Helminth Infections and HIV: A Double Hit

Jill E. Weatherhead, MD; Laila Woc-Colburn, MD

Disclosures

October 21, 2014

Strongyloidiasis

Acute infection manifests during initial migration of Strongyloides larvae through the venous peripheral blood system. They then travel through the lung parenchyma, ascending the bronchotracheal tree, and are subsequently swallowed to gain access to the small intestine. After initial infection, mature females in the duodenum produce rhabditiform larvae through parthenogenesis. Rhabditiform larvae in the intestinal tract can develop into infective filariform larvae and reinfect the host through penetration of intestinal mucosa, a process called "autoinfection" that supports chronic strongyloidiasis even after remote exposure.

Patients with chronic strongyloidiasis are typically asymptomatic or have minor intermittent gastrointestinal symptoms, such as diarrhea, vomiting, or constipation, over time. Chronic strongyloidiasis can progress to serious infection in the event of alteration of the host immune system, including restoration of the host immune system during initiation of HAART.

IRIS after initiation of HAART in patients with chronic strongyloidiasis increases replication of larvae and promotion of typical symptoms of chronic strongyloidiasis. Increased autoinfection and larvae migration through the gastrointestinal mucosa and into pulmonary tissue occurs secondary to a reduction of host mucosal surveillance as a result of steroid use, inducing exaggerated gastrointestinal and pulmonary symptoms that are termed "hyperinfection syndrome." The term "disseminated disease" refers to larvae that are found in organs not involved in the standard life cycle of Strongyloides.

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