Serwy Daniel Miceli, Conde Maria Eduarda Rocha, Alencar Ana Luiza Carneiro, Novaes Roberto Leonan Morim, Lima-Junior Josué da Costa, da Mota Fabio Faria, Carvalho-Assef Ana Paula, Galvao Teca Calcagno, Zahner Viviane
Fiocruz, Laboratório de Bacteriologia Aplicada a Saúde Única e Resistência Antimicrobiana, Instituto Oswaldo Cruz, Rio de Janeiro, RJ, Brazil.
Fiocruz, Laboratório de Imunoparasitologia, Instituto Oswaldo Cruz, Rio de Janeiro, RJ, Brazil.
Mol Ecol. 2026 Jan;35(2):e70234. doi: 10.1111/mec.70234.
This study investigates the genetic diversity and evolutionary mechanisms driving polymyxin resistance in Klebsiella pneumoniae, a critical priority pathogen. By analysing mgrB, phoPQ and pmrAB genes in susceptible (PM-S) and resistant (PM-R) populations through neutrality tests (Tajima D, Fu & Li's D) we uncovered polygenic adaptation and positive selection as a key driver of resistance. High genetic diversity was observed across all loci, with mgrB insertions dominating PM-R populations. Negative Tajima and Fu & Li's D values and excess rare alleles revealed recent population expansions linked to the reintroduction of polymyxins in the 2010s. Positive selection via selective sweeps was detected in PM-R isolates, exemplified by the rapid spread of haplotype 27, which presents mgrB insertions, the major determinant of LPS modification pathway hyperactivation. The expansion of this haplotype suggests that horizontal gene transfer accelerates resistance dissemination. The elevated genetic diversity observed in the phoPQ and pmrAB systems among isolates harbouring mgrB alterations may reflect reduced adaptive fitness costs, enabling the preservation of genomic variability despite sustained selective pressures. Our results demonstrate that polymyxin resistance arises through polygenic adaptation and positive selection, combining de novo mutations, recombination and selection-driven sweeps. These dynamics threaten to exacerbate resistance in hospital environments, emphasising the need for genomic surveillance and alternative therapies. This study bridges molecular evolution and clinical epidemiology, offering insights into the resilience of K. pneumoniae and the ecological drivers of antimicrobial resistance.
本研究调查了肺炎克雷伯菌(一种关键的优先病原体)中多粘菌素耐药性的遗传多样性和驱动其进化的机制。通过中性检验( Tajima D、Fu & Li's D)分析敏感(PM-S)和耐药(PM-R)群体中的mgrB、phoPQ和pmrAB基因,我们发现多基因适应和正选择是耐药性的关键驱动因素。在所有基因座上均观察到高遗传多样性,mgrB插入在PM-R群体中占主导地位。负的Tajima和Fu & Li's D值以及过量的稀有等位基因揭示了与2010年代多粘菌素重新引入相关的近期种群扩张。在PM-R分离株中检测到通过选择性清除的正选择,以单倍型27的快速传播为例,该单倍型存在mgrB插入,这是脂多糖修饰途径过度激活的主要决定因素。这种单倍型的扩张表明水平基因转移加速了耐药性的传播。在携带mgrB改变的分离株中,phoPQ和pmrAB系统中观察到的遗传多样性增加可能反映了适应性适合度成本的降低,尽管存在持续的选择压力,但仍能保留基因组变异性。我们的结果表明,多粘菌素耐药性是通过多基因适应和正选择产生的,结合了从头突变、重组和选择驱动的清除。这些动态变化可能会加剧医院环境中的耐药性,强调了基因组监测和替代疗法的必要性。本研究架起了分子进化与临床流行病学之间的桥梁,为肺炎克雷伯菌的适应性以及抗菌药物耐药性的生态驱动因素提供了见解。