暴露于甲的次致命性暴露导致过度病毒性L. monocytogenes的生物制剂-抗生素交叉耐药性
Joshua Macleod1,2, Zak Hamid1,2, Benjamin E Johns3
1Microbiology and Infection Research Group, School of Sport and Health Sciences, Cardiff Metropolitan University, Cardiff, CF5 2YB, United Kingdom.
Journal of applied microbiology
|September 24, 2025
概括
在Listeria monocytogenes中对甲 (BAC) 的次致命暴露可能导致对抗生素的交叉耐药性. 这种由遗传突变驱动的适应,引发了人们对食品安全中的生物制剂-抗生素交叉耐药性的担忧.
科学领域:
- 食品微生物学 食品微生物学
- 抗微生物耐药性 抗微生物耐药性
- 细菌的适应 细菌的适应
背景情况:
- 李斯特菌 (Listeria monocytogenes) 是一个重要的食物传播病原体.
- 杀虫剂在食品制造环境 (FME) 中被广泛使用.
- 微致命的生物制剂暴露可能会诱导细菌的适应和交叉耐药性.
研究的目的:
- 为了调查杀性化 (BAC) 度是否会在Listeria monocytogenes中引起对抗生素的交叉耐药性.
- 通过适应性实验室进化 (ALE) 模型探索这种适应的基因机制.
主要方法:
- 六种Listeria monocytogenes和两种Listeria innocua菌株接受了为期30天的亚致命BAC适应性实验室进化 (ALE).
- 对各种生物制剂和抗生素进行了敏感性测试.
- 全基因组测序和变异调用是在适应的分离物上进行的.
主要成果:
- 适应BAC的分离体对BAC,诺基诺和co-trimoxazole的敏感性降低.
- 基因分析发现了fepR和基因间区域的突变,与生物制剂和抗生素敏感性降低有关.
- 这些突变与诺基诺排泄FepA有关.
结论:
- 亚致死性BAC暴露可以选择对生物制剂和抗生素敏感性降低的变体.
- fepR基因与生物制剂-抗生素交叉耐药性有关.
- 这凸显了食物传播病原体中抗菌素耐药性发展的潜在风险.
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