Long-lasting impact of antibiotic treatment for Chlamydia trachomatis on the vaginal microbiome in young women Jeanne Tamarelle1, Bing Ma2,3, Pawel Gajer2,3, Mike S. Humphrys2, Elisabeth Delarocque-Astagneau1, Larry J. Forney4, Patrik Bavoil5, Jacques Ravel2,3 1UMR1181, Université Versailles-Saint-Quentin-en-Yvelines/Institut Pasteur/INSERM; 2Institute for Genome Sciences, University of Maryland School of Medicine; 3Department of Microbiology and Immunology, University of Maryland School of Medicine; 4Department of Biological Sciences, University of Idaho; 5Department of Microbial Pathogenesis, University of Maryland School of Dentistry
Chlamydia trachomatis infection is the most widespread bacterial sexually transmitted infection (STI) worldwide. Antibiotics (ATB) are efficient against this infection, however reinfection is common. Dysbiotic vaginal microbiota has been associated with susceptibility to infection, and ATB treatment for C. trachomatis may negatively affect the vaginal microbiota, maintaining risk for subsequent infection. We conducted a study of the vaginal microbiota composition and structure in a cohort of 149 women with genital C. trachomatis infection followed-up quarterly for 9 months (CHARM study). Vaginal microbial communities dominated by L. iners (community state type (CST) III) or a diversity of anaerobes including G. vaginalis (CST-IV) were shown to be over-represented in CT-positive women before ATB. Three months post-ATB treatment, we observed an increase of CST-III, followed by a slight progressive decrease at 6 and 9-month post-treatment. At the species-level, we noted that L. iners distinguishes itself from other vaginal Lactobacillus spp. as it is the only Lactobacillus that expands post-treatment. ATB sensitivity tests demonstrated that most L. iners and G. vaginalis strains are resistant to azithromycin, while other vaginal Lactobacillus spp., including L. crispatus, L. jensenii, and L. gasseri, are azithromycin-sensitive. We speculate that azithromycin treatment for C. trachomatis infection drives the composition of the vaginal microbiota toward communities dominated by L. iners or G. vaginalis, causing reduced community resilience and vaginal dysbiosis, and ultimately high STI susceptibility. These results advocate for the need to examine systematically vaginal microbial communities in relation to STIs, in both research and clinical practice, and develop post-ATB interventions to restore a protective vaginal microbiota.
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