Sunday, October 25, 2015

Genital Infections & Risk of Premature Rupture of Membranes in Mulago Hospital, Uganda: A Case Control Study

Inflammatory mediators that weaken and cause membrane rupture are released during the course of genital infections among pregnant women. We set out to determine the association of common genital infections (Trichomonas vaginalis, syphilis, Neisseria gonorrhea, Chlamydia trachomatis, Group B Streptococcus, Bacterial vaginosis, Herpes Simplex Virus Type 2 and candidiasis) and premature rupture of membranes in Mulago hospital, Uganda.

We conducted an unmatched case-control study among women who were in the third trimester of pregnancy at New Mulago hospital, Uganda. The cases had PROM and the controls had intact membranes during latent phase of labour in the labour ward. We used interviewer-administered questionnaires to collect data on socio-demographic characteristics, obstetric and medical history. Laboratory tests were conducted to identify T. vaginalis, syphilis, N. gonorrhea, C. trachomatis, Group B Streptococcus, Bacterial vaginosis, Herpes Simplex Virus Type 2 (HSV-2) and candidiasis. Logistic regression models were used to estimate the odds ratios (OR) and 95 % CI of the association between genital infections and PROM.

There was an association between PROM and abnormal vaginal discharge, presence of candidiasis and T. vaginalis. However, there was no association between PROM and presence of C. trachomatis and HSV-2 serostatus. Few or no patients with Bacterial vaginosis, Neisseria gonorrhoea, Group B streptococcus or syphilis were identified among the cases and controls. Co-infection of Trichomoniasis and candidiasis was not associated with PROM. Co infection with T. vaginalis and C. trachomatis was associated with PROM.

Trichomonas vaginalis alone, T. vaginalis with C. trachomatis co-infection and abnormal per vaginal discharge were found as risk factors for PROM. There was no association of HSV-2 serostatus, syphilis, N. gonorrhea, C. trachomatis, Group B Streptococcus and Bacterial vaginosis with PROM. Candidiasis seemed to have a protective effect on PROM.

Table 3

Genital infections and risk for PROM in Mulago Hospital
VariableUnadjusted odds ratio (95 % CI)Adjusted odds ratio (95 %) in model 1Adjusted odds ratio (95 %) in model 2aAdjusted odds ratio (95 %) in model 3b
Abnormal vaginal discharge
 Yes2.02 (1.10–3.70)2.30 (1.18–4.47)2.30 (1.18–4.40)2.30 (1.18–4.46)
 No
HIV status
 Positive0.99 (0.42–2.34)1.38 (0.51–3.75)1.30 (0.51–3.72)1.38 (0.51–3.75)
 Negative
Trichomonas vaginalis
 Positive2.98 (1.18–7.56)4.22 (1.51–11.80)3.70 (0.92–14.90)
 Negative
Chlamydia trachomatis
 Positive2.05 (0.37–11.49)1.91 (0.30–12.22)1.92 (0.30–12.20)
 Negative
Candida
 Positive0.27 (0.14–0.52)0.22 (0.10–0.46)0.16 (0.02–1.22)0.22 (1.51–11.83)
 Negative
HSV-2
 Positive1.15 (0.63–2.09)0.95 (0.48–1.88)0.94 (0.48–1.87)0.95 (0.48–1.88)
 Negative
 Trichomonas and candida0.49 (0.27–0.90)1.34 (0.16–11.10)1.34 (0.16–11.10)
 Trichomonas and Chlamydia3.09 (1.21–7.84)4.22 (1.51–11.83)
In this table we have three models after multivariable analysis. Model 1 included abnormal vaginal discharge, HIV status Trichomonas vaginalis, Chlamydia trachomatis, candidiasis and HSV-2 serostatus. The italicized odds ratios were either independent risk factors for PROM (abnormal vaginal discharge and Trichomonas) or protective factors (candidiasis). Model 2 is included to assess whether co-infection with Trichomoniasis and candidiasis was a risk factor for premature rupture of membranes and found that this interaction was not a risk factor for PROM at multivariable analysis. Model 3 is included to assess whether co-infection with Trichomonas vaginalis and Chlamydia trachomatis was associated with PROM and it is shown that this interaction is a risk factor for PROM
aThe model 2 assesses interactions between Trichomonas vaginalis and candidiasis
bThe model 3 assesses interaction between Trichomonas vaginalis and Chlamydia trachomatis

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  • 1Department of Obstetrics and Gynecology, School of Medicine, Makerere University College of Health Sciences, P O Box 7072, Kampala, Uganda. sarahug@gmail.com.
  • 2Department of Obstetrics and Gynecology, School of Medicine, Makerere University College of Health Sciences, P O Box 7072, Kampala, Uganda. dankkaye@yahoo.com.
  • 3Department of Microbiology, Makerere University College of Health Sciences, P O Box 7072, Kampala, Uganda. fxb18@case.edu.
  • 4School of Public Health, Makerere University College of Health Sciences, P O Box 7072, Kampala, Uganda. naz@musph.ac.ug.
  • 5Department of Obstetrics and Gynecology, School of Medicine, Makerere University College of Health Sciences, P O Box 7072, Kampala, Uganda. flomir2002@yahoo.com.  


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