Plasmid-Mediated QnrS2 Determinant from a Clinical Aeromonas veronii Isolate

Abstract

ᰔThe main objective of this study was to determine the prevalence of the Qnr determinants in clinical and environmental Aeromonas spp. A total of 52 Aeromonas sp. isolates identified by biochemical methods (5), 25 isolated from natural waters (1) and 27 isolated from clinical samples from hospitals in Valencia, Spain, were tested for quinolone resistance by the disk diffusion method (4) (nalidixic acid, 30 g; oxolinic acid, 2 g; flumequine, 30 g; ciprofloxacin, 5 g; and levofloxacin, 5 g). Among the studied isolates, 27 showed resistance to nalidixic acid and susceptibility to ciprofloxacin, 24 isolates were susceptible to both nalidixic acid and ciprofloxacin, and only 1, the A. veronii A272 clinical isolate, was resistant to both nalidixic acid and ciprofloxacin. The isolates resistant to nalidixic acid were also resistant to oxolinic acid and flumequine. Moreover, A. veronii A272 was the only one resistant to levofloxacin. Screening of the qnrA, qnrB, and qnrS genes was performed by multiplex PCR using a set of specific primers for all isolates. Bacterial strains positive for each qnr gene were used as positive controls (Klebsiella pneumoniae UAB1 for qnrA, Escherichia coli J53 pMG252 for qnrB, and E. coli J53 pMG298 for qnrS) and were run in each batch of tested samples. Only an A. veronii clinical isolate (A. veronii A272) presented a qnr gene, which showed 100% homology with the qnrS2 gene previously reported in an isolate from the bacterial community of a wastewater treatment plant in Germany (2) and in a non-Typhi Salmonella clinical isolate in the United States (6).The qnrS2-carrying strain was identified as A. veronii by sequencing of the 16S rRNA gene (10). The MICs for nalidixic acid, ciprofloxacin, and norfloxacin were determined using the Etest method (AB Biodisk, Solna, Sweden). CLSI breakpoints were used to define susceptibility (4). The MICs showed by this strain were Ͼ256 mg/liter, 8 mg/liter, and 12 mg/liter to nalidixic acid, ciprofloxacin, and norfloxacin, respectively (Table 1). PCR amplification of the quinolone resistance-determining regions of the gyrA and parC genes was performed with primers previously described (7). A. veronii CECT 4260 and CECT 4258 strains, susceptible to quinolones, were included. The nucleotide and deduced protein sequences were analyzed with

The GenusAeromonas: Taxonomy, Pathogenicity, and Infection

“…Quinolone resistance has also been associated with the plasmid-mediated 218-amino-acid QnrA protein. Two reports have detected QnrS determinants (41% to 60% amino acid identity with QnrA) in two environmental isolates of A. media and A. caviae and in one clinical isolate of A. veronii (30,256). In the latter instance, the A. veronii strain was resistant not only to nalidixic acid but also to ciprofloxacin and levofloxacin.…”

Plasmid-Mediated Quinolone Resistance; Interactions between Human, Animal, and Environmental Ecologies

“…isolates, respectively (Ahmed et al, 2007; Cattoir et al, 2008b; Sanchez-Cespedes et al, 2008). Interestingly, qnrS and mostly qnrB genes were identified from zoo animals, mostly including reptiles (Ahmed et al, 2007).…”

Prevalence of Plasmid-Mediated Quinolone Resistance Determinants over a 9-Year Period

“…Since then, four major groups of qnr determinants, qnrA, qnrB, qnrC, and qnrS, have been identified (7,29), and two additional plasmid-mediated quinolone resistance (PMQR) genes have been describedaac(6Ј)-Ib-cr, which encodes a variant aminoglycoside acetyltransferase that modifies ciprofloxacin (21), and qepA, which encodes an efflux pump belonging to the major facilitator subfamily (19,32). These PMQR determinants are increasingly being identified worldwide in clinical isolates of Enterobacteriaceae (4,11,17,22,23,27) and in clinical and environmental Aeromonas species isolates (1,26).…”