Abstract
Ciprofloxacin resistant Shigella sonnei across the globe have been increasing alarmingly. In order to understand the emergence of S.sonnei with respect to ciprofloxacin resistance in our patient population, the following study was carried out. Of the 184 Shigella sp. Isolated from 2012 to 2015, 34 S.sonnei which were confirmed by standard methods and subjected to antimicrobial susceptibility testing were selected. The minimum inhibitory concentrations (MICs) of 16/34 quinolone resistant isolates tested ranged from 4micrograms/ml to 16micrograms/ml for ciprofloxacin, from 16 micrograms/ml to 64 micrograms/ml for ofloxacin and from 16micrograms/ml to 64micrograms/ml for levofloxacin. Sequence determination of the quinolone resistance determining regions of gyrA, gyrB, parC, and parE genes showed mutations in GyrA at Gln69/Trp, Phe71/Ser, Ser72/Pro, Met75/Leu, Ser90/Cys, Met94/Leu, His106/Pro, Asn161/His, Thr163/Ala and in ParC at Ala64/Asp. Among the plasmid-mediated quinolone resistance (PMQRs) targets investigated,qnrB was the most (93.7%) prevalent followed by qnrC (18.7%). None hadqnrA, qnrS and qepA. Two (0.1%) of the isolates harboured theaac(6’)-lb gene. Drug accumulation assay detected the presence of efflux pump activity in 9/15 (60%) among ciprofloxacin resistant isolates. All isolates harboured the ipaH gene followed by ial (17.6%), sen (11.7%), set1A&set1B (5.8%) genes. None had stx1 element. PCR for Enterobacterial repetitive intergenic consensus (ERIC) sequences resulted in 4 unique clusters, of which Type III was the most (44%) dominant but there was no correlation between the ERIC types and the antibiotic resistance pattern or the virulence profile. A documented increase in S.sonnei harbouring the qnrgenes and some unusual genes like set1Aand indicate an ongoing process of horizontal gene transfer. The accumulation of novel mutations in GyrA and ParC in the presence of efflux pump and PMQR genes contributed to the raised MIC to quinolones. These findings are crucial in our understanding of quinolone resistance in these isolates.
Highlights
Shigellosis is very contagious and can spread through communities at a fast rate posing a health threat globally
Among the plasmid-mediated quinolone resistance (PMQRs) targets investigated,qnrB was the most (93.7%) prevalent followed by qnrC (18.7%)
Resistance to quinolones is mediated by mutations in the chromosomal genes called the quinolone resistance determining regions (QRDRs) of DNA gyrases namely, gyrA and gyrB and the Type IV topoisomerases namely, parC and parE or the presence of plasmid genes called the plasmid mediated quinolone resistance regions (PMQRs) namely the qnr (qnrA, qnrB, qnrC, qnrD, qnrS, qep, aac(6’)lb-cr) genes
Summary
Shigellosis is very contagious and can spread through communities at a fast rate posing a health threat globally. Shigellosis can be caused by any of the known serogroups of Shigella. Though S.sonnei has been attributed to cause disease mostly in developed countries the current scenario speaks otherwise as it is marked by spread of this agent due to travel to endemic places. Several reports from the Indian subcontinent and south-east Asian countries have revealed a changing scenario regarding the shift in serogroups of Shigella. The emergence of ciprofloxacin resistance has been reported since 2002 with the clonal spread of a ciprofloxacin resistant S.dysenteriae serotype 1 from Kolkata to other places followed by S.flexneri 2a and S.flexneri 3a in 2004 and in S.sonnei in 2007 [2]. There are increasing reports regarding ciprofloxacin resistant Shigella across the globe which can be attributed to increased frequency in international travels, low infective dose and ease of accepting antibiotic resistance genes by horizontal gene transmission [5]
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