Relationship Between Drug Resistance Characteristics and Biofilm Formation in Klebsiella Pneumoniae Strains

Abstract

Objective To conduct epidemiological analysis of Klebsiella pneumoniae ( K. pneumoniae ) with hypervirulence , and to investigate its drug resistance phenotype, Extended-spectrum β-lactamase ( ESBLs ) gene, virulence factor, capsular serotype and biofilm formation, so as to provide theoretical basis for further understanding of the drug resistance mechanism of K. pneumoniae with hypervirulence . Methods K. Pneumoniae were isolated from clinical samples collected from inpatients. All strains were identified by VITEK2 Compact using fully automatic microbial analyzer, the minimal inhibitory concentration ( MIC ) of antibiotics was determined by microbroth dilution test. The double disk diffusion method was used to detect the production of ESBLs , modified carbapenem inactivation method ( mCIM ) was used to detect the production of carbapenemase , and hypermucoviscosity phenotype was detected by wire drawing test. PCR was used to detect ESBLs gene, virulence factor and capsular serotype. Crystal violet staining was used to detect the ability of biofilm formation. Results The ESBLs genes detected in this study included strains blaTEM 35 (36.5%), blaSHV 51 (53.1%), and blaCTX-M 49 (51.0%). Most strains carried multiple ESBLs genes , but not all of them produce ESBLs. K1 and K2 accounted for 14.6% and 11.5% respectively. Most (91.7%) strains carried the fimH gene, and the other virulence genes were ybtS (53.1%), entB (46.9%), rmpA (41.7%), aerobactin (32.3%), allS (15.6%), kfu (15.6%). Of all the Klebsiella pneumoniae strains, 33 (34.4%) exhibited ESBLs phenotype, 16 (16.7%) were carbapenemase-producing, and 20 (20.8%) with ESBLs phenotype tested were resistant to all four drugs. The correlation between ESBLs-producing strains and biofilm formation was significantly increased compared to strains without ESBLs phenotype ( P =0.035). Conclusion Compared to hypervirulent Klebsiella pneumoniae ( hvKP ), classical Klebsiella pneumoniae ( cK...

Comparison of virulence factors between ESBL and non-ESBL producing Klebsiella pneumoniae isolates

“…In addition, allS, K1(magA), rmpA, iutA and aero virulence genes were only detected in hypermucoviscous K. pneumoniae isolates and the carriage of K2 gene was higher in hypermucoviscous K. pneumoniae compared to non hypermucoviscous isolates with significance of differences (p≤ 0.05). These findings were similar to the previous studies ( 7 , 35 – 37 ).…”

Extensive Expression of the Virulome Related to Antibiotic Genotyping in Nosocomial Strains of Klebsiella pneumoniae

“…High percentages for the streptomycin-(aadA1) and gentamicin-(aac(3)-IV) resistance gene were also detected in strains from patients with hospital-acquired infections (pneumonia) and communityacquired infections (UTI, respiratory infection, and infected ulcer). The overall number of bla TEM (144/150) and bla CXTX-9 (10/150) coincide with those described in K. pneumoniae strains isolated from Mexican patients in a health facility [35], while the numbers of bla SHV (96/150), bla CTXM-1 (67/150), and bla TEM (144/150) are higher than those described in K. pneumoniae strains isolated from hospital-acquired infections in other parts of the world [36,37]. The wide distribution of the resistance genotype to other non-beta-lactam antibiotics, such as tetracycline (tet(A)), sulfonamide (sul1), gentamicin (aac(3)-IV), and streptomycin (aadA1) detected in K. pneumoniae strains from patients with hospital-and community-acquired infections coincides with the high MDR phenotype found in Mexico in hospital strains of K. pneumoniae from bacteremia, UTIs, respiratory infection, and other infections [35,38].…”

Microbial Biofilm: A Review on Formation, Infection, Antibiotic Resistance, Control Measures, and Innovative Treatment

“…Similar observations were made with Klebsiella pneumoniae . This strain is sensitive when isolated from an aqueous solution but extremely resistant to specific antibiotics when tested from a biofilm [ 130 ]. Delayed or inadequate diffusion of the anti-microbial agents through the biofilms, varied growth rate of the biofilm microbial organisms, and other functional alterations are responsible for the development of antimicrobial resistance.…”