14 research outputs found

    Chlamydia and gonorrhoea in pregnant Batswana women: time to discard the syndromic approach?

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    <p>Abstract</p> <p>Background</p> <p>Chlamydia and gonorrhoea are major causes of morbidity among women in developing countries. Both infections have been associated with pregnancy-related complications, and case detection and treatment in pregnancy is essential. In countries without laboratory support, the diagnosis and treatment of cervical infections is based on the syndromic approach. In this study we measured the prevalence of chlamydia and gonorrhoea among antenatal care attendees in Botswana. We evaluated the syndromic approach for the detection of cervical infections in pregnancy, and determined if risk scores could improve the diagnostic accuracy.</p> <p>Methods</p> <p>In a cross-sectional study, 703 antenatal care attendees in Botswana were interviewed and examined, and specimens were collected for the identification of <it>C trachomatis</it>, <it>N gonorrhoeae </it>and other reproductive tract infections. Risk scores to identify attendees with cervical infections were computed based on identified risk factors, and their sensitivities, specificities, likelihood ratios and predictive values were calculated.</p> <p>Results</p> <p>The prevalence of chlamydia was 8%, and gonorrhoea was found in 3% of the attendees. Symptoms and signs of vaginal discharge did not predict cervical infection, and a syndromic approach failed to identify infected women. Age (youth) risk factor most strongly associated with cervical infection. A risk score with only sociodemographic factors had likelihood ratios equivalent to risk scores which incorporated clinical signs and microscopy results. However, all the evaluated risk scores were of limited value in the diagnosis of chlamydia and gonorrhoea. A cut-off set at an acceptable sensitivity to avoid infected antenatal care attendees who remained untreated would inevitably lead to considerable over-treatment.</p> <p>Conclusion</p> <p>Although in extensive use, the syndromic approach is unsuitable for diagnosing cervical infections in antenatal care attendees in Botswana. None of the evaluated risk scores can replace this management. Without diagnostic tests, there are no adequate management strategies for <it>C trachomatis </it>and <it>N gonorrhoeae </it>in pregnant women in Botswana, a situation which is likely to apply to other countries in sub-Saharan Africa. Screening for cervical infections in pregnant women is an essential public health measure, and rapid tests will hopefully be available in developing countries within a few years.</p

    Prevalence and risk factors of cervicovaginal HIV shedding among HIV-1 and HIV-2 infected women in Dakar, Senegal

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    Objectives: To assess the risk determinants and prevalence of cervicovaginal shedding of HIV-1 and HIV-2 among women in Dakar, Senegal. Methods: We conducted a cross sectional study of 153 HIV seropositive female sex workers (FSW) and another 142 HIV seropositive women attending an infectious diseases unit, based on an interview, physical examination, and laboratory screening for major sexually transmitted infections (STI). Cervicovaginal lavage fluid was tested for HIV-RNA by means of nested PCR. Links between cervicovaginal shedding of HIV-1 and HIV-2 and sociodemographic, clinical, and laboratory variables were identified by using odd ratios and 95% confidence intervals. Logistic regression analysis was used to identify independent links with HIV shedding. Results: The detection rate of HIV-RNA in cervicovaginal lavage fluid was low among FSW, with no difference between HIV-1 (7/90: 8%) and HIV-2 (3/48: 6%). The rate was far higher among the other women (41%, 48/117; 33%, 7/21 for HIV-1 and HIV-2, respectively). In multivariate analysis, high plasma viral load (>40 000 copies/ml) (AOR = 2.4 (1.0–5.6) p = 0.04) and basic vaginal pH (AOR = 2.2 (1.3–3.7) p = 0.002) were independently associated with HIV-1 shedding. For HIV-2 a CD4 count < 200 cells x 10(6)/l was the only factor associated with the shedding of HIV-2 (AOR = 9.0 (0.9–93)). The genital shedding rate was higher with HIV-1 than with HIV-2 (OR = 2.1 (0.9–4.8), but this difference disappeared after adjustment for the CD4+ cell count (AOR = 1.2 (0.5–2.9)). Conclusion: Advanced disease stage and immunosuppression are the major risk determinants for shedding of both HIV-1 and HIV-2. Basic vaginal pH is also a risk determinant for HIV-1 shedding. Key Words: cervicovaginal shedding; HIV; Senega

    Spatial phylodynamics of HIV-1 epidemic emergence in east Africa

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    DESIGN: We sought to investigate the evolutionary and historical reasons for the different epidemiological patterns of HIV-1 in the early epidemic. In order to characterize the demographic history of HIV-1 subtypes A and D in east Africa, we examined molecular epidemiology, geographical and historical data.METHODOLOGY: We employed high-resolution phylodynamics to investigate the introduction of HIV-1A and D into east Africa, the geographic trends of viral spread, and the demographic growth of each subtype. We also used geographic information system data to investigate human migration trends, population growth, and human mobility. RESULTS: HIV-1A and D were introduced into east Africa after 1950 and spread exponentially during the 1970s, concurrent with eastward expansion. Spatiotemporal data failed to explain the establishment and spread of HIV based on urban population growth and migration. The low prevalence of the virus in the Democratic Republic of Congo before and after the emergence of the pandemic was, however, consistent with regional accessibility data, highlighting the difficulty in travel between major population centers in central Africa. In contrast, the strong interconnectivity between population centers across the east African region since colonial times has likely fostered the rapid growth of the epidemic in this locale. CONCLUSION: This study illustrates how phylodynamic analysis of pathogens informed by geospatial data can provide a more holistic and evidence-based interpretation of past epidemics. We advocate that this 'landscape phylodynamics' approach has the potential to provide a framework both to understand epidemics' spread and to design optimal intervention strategies
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