# Antibiotic susceptibility and resistance genes in Escherichia coli from broilers reared in a low-antibiotic-use production system

**Authors:** Homayoon Davam, Désirée S. Jansson, Emma Nord, Jesper Rydén, Ingrid Hansson

PMC · DOI: 10.1016/j.psj.2026.106764 · 2026-03-12

## TL;DR

This study examines antibiotic resistance in Escherichia coli from broiler chickens in a low-antibiotic-use system, finding higher resistance in non-disease-related isolates.

## Contribution

The study reveals that non-clinical E. coli isolates may act as reservoirs for antibiotic resistance genes in low-antibiotic-use systems.

## Key findings

- Non-clinical E. coli isolates showed higher resistance rates to certain antibiotics compared to clinical isolates.
- Resistance in non-clinical isolates was strongly correlated with the presence of known AMR genes or mutations.
- Factors like horizontal gene transfer and environmental contamination may contribute to AMR dissemination in low-antibiotic systems.

## Abstract

Antimicrobial resistance (AMR) is a major global concern for animal and human health. This study investigated the occurrence and patterns of AMR in Escherichia coli (E. coli) isolated from Swedish broiler flocks reared under low-antibiotic-use conditions. During routine necropsy examinations of 80 broilers from 40 flocks with increased mortality associated with colibacillosis, liver samples were collected for bacteriological analysis. E. coli isolated from the liver were classified as clinical E. coli. In addition, boot sock samples were taken to collect feces from the litter of 60 broiler flocks with no signs of disease or increased mortality. E. coli isolates (n = 109) obtained from boot sock samples were classified as non-clinical E. coli. Susceptibility to 15 antibiotics was assessed using broth microdilution, and resistance-associated genes and mutations were identified through whole-genome sequencing (WGS). Overall resistance was low, with all isolates susceptible to 9 of the 15 tested antibiotics: meropenem, azithromycin, amikacin, gentamicin, tigecycline, ceftazidime, cefotaxime, chloramphenicol, and colistin. Resistance was significantly more frequent in non-clinical than clinical isolates for the six antibiotics with detected resistance (P < 0.05) and was strongly correlated with the presence of known AMR genes or mutations. Among clinical isolates, 93.7% were fully susceptible to all tested antibiotics, compared with 49.5% of non-clinical isolates. The highest resistance rates were observed in non-clinical isolates against ampicillin (34%), sulfamethoxazole (32.1%), and trimethoprim (28.4%). The results of this study indicate that in low-antibiotic-use production systems, factors beyond direct antibiotic use—such as horizontal gene transfer, vertical transmission, and environmental contamination—may contribute to AMR dissemination. Higher AMR rates in non-clinical isolates suggest that these isolates may serve as reservoirs of resistance genes. This highlights the importance of monitoring commensal E. coli and farm environments to support AMR mitigation and sustainable broiler production.

## Linked entities

- **Chemicals:** meropenem (PubChem CID 441130), azithromycin (PubChem CID 447043), amikacin (PubChem CID 37768), gentamicin (PubChem CID 3467), tigecycline (PubChem CID 54686904), ceftazidime (PubChem CID 5481173), cefotaxime (PubChem CID 5742673), chloramphenicol (PubChem CID 5959), colistin (PubChem CID 5311054), ampicillin (PubChem CID 6249), sulfamethoxazole (PubChem CID 5329), trimethoprim (PubChem CID 5578)
- **Diseases:** colibacillosis (MONDO:0020920)
- **Species:** Escherichia coli (taxon 562), Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** ESBL [NCBI Gene 13906541], dfrA1 [NCBI Gene 10549022], aph [NCBI Gene 4364198], aadA1 [NCBI Gene 13906545], tet(A) [NCBI Gene 15152827], BlaTEM-1 [NCBI Gene 9537966], sul2 [NCBI Gene 7324562]
- **Diseases:** AMR (MESH:D060467), bacterial infections (MESH:D001424), infection (MESH:D007239), MDR (MESH:D018088), necrotic enteritis (MESH:D004751)
- **Chemicals:** ceftazidime (MESH:D002442), quinolone (MESH:D015363), glycerol (MESH:D005990), carbapenem (MESH:D015780), beta-lactam (MESH:D047090), ampicillin (MESH:D000667), cefotaxime (MESH:D002439), phenoxymethylpenicillin (MESH:D010404), trimethoprim (MESH:D014295), nalidixic acid (MESH:D009268), chloramphenicol (MESH:D002701), azithromycin (MESH:D017963), amikacin (MESH:D000583), streptomycin (MESH:D013307), BPW (-), meropenem (MESH:D000077731), gentamicin (MESH:D005839), trimethoprim-sulfamethoxazole (MESH:D015662), tigecycline (MESH:D000078304), tetracycline (MESH:D013752), aminoglycoside (MESH:D000617), sulfamethoxazole (MESH:D013420), Ciprofloxacin (MESH:D002939), sulfonamide (MESH:D013449), cephalosporin (MESH:D002511)
- **Species:** Gallus gallus (bantam, species) [taxon 9031], Homo sapiens (human, species) [taxon 9606], Enterobacterales (order) [taxon 91347], Escherichia coli (E. coli, species) [taxon 562], Campylobacter (genus) [taxon 194]
- **Mutations:** S83L, C for 18-24, p.I355T, p.S57T
- **Cell lines:** ATCC 25922 — Homo sapiens (Human), Lung adenocarcinoma, Cancer cell line (CVCL_0023)

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Source: https://tomesphere.com/paper/PMC13018936