Life sciences · Journal article

Virulence and Antimicrobial Resistance in Campylobacter jejuni and Campylobacter coli

Antibiotics · August 26, 2026

Hypothesis-Generating Why this matters to you Expert discussion

Raises a question worth testing. It does not answer one.

AI Summary

This is a narrative review of virulence and antimicrobial resistance mechanisms in Campylobacter jejuni and C. coli, integrating gene-carriage surveys, strain variation, and resistance-fitness relationships. The authors conclude that available data do not establish that antimicrobial resistance generally predicts more severe human disease, despite documented alterations in colonization or competitive fitness for specific mutations (gyrA Thr-86-Ile and CmeABC).

What was studied

Narrative review. Campylobacter jejuni and Campylobacter coli; human campylobacteriosis cases in the context of One Health reservoirs (animal, food, environmental)..

Key findings

Motility and adhesion have the most reproducible support during colonization and epithelial contact Biofilm formation, quorum sensing, and T6SS-associated phenotypes vary substantially across strains and models gyrA Thr-86-Ile and CmeABC can alter colonization or competitive fitness, but available data do not show that resistance generally predicts more severe human disease

Safety

Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.

Who this may help

Clinicians should recognize that antimicrobial resistance in Campylobacter does not necessarily correlate with increased disease severity in humans. Surveillance and intervention priorities should be reassessed in light of the documented fitness-resistance trade-offs and ecological distribution rather than assuming resistance-virulence coupling.

Plain-language summary

A narrative review synthesizing existing knowledge on virulence mechanisms and resistance pathways in Campylobacter species; raises questions about resistance-fitness relationships but does not present new empirical evidence or a definitive causal link to human disease severity.

Study design

As stated by the source record.

MethodsNarrative review

Clinical bottom line

Caveats

No new empirical data or clinical trials presented; conclusions depend on synthesis of existing literature
Authors explicitly note that for C. coli, gene-carriage surveys often substitute for functional evidence, introducing proxy measurement uncertainty
No quantitative meta-analysis or systematic review methodology employed; consistency of findings across studies not formally assessed
Human disease severity outcome data not reported; conclusions about resistance-disease severity are stated as negative findings ('data do not show') rather than from direct measurement

Evidence assessment

Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.

Study design

insufficient

Narrative review; no primary data collection or experimental design reported.

Directness

limited

Discusses virulence factors and resistance mechanisms; connection to clinical human outcomes is indirect and acknowledged as uncertain.

Consistency

moderate

Acknowledges substantial variation in biofilm, quorum sensing, and T6SS phenotypes across strains and models.

Risk of bias

insufficient

Narrative review; no formal bias assessment or quality appraisal methodology described.

Sample adequacy

insufficient

Review synthesizes literature; no primary sample size or population defined.

What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.

Source abstract

Campylobacter jejuni and Campylobacter coli account for most recognized cases of human campylobacteriosis. For C. coli, gene-carriage surveys often stand in for direct tests of function; this distinction is maintained throughout the review. Virulence is discussed as a sequence of events rather than as a catalogue of factors. Motility and adhesion have the most reproducible support during colonization and epithelial contact, whereas biofilm formation, quorum sensing, and T6SS-associated phenotypes vary substantially across strains and models. We then consider host–cell injury, persistence, transmission, and the uncommon post-infectious outcomes linked to sialylated LOS. Antimicrobial resistance is treated in parallel, with emphasis on target-site change, ribosomal protection or methylation, enzymatic inactivation, and CmeABC-mediated efflux. The One Health model places both species within overlapping animal, food, and environmental reservoirs rather than assigning C. jejuni exclusively to poultry or C. coli to swine. A narrower conclusion emerges from the resistance-fitness literature: gyrA Thr-86-Ile and CmeABC can alter colonization or competitive fitness, but the available data do not show that resistance generally predicts more severe human disease. This distinction frames the proposed priorities for surveillance and intervention.

Follow from this

Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.

Hyokeun SongJinkyung LeeMinchae Kang