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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 occasionally in sputum or by detection of antibodies in blood. Treatment is with ivermectin or albendazole.
Strongyloidiasis is endemic throughout the tropics and subtropics, including rural areas of the southern US, at sites where bare skin is exposed to contaminated soil and conditions are unsanitary. Strongyloides fülleborni, which infects chimpanzees and baboons, can cause limited infections in humans.
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 the larvae are excreted in the stool. After a few days in soil, they develop into infectious filariform larvae. Like hookworms, Strongyloides larvae penetrate human skin, 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 into 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 (external autoinfection). Autoinfection explains why strongyloidiasis can persist for many decades and helps account for the extremely high worm burdens in the hyperinfection syndrome.
Hyperinfection may result from a newly acquired Strongyloides infection or from activation of a previously asymptomatic one. In either case, it can result in disseminated disease involving organs not usually part of the parasite’s normal life cycle (eg, CNS, skin, liver, heart). Hyperinfection usually occurs in patients who are taking corticosteroids or who have impaired cell-mediated immunity, particularly those infected with the human T-lymphotropic virus 1 (HTLV-1). However, hyperinfection and disseminated strongyloidiasis are less common than might be predicted among patients with HIV/AIDS, even those living in areas where Strongyloides is highly endemic.
Infection may be asymptomatic.
Larva currens (creeping infection) is a form of cutaneous larva migrans specific to Strongyloides infection; it results from autoinfection. The eruption begins in the perianal region and rapidly spreads, causing intense pruritus, but nonspecific maculopapular or urticarial eruptions may also occur.
Pulmonary symptoms are uncommon, although heavy infections may cause Löffler syndrome, 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.
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 organs 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 reflect disruption of bowel mucosa, carriage of bacteria on migrating larvae, or both. Liver infection may result in cholestatic and granulomatous hepatitis. Infection may be fatal in immunocompromised patients, even with treatment.
Microscopic examination of a single stool sample detects larvae in about 25% of uncomplicated infections. Repeated examination of concentrated stool samples raises the sensitivity; as many as 7 negative stool samples are recommended to exclude the diagnosis. The agar plate method has a sensitivity of > 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 the proximal small bowel by aspiration may be positive in low-level infections and should be done endoscopically to permit biopsy of suspicious duodenal and jejunal lesions. In 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.
Several immunodiagnostic tests are available for strongyloidiasis. Enzyme immunoassay (EIA) is recommended because of its greater sensitivity (> 90%). IgG antibodies can usually be detected even in immunocompromised patients with disseminated strongyloidiasis, but the absence of detectable antibodies does not exclude infection. Cross-reactions in patients with filariasis or other nematode infections may result in false-positive tests. Antibody test results cannot be used to differentiate current from past infection. A positive test warrants continuing efforts to establish a parasitologic diagnosis. Serologic monitoring may be useful in follow-up because antibody levels decrease within 6 mo of successful chemotherapy. Sensitive and specific PCR-based methods for the diagnosis of S. stercoralis in stool samples are being developed and are available in research settings.
Eosinophilia is often present but can be suppressed by drugs such as corticosteroids or cytotoxic chemotherapeutic drugs.
Ivermectin 200 mcg/kg po once/day for 2 days is used for uncomplicated infection and is generally well-tolerated. Albendazole 400 mg po bid for 7 days is an alternative. In immunocompromised patients, prolonged therapy or repeated courses may be needed. Combined therapy with albendazole and ivermectin has been used for hyperinfection. In severely ill patients who are unable to take oral drugs, rectal preparations of ivermectin have been used.
Cure should be documented by repeated stool examinations.
Prevention of primary infections is the same as for hookworms. To prevent potentially fatal hyperinfection syndrome, clinicians should do several stool examinations and serologic testing in patients with possible exposure to Strongyloides (even in the distant past), with unexplained eosinophilia, or with symptoms that suggest strongyloidiasis before corticosteroids or other immunosuppressants are used. If patients are infected, treatment for strongyloidiasis should be instituted and parasitologic cure should be documented before immunosuppression. Immunosuppressed people who have recurrent strongyloidiasis require additional courses of treatment until cured.
Strongyloides larvae penetrate human skin when people walk barefoot on infested soil.
Larvae travel through the bloodstream to the lungs, penetrate the alveoli, ascend the respiratory tract, are swallowed, and then mature in the intestines; adult worms produce ova that hatch in the intestines, releasing larvae; they can develop into infective filariform larvae, which may cause external or internal autoinfection, perpetuating the cycle.
Patients who are taking corticosteroids or who have impaired cell-mediated immunity may develop potentially fatal hyperinfection syndrome—disseminated disease involving the lungs, intestines, skin, and organs that are not part of the parasite’s normal life cycle (eg, CNS, liver, heart).
Symptoms include rash, pulmonary symptoms (including cough and wheezing), and abdominal pain with diarrhea.
Diagnose by microscopic examination of multiple stool samples, the agar plate method, or duodenal aspirate. Larvae may be identified in sputum in patients with hyperinfection.
Treat with ivermectin for 2 days or with albendazole for 7 days; hyperinfection syndrome requires prolonged or repeated courses.
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