Severe strongyloidiasis complicated by meningitis and hydrocephalus in an HTLV-1 carrier with increased proviral load.

We report a 47-year-old Japanese man who was a human T-cell leukemia virus type 1 (HTLV-1) carrier with strongyloidiasis, and who was born in an area endemic for both Strongyloides stercoralis ( S. stercoralis) and HTLV-1. He presented with edema of both legs. Laboratory examination on admission revealed hypoalbuminemia, and S. stercoralis rhabditiform larvae were found by stool microscopy. Purulent meningitis, which was suspected to be due to disseminated strongyloidiasis, developed during the first and second treatment for S. stercoralis infection. After the meningitis was alleviated, hydrocephalus with gait disturbance developed, and these features were attenuated by a ventriculo-peritoneal shunt. Impaired immunity and increased HTLV-1 proviral load, with an increased titer of HTLV-1 antibody, were observed in this patient. These results suggest that HTLV-1 proviral load and/or antibody titer of HTLV-1 can be used for the identification of carriers who are at increased risk of developing severe strongyloidiasis among those patients who are infected with both S. stercoralis and HTLV-1.

Involvement of IL-2/IL-2R system activation by parasite antigen in polyclonal expansion of CD4(+)25(+) HTLV-1-infected T-cells in human carriers of both HTLV-1 and S. stercoralis.

The intermediate state of HTLV-1 infection, often found in individuals dually infected with Strongyloides stercoralis (S. stercoralis) and HTLV-1, is assumed to be a preleukemic state of adult T-cell leukemia (ATL). To investigate the effects of S. stercoralis superinfection on the natural history of HTLV-1 infection, we characterized peripheral blood samples of these individuals in Okinawa, Japan, an endemic area for both HTLV-1 and S. stercoralis and we studied effects of the parasite antigen on T-cells. The dually infected individuals showed a significantly higher provirus load and an increase in CD4(+)25(+) T cell population, with a significant, positive correlation. This increase was attributable to polyclonal expansion of HTLV-1-infected cells, as demonstrated by inverse-long PCR analysis of the integration sites. S. stercoralis antigen activated the IL-2 promoter in reporter gene assays, induced production of IL-2 by PBMC in vitro, and supported growth of IL-2 dependent cell lines immortalized by HTLV-1 infection or the transduction of Tax. Taken collectively, these results indicate that S. stercoralis infection induces polyclonal expansion of HTLV-1-infected cells by activating the IL-2/IL-2R system in dually infected carriers, an event which may be a precipitating factor for ATL and inflammatory diseases.