Objective To define an entity of abnormal vaginal flora: aerobic vaginitis.Design Observational study.Setting University Hospital Gasthuisberg, Leuven, Belgium.Sample 631 women attending for routine prenatal care or attending vaginitis clinic.Methods Samples were taken for fresh wet mount microscopy of vaginal fluid, vaginal cultures and measurement of lactate, succinate and cytokine levels in vaginal fluid. Smears deficient in lactobacilli and positive for clue cells were considered to indicate a diagnosis of bacterial vaginosis. Aerobic vaginitis was diagnosed if smears were deficient in lactobacilli, positive for cocci or coarse bacilli, positive for parabasal epithelial cells, and/or positive for vaginal leucocytes (plus their granular aspect). Results Genital complaints include red inflammation, yellow discharge, vaginal dyspareunia. Group B streptococci, escherichia coli, staphylococcus aureus and trichomonas vaginalis are frequently cultured.Vaginal lactate concentration is severely depressed in women with aerobic vaginitis, as in bacterial vaginosis, but vaginal succinate is not produced. Also in contrast to bacterial vaginosis, aerobic vaginitis produces a host immune response that leads to high production of interleukin-6, interleukin-1-b and leukaemia inhibitory factor in the vaginal fluid. Conclusion Aerobic vaginitis is associated with aerobic micro-organisms, mainly group B streptococci and E. coli. Its characteristics are different from those of bacterial vaginosis and elicit an important host response. The most severe form of aerobic vaginitis equals desquamative inflammatory vaginitis. In theory, aerobic vaginitis may be a better candidate than bacterial vaginosis as the cause of pregnancy complications, such as ascending chorioamnionitis, preterm rupture of the membranes and preterm delivery.
The causal relationship between persistent infection with high-risk HPV and cervical cancer has resulted in the development of HPV DNA detection systems. The widely used MY09/11 consensus PCR targets a 450bp conserved sequence in the HPV L1 gene, and can therefore amplify a broad spectrum of HPV types. However, limitations of these consensus primers are evident, particularly in regard to the variability in detection sensitivity among different HPV types. This study compared MY09/11 PCR with type-specific PCRs in the detection of oncogenic HPV types. The study population comprised 15, 774 patients. Consensus PCR failed to detect 522 (10.9%) HPV infections indicated by type-specific PCRs. A significant correlation between failure of consensus PCR and HPV type was found. HPV types 51, 68 and 45 were missed most frequently. The clinical relevance of the HPV infections missed by MY09/11 PCR was reflected in the fraction of cases with cytological abnormalities and in follow-up, showing 104 (25.4%) CIN2+ cases. The MY09/11 false negativity could be the result of poor sensitivity, mismatch of MY09/11 primers or disruption of L1 target by HPV integration or DNA degradation. Furthermore, MY09/11 PCR lacked specificity for oncogenic HPVs. Diagnostic accuracy of the PCR systems, in terms of sensitivity (MY09/11 PCR: 87.9%; type-specific PCRs: 98.3%) and specificity (MY09/11 PCR: 38.7%; type-specific PCRs: 76.14%), and predictive values for histologically confirmed CIN2+, suggest that type-specific PCRs could be used in a clinical setting as a reliable screening tool.
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