Impact of ompK35 and ompK36 downregulation on antibiotic resistance in clinical carbapenem-resistant Klebsiella pneumoniae isolates.

The increase in the prevalence of carbapenem-resistant Klebsiella pneumoniae strains (CRKP) has led to higher mortality and hospitalization of patients in health care facilities. This study investigates the resistance in CRKP, highlighting the involvement of carbapenemases, extended-spectrum β-lactamases (ESBLs), and AmpC β-lactamases, alongside the contribution of ompK35 and ompK36 porin genes in diminished antibiotic susceptibility. In the present study, 44 CRKP isolates were obtained from clinical samples, and antimicrobial susceptibility of isolates was determined. The presence of ESBLs, carbapenemase, and AmpC β-lactamases was identified through phenotypic testing. The ompK35 and ompK36 genes were identified using the polymerase chain reaction (PCR) technique, while their expression levels were evaluated through quantitative real-time PCR (q-PCR). ESBLs, carbapenemases, and AmpC β-lactamases were identified in 75%, 84%, and 13.6% of the isolates, respectively. The ompK35 was detected in 59.1% and ompK36 was detected in 56.8% of the CRKP isolates. A decresing in the expression of ompK35 and ompK36 was associated with elevated minimum inhibitory concentrations (MICs) for cefotaxime and cefepime, although no correlation was observed with imipenem. The high prevalence of ESBLs and carbapenemase production and the decreased expression of ompK35 and ompK36 correlated with decreased susceptibility to cefepime and cefotaxime, highlighting the co-exist of different of mechanisms resistance in CRKP. These results emphasize the necessity for continued surveillance and developing specific therapeutic strategies to tackle CRKP infections effectively.