Association of classical sexually transmitted infections and genital mycoplasmas detection with high-risk human papillomavirus and cervical lesions among women undergoing cervical cancer screening in Ethiopia

Persistent high-risk human papillomavirus (hrHPV) infection is the necessary cause of cervical cancer. A small proportion of HPV infections may progress to high-grade cervical lesions or cancer. Genital mycoplasma and sexually transmitted infections (STIs) may be associated with HPV persistence and progression. These detections or infections may also reduce the diagnostic accuracy of visual inspection-based screening by increasing local inflammation. In Ethiopia, there is still limited evidence on the association of STIs and genital mycoplasmas with hrHPV, cervical lesions, and visual inspection with acetic acid or Lugol’s iodine (VILI/VILI). This study assessed the prevalence of certain classical STIs and genital mycoplasma, their association with hrHPV infection, cervical lesions, and VIA/VILI outcomes among women undergoing HPV-based cervical cancer screening. Vaginal self-samples from 885 Ethiopian women were tested for 14 hrHPV types, C. trachomatis (CT), N. gonorrhoeae (NG), T. vaginalis (TV), and four genital mycoplasmas using real-time PCR. One hundred and fifty-six women who tested positive for hrHPV underwent VIA/VILI, and 116 women underwent histology examinations. Frequencies and percentages were used to summarize descriptive statistics of categorical variables. The prevalence estimates were provided with 95% confidence intervals (CIs), using the Wilson score method. Associations were assessed by the chi-square test and logistic regression analysis between the independent and outcome variables. A Firth-penalized multivariable logistic regression analysis was also used for histological results and independent variables. Among the study participants, 568 women (64.2%) had at least one sexually transmitted microbe (STM) (95% CI: 61–67). Classical STIs were detected in 4.3% (95% CI: 3.1–5.8), and genital mycoplasmas in 64% (95% CI: 60.7–67.1) of participants. U. parvum was the most frequently detected species. High-risk HPV infection was associated with genital mycoplasma detection (AOR = 1.7, 95% CI: 1.3–2.3, p = 0.001), C. trachomatis infection (AOR = 5.4, 95% CI: 1.4–21, p = 0.014), M. hominis detection (AOR = 2.0, 95% CI: 1.4-3.0, p = 0.001), and HIV infection (AOR = 3.2, 95% CI: 1.8–5.5, p < 0.001). CIN2 + lesions were associated with both hrHPV (AOR = 6.77, 95% CI: 1.2–75.4, P = 0.03) and HIV infection (AOR = 8.92, 95% CI: 1.5–72.2, P = 0.02). Neither STIs nor genital mycoplasma detection were associated with VIA/VILI outcomes. Classical STIs were low among the women included in the study. However, one out of five women were infected with hrHPV, and 64% of the women were harbored genital mycoplasma. HrHPV infection was associated with genital mycoplasma detection, C. trachomatis infection , M. hominis detection, and HIV infection. HrHPV and HIV infections were associated with CIN2 + lesions, whereas classical STIs and genital mycoplasma were not associated with cervical abnormalities. There was no association between STIs or the detection of genital mycoplasma and the outcomes of VIA/VILI. Overall, this study emphasizes the importance of considering HPV–HIV co-infections in cervical cancer prevention strategies.