Changes in the etiology of sexually transmitted diseases in Botswana between 1993 and 2002: implications for the clinical management of genital ulcer disease.
ABSTRACT In recent years, increasing evidence has accumulated that suggests the majority of cases of genital ulcer disease in sub-Saharan Africa are due to viral and not bacterial infections. Although many cross-sectional studies support such a trend, few serial cross-sectional data are available to show the evolution of genital ulcer disease over time.
We surveyed the prevalence of sexually transmitted diseases (STDs) among patients with STD symptoms and women recruited from family planning clinics in 3 cities in Botswana in 2002 and compared our findings with those from a survey of a similar population conducted in 1993.
The observed proportion of cases of genital ulcer disease due to chancroid decreased from 25% in 1993 to 1% in 2002, whereas the proportion of ulcers due to herpes simplex virus increased from 23% in 1993 to 58% in 2002. Although the proportion of ulcers due to syphilis was similar for both surveys, the rate of positive serologic test results for syphilis among patients with genital ulcer disease decreased from 52% in 1993 to 5% in 2002. During this period, decreases in the prevalence of gonorrhea, syphilis-reactive serologic findings, chlamydial infection, and trichomoniasis were also detected among patients with STDs and women from family planning clinics. These changes remained significant after estimates were adjusted for the sensitivity and specificity of diagnostic tests.
Our findings suggest a decrease in the prevalence of bacterial STDs and trichomoniasis, a reduction in the proportion of ulcers due to bacterial causes, and an increase in the proportion of ulcers due to herpes simplex virus during the period 1993-2002. These changes should be taken into consideration when defining new guidelines for the syndromic management of genital ulcer disease.
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ABSTRACT: Chancroid, caused by Haemophilus ducreyi, has declined in importance as a sexually transmitted pathogen in most countries where it was previously endemic. The global prevalence of chancroid is unknown as most countries lack the required laboratory diagnostic capacity and surveillance systems to determine this. H. ducreyi has recently emerged as a cause of chronic skin ulceration in some South Pacific islands. Although no antimicrobial susceptibility data for H. ducreyi have been published for two decades, it is still assumed that the infection will respond successfully to treatment with recommended cephalosporin, macrolide or fluoroquinolone-based regimens. HIV-1-infected patients require careful follow-up due to reports of treatment failure with single dose regimens. Buboes may need additional treatment with either aspiration or excision and drainage.Expert Review of Anticancer Therapy 03/2014; DOI:10.1586/14787210.2014.892414 · 3.06 Impact Factor
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ABSTRACT: Congenital syphilis is a devastating disease that can be prevented by screening and treatment of infected pregnant women. The WHO is leading a global initiative to eliminate mother-to-child-transmission of syphilis with a goal of ≤50 congenital syphilis cases per 100,000 live births and targets of 95% antenatal care, 95% syphilis testing, and 95% treatment coverage. We estimated current congenital syphilis rates for 43 African countries, and additional scenarios in a subset of 9 countries. Our analysis suggested that only 4 of 43 countries are likely to currently have a congenital syphilis rate ≤50 per 100,000 live births, and none of the 9 countries could reach this goal even in 5 different scenarios with improved services. To achieve the eliminate mother-to-child-transmission goal, it appears necessary to intervene beyond services for pregnant women, and decrease prevalence of syphilis in the general population as well.Expert Review of Anticancer Therapy 06/2014; 12(6):705-14. DOI:10.1586/14787210.2014.919221 · 3.06 Impact Factor
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ABSTRACT: Genital HSV reactivation is thought to be anatomically and temporally localized, coincident with limited ganglionic infection. Short, subclinical shedding episodes are the most common form of HSV-2 reactivation, with host clearance mechanisms leading to rapid containment. The anatomic distribution of shedding episodes has not been characterized.To precisely define patterns of anatomic reactivation, we divided the genital tract into a 22-region grid and obtained daily swabs for 20 days from each region in 28 immunocompetent, HSV-2 seropositive persons. HSV was detected via PCR and sites of asymptomatic HSV shedding were biopsied within 24 hours. CD4+ and CD8+ T cells were quantified by immunofluorescence, and HSV specific CD4+ T cells were identified by intracellular cytokine cytometry.HSV was detected in 868 (7%) of 11,603 genital swabs at a median of 12 sites per person (range 0-22). Bilateral HSV detection occurred on 83 (67%) days with shedding, and the median quantity of virus detected/day was associated with the number of sites positive (p<0.001). In biopsies of asymptomatic shedding sites, we found increased numbers of CD8+ T cells compared to control tissue (27 vs. 13 cells/mm(2), p=0.03) and identified HSV specific CD4+ T cells.HSV reactivations emanate from widely separated anatomic regions of the genital tract and are associated with a localized cellular infiltrate that was demonstrated to be HSV-specific in 3 cases. These data provide evidence that asymptomatic HSV-2 shedding contributes to chronic inflammation throughout the genital tract. This detailed study of the anatomic patterns of genital HSV-2 shedding demonstrates that HSV-2 reactivation can be detected at multiple, bilateral sites in the genital tract, suggesting that HSV establishes latency throughout the sacral ganglia. In addition, genital biopsies from sites of asymptomatic HSV shedding have increased numbers of CD8+ T cells compared to control tissue, and HSV-specific CD4+ T cells are found at sites of asymptomatic shedding. These findings suggest that that widespread asymptomatic genital HSV-2 shedding is associated with a targeted host immune response and contributes to chronic inflammation throughout the genital tract.Journal of Virology 02/2014; DOI:10.1128/JVI.03285-13 · 4.65 Impact Factor