Colistin Resistance Mediated by mcr-1 in ESBL-Producing, Multidrug Resistant Salmonella Infantis in Broiler Chicken Industry, Italy (2016-2017)

Abstract

Colistin-resistance mediated by mobilisable and plasmid-borne mcr genes has emerged worldwide, threatening the efficacy of colistin, a last resort antibiotic increasingly used for treating human invasive infections by multidrug-resistant or extensively drug-resistant Enterobacteriaceae. In this study, we report the first evidence of mcr-1-mediated colistin resistance in four multidrug resistant (MDR) out of 324 Salmonella infantis from the Italian antimicrobial resistance (AMR) monitoring (2001-2017) in broilers and broiler meat. Two were also Extended Spectrum Beta-Lactamases (ESBL)-producing isolates. Characterization by whole genome sequencing (WGS), located mcr-1.1 on an incX4 plasmid. Phylogenetic analysis of these isolates with selected Italian S. Infantis previously isolated from animals, meat and human clinical cases with unknown epidemiological relationship, demonstrated that ESBL-producing, mcr-1-positive isolates belonged to the emerging pESI-like-positive-ESBL-producing clone described in Italy in 2015.

Keywords: ESBL (Extended Spectrum Beta-Lactamases); Salmonella Infantis; broiler meat; broilers; colistin resistance; mcr genes; plasmids; whole genome sequencing.

Figure 1

Single-nucleotide polymorphism (SNP)-based phylogeny of 16 selected ESC-resistant, ESBL-producing, and ESC-susceptible Salmonella Infantis mainly from broiler chicken, broiler meat, and humans in Italy (2006–2017). Colors of the isolate ID indicate the sample host: red: human; purple: broiler meat; blue: broiler chicken; pink: pig; green: guinea fowl. Full purple dot: presence of the mutation D87G in the gyrA gene; empty purple dot: presence of the mutation S83Y in the gyrA gene. Full green dot: presence of bla_CTX−M−1 ESBL gene; Empty green dot: presence of bla_CTX−M−65 ESBL gene. Full light blue dot: presence of mcr-1.1. Numbers in the figure indicate the number of SNPs difference between two isolates or between clusters. Two clusters were identified based on the number of SNPs: Cluster A, with a difference of 1-18 SNPs between the isolates, and Cluster B with a difference of 7 SNPs between the isolates. Isolates of Cluster A and Cluster B differed at least by 42 SNPs. Details of the 16 isolates are indicated in the Supplementary Table 1.