Case-control study of vulvar vestibulitis risk associated with genital infections.

OBJECTIVE: To evaluate the risk of vulvar vestibulitis syndrome (VVS) associated with genital infections in a case-control study. METHODS: Diagnosed cases with VVS (n = 69) and age-frequency-matched healthy controls (n = 65) were enrolled from gynecology clinics in a university medical hospital during 1999. They were compared for potential risk factors and symptoms of disease. RESULTS: VVS cases had a significantly higher risk of physician-reported bacterial vaginosis (BV) (odds ratio, OR = 9.4), Candida albicans (OR = 5.7), pelvic inflammatory disease (PID) (OR = 11.2), trichomoniasis (OR = 20.6), and vulvar dysplasia (OR = l5.7) but no risk associated with human papillomavirus (HPV), ASCUS, cervical dysplasia, genital warts, chlamydia, genital herpes or gonorrhea. Genital symptoms reported significantly more often with VVS included vulvar burning (91 vs. 12%), dyspareunia (81 vs. 15%), vulvar itching (68 vs. 23%) and dysuria (54 vs. 19%) (p < 0.0001). CONCLUSION: A history of genital infections is associated with an increased risk of VVS. Long-term follow-up case-control studies are needed to elucidate etiologic mechanisms, methods for prevention and effective treatment

Comparative Study of Intravaginal Metronidazole and Triple-Sulfa Therapy for Bacterial Vaginosis

Objective: We sought to compare the efficacy of metronidazole gel vs. triple-sulfa cream in the treatment of bacterial vaginosis (BV)

Group B <em>Streptococcus </em>engages an inhibitory siglec through sialic acid mimicry to blunt innate immune and inflammatory responses <em>in vivo</em>

Group B Streptococcus (GBS) is a common agent of bacterial sepsis and meningitis in newborns. The GBS surface capsule contains sialic acids (Sia) that engage Sia-binding immunoglobulin-like lectins (Siglecs) on leukocytes. Here we use mice lacking Siglec-E, an inhibitory Siglec of myelomonocytic cells, to study the significance of GBS Siglec engagement during in vivo infection. We found GBS bound to Siglec-E in a Sia-specific fashion to blunt NF-κB and MAPK activation. As a consequence, Siglec-E-deficient macrophages had enhanced pro-inflammatory cytokine secretion, phagocytosis and bactericidal activity against the pathogen. Following pulmonary or low-dose intravenous GBS challenge, Siglec-E KO mice produced more pro-inflammatory cytokines and exhibited reduced GBS invasion of the central nervous system. In contrast, upon high dose lethal challenges, cytokine storm in Siglec-E KO mice was associated with accelerated mortality. We conclude that GBS Sia mimicry influences host innate immune and inflammatory responses in vivo through engagement of an inhibitory Siglec, with the ultimate outcome of the host response varying depending upon the site, stage and magnitude of infection