Correlation between antimicrobial resistance and biofilm formation capability among Klebsiella pneumoniae strains isolated from hospitalized patients in Iran

Abstract

Background Klebsiella pneumoniae is a common cause of nosocomial infections. Antibiotic resistance and ability to form biofilm, as two key virulence factors of K. pneumoniae, are involved in the persistence of infections. The purpose of this study was to investigate the correlation between antimicrobial resistance and biofilm formation capability among K. pneumoniae strains isolated from hospitalized patients in Iran. Methods Over a 10-month period, a total of 100 non-duplicate K. pneumoniae strains were collected. Antibiotic susceptibility was determined by Kirby–Bauer disk diffusion method according to CLSI. Biofilm production was assessed by tissue culture plate method. Finally, polymerase chain reaction was conducted to detect four families of carbapenemase: blaIMP, blaVIM, blaNDM, blaOXA−48; biofilm formation associated genes: treC, wza, luxS; and K. pneumoniae confirming gene: rpoB. Results Most of the isolates were resistant to trimethoprim-sulfamethoxazole (52 %), cefotaxime (51 %), cefepime (43 %), and ceftriaxone (43 %). Among all the 100 isolates, 67 were multidrug-resistant (MDR), and 11 were extensively drug-resistant (XDR). The prevalence of the blaVIM, blaIMP, blaNDM, and blaOXA−48 genes were 7 , 11 , 5 , and 28 %, respectively. The results of biofilm formation in the tissue culture plate assay indicated that 75 (75 %) strains could produce biofilm and only 25 (25 %) isolates were not able to form biofilm. Among these isolates, 25 % formed fully established biofilms, 19 % were categorized as moderately biofilm-producing, 31 % formed weak biofilms, and 25 % were non-biofilm-producers. The antimicrobial resistance among biofilm former strains was found to be significantly higher than that of non-biofilm former strains (p < 0.05). Molecular distribution of biofilm formation genes revealed that 98 , 96 , and 34 % of the isolates carried luxS, treC, and wza genes, respectively. Conclusions The rise of antibiotic resistance among biofilm-producer strains demonstrates a serious concern about limited treatment options in the hospital settings. All of the data suggest that fundamental actions and introduction of novel strategies for controlling of K. pneumoniae biofilm-related infections is essential.

Frequency of Virulence Genes and Their Association with Biofilm Formation Ability in Klebsiella pneumoniae Isolated from Wound Infections

“…In our study, the most prevalent genes were entB (95.9%), mH (94.6%), mrkD (90.5%), and mrkA (75.7%). Consistently, previous studies have shown that mH, mrkD, mrkA and entB genes are among the most common virulence genes in K. pneumoniae strains (Sei et al 2016;Shadkam et al 2021). The rate of the entB was similar to the report of Mirzaie et al (Mirzaie and Ranjbar 2021).…”

High Acquisition Rate of Gram-Negative Multi-Drug Resistant Organism Colonization During Hospitalization: A Perspective from a High Endemic Setting

“…However, there are many studies that showed isolation of Enterobacterales, non-fermenting P. aeruginosa and A. baumannii from clinical samples and established infection from rectal colonization. [34][35][36][37] Some studies from Mongolia also showed presence of extended-spectrum β-lactamase-producing E. coli, Klebsiella spp. and A. baumannii from clinical samples.…”

In Vitro and In Vivo Studies on the Antibacterial Activity and Safety of a New Antimicrobial Peptide Dermaseptin-AC

“…However, for P. aeruginosa and K. pneumonia , these values were higher ( P. aeruginosa MIC = 4 μM, MBC = 8 μM; K. pneumoniae MIC = 2 μM, MBC = 8 μM). A possible reason is that P. aeruginosa and K. pneumoniae tend to secrete extracellular polysaccharide matrix, which hinders the effect of peptides on bacteria ( 16 , 17 ). Studies have shown that capsular polysaccharides released by K. pneumoniae and alginate secreted by P. aeruginosa shield AMPs, causing conformational changes in them and preventing their interaction with microbial membranes ( 18 ).…”