Spread of the qnrVC Quinolone Resistance Determinant in Vibrio cholerae

Abstract

We read with great interest the recently published paper by Kim et al. (3) that reported a new qnr gene cassette, qnrVC3, inserted in the mobile integrative conjugative element SXT, found in Vibrio cholerae. qnrVC3 presented 99% identity to the first described qnr gene cassette (qnrVC1) found in a V. cholerae strain (VC627) from Brazil, reported by us (2). After publication of the qnrVC3 sequence, we verified that the submitted qnrVC1 sequence, in fact, did not contain the mismatches that raised the amino acid changes compared to the qnrVC3 sequence. We immediately performed an update, and the real sequence is under the same GenBank accession number, EU436855. Therefore, we concluded that qnrVC1 and qnrVC3 are identical since they share 100% identity at the amino acid level and presented only a unique synonymous mutation in the nucleotide sequence. Moreover, taking into account that a gene cassette is characterized by a particular attC site (4), the presence of the same attC site, which is a V. cholerae repeat (VCR)-like site from superintegrons, together with the same 5Ј untranscribed region (5ЈUTR) (including the putative promoter) (2), confirmed that qnrVC1 and qnrVC3 are in fact the same gene cassette.The genetic contexts of qnrVC tissue (2, 3) indicate the dynamics of mobilization and the evolution of this gene cassette. First, it was found in a typical class 1 integron (2). Kim et al. (3) verified this cassette in an integrated conjugative element (ICE) embedded in the chromosome. Comparing the two results, it can be concluded that this high mobility increases the chance of qnrVC spread, not only among V. cholerae strains. These results together also support the functionality of the attC sites in being recognized by IntI1, present in the genetic context of both qnrVC1 and qnrVC3 (2, 3), since this enzyme efficiently catalyzes attI ϫ VCR recombination (1).In conclusion, the results presented by Kim et al. reinforced the importance of qnrVC as a quinolone resistance determinant and its mobilization ability resulting in the spread of this resistance trait with such an impact on public health. This study was supported by FAPERJ and CNPq fellowships.

Genetic and Phenotypic Virulence Potential of Non-O1/Non-O139 Vibrio cholerae Isolated from German Retail Seafood

“…Antibiotic resistance could be simultaneously shown against three antibiotic classes (beta-lactams, for example, penicillin, cephalosporin, and carbapenem; polymyxins; and sulfonamides) for five seafood-associated NOVC (16-VB00021, 16-VB00024, 16-VB00025, 17-VB00441, and 19-VB00051). Relevant gene distribution could explain some results from antibiotic in vitro assays, including blaCARB presence and AMP resistance [73,74], almG presence and COL resistance [75], qnrVCs presence and quinolone (CIP and NAL) resistance [76], varG and IMIPEN resistance [77], and dfrA31 presence and TMP resistance [78]. However, AST result cannot be fully explained by genetic information: the COL resistance rate is 87%, while all NOVC strains used in this study contain almG; blaCARB was not found in the three AMP resistant strains; and all catB9 harboring strains have no in vitro resistance to CHL.…”