Factors associated with symptomatic vulvovaginal candidiasis: a study among women attending a primary healthcare clinic in KwaZulu-Natal, South Africa

  • T Apalata
  • B Longo-Mbenza
  • AW Sturm
  • WH Carr
  • P Moodley
Keywords: Human immunodeficiency virus‑related immune suppression, Vulvovaginal candidiasis, Primary healthcare clinic

Abstract

Background: Symptomatic vulvovaginal candidiasis (VVC) is one of the most common problems leading women to seek advice in primary healthcare facilities.
Aim: The aim of this study is to describe the associations between some hypothesized factors and the presence of symptomatic VVC.
Subjects and Methods: An analytical cross‑sectional study was conducted. A total of 90 women diagnosed with symptomatic VVC and 108 women without symptomatic VVC were recruited when attending Umlazi D clinic, a primary health clinic in KwaZulu‑Natal, South Africa between June 2011 and December 2011. Confirmed symptomatic VVC was determined by Gram stain and microbiological culture of vaginal swabs. For human immunodeficiency virus (HIV)‑infected women, HIV ribonucleic acid load in plasma and genital fluid was determined by real‑time‑polymerase chain reaction (BioMerieux, Lyon, France). CD4 counts were obtained from patients’ medical records. Data were analyzed using the statistical package for the social sciences (SPSS) version 21.0 (SPSS Inc.; Chicago, IL, USA). Multiple logistic regression models were used to exclude univariate confounders. All tests were two‑sided and a P < 0.05 was considered to be significant.
Results: A total of 90% (81/90) of patients with symptomatic VVC complained of vulval itching, soreness and vaginal discharge when compared to 75.9% (82/108) of patients without symptomatic VVC (P < 0.01).Whilst pregnancy was independently associated with symptomatic VVC (P < 0.01), the latter was inversely related to Nugent’s scores (P < 0.01). When compared with HIV negative women, the odds for symptomatic VVC increased among women with HIV‑associated immunocompromise (CD4 counts < 200 cells/mm3, P < 0.001), significantly shedding HIV in their genital tracts (P = 0.04), with plasma HIV load > 1000 copies/mL (P < 0.001). There was a significant negative association between the use of highly active anti‑retroviral therapy and the presence of symptomatic VVC in HIV‑infected women (P < 0.01).
Conclusion: Although symptomatic VVC is not classified as acquired immunodeficiency syndrome‑related condition, HIV‑related immune compromised women and particularly those who are anti‑retroviral therapy‑naïve are likely to develop symptomatic VVC.

Keywords: Human immunodeficiency virus‑related immune suppression, Vulvovaginal candidiasis, Primary healthcare clinic

Published
2015-01-29
Section
Articles

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print ISSN: 2141-9248