Abstract

BackgroundAnimal studies have demonstrated that functional immune responses, as determined by the levels of CD4+ cell counts and anti-schistosome antibodies responses, determine the efficacy of praziquantel. Based on this evidence, it has been hypothesised that the immunodeficiency effects of the human immunodeficiency virus (HIV)-1 infection may affect the efficacy of praziquantel in co-infected human hosts. Thus, the present study assessed the efficacy of praziquantel by comparing parasitological cure rates and the reduction in infection intensity in HIV-1 seronegative individuals infected with S. mansoni and HIV-1 seropositive individuals co-infected with S. mansoni, following treatment with a single oral dose of praziquantel.MethodsThis was a prospective longitudinal study which included, at baseline, 555 S. mansoni infected adults aged 21–55 years, who were either co-infected or not with HIV-1 and who lived in fishing villages along Lake Victoria in Northwest Tanzania. These individuals were treated with a single oral dose of praziquantel (40 mg/kg) and, at 12 weeks, single stool samples were obtained and examined for S. mansoni eggs using the Kato-Katz technique. Finger prick and venous blood samples were collected for HIV-1 screening and CD4+ cell quantification.ResultsThe parasitological cure rate did not differ significantly from the HIV-1 serostatus (P = 0.12): among the co-infected individuals, the cure rate was 48.3% (14/29), and among the individuals infected only with S. mansoni, the cure rate was 62.6% (329/526). The egg reduction rate did not vary with the HIV-1 serostatus (P = 0.22): 77.22% for HIV-1 seronegative and 75% for HIV-1 seropositive individuals. The level of CD4+ cell counts (median 228 cells/μL: range 202–380 cells) did not influence the cure rate (P = 0.23) or the reduction in the intensity of the infection (P = 0.37).ConclusionThe HIV-1 infection per se or its moderate immunodeficiency effects, demonstrated by the range of CD4+ cell counts observed in co-infected individuals, did not affect praziquantel efficacy, as measured by the parasitological cure rate and the reduction in intensity of infection in the present study cohort.Electronic supplementary materialThe online version of this article (doi:10.1186/2049-9957-3-47) contains supplementary material, which is available to authorized users.

Highlights

  • Animal studies have demonstrated that functional immune responses, as determined by the levels of CD4+ cell counts and anti-schistosome antibodies responses, determine the efficacy of praziquantel

  • There were no differences in pre-treatment geometrical mean egg per gram of faeces (GM-epg) between the 555 individuals who were present (174.21 epg, 95% CI; 154.14– 196.87) and the 299 individuals who were absent (200.92 epg, 95% CI: 167.97–240.34) (t = −1.4012, P = 0.16)

  • In relation to the parasitological cure rate and the reduction in the intensity of infection, individuals co-infected with human immunodeficiency virus (HIV)-1 and S. mansoni responded to praziquantel treatment the same as HIV-1 seronegative individuals infected with S. mansoni did

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Summary

Introduction

Animal studies have demonstrated that functional immune responses, as determined by the levels of CD4+ cell counts and anti-schistosome antibodies responses, determine the efficacy of praziquantel. Preimmunisation of S. mansoni animals models with parasite antigens to generate parasite-specific antibodies [18,19], or the passive transfer of immune serum from immunocompetent animal models, increases praziquantel efficacy [17,19,20]. This indicates that a functional and intact immune response is required to enhance praziquantel efficacy [19]

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