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Strongyloidiasis
is infection with Strongyloides stercoralis.
Findings include rash and pulmonary symptoms (including cough and wheezing),
eosinophilia, and abdominal pain with diarrhea. Diagnosis is by
finding larvae in stool or small-bowel contents or by the detection
of antibodies in blood. Treatment is with ivermectin, thiabendazole,
or albendazole.
Etiology
and Pathophysiology
Strongyloidiasis is endemic throughout the tropics and subtropics, including rural areas of the southern US, at sites where there is exposure of bare skin to contaminated soil and unsanitary conditions.
Adult worms live in the mucosa and submucosa of the duodenum and jejunum. Released eggs hatch in the bowel lumen, liberating rhabditiform larvae. Most of these larvae are excreted in the stool. After a few days in soil, they develop into infectious filariform larvae. Like hookworms, Strongyloides larvae penetrate the skin of humans, migrate via the bloodstream to the lungs, break through pulmonary capillaries, ascend the respiratory tract, are swallowed, and reach the intestine, where they mature in about 2 wk. In the soil, larvae that do not contact humans may develop to free-living adult worms that can reproduce for several generations before their larvae reenter a human host.
Some rhabditiform larvae convert within the intestine to infectious filariform larvae that immediately reenter the bowel wall, short-circuiting the life cycle (internal autoinfection). Sometimes filariform larvae are passed in stool and reenter through the skin of the buttocks and thighs. Autoinfection can result in extremely high worm burdens (hyperinfection syndrome) and explains why strongyloidiasis persists for many decades. Hyperinfection usually occurs in patients taking corticosteroids or with impaired cell-mediated immunity, particularly those infected with the human T-lymphotropic virus 1 (HTLV-1). Hyperinfection may represent activation of a previously asymptomatic or newly acquired Strongyloides infection. However, disseminated strongyloidiasis is less common than might be predicted among patients with AIDS, even those living in areas where Strongyloides is highly endemic.
Symptoms and Signs
Infection may be asymptomatic. Cutaneous symptoms sometimes result from an allergic reaction to migrating larvae; larva currens, a serpiginous, migratory, urticarial lesion, is pathognomonic, but nonspecific maculopapular or urticarial eruptions may occur. Pulmonary symptoms are uncommon, although heavy infections may produce Löffler's pneumonia, with cough, wheezing, and eosinophilia. GI symptoms include anorexia, epigastric pain and tenderness, diarrhea, nausea, and vomiting. In heavy infections, malabsorption and protein-losing enteropathy may result in weight loss and cachexia.
The hyperinfection syndrome can result in disseminated disease involving the CNS, lungs, skin, liver, and heart. Immunosuppression increases risk. GI and pulmonary symptoms are often prominent. Ileus, obstruction, massive GI bleeding, severe malabsorption, and peritonitis may occur. Pulmonary symptoms include dyspnea, hemoptysis, and respiratory failure. Infiltrates may be seen on chest x-ray. Other symptoms depend on the organ involved. CNS involvement includes parasitic meningitis, brain abscess, and diffuse invasion of the brain. Secondary gram-negative meningitis and bacteremia, which occurs with high frequency, probably reflects disruption of bowel mucosa and/or carriage of bacteria on migrating larvae. Liver infection may result in cholestatic and granulomatous hepatitis. Infection may be fatal in immunocompromised patients, even with treatment.
Diagnosis
Microscopic visualization of larvae in a single stool sample is successful about 25% of the time in uncomplicated infections. Repeated examination of concentrated stool or the agar-plate method raises the sensitivity to ≥ 85%. If the specimen stands at room temperature for several hours, rhabditiform larvae may transform into longer filariform larvae, leading to erroneous diagnosis of hyperinfection. Sampling of proximal small bowel by aspiration may be positive in low-level infections. The latter should be done endoscopically to permit biopsy of suspicious duodenal and jejunal lesions. In the hyperinfection syndrome, filariform larvae may be found in stool, duodenal contents, sputum, and bronchial washings, and uncommonly in CSF, urine, or pleural or ascitic fluid. Chest x-rays may show diffuse interstitial infiltrates, consolidation, or abscess.
Enzyme-linked immunosorbent assay (ELISA) for serum anti–S. stercoralis antibodies is > 90% sensitive but may be falsely positive in patients infected with other intestinal nematodes or filariasis. Specificity varies with the assay used.
Eosinophilia is often present but can be suppressed by drugs such as corticosteroids or cytotoxic chemotherapeutic agents.
Treatment
and Prevention
Ivermectin (200 μg/kg po once/day for 1 or 2 days or single doses given at an interval of 2 wk) is effective for uncomplicated infection and is generally well tolerated. Doses of 200 μg/kg once/wk for 4 wk have been used for hyperinfection. Albendazole (400 mg bid for 2 days) is an alternative, but failures occur. Albendazole and ivermectin can be used together in hyperinfections. Cure should be documented by repeated stool examinations.
Thiabendazole was the drug of choice for strongyloidiasis, but it is more toxic than ivermectin and is no longer commercially available in the US. When thiabendazole is used, uncomplicated infection is treated with 25 mg/kg po bid for 2 days (maximum 3 g/day) and results in 80 to 90% cure. Repeated courses may be required. In hyperinfection syndrome, 25 mg/kg po bid should be given for a minimum of 5 to 7 days, but therapy should be continued for at least several days after parasites have disappeared from all sites. Adverse effects of thiabendazole , which are frequent and occasionally disabling, are nausea, vomiting, abdominal pain, dizziness, headache, paresthesia, malaise, pruritus, and flushing. Cure should be documented by repeated stool examination.
Prevention of primary infections is the same as for hookworms. To prevent potentially fatal hyperinfection syndrome, patients with possible exposure to Strongyloides (even in the distant past), patients with unexplained eosinophilia, and patients with symptoms suggestive of strongyloidiasis should undergo several stool examinations and serologic testing before receiving corticosteroids or other immunosuppressants. If infected, treatment for strongyloidiasis should be instituted and parasitologic cure documented before immunosuppression. Immunosuppressed people who have recurrent strongyloidiasis require additional courses of treatment until cured.
Last full review/revision November 2005
Content last modified November 2005
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