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* Department of Gynecology and Obstetrics, Emory University, Atlanta, GA;
Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Correspondence to: Dr Jane R Schwebke, University of Alabama at Birmingham, 703 19th Street South, ZRB 239, Birmingham, AL 35294, USA Email: schwebke{at}uab.edu
The cause of bacterial vaginosis remains controversial. The two leading hypotheses are that Gardnerella vaginalis is the specific aetiologic agent versus the polymicrobial hypothesis that G. vaginalis acts in concert with other bacteria, principally anaerobes, to produce the disease. Here we reassess the prevailing polymicrobial hypothesis, finding it conceptually problematical. No host initiating factors as postulated have been identified, nor is there conclusive evidence that G. vaginalis lacks diagnostic specificity for the disease. The polymicrobial hypothesis, presupposing a unique disruption of vaginal microecology, is inconsistent with the epidemiological profile of the syndrome, which is that of a sexually transmitted disease. The epidemiological and clinical similarities between bacterial vaginosis and trichomoniasis suggest a similar pathogenetic process; i.e., primary causation by a specific agent, with secondary anaerobic activation and resultant amine production.
Key Words: bacterial vaginosis polymicrobial Gardnerella
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