Urogenital schistosomiasis secondary to S haematobium, a water-borne parasitic blood fluke, causes ulcerative lesions and inflammation on the cervix and vagina in females, and leukocytospermia and gross hematospermia in males. Chronic inflammatory disease caused by granulomatous reactions to Schistosoma eggs promotes HIV acquisition in the urogenital tract in females. There is growing evidence that urogenital schistosomiasis in men may also cause increased acquisition of HIV infection.
Schistosomiasis species are common in areas of high prevalence of HIV throughout the world. In sub-Saharan Africa, 220 million people are infected with the parasite, of whom 112 million are infected with S haematobium.
Schistosomiasis tends to infect people during childhood, maintaining chronic infection into adolescence and young adulthood. Like other parasitic infections, schistosomiasis activates a strong Th2 response, which in theory increases the susceptibility to such infections as HIV. Schistosomiasis, specifically intestinal disease, has also been shown to have effects on the immune modulation of HIV.
A prominent up-regulation of T cells in the intestinal mucosa can inhibit the ability of CD8 cells to control HIV viral replication, which may increase HIV progression concurrent with schistosomiasis. Of note, in patients with profound HIV infection with low CD4 counts, there is suppression of egg excretion efficiency even with heavy schistosomiasis burden.[7,10,11] As CD4 counts decline in progressive HIV infection, the granulomatous response to schistosoma eggs is muted and migration of the eggs through the mucosa is stunted, inhibiting their excretion. This reduced egg excretion in HIV-1 infected individuals with low CD4 counts leads to a gross underestimate of schistosomiasis prevalence when conventional stool egg count methods are used for detection.
Although there is no evidence that treated infection is more severe in HIV-infected persons, data now show that female and male urogenital schistosomiasis caused by S haematobium increases the risk for HIV transmission by three to four times.[4,7,12] In endemic areas, up to 75% of infected individuals have genital schistosomiasis, acquired primarily during childhood. It is thought that activation of the immune system in the genital mucosa facilitates virus binding to HIV-susceptible cells and allows for subsequent HIV entry into the cell.[10,12]
Urogenital schistosomiasis, like certain sexually transmitted infections, is now considered a cofactor for HIV transmission. Because of the association between schistosomiasis and HIV acquisition, treatment of schistosomiasis has been proposed to slow the spread of HIV in communities, especially those with limited access to HAART. Unfortunately, once a patient is coinfected with HIV and schistosomiasis, the effectiveness of appropriate antihelminth therapy is reduced and susceptibility to reinfection remains increased.[7,10,11] Thus, primary prevention and treatment of schistosomiasis should target children, in whom acquisition of schistosomiasis is most prominent.[7,10]
Medscape Infectious Diseases © 2014
Cite this: Helminth Infections and HIV: A Double Hit - Medscape - Oct 21, 2014.