Background. Data on the incidence of Trichomonas vaginalis and use of hormonal contraception (HC) are limited. Methods. 2,374 sexually active women aged 15–49 years from cohort surveys in Rakai, Uganda, were included. Incidence of T. vaginalis was estimated per 100 person years (py) and association between HC (DMPA, Norplant, and oral contraceptives) and T. vaginalis infection was assessed by incidence rate ratios (IRR), using Poisson regression models. Results. At baseline, 34.9% had used HC in the last 12 months, 12.8% HIV+, 39.7% with high BV-scores (7–10), and 3.1% syphilis positive. The 12-month incidence of T. vaginalis was 2.4/100？py; CI (1.90, 3.25). When stratified by type of HC used, compared to women who did not use HC or condoms, incidence of T. vaginalis was significantly higher among users of Norplant (adj.IRR = 3.01, CI: 1.07–8.49) and significantly lower among DMPA users (adj.IRR = 0.55, CI: 0.30, 0.98) and women who discontinued HC use at follow-up (adj.IRR = 0.30, CI: 0.09, 0.99). HIV infection was associated with an increase in incidence of T. vaginalis (adj.IRR = 2.34, CI: 1.44, 3.78). Conclusions. Use of Norplant and being HIV+ significantly increased the risk of T. vaginalis, while use of DMPA and discontinuation of overall HC use were associated with a decreased incidence of T. vaginalis. 1. Introduction Trichomonas vaginalis (T. vaginalis) is the most common curable sexually transmitted infection (STI), and despite high prevalence rates ranging from 5–75%, and adverse health consequences such as pelvic inflammatory disease and adverse pregnancy outcomes, it has received little attention globally [1]. Sub-Saharan Africa continues to bear a disproportionate burden of the HIV disease with an estimated 22.5 million people living with HIV [2] and T. vaginalis has been shown to increase the odds of HIV acquisition between 1.5-fold and 3-fold [3, 4]. Dual use of efficacious contraceptives and condoms continues to be encouraged to prevent unwanted pregnancies and the high rates of HIV and STIs; however, dual use continues to be uncommon, especially among stable unions. The use of hormonal contraception (HC) and especially injectable contraceptives (ICs) is gaining popularity in Sub-Saharan Africa [5], and the two latest Ugandan demographic and health survey (DHS) show an increase in use of HCs among currently married women aged 15 to 49 years from 13.4% in 2005/6 [6] to 19.7% in 2011 [7]. Given that T. vaginalis is highly asymptomatic in females and their male partners and rates of reinfection are consequently high, efforts need to focus
References
[1]
B. van der Pol, “Trichomonas vaginalis infection: the most prevalent nonviral sexually transmitted infection receives the least public health attention,” Clinical Infectious Diseases, vol. 44, no. 1, pp. 23–25, 2007.
[2]
UNAIDS, “UNAIDS Report on the Global AIDS Epidemic—2010,” Report, UNAIDS/10.11E|JC1958E, UNAIDS, Geneva, Switzerland, 2010.
[3]
B. van der Pol, C. Kwok, B. Pierre-Louis et al., “Trichomonas vaginalis infection and human immunodeficiency virus acquisition in African women,” Journal of Infectious Diseases, vol. 197, no. 4, pp. 548–554, 2008.
[4]
R. S. McClelland, L. Sangaré, W. M. Hassan et al., “Infection with Trichomonas vaginalis increases the risk of HIV-1 acquisition,” Journal of Infectious Diseases, vol. 195, no. 5, pp. 698–702, 2007.
[5]
A. A. Creanga, D. Gillespie, S. Karklins, and A. O. Tsui, “Low use of contraception among poor women in Africa: an equity issue,” Bulletin of the World Health Organization, vol. 89, no. 4, pp. 258–266, 2011.
[6]
Uganda Bureau of Statistics (UBOS), “Uganda Demographic and Health Survey 2004-5,” Report, 2006.
[7]
Uganda Bureau of Statistics (UBOS) and Macro International Inc., Uganda Demographic and Health Survey, 2011, UBOS and Macro International Inc., Calverlton, Md, USA, 2012.
[8]
C. B. Polis, S. J. Phillips, and K. M. Curtis, “Hormonal contraceptive use and female-to-male HIV transmission: a systematic review of the epidemiologic evidence,” AIDS, vol. 27, no. 4, pp. 493–505, 2012.
[9]
R. Heffron, D. Donnell, H. Rees et al., “Use of hormonal contraceptives and risk of HIV-1 transmission: a prospective cohort study,” The Lancet Infectious Diseases, vol. 12, no. 1, pp. 19–26, 2012.
[10]
WHO, Hormonal Contraception and HIV: Technical Statement, Department of Reproductive Health and Research, WHO, Geneva, Switzerland, 2012.
[11]
J. M. Baeten, P. M. Nyange, B. A. Richardson et al., “Hormonal contraception and risk of sexually transmitted disease acquisition: results from a prospective study,” The American Journal of Obstetrics and Gynecology, vol. 185, no. 2, pp. 380–385, 2001.
[12]
B. I. Nsofor, C. S. S. Bello, and C. C. Ekwempu, “Sexually transmitted disease among women attending a family planning clinic in Zaria, Nigeria,” International Journal of Gynecology and Obstetrics, vol. 28, no. 4, pp. 365–367, 1989.
[13]
A. Pettifor, S. Delany, I. Kleinschmidt, W. C. Miller, J. Atashili, and H. Rees, “Use of injectable progestin contraception and risk of STI among South African women,” Contraception, vol. 80, no. 6, pp. 555–560, 2009.
[14]
M. J. Wawer, N. K. Sewankambo, D. Serwadda et al., “Control of sexually transmitted diseases for AIDS prevention in Uganda: a randomised community trial,” The Lancet, vol. 353, no. 9152, pp. 525–535, 1999.
[15]
M. J. Wawer, R. H. Gray, N. K. Sewankambo et al., “A randomized, community trial of intensive sexually transmitted disease control for AIDS prevention, Rakai, Uganda,” AIDS, vol. 12, no. 10, pp. 1211–1225, 1998.
[16]
S. N. Mavedzenge, B. van der Pol, H. Cheng et al., “Epidemiological synergy of Trichomonas vaginalis and HIV in Zimbabwean and South African women,” Sexually Transmitted Diseases, vol. 37, no. 7, pp. 460–466, 2010.
[17]
J. R？ttingen, W. D. Cameron, and G. P. Garnett, “A systematic review of the epidemiologic interactions between classic sexually transmitted diseases and HIV: how much really is known?” Sexually Transmitted Diseases, vol. 28, no. 10, pp. 579–597, 2001.
[18]
S. Cu-Uvin, J. W. Hogan, A. M. Caliendo, J. Harwell, K. H. Mayer, and C. C. J. Carpenter, “Association between bacterial vaginosis and expression of human immunodeficiency virus type 1 RNA in the female genital tract,” Clinical Infectious Diseases, vol. 33, no. 6, pp. 894–896, 2001.
[19]
L. Lavreys, V. Chohan, J. Overbaugh et al., “Hormonal contraception and risk of cervical infections among HIV-1-seropositive Kenyan women,” AIDS, vol. 18, no. 16, pp. 2179–2184, 2004.
[20]
C. S. Morrison, P. Bright, E. L. Wong et al., “Hormonal contraceptive use, cervical ectopy, and the acquisition of cervical infections,” Sexually Transmitted Diseases, vol. 31, no. 9, pp. 561–567, 2004.
[21]
F. Barbone, H. Austin, W. C. Louv, and W. J. Alexander, “A follow-up study of methods of contraception, sexual activity, and rates of trichomoniasis, candidiasis, and bacterial vaginosis,” The American Journal of Obstetrics and Gynecology, vol. 163, no. 2, pp. 510–514, 1990.
[22]
J. S. Hunt, L. Miller, and J. S. Platt, “Hormonal regulation of uterine macrophages,” Developmental Immunology, vol. 6, no. 1-2, pp. 105–110, 1998.
[23]
L. Miller, D. L. Patton, A. Meier, S. S. Thwin, T. M. Hooton, and D. A. Eschenbach, “Depomedroxyprogesterone-induced hypoestrogenism and changes in vaginal flora and epithelium,” Mechanisms of Development, vol. 96, no. 2, pp. 431–439, 2000.
[24]
R. N. Fichorova, R. T. Trifonova, R. O. Gilbert et al., “Trichomonas vaginalis lipophosphoglycan triggers a selective upregulation of cytokines by human female reproductive tract epithelial cells,” Infection and Immunity, vol. 74, no. 10, pp. 5773–5779, 2006.
[25]
L. C. Ford, H. A. Hammill, R. J. DeLange et al., “Determination of estrogen and androgen receptors in Trichomonas vaginalis and the effects of antihormones,” The American Journal of Obstetrics and Gynecology, vol. 156, no. 5, pp. 1119–1121, 1987.
[26]
J. Cleland and M. M. Ali, “Sexual abstinence, contraception, and condom use by young African women: a secondary analysis of survey data,” The Lancet, vol. 368, no. 9549, pp. 1788–1793, 2006.
