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P3.090 Bacterial Vaginosis and the Risk of Trichomonas Vaginalis Acquisition Among HIV-1 Negative Women
  1. J E Balkus1,2,
  2. B A Richardson1,2,
  3. L K Rabe3,
  4. T Taha4,
  5. N Mgodi5,
  6. M P Kasaro6,
  7. L A Maslankowski7,
  8. G Ramjee8,
  9. I F Hoffman9,
  10. S S Abdool Karim10,11
  1. 1Fred Hutchinson Cancer Research Center, Seattle, WA, United States
  2. 2University of Washington, Seattle, WA, United States
  3. 3Magee Women’s Research Institute, Pittsburgh, PA, United States
  4. 4Johns Hopkins School of Public Health, Baltimore, MD, United States
  5. 5University of Zimbabwe, Harare, Zimbabwe
  6. 6Center for Infectious Disease Research in Zambia, Lusaka, Zambia
  7. 7University of Pennsylvania, Philadelphia, PA, United States
  8. 8South Africa Medical Research Council, Durban, South Africa
  9. 9University of North Carolina, Chapel Hill, NC, United States
  10. 10University of KwaZulu-Natal, Durban, South Africa
  11. 11Columbia University, New York, NY, United States


Background The vaginal microbiota may play a role in mediating susceptibility to sexually transmitted infections, including Trichomonas vaginalis (TV). This analysis evaluated the association between bacterial vaginosis (BV) and incident TV among women enrolled in a biomedical HIV prevention trial.

Methods Data were analysed from HIV-1 seronegative women participating in HIV Prevention Trials Network Protocol 035. At quarterly visits for up to 30 months, participants completed structured interviews and specimens were collected for genital tract infection testing. TV was detected by saline microscopy. BV was characterised by Gram stain using the Nugent score (BV = 7–10; intermediate = 4–6; normal = 0–3 [reference group]). Cox proportional hazards models stratified by study site were used to assess the association between BV at the prior quarterly visit and TV acquisition. Participants were censored at their first TV infection or if they became pregnant or HIV-infected.

Results This secondary analysis included 2,804 participants from Malawi, South Africa, USA, Zambia and Zimbabwe who contributed 13,977 follow-up visits. BV was detected at 5,184 (37.1%) visits and TV was detected at 352 (2.5%) visits. After adjusting for age, marital status, hormonal contraceptive use, sexual activity and TV at baseline, intermediate microbiota and BV at the prior visit were independently associated with an increased risk of TV (intermediate microbiota: adjusted hazard ratio [aHR] = 1.74, 95% confidence interval [CI] 1.22, 2.47; BV: aHR = 3.25, 95% CI 2.53–4.17). TV at baseline was also associated with an increased risk of TV (aHR = 2.54; 95% CI 1.91, 3.36). Sensitivity analyses excluding 202 women with baseline TV showed similar results (BV: aHR = 3.18; 95% CI 2.42 – 2.19).

Conclusions Women with a Nugent score > 3 were at an increased risk of acquiring TV. If this relationship is causal, interventions that decrease the incidence of BV and promote a normal vaginal microbiota could potentially contribute to reductions in TV incidence.

  • bacterial vaginosis
  • epidemiology
  • Trichomonas vaginalis

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