Clinical Study Determinants of Symptomatic Vulvovaginal Candidiasis among Human Immunodeficiency Virus Type 1 Infected Women in Rural KwaZulu-Natal, South Africa Teke Apalata, 1,2 William H. Carr, 3,4 Willem A. Sturm, 1 Benjamin Longo-Mbenza, 2 and Prashini Moodley 1 1 Department of Infection Prevention and Control and Medical Microbiology, School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Private Bag 7, Congella, Durban 4013, South Africa 2 Department of Medical Microbiology, Faculty of Health Sciences, Walter Sisulu University, Private Bag X1, Mthatha, Eastern Cape 5117, South Africa 3 HIV Pathogenesis Programme (HPP), Department of Paediatrics and Child Health, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Private Bag 7, Congella, Durban 4013, South Africa 4 Department of Biology, Medgar Evers College, City University of New York, Brooklyn, NY 11225, USA Correspondence should be addressed to Teke Apalata; 203520405@stu.ukzn.ac.za Received 13 May 2013; Revised 11 November 2013; Accepted 17 December 2013; Published 9 April 2014 Academic Editor: Harold Wiesenfeld Copyright © 2014 Teke Apalata et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. We sought to determine the association between HIV-induced immunosuppression, virologic correlates, and vulvovaginal candidiasis (VVC). Methods. his is a retrospective cohort study, where HIV infected and uninfected women were studied with VVC being the primary outcome. Ninety-seven HIV-infected and 101 HIV-uninfected women were enrolled between June and December 2011. Cases of VVC were conirmed. HIV RNA load was determined by RT-PCR and CD4 counts were obtained from medical records. Results. Fity-two of 97 (53.6%) HIV-infected and 38/101 (37.6%) HIV-uninfected women were diagnosed with VVC ( = 0.032). he relative risk for VVC amongst HIV-infected patients was 1.53 (95% CI: 1.04–2  = 0.024). Cases of VVC increased at CD4+ T cell count below 200 cells/mm 3 ( < 0.0001) and plasma HIV RNA load above 10 000 copies/mL ( < 0.0001). VVC was associated with increased genital shedding of HIV ( = 0.002), and there was a linear correlation between plasma HIV load and genital HIV shedding ( = 0.540;  2 = 0.292;  < 0.0001). Women on HAART were 4-fold less likely ( = 0.029) to develop VVC. Conclusion. CD4 counts below 200 cells/mm 3 and plasma HIV loads ≥10 000 copies/mL were signiicantly associated with VVC. 1. Introduction Symptomatic vulvovaginal candidiasis (VVC) is caused by a number of species belonging to the genus Candida which are commensal fungi of the gastrointestinal tract and vagina. Candida albicans has been reported as the cause of symp- tomatic VVC in 85%–95% of cases, whilst C. glabrata rep- resents the most common cause of nonalbicans candida vaginitis [1]. Whilst 75% of healthy women develop symptomatic VVC at least once during their reproductive age, it is estimated that 5%–8% of women develop recurrent vulvovaginal candidiasis (RVVC). he latter is deined as the occurrence of four or more episodes of symptomatic VVC per year [1]. In HIV infected patients, whilst oroesophageal candidi- asis is known to appear at any time during the course of progression of HIV infection, symptomatic VVC develops signiicantly later [2]. It has been shown that oroesophageal candidiasis occurs as a result of the loss of mucosal and systemic cell-mediated immunity, while animal studies, in vitro experiments, and clinical trials indicate that systemic cell-mediated immunity does not play a protective role against candida vaginitis [3–5]. Hindawi Publishing Corporation Infectious Diseases in Obstetrics and Gynecology Volume 2014, Article ID 387070, 10 pages http://dx.doi.org/10.1155/2014/387070