Introduction: The non-fermenters of clinical significance Acinetobacter baumannii and Pseudomonas aeruginosa, usually considered as opportunistic pathogens, nowadays emerge to evolve in some of the most problematic causative agents of infections. The therapeutic restrictions are determined on one hand due to their intrinsic resistance to a great variety of antibiotics and on the other, due to the arising acquired resistance.
Aim: The aim of this article is to analyze the most often detected mechanisms of carbapenem resistance among non-fermenters in the country and to recommend options to manage the therapeutic restrictions.
Methods: Both methods - phenotypic and genetic, are usually combined to evaluate the mechanisms of resistance to carbapenems. As phenotypic tests for detection of common carbapenemases a Modified Hodge test and a Carba NP-test are used. A classical PCR investigation is used to detect the most frequent carbapenemases for both microorganisms and a qRT-PCR to assess the expression of main efflux pumps, the intrinsic AmpC and the transmembrane receptor OprD in Pseudomonas.
Results and Discussion: Two independent studies proved that in Bulgarian clinical isolates P. aeruginosa, the increased expression or overexpression of MexXY-OprM efflux pump, is the main mechanism of determining carbapenem resistance. The main reason for carbapenem resistance in A. baumannii isolates is the production of OXA-23 carbapenemases. The newest therapeutic strategies include the use of sulbactam for infections provoked by OXA-23 producing A.baumannii due to the lack of activity of these carbapenemases against it and the intrinsic effect of this beta-lactamase inhibitor against Acinetobacter spp. Antibiotic schemes including colistin, rifampicin and phosphomycin could be an appropriate alternative for infections provoked by both Pseudomonas and Acinetobacter.
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