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<p>Outbreaks of cholera are caused by the highly transmissive pathogen <i>Vibrio cholerae</i>. Infant mouse studies have elucidated many aspects of <i>V. cholerae</i> pathogenesis; however, the components of pathogenesis that feed-forward to promote transmission have remained enigmatic because animal models routinely bypass the mechanisms of inter-animal transmission by directly inoculating cultured bacteria into the stomach. Here, a transposon screen reveals that inactivation of the <i>V. cholerae</i> motility-linked gene <i>motV</i> increases infant mouse intestinal colonization. Compared to wild-type <i>V. cholerae</i>, a Δ<i>motV</i> mutant, which exhibits heightened motility in the form of constitutive straight swimming, localizes to the crypts earlier in infection and over a larger area of the small intestine. Aberrant localization of the mutant is associated with an increased number of <i>V. cholerae</i> initiating infection, and elevated pathogen burden, diarrhea, and lethality. Moreover, the deletion of <i>motV</i> causes <i>V. cholerae</i> to transmit from infected suckling mice to naïve littermates more efficiently. Even in the absence of cholera toxin, the Δ<i>motV</i> mutant continues to transmit between animals, although less than in the presence of toxin, indicating that phenotypes other than cholera toxin-driven diarrhea contribute to transmission. Collectively, this work provides experimental evidence linking intra-animal bottlenecks, colonization, and disease to inter-animal transmission.</p>

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Vibrio cholerae motility is associated with inter-animal transmission

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月27日

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  • Ian W. Campbell,
  • Ruchika Dehinwal,
  • Alexander A. Morano,
  • Katherine G. Dailey,
  • Franz G. Zingl,
  • Matthew K. Waldor

摘要

Outbreaks of cholera are caused by the highly transmissive pathogen Vibrio cholerae. Infant mouse studies have elucidated many aspects of V. cholerae pathogenesis; however, the components of pathogenesis that feed-forward to promote transmission have remained enigmatic because animal models routinely bypass the mechanisms of inter-animal transmission by directly inoculating cultured bacteria into the stomach. Here, a transposon screen reveals that inactivation of the V. cholerae motility-linked gene motV increases infant mouse intestinal colonization. Compared to wild-type V. cholerae, a ΔmotV mutant, which exhibits heightened motility in the form of constitutive straight swimming, localizes to the crypts earlier in infection and over a larger area of the small intestine. Aberrant localization of the mutant is associated with an increased number of V. cholerae initiating infection, and elevated pathogen burden, diarrhea, and lethality. Moreover, the deletion of motV causes V. cholerae to transmit from infected suckling mice to naïve littermates more efficiently. Even in the absence of cholera toxin, the ΔmotV mutant continues to transmit between animals, although less than in the presence of toxin, indicating that phenotypes other than cholera toxin-driven diarrhea contribute to transmission. Collectively, this work provides experimental evidence linking intra-animal bottlenecks, colonization, and disease to inter-animal transmission.