Detection of OMPKs 36/37 porins and other resistance determinants in extended spectrum beta-lactamases (ESBLs) -producing K. pneumoniae

Abstract

The rise of β-lactamases and loss of porin by multidrug-resistant Klebsiella pneumoniae is an important global issue. This work aimed to reveal how the loss of outer membrane porin (OMP) contributes to resistance in Klebsiella pneumoniae to certain antibiotic drugs. In this study, standard microbiological techniques of phenotypic procedures were used to isolate K. pneumoniae (P10) from the hospital wastewater sample. A double disk synergy test was used for the phenotypic detection of ESBL. Whole-genome sequencing (WGS) was conducted on the Illumina platform, and the resulting raw read was de novo assembled using RAPT NCBI. The landscape of antibiotic resistance inside the genome was examined using online bioinformatics tools. The biochemical tests identified the isolate to be K. pneumoniae with 100% resistance to ceftazidime, cefepime, augmentin, and intermediate resistance to meropenem but was susceptible to gentamicin. The isolate was confirmed as an ESBL-producer by an enlarged inhibitory zone towards Augmentin-clavulanic acid. WGS results showed the isolate harbors blaTEM, and blaSHV with Ompk 36 and Ompk 37 porin loss. The K. pneumoniae (P10) isolate exhibited a multidrug-resistant profile characterized by ESBL production, additional resistance genes, and loss of OmpK36/37 porins, collectively conferring resistance to a wide range of antibiotics including carbapenem and posing significant challenges for clinical management and infection control.