs.
Symptoms and Signs
Acute schistosome dermatitis:
Most infections are asymptomatic. A pruritic papular rash (see Dermatitis Caused by Avian and Animal Schistosomes) can develop where cercariae penetrate the skin in previously sensitized people.
Acute Katayama fever:
Katayama fever may occur with onset of egg laying, typically 2 to 4 wk after heavy exposure. Symptoms include fever, chills, cough, nausea, abdominal pain, malaise, myalgia, urticarial rashes, and marked eosinophilia, resembling serum sickness. Manifestations are more common and usually more severe in visitors than in residents of endemic areas and typically last for several weeks.
Chronic schistosomiasis results primarily from host responses to eggs retained in tissues. Early on, intestinal mucosal ulcerations caused by S. mansoni or S. japonicum may bleed and result in bloody diarrhea. As lesions progress, focal fibrosis, strictures, fistulas, and papillomatous growths may develop in the intestine.
Granulomatous reactions to eggs of S. mansoni and S. japonicum in the liver usually do not compromise liver function, but they may cause fibrosis and cirrhosis, which can lead to portal hypertension and subsequent hematemesis due to esophageal varices. Eggs in the lungs may produce granulomas and focal obliterative arteritis, which may ultimately result in pulmonary hypertension and cor pulmonale.
With S. haematobium, ulcerations in the bladder wall may cause dysuria, hematuria, and urinary frequency. Over time, chronic cystitis develops. Strictures may lead to hydroureter and hydronephrosis. Papillomatous masses in the bladder are common, and squamous cell carcinoma may develop. Blood loss from both GI and GU tracts frequently results in anemia.
Secondary bacterial infection of the GU tract is common, and persistent Salmonella septicemia may occur with S. mansoni. Several species, notably S. haematobium, can cause genital disease in both men and women, resulting in numerous symptoms including infertility. Neurologic complications can occur even in light Schistosoma infections. Eggs or adult worms lodged in the spinal cord can cause transverse myelitis, and those in the brain can produce focal lesions and seizures.
Stool or urine (S. haematobium, occasionally S. japonicum) is examined for eggs. Repeated examinations using concentration techniques may be necessary. Geography is a primary determinant of species, so a history of exposure should be communicated to the laboratory. If the clinical picture suggests schistosomiasis but no eggs are found after repeated examination of urine or feces, intestinal or bladder mucosa can be biopsied to check for eggs.
Depending on the antigens used, serologic tests may be sensitive and specific for infection, but they do not provide information about worm burden, clinical status, or prognosis.
Single-day oral treatment with praziquantel (20 mg/kg bid for S. haematobium, S. mansoni, and S. intercalatum; 20 mg/kg tid for S. japonicum and S. mekongi) is recommended. However, treatment does not affect developing schistosomula and thus may not abort an early infection. Adverse effects are generally mild and include abdominal pain, diarrhea, headache, and dizziness. Therapeutic failures have been reported, but it is difficult to determine whether they are due to reinfection or drug-resistant strains.
Treatment of Katayama fever is uncertain. Praziquantel is not particularly effective early in infection; corticosteroids can ameliorate severe symptoms.
Patients should be examined for living eggs 3 and 6 mo after treatment. Retreatment is indicated if egg excretion has not decreased markedly.
Scrupulously avoiding contact with contaminated freshwater prevents infection. The sanitary disposal of urine and feces reduces the likelihood of infection. Adult residents of endemic areas are more resistant to reinfection than children, suggesting the possibility of acquired immunity. Vaccine development is under way.
Dermatitis Caused by Avian and Animal Schistosomes
(Cercarial Dermatitis; Clam Digger's Itch; Swimmer's Itch)
Cercarial dermatitis, a skin condition, occurs when Schistosoma sp that cannot develop in humans penetrate the skin during contact with contaminated freshwater or brackish water.
Cercariae of Schistosoma sp that infect birds and mammals other than humans can penetrate the skin. Although the organisms do not develop in humans, humans may become sensitized and develop pruritic maculopapular, then vesicular skin lesions at the site of penetration. Skin lesions may be accompanied by a systemic febrile response that runs for 5 to 7 days and resolves spontaneously.
Cercarial dermatitis occurs worldwide. In North America, ocean-related schistosome dermatitis (clam digger's itch) occurs on all Atlantic, Gulf, Pacific, and Hawaiian coasts. It is common in muddy flats off Cape Cod. Freshwater schistosome dermatitis (swimmer's itch) is common in the Great Lakes region.
Diagnosis is based on clinical findings. Most cases do not require medical attention.
Treatment is symptomatic with cool compresses, baking soda, or antipruritic lotions. Topical corticosteroids can also be used.
Last full review/revision July 2013 by Richard D. Pearson, MD
Content last modified October 2013