Genomic, Antimicrobial Resistance, and Public Health Insights into Enterococcus spp. from Australian Chickens.

Mark O’Dea,Anthony Pavic,Rebecca Abraham,Geoffrey W Coombs,Shafi Sahibzada,Tanya Laird,Kylie Hewson,Stanley Pang,Taha Harris,Sam Abraham,Terence Lee,David Jordan,Brad Fenwick

doi:10.1128/jcm.00319-19

Abstract

Due to Australia's management of antimicrobial use in poultry, particularly the discontinued use of avoparcin for nearly 20 years, it is hypothesized that vancomycin-resistant enterococci associated with human disease are not derived from poultry isolates. This study evaluated antimicrobial resistance (AMR) of five enterococcal species isolated from Australian meat chickens, genomic features of Enterococcus faecium and Enterococcus faecalis, and the phylogenetic relationship of the poultry-derived E. faecium with isolates from human sepsis cases. All enterococcal isolates from chicken ceca were subjected to antimicrobial susceptibility testing. E. faecium and E. faecalis underwent whole-genome sequencing. E. faecium was compared at the core genome level to a collection of human isolates (n = 677) obtained from cases of sepsis over a 2-year period spanning 2015 to 2016. Overall, 205 enterococci were isolated consisting of five different species. E. faecium was the most frequently isolated species (37.6%), followed by E. durans (29.7%), E. faecalis (20%), E. hirae (12.2%), and E. gallinarum (0.5%). All isolates were susceptible to vancomycin and gentamicin, while one isolate was linezolid resistant (MIC 16 mg/liter). Core genome analysis of the E. faecium demonstrated two clades consisting predominantly of human or chicken isolates in each clade, with minimal overlap. Principal component analysis for total gene content revealed three clusters comprised of vanA-positive, vanB-positive, and both vanA- and vanB-negative E. faecium populations. The results of this study provide strong evidence that Australian chicken E. faecium isolates are unlikely to be precursor strains to the currently circulating vancomycin-resistant strains being isolated in Australian hospitals.

Highlights

Due to Australia’s management of antimicrobial use in poultry, the discontinued use of avoparcin for nearly 20 years, it is hypothesized that vancomycin-resistant enterococci associated with human disease are not derived from poultry isolates
Despite studies demonstrating transmission pathways for hospital associated vancomycin-resistant E. faecium (VREfm) clones such as ST203, ST796, and ST80 [5], the poultry industry has been examined as a source of antimicrobial-resistant enterococci causing disease in humans, owing to the pervasiveness of chicken meat in the diet of humans, and the widely documented use of antimicrobials within the poultry production cycle
Using whole-genome sequencing, we investigated the evolution and genetic traits of a collection of Australian isolates of E. faecium obtained from cases of sepsis in humans to understand whether E. faecium originating in chicken was a possible cause

Summary

Introduction

Due to Australia’s management of antimicrobial use in poultry, the discontinued use of avoparcin for nearly 20 years, it is hypothesized that vancomycin-resistant enterococci associated with human disease are not derived from poultry isolates. A characteristic of enterococci that allows them to readily transfer between hosts is their enhanced ability to survive conditions outside hosts that would be fatal to most other vegetative bacteria [1] Certain species, such as Enterococcus faecalis and E. faecium, are a prominent cause of opportunistic infections in humans causing disease that ranges in severity from mild to fatal [2]. Despite studies demonstrating transmission pathways for hospital associated VREfm clones such as ST203, ST796, and ST80 [5], the poultry industry has been examined as a source of antimicrobial-resistant enterococci causing disease in humans, owing to the pervasiveness of chicken meat in the diet of humans, and the widely documented use of antimicrobials within the poultry production cycle. Previous studies have shown transposons containing vancomycin-resistant genes were the likely cause of VREfm identified in poultry farmers and abattoir workers in the Netherlands [15], and the vanA gene can be transferred from poultry enterococci to human enterococci in vivo [16]

Methods

Results

Conclusion