Woodland Breyer, Roy Chowdhury Piklu, O'Rourke Matthew B, Padula Matthew P
School of Life Sciences and Proteomics, Lipidomics and Metabolomics Core Facility, Faculty of Science, University of Technology Sydney, Ultimo, NSW, 2007, Australia.
Australian Institute for Microbiology and Infection, University of Technology Sydney, Ultimo, NSW, 2007, Australia.
Talanta. 2026 Jan 1;296:128480. doi: 10.1016/j.talanta.2025.128480. Epub 2025 Jun 17.
Klebsiella pneumoniae is a Gram-negative bacterium and a major cause of nosocomial infections such as urinary tract infections (UTIs), pneumonia and meningitis. Although these infections are commonly treated with the β-lactam group of antibiotics and combinations of it, (multi-)drug resistance in K. pneumoniae has steadily increased in the last few decades. Resistance to the β-lactam class of antibiotics is primarily mediated through the activation of narrow and extended-spectrum β-lactamase enzymes and changes within the bacterial cell envelope. Antimicrobial Resistance (AMR) has become a large global public health problem and economic burden. Carbapenem-resistant and extended-spectrum β-lactamase-producing K. pneumoniae have been classified as critical pathogens for which improved diagnostics and treatments are urgently needed. In order to develop new diagnostics and treatments, the resistance profiles of K. pneumoniae on a molecular level needs to be understood. Despite the identification of several genes, transcripts, proteoforms and their associated roles in resistance mechanisms, global resistance phenotypes are steadily evolving and consequently lack comprehensive understanding. This review discusses the role of genomics, transcriptomics, and proteomics in understanding resistance mechanisms and the associated molecular characteristics using carbapenem-resistant and extended-spectrum β-lactamase-producing K. pneumoniae as a model pathogen to further our current understanding of AMR. Furthermore, we also highlight the need for a holistic approach (i.e., combining 'omics technologies and data) to provide an in-depth understanding of the global resistance phenotype of K. pneumoniae in AMR.
肺炎克雷伯菌是一种革兰氏阴性菌,是医院感染的主要病因,如尿路感染(UTIs)、肺炎和脑膜炎。尽管这些感染通常用β-内酰胺类抗生素及其组合进行治疗,但在过去几十年中,肺炎克雷伯菌的(多重)耐药性一直在稳步上升。对β-内酰胺类抗生素的耐药性主要通过窄谱和广谱β-内酰胺酶的激活以及细菌细胞壁的变化来介导。抗菌药物耐药性(AMR)已成为一个重大的全球公共卫生问题和经济负担。耐碳青霉烯类和产超广谱β-内酰胺酶的肺炎克雷伯菌已被列为急需改进诊断和治疗方法的关键病原体。为了开发新的诊断和治疗方法,需要从分子水平了解肺炎克雷伯菌的耐药谱。尽管已经鉴定出了几个基因、转录本、蛋白质变体及其在耐药机制中的相关作用,但全球耐药表型仍在不断演变,因此缺乏全面的了解。本综述以耐碳青霉烯类和产超广谱β-内酰胺酶的肺炎克雷伯菌作为模型病原体,讨论了基因组学、转录组学和蛋白质组学在理解耐药机制及相关分子特征方面的作用,以加深我们目前对AMR的理解。此外,我们还强调了采用整体方法(即结合“组学”技术和数据)来深入了解肺炎克雷伯菌在AMR中的全球耐药表型的必要性。