Primary Distribution: Scattered areas of sub-Saharan, tropical, South, and North Africa; Middle East; West India; Central and Eastern China; Philippine Islands and nearby islands; numerous areas of the world, with variants and locations noted below under vectors and agents.
Agents and Vectors: Schistosomes (Schistosoma sp.) are flatworms or blood flukes (trematodes) carried by freshwater snails (the intermediate host). Humans pass eggs via stool or urine into the water where the parasites grow inside the snails. The parasite then leaves the snail in the form of cercaria and directly penetrates the skin of persons working (e.g., planting rice), bathing, or swimming in the water. The worms then grow inside vessels, bladder, or intestines, resulting in symptoms (from the worms and retained eggs) as well as means of repeating the life cycle. Important species of Schistosoma are:
Other species also exist, but are of lesser public health importance.
Incubation: Symptoms of acute schistosomiasis begin about a month after infection.
Clinical Findings and Treatment
Signs and Symptoms: There are several syndromes, not all of which are evident in all infected persons. The last (chronic) stage varies according to species, i.e., S. japonica, S. mansoni, and S. mekongi primarily affect liver and intestines; while S. haematobium primarily affects the urinary tract. In general, patients with chronic schistosomiasis tend to present in developed countries with lethargy, colicky abdominal pain, mucoid/bloody diarrhea, or dysuria and hematuria.
Salmonella infection concurrent with schistosomiasis is common and is resistant to treatment unless the schistosomiasis is also treated.
Complications: Progression of liver, kidney, or other dysfunction may occur for many years after transmission has been interrupted - especially with heavy infection and re-exposure. Central nervous system lesions occur, but rarely.
Laboratory Findings: Eosinophilia, leukocytosis, mild anemia, hypoalbuminemia are common. Increased immune complexes, IgM, IgE, and IgG are also found. Patients with S. haematobium commonly exhibit albuminuria and red cells.
Diagnosis: Note that periportal fibrosis, glomerulonephritis, and other manifestations and complications are diagnosed separately. Diagnosis of S. japonicum and S. mansoni is by the presence of ova in feces or tissue. Diagnosis of S. haematobium is by the presence of ova in urine or tissue. However, ova loads are not always sufficient for diagnosis, especially in long-standing chronic illness. Immunofluorescent antibody tests and antigen detection assays are increasingly used. "Fetal head" bladder calcification may be shown in x-rays of patients with chronic S. haematobium infection.
Differential Diagnosis: Any prolonged febrile illness; typhoid fever, strongyloidosis, trichuriasis; other causes of hepatic, renal, GI, or urinary tract dysfunction - including carcinoma.
Treatment: For S. haematobium and S. mansoni, praziquantel 20/kg po bid for one day; for S. japonica and S. mekongi, praziquantel 20/kg po tid for one day are the treatments of choice. S. mansoni may also be treated with oxamniquine in a single po dose (with food) of 15 mg/kg. S. haematobium in North and East Africa may be treated with metrifonate 7.5-10 mg/kg every other week for a total of 3 doses.
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