Candida species are one of the commonest causes of vaginitis in healthy women of reproductive age. Vulvovaginal candidiasis (VVC) is characterized by vulvovaginal itching, redness and discharge. Candida albicans, which is a common genito-urinary tract commensal, has been the prominent species and remains the most common fungal agent isolated from clinical samples of patients diagnosed with VVC. In recent times, however, there has been a notable shift in the etiology of candidiasis with non-albicans Candida (NAC) species gaining prominence. The NAC species now account for approximately 10% to as high as 45% of VVC cases in some studies. This is associated with treatment challenges and a slightly different clinical picture. NAC species vaginitis is milder in presentation, often occur in patients with underlying chronic medical conditions and symptoms tend to be more recurrent or chronic compared with C. albicans vaginitis. C. glabrata is the most common cause of NAC-VVC. C. tropicalis, C. krusei, C. parapsilosis, and C. guilliermondii are the other commonly implicated species. Treatment failure is common in NAC-VVC, since some of these species are intrinsically resistant or show low susceptibilities to commonly used antifungal agents. This article reviews the etiology, pathogenesis, clinical features, diagnosis, and management of NAC vulvovaginitis.

The prevalence of plasmid-mediated resistance to tetracycline, and to a lesser extent penicillin, is high and neither drug is likely to have any future role in the treatment of gonorrhoea in South Africa. A novel β-lactamase plasmid was detected during the study and requires further characterization.

Introduction tuberculosis (TB) is the commonest opportunistic infection and cause of death in patients with Human Immunodeficiency Virus (HIV) in developing countries. World Health Organization (WHO) recommends 85% treatment success rate for all TB cases as an indicator of TB control. The study aimed at determining TB treatment success rate among TB-HIV co-infected patients and identifying predictors of successful treatment among patients in TB treatment sites in Abeokuta, Nigeria. Methods it was a cross-sectional study among HIV-TB co-infected patients in the two major health facilities in Abeokuta, Nigeria. Socio-demographic characteristics with treatment history were obtained using a semi-structured questionnaire. Sputum samples were collected and tested for acid-fast bacilli (AFB) using a standard method according to national guideline for TB treatment to determine treatment success rate. Treatment success was defined as any HIV positive patient with a diagnosis of TB by acid-fast bacilli (AFB) smear positivity at diagnosis, who after 6 months of complete treatment becomes smear negative. Adjusted odds ratio was used to identify independent predictors of successful treatment outcome with confidence interval set at 95% and level of significance set at P < 0.05. Results a total of 109 HIV-TB co-infected patients were enrolled for this study. Fifty-nine (54.1%) were females, 106 (97.3%) were newly treated for TB. Eighty-five (78.0%) were treated in a private health facility. A total of 91 had successful treatment outcome with a treatment success rate (TSR) of 83.5%. Eleven (10.1%) died, 5 (4.6%) defaulted, 1 (0.9%) failed treatment, 1 (0.9%) was transferred out. Successful treatment was associated with being newly registered (i.e. receiving TB treatment under the DOTS program for the first time), receiving TB treatment for the first time (adjusted OR = 18, 95%CI: 1.5-482.3) and being treated at a private health facility (adjusted OR = 14.1, 95%CI 4.27-48.4). Conclusion treatment success rate of TB among HIV-TB co-infected patients in this study slightly falls below the WHO target. Registration status and health facility type were predictors of treatment outcome among study patients. Patients and healthcare workers in public facilities were educated on HIV-TB co-infection management.

Sequencing of a novel β-lactamase-encoding plasmid (pEM1) found in PPNG isolates in Johannesburg shows it to be a deletion derivative of the prototype Asia plasmid, the deletion most likely arising as a result of DNA rearrangements. The majority of Johannesburg plasmid-containing PPNG isolates were, or were very closely related to, ST502.