This is our Friday rubric: every week a new Science Page from the Bob Morrison’s Swine Health Monitoring Project. The previous editions of the science page are available on our website.
This week we are sharing a report from Dr. Shivdeep Singh Hayer from the STEMMA lab, on the emerging enrofloxacin and ceftiofur resistance in E.coli in swine.
- Nearly one-third of clinical E. coli isolates collected from swine samples were ceftiofur or enrofloxacin resistant
- Genetic analysis revealed presence of rarely reported genes in antimicrobial resistant isolates
- Most of the isolates were multi-drug resistant on both routine lab tests and genetic analysis
In a previous study, we analyzed the antimicrobial resistance in Escherichia coli isolates recovered from swine clinical samples from across USA during 2006-2016 at the University of Minnesota Veterinary Diagnostic Laboratory (UMN-VDL), and found a 47% annual increase in the prevalence of enrofloxacin resistance (from 1.5% in 2006 to 32% in 2016) while no trend was observed for the resistance to ceftiofur (that ranged between 32-39%). A follow-up study was conducted to evaluate the genetic basis of resistance against enrofloxacin and ceftiofur in E. coli isolates using whole genome sequencing (WGS).
153 swine clinical E. coli isolates collected in 2014-15 from 14 states across USA were selected and genes causing ceftiofur and enrofloxacin resistance were identified using WGS.
21 (out of 106) enrofloxacin-resistant isolates from 6 states harbored diverse plasmid mediated quinolone resistance (PMQR) genes (qnrB19, qnrB2, qnrS1, qnrS2 and qnrS15). The presence of PMQR genes alone was associated with clinical levels of resistance.
The most prevalent genes associated with ceftiofur resistance were blaCMY-2 (89/106, 84%). Moreover, 24 ceftiofur-resistant isolates harbored various blaCTX-M and blaSHV genes.
Additionally, bacteria carrying blaCTX-M and qnr genes also contained genes coding for resistance mechanisms against other antimicrobial classes and were commonly resistant against ampicillin, tetracyclines, gentamycin, trimethoprim and sulfonamides.
These genes (blaCTX-M, qnr) have been rarely reported from farm animals in USA and have been implicated as important genetic mechanisms behind extended spectrum cephalosporin and fluoroquinolone resistance in human and animal populations in several countries. These genes are present on plasmids, making their dissemination across bacterial populations faster by horizontal transfer.
The presence of multiple antimicrobial resistance genes on the same plasmids also makes mitigation of this problem more difficult because of the possibility that using one antimicrobial class will exert positive selection pressure for resistance against other antimicrobial classes.