The spread of bla(OXA-48) and bla(OXA-244) carbapenemase genes among Klebsiella pneumoniae, Proteus mirabilis and Enterobacter spp. isolated in Moscow, Russia

BACKGROUND: The spread of carbapenemase-producing Enterobacteriaceae (CPE) is a great problem of healthcare worldwide. Study of the spread for bla(OXA-48-like) genes coding epidemically significant carbapenemases among hospital pathogens is important for the regional and global epidemiology of antimicrobial resistance. METHODS: Antibacterial resistant isolates of Klebsiella pneumoniae (n = 95) from 54 patients, P.mirabilis (n = 32) from 20 patients, Enterobacter aerogenes (n = 6) from four patients, and Enterobacter cloacae (n = 4) from four patients were collected from January, 2013 to October, 2014 in neurosurgical intensive care unit (ICU) of the Burdenko Neurosurgery Institute, Moscow. Characteristics of the isolates were done using susceptibility tests, PCR detection of the resistance genes, genotyping, conjugation, DNA sequencing, and bioinformatic analysis. RESULTS: Major strains under study were multi drug resistant (MDR), resistant to three or more functional classes of drugs simultaneously—98.9 % K. pneumoniae, 100 % P.mirabilis, one E.aerogenes isolate, and one E.cloacae isolate. Molecular-genetic mechanism of MDR in K.pneumoniae and P.mirabilis isolates were based on carrying of epidemic extended-spectrum beta-lactamase bla(CTX-M-15) gene (87.2 and 90.6 % accordingly), carbapenemase bla(OXA-48-like) gene (55.3 and 23.3 % accordingly), and class 1 (54.8 and 31.3 % accordingly) and class 2 (90.6 % P. mirabilis) integrons. The bla(OXA-48-like)-positive K. pneumoniae were collected during whole two-year surveillance period, while P. mirabilis and Enterobacter spp. carrying bla(OXA-48-like) genes were detected only after four and 18 months after the research start, respectively. The bla(OXA-48-like) gene acquisition was shown for P. mirabilis isolates collected from five patients and for E. cloacae isolate collected from one patient during their stay in the ICU, presumably from bla(OXA-48-like)-positive K. pneumoniae. The source of the bla(OXA-244) gene acquired by E. aerogenes isolates and the time of this event were not recognized. CONCLUSIONS: The expanding of CPE in the surveyed ICU was associated with the spread of bla(OXA-48) and bla(OXA-244) carbapenemase genes documented not only among K.pneumoniae, well-known bacterial host for such genes, but among P.mirabilis, E.aerogenes, and E. cloacae.