Resistance patterns and integron cassette arrays of Enterobacter cloacae complex strains of human origin.

The aim of this research was to analyse the resistance patterns and characterize the distribution and genetic content of resistance integrons within Enterobacter cloacae complex strains originating from hospitalized patients. The strains were included in the E. cloacae complex study following sequence analysis of the hsp60 gene. The determination of resistance towards eight classes of antimicrobials was followed by PCR detection of integrons and analyses of the size and sequences of their variable parts. The majority of 69 clinical strains of the E. cloacae complex were identified as Enterobacter hormaechei. They were isolated from a variety of samples, including urine, wounds, blood and stools. The remaining isolates belonged to E. cloacae clusters III and IV, E. cloacae subsp. cloacae and Enterobacter kobei. Fifty-two isolates (75.4 %) were resistant to more than three unrelated antibiotics. The resistance for each antibiotic, except imipenem, was significantly associated with the presence of integrons. Class 1 integrons were detected in 55 % of isolates: 63.3 % of 'E. hormaechei subsp. steigerwaltii', 50 % of E. cloacae cluster III, 40 % of 'E. hormaechei subsp. oharae', 33 % belonging to E. cloacae cluster IV and 20 % of 'E. hormaechei subsp. hormaechei' were intI1-positive. All of the integrons were located on transferable genetic elements. The transferred resistance primarily included that to aminoglycosides, ticarcillin, piperacillin, sulfamethoxazole, trimethoprim and tetracycline. Sequence analysis of the variable regions of integrons identified two groups of genes: those encoding aminoglycoside adenylotransferases responsible for resistance to aminoglycosides, and dfr cassettes conferring resistance to trimethoprim. Integrons of the E. cloacae complex showed limited variability of genes encoding resistance to therapeutics and were stable in structure with the following cassette arrays: dfrA12-orfF-aadA2, aadB-aadA2, dfrA1-aadA1 and aacA4-aadA1. Hospital-dependent differences in type and arrays of gene cassettes were observed, which seemed to be conserved and not liable to changes.