Strongyloidiasis is a soil-transmitted helminth infection that is concentrated in tropical and subtropical regions of the world, with an estimated prevalence of 50 million infections worldwide. Studies have shown that patients with certain types of cell-mediated immunosuppression, such as those taking corticosteroids, have high rates of hyperinfection and disseminated strongyloidiasis. As a result, HIV/AIDS was originally considered a significant risk factor for strongyloidiasis hyperinfection syndrome and disseminated strongyloidiasis as well.
At the beginning of the HIV/AIDS epidemic, strongyloidiasis was listed as an opportunistic infection in patients with advancing AIDS.[6,7] However, unlike corticosteroid use leading to severe strongyloidiasis, the association of advanced HIV and severe strongyloidiasis infection has not been validated. As a result, the Centers for Disease Control and Prevention and the World Health Organization removed hyperinfection and disseminated strongyloidiasis from the list of AIDS-defining illnesses.[5,7,8]
The lack of an association between cellular immunosuppression in end-stage HIV/AIDS and strongyloidiasis hyperinfection syndrome results from the intricate mucosal immune response found in the intestine of the human host. Progression from chronic intestinal strongyloidiasis to hyperinfection and disseminated strongyloidiasis depends on an intact immune system that allows for development of the rhabditiform larvae into infectious larvae in the gut, promoting autoinfection. Immune suppression from HIV/AIDS has been postulated to halt this larvae development process and impair progression into the autoinfection cycle.
Of interest, initiation of HAART in a patient with HIV and Strongyloides coinfection could have deleterious effects. Documentation of IRIS has occurred after initiation of HAART in patients presenting with Strongyloides hyperinfection syndrome or worsening of chronic strongyloidiasis symptoms.[5,7]
Despite the paucity of more severe disease, patients with HIV, even with high CD4 counts, have been shown to have a higher (21 times) prevalence of intestinal strongyloidiasis. This suggests that HIV has an impact on the susceptibility to infection.[5,8] Furthermore, patients with HIV and Strongyloides coinfection might also have a slower response to antihelminth therapy, requiring repeated dosing of ivermectin for clearance of the infection.
Fewer data are available to support the interaction between HIV and soil-transmitted helminth infections, such as hookworm, ascariasis, trichuriasis, and enterobiasis. Similar to strongyloidiasis, several areas of the world have a high prevalence of soil-transmitted helminth parasitic infection among HIV-infected patients. Despite these overlaps, data to support the effects of concurrent infection on the human host are lacking.
The parasite hookworm is commonly identified in HIV-infected patients, and like HIV-1 infection alone, hookworm can cause a significant hypochromic microcytic anemia. Despite similar symptom profiles, no correlation between anemia and hookworm has been documented in HIV-infected patients.
Similarly, trichuriasis and ascariasis have been well documented in patients with HIV-1 infection. Some studies have shown more difficulty in treating coinfected patients, and others demonstrate higher HIV viral loads in these patients, but these data have not been consistently reproducible. As with other helminth infections, such soil-transmitted helminths as ascariasis, trichuriasis, and hookworm have profound effects on the Th2 immune response; this supports the possibility that interactions between soil-transmitted helminths and HIV-1 infection exist, but this requires further investigation.
Medscape Infectious Diseases © 2014
Cite this: Helminth Infections and HIV: A Double Hit - Medscape - Oct 21, 2014.