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<p>Antibiotics disrupt mucosal microbial communities, yet the effects on microbiomes infected with <i>Chlamydia trachomatis</i> (<i>Ct</i>) remain poorly understood. Some data exist on vaginal microbiomes, but none exist for the endocervix or rectum that are primary sites of infection. We applied metagenomic shotgun sequencing to vaginal, endocervical and rectal samples collected longitudinally from women who cleared their infection post-treatment (<i>n</i> = 10), had persistent infection (<i>n</i> = 11), or remained uninfected (<i>n</i> = 18) to evaluate azithromycin-induced changes in microbial composition, function, and the resistome over time. Our results show shifts in composition and function post-treatment that support persistent <i>Ct</i>, nonsynonymous <i>Ct</i> L22 amino acid substitutions that may be linked to azithromycin resistance, and significant endocervical increases in azithromycin resistance genes in <i>Lactobacillus iners</i> and <i>Gardnerella vaginalis</i> strains with moderate/high biofilm formation potential. These findings highlight the unintended ecological consequences of azithromycin treatment, including likely resistance gene propagation, emphasizing the need for novel treatment and microbiome-preserving strategies.</p>

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Azithromycin alters the microbiome composition, function and resistome in women with Chlamydia trachomatis infections

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月13日

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  • Sankhya Bommana,
  • Olusola Olagoke,
  • Yi-Juan Hu,
  • Ruohong Wang,
  • Mike Kama,
  • Morgan Dehdashti,
  • Reshma Kodimerla,
  • Timothy D. Read,
  • Deborah Dean

摘要

Antibiotics disrupt mucosal microbial communities, yet the effects on microbiomes infected with Chlamydia trachomatis (Ct) remain poorly understood. Some data exist on vaginal microbiomes, but none exist for the endocervix or rectum that are primary sites of infection. We applied metagenomic shotgun sequencing to vaginal, endocervical and rectal samples collected longitudinally from women who cleared their infection post-treatment (n = 10), had persistent infection (n = 11), or remained uninfected (n = 18) to evaluate azithromycin-induced changes in microbial composition, function, and the resistome over time. Our results show shifts in composition and function post-treatment that support persistent Ct, nonsynonymous Ct L22 amino acid substitutions that may be linked to azithromycin resistance, and significant endocervical increases in azithromycin resistance genes in Lactobacillus iners and Gardnerella vaginalis strains with moderate/high biofilm formation potential. These findings highlight the unintended ecological consequences of azithromycin treatment, including likely resistance gene propagation, emphasizing the need for novel treatment and microbiome-preserving strategies.