Infectious complications caused by antibiotic-resistant strains in burn injury patients account for 30—75% of all deaths. For optimal clinical control important to know the susceptibility profile, the mechanisms of antimicrobial resistance and the predominant genetic lineage.
THE AIMED
At studying the mechanisms of antibiotic resistance of the main causative agents of pyoinflammatory complications in patients with burns.
MATERIALS AND METHODS
In 2011—2017 were examined 90 patients with deep burns who were treated at the Regional Clinical Hospital. Materials investigated by bacteriological method, MALDI-TOF. Antibiotic sensitivity was studied by methods: disk-diffusion; PCR; E-test; serial dilutions in Muller-Hinton broth. Genotyping and determination of resistance mechanisms: PCR, sequencing.
RESULTS
The prevalence of a mixed flora of multi- and extremely resistant pathogens, representatives of the ESKAPE group, has been established. 66.7% of P. aeruginosa strains (n=9) had blaVIM, 22.2% of strains — blaCTX-M. 50% of A. baumannii strains (n=8) — blaOXA-24-like, 25% — blaOXA-23-like, 100% — blaOXA-51-like, ompA, adeR. 50% of K. pneumonia strains (n=2) had blaTEM and blaCTX-M, 100% — blaSHV, ompK36. MRSA PVL- isolates (n=10), belong to the ST239;spat037;SCCmecIIIA;tst variant, had the aacA-aphD, aadD resistance genes; ermA; tetM; cat (plasmid 2.5 kb); mutations were revealed in GyrA-Ser84Leu and GrlA-Ser80Phe, as well as in rpoB-His481Asn, Ile527Met.
CONCLUSION
The distribution of P. aeruginosa, A. baumannii and K. pneumoniae strains with carbapenemases and other mechanisms among burns patients was presented. MRSA strains are due to the presence of mutations in chromosomal genes and had resistance genes.