Access Microbiol. 2025 Jun 30;7(6). doi: 10.1099/acmi.0.000999.v3. eCollection 2025.
Interactions between environmental protists and bacteria play a crucial role in shaping bacterial survival strategies and pathogenic potential. Certain bacteria have evolved mechanisms to resist predation by protists such as , allowing them to persist intracellularly and, in some cases, enhance their virulence. We hypothesize that species may also play a role in promoting antimicrobial resistance (AMR) in amoeba-resistant bacteria. This study investigated whether enhanced AMR development in under lethal ciprofloxacin concentrations. was co-incubated with and maintained in ciprofloxacin concentrations starting at 2 µg ml, four times the planktonic MIC, which was incrementally increased as resistance emerged. The survival of the co-incubated and the development of resistance were monitored, and antimicrobial susceptibility tests were conducted using multiple antibiotics. co-incubated with in the presence of ciprofloxacin became increasingly resistant in a dose-dependent manner, with the MIC increasing from 0.5 to 20 µg ml after 17 days. Contrastingly, the naïve strain did not survive sustained exposure at 2 µg ml. Co-incubated bacteria maintained under ciprofloxacin pressure developed resistance to ciprofloxacin, chloramphenicol, azithromycin and enrofloxacin while retaining susceptibility to streptomycin and tetracycline. Co-incubation in the absence of ciprofloxacin did not promote resistance in , suggesting that the combination of extracellular drug pressure and intracellular survival is important in driving resistance. These findings indicate that intracellular survival within can significantly accelerate AMR development in under fluoroquinolone pressure. Further research into the molecular mechanisms involved is warranted to inform strategies for mitigating AMR emergence in clinical and environmental contexts.
环境原生生物与细菌之间的相互作用在塑造细菌的生存策略和致病潜力方面起着至关重要的作用。某些细菌已经进化出抵御原生生物捕食的机制，例如，使它们能够在细胞内持续存在，并且在某些情况下增强其毒力。我们假设[具体物种名称]物种也可能在促进对变形虫具有抗性的细菌的抗菌耐药性（AMR）方面发挥作用。本研究调查了在致死浓度的环丙沙星作用下，[具体物种名称]是否会增强[细菌名称]的AMR发展。将[细菌名称]与[具体物种名称]共同孵育，并维持在起始浓度为2μg/ml的环丙沙星中，这是浮游菌最低抑菌浓度（MIC）的四倍，随着耐药性的出现，浓度逐渐增加。监测共同孵育的[细菌名称]的存活情况和耐药性的发展，并使用多种抗生素进行药敏试验。在环丙沙星存在下与[具体物种名称]共同孵育的[细菌名称]以剂量依赖的方式变得越来越耐药，17天后MIC从0.5μg/ml增加到20μg/ml。相比之下，未经处理的菌株在2μg/ml的浓度下无法在持续暴露中存活。在环丙沙星压力下维持的共同孵育细菌对环丙沙星、氯霉素、阿奇霉素和恩诺沙星产生了耐药性，同时对链霉素和四环素仍保持敏感。在没有环丙沙星的情况下共同孵育不会促进[细菌名称]产生耐药性，这表明细胞外药物压力和细胞内存活的结合在推动耐药性方面很重要。这些发现表明，在氟喹诺酮压力下，在[具体物种名称]内的细胞内存活可以显著加速[细菌名称]的AMR发展。有必要对所涉及的分子机制进行进一步研究，以为减轻临床和环境背景下AMR出现的策略提供信息。
