Bacterial vaginosis is a polymicrobial clinical syndrome of non-inflammatory genesis characterized by a dramatic decrease or complete absence of protective lactoflora.
It is replaced by a massive association of obligate and facultative anaerobic microorganisms.
The pathogenesis is based on the formation of a dense polymicrobial biofilm on the surface of the vaginal epithelium. The primary colonizer is Gardnerella vaginalis, which creates a polymeric matrix into which other anaerobes (Atopobium vaginae, Mobiluncus spp., Prevotella spp.) are incorporated. These bacteria produce proteolytic enzymes, mucinases and sialidases that destroy the protective mucosal barrier of the cervix and vagina.
The specific “fishy” odor is due to the production of volatile amines (putrescine, cadaverine, trimethylamine) during anaerobic metabolism of amino acids. The absence of leukocytic reaction (inflammation) is due to the ability of Gardnerella to produce hemolysin, which destroys leukocytes and blocks chemotaxis.
It is diagnosed based on Amsel criteria (presence of homogeneous gray-white discharge, pH > 4.5, positive aminotest, presence of key cells) or on the Nugent microbiologic scale.
Bacterial vaginosis is associated with a high risk of ascending infection (UTI), postoperative complications (cultitis, endometritis), preterm labor, premature rupture of fetal membranes, and increased susceptibility to HIV and other STIs.
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