Clinical Pearls & Morning Reports
Published January 22, 2020
Strongyloides stercoralis is a nematode that causes strongyloidiasis, which can be asymptomatic or manifested by a range of symptoms, including shock. Mild infections are most likely to be characterized by nonspecific gastrointestinal symptoms or incidentally identified peripheral eosinophilia. Read the latest Case Records of the Massachusetts General Hospital here.
Q: How do humans become infected with S. stercoralis?
A:S. stercoralis is endemic in large parts of the tropics and subtropics. Infection begins with inoculation of the skin with filariform larvae that reside in the soil. The larvae migrate through the skin into the bloodstream, which carries them to the lungs. The organisms then penetrate the alveolar wall and ascend the bronchi and trachea until they reach the pharynx, where they are swallowed and subsequently come to rest in the proximal small bowel. The larvae mature into adult worms that inhabit the mucosa of the gut, where they shed eggs that hatch into rhabditiform larvae that are eventually excreted in the stool.
Q: Is “autoinfection” a feature of strongyloidiasis?
A: A well-known characteristic of strongyloides is that it can complete its life cycle within the human host. In this autoinfection cycle, the rhabditiform larvae mature into invasive filariform larvae in the small bowel and colon and then burrow through the bowel wall or perianal skin to restart the life cycle within the same host. In this way, the infection can last for decades after the patient has left the region where the organism is endemic.
A: There are several gastrointestinal manifestations of strongyloides infection, including epigastric pain, nausea, and vomiting, features that mimic peptic-ulcer disease. Watery diarrhea is a common manifestation that may be accompanied by frank malabsorption of fat and vitamin B12. Malabsorption syndrome can mimic celiac disease or tropical sprue and may manifest as a protein-losing enteropathy, characterized by hypoalbuminemia and peripheral edema. Among patients with a high burden of disease, pulmonary, gastrointestinal, and skin symptoms can be present, and infections such as bacteremia and meningitis with enteric organisms can occur owing to translocation of bacteria enabled by migration of the adult worm or larvae out of the intestinal lumen. The severity of symptoms is closely related to the patient’s cell-mediated immune status. Hyperinfection syndrome is associated with a greatly increased worm burden, which often occurs in the context of immunosuppression or human T-cell lymphotropic virus type 1 (HTLV-1) infection. Additional risk factors that increase the likelihood of strongyloidiasis include glucocorticoid use and other forms of immunosuppression that result in decreased cell-mediated immunity.
A: Treatment options for strongyloidiasis have not been well studied. For uncomplicated infection, the Centers for Disease Control and Prevention recommends a weight-based dose of ivermectin (200 μg per kilogram of body weight), administered once daily for 1 or 2 days. Persistent symptoms after ivermectin treatment should arouse suspicion for treatment failure. For hyperinfection or disseminated disease, treatment with ivermectin at a daily dose of 200 μg per kilogram is recommended, at least until stool examinations are negative and symptoms are resolved; repeat examination of the stool is recommended thereafter to test for relapse. Because persons who have compromised cell-mediated immunity, including those with HTLV-1 infection, are at risk for treatment failure, continued monitoring of these patients is recommended.