Beta-lactam and quinolone resistance markers in uropathogenic strains isolated from renal transplant recipients

Abstract

Our objectives were to investigate the extended-spectrum beta-lactamases (ESBLs) and carbapenemases (CR) genetic determinants and to assess the association between ESBL production and quinolone resistance in bacterial strains isolated from renal transplant recipients with urinary tract infections. Material and methods: A number of 30 isolates were recovered from urine specimens of patients with renal transplant from October 2015 to March 2016. The isolates were analyzed for ESBL production using double disc synergy test and for CR production by the Hodge test. Phenotypically confirmed isolates were screened by PCR for the identification of ESBL, CR and fluoroquinolone resistance genes. Results: The 30 clinical bacterial strains isolated from urinary tract infections in renal transplant recipients were identified as Klebsiella pneumoniae (17), Pseudomonas aeruginosa (7), Morganella morganii (2), Escherichia coli (2), Edwardsiella tarda (1) and Enterobacter cloacae (1). Out of them, 22 isolates were ESBL producers and 20 multi-drug resistant (MDR) (i.e., 13 K. pneumoniae and 7 P. aeruginosa strains). More than half of the ESBL clinical strains (14/22, 63.63%) revealed at least one ESBL gene, the most frequent being blaCTX-M type (18/22, 81.81%), either alone (4/22, 18.18%) or in combination with another ESBL gene (17/22, 77.27%), followed by blaTEM (13/22, 59.09%). The blaOXA-48 was present in 10 isolates (33.33%). The most frequent association of ESBLs and CR genes (5/14, 35.71%) was revealed by blaCTX-M- blaTEM - blaOXA-48, encountered particularly among K. pneumoniae isolates (4/17, 23.52%). The qnrB gene was identified in five strains, i.e. one P. aeruginosa ESBL isolate (expressing the blaCTX-M gene) and four K. pneumoniae ESBL isolates (harboring the blaCTX-M - blaTEM genes combination). Conclusions: The uropathogenic strains isolated from renal transplant recipients exhibited high rates of MDR and beta-lactam resistance. The selective pressure exerted by quinolones could enable uropathogenic bacteria to acquire resistance to this class of antibiotics.