Resistant Campylobacter clones spread between nearby Finnish broiler farms rather than passing down from breeder flocks

Transient surges of fluoroquinolone-resistant Campylobacter jejuni in Finnish broiler production were driven mainly by the regional, clonal spread of successful resistant lineages between geographically proximate farms, not by vertical transmission from breeder flocks to their broiler descendants. That is the central conclusion of a genomic surveillance study published in Acta Veterinaria Scandinavica, in which researchers at the Finnish Food Authority and collaborators sequenced 333 C. jejuni isolates collected from breeder and broiler flocks at slaughter between 2014 and 2019. The finding matters because poultry is a leading reservoir of this zoonotic foodborne pathogen, and understanding how resistance emerges in a production system that uses almost no antibiotics offers rare insight into how resistant strains persist and move even without drug pressure.

Finland provided an unusually clean setting for the question. Antimicrobial use in Finnish broiler production is minimal: broiler flocks had not been medicated with antibiotics since 2010, and quinolones have not been used anywhere in the broiler production chain since 2007 and, as far as the industry records show, not before then either. Yet national monitoring recorded episodic peaks of resistance in broiler isolates during the study window, with the highest rates in 2014 at 25.0 percent against ciprofloxacin and 17.0 percent against tetracycline. Resistance appeared in 2014, 2016, 2018, and 2019, with little or none detected in 2015 and 2017. Breeders were treated more often, with antibiotics used on between 2.7 and 20.2 percent of breeder flocks annually, mostly penicillin but also amoxicillin, oxytetracycline, and sulfamethoxazole–trimethoprim, which made the breeder route a plausible hypothesis worth testing.

The team assembled a dataset of 145 breeder and 188 broiler isolates, covering all campylobacter-positive breeder flocks over the period and a strategically selected 34 to 74 percent of positive broiler flocks each year, with resistant isolates deliberately over-sampled to maximize the chance of pairing resistant and susceptible strains of the same genotype. Every isolate was sequenced with Illumina technology and characterized by multilocus sequence typing, an ad hoc core-genome MLST schema of 1,292 loci, resistance-gene prediction against the ResFinder and PointFinder databases, and maximum-likelihood phylogenomics. The collection revealed 15 clonal complexes and 95 sequence types, with ST-45 dominating both flock types: 51.0 percent of breeder and 43.6 percent of broiler isolates belonged to ST-45 clonal complex, and ST-45 itself was the single most common sequence type throughout.

Resistance was strikingly lineage-associated. Among ST-206 clonal complex isolates, 94.3 percent carried a quinolone-resistance genotype and 40.0 percent carried tetracycline resistance, whereas only 3.2 percent of ST-45 clonal complex isolates were quinolone-resistant and all were tetracycline-susceptible. More than half of ST-21 clonal complex isolates, 52.9 percent, were quinolone-resistant but tetracycline-susceptible. The genetic determinants tracked phenotypic resistance closely in broiler isolates, with sensitivities of 96.0 to 100.0 percent and specificities of 99.4 to 100.0 percent for the tested drugs. Nearly all quinolone-resistant isolates carried the classic gyrA T86I mutation, although five broiler ST-45 isolates carried the less common T86A change, which conferred nalidixic acid resistance but not ciprofloxacin resistance, a nuance the authors note can be missed if resistance is inferred from standard databases alone.

Core-genome MLST identified 54 clusters of two to fourteen isolates differing by at most 11 alleles, and seven of these clusters were resistant. The spatial pattern was decisive. The largest resistant cluster comprised 14 broiler isolates of ST-2104, sampled mainly in July and August 2018, from six farms all located within 38 kilometres of one another in the Ostrobothnia region. The second largest contained 14 isolates of ST-122, mostly from broilers, sampled across late 2014, 2015, and early 2016, from 13 farms within 55 kilometres, again in Ostrobothnia. Some of the same farms appeared in multiple resistant clusters over consecutive years, and the distance between farms in resistant clusters of ST-206 and ST-21 clonal complex was typically 55 kilometres or less. By contrast, clusters of the susceptible ST-45 clonal complex sometimes spanned up to 243 kilometres, hinting that different genotypes may travel by different environmental routes.

The vertical transmission hypothesis fared poorly. Thirteen breeder isolates shared a sequence type with an epidemiologically linked isolate from a descendant broiler flock, but twelve of the thirteen were ST-45 and genotypically susceptible to quinolones and tetracycline. Although several breeder isolates belonged to core-genome clusters, none of those clusters contained a breeder isolate together with its epidemiologically associated broiler isolate, which directly contradicts the possibility of resistant strains passing from parent stock through the egg. Almost all quinolone-resistant breeder isolates, four of five, instead fell into two resistant clusters that also contained broiler isolates, while most tetracycline-resistant breeder isolates were sporadic findings outside any cluster. The authors also note that Finnish breeder isolates appeared to represent mainly local populations rather than imported lineages, since Finnish C. jejuni populations in 2014 were previously shown to be genetically distinct from those circulating in other European countries, even as the country switched from importing grandparent flocks to importing parent stock as day-old chicks.

Why did resistant clones thrive without drug selection? The study cannot fully answer that, but the authors point to prior evidence that quinolone resistance imposes only a minor fitness cost on C. jejuni in the chicken gut and may even be advantageous, and resistant campylobacters have been detected in poultry in other countries that do not use fluoroquinolones in livestock. The tetracycline story had a different texture. Most broiler isolates carried the tet(O/32/O) mosaic gene together with the gyrA T86I mutation, and this mosaic variant was found exclusively in ST-122 isolates, thirteen from broilers and one from a breeder, underscoring the clonality of the co-resistant broiler strains. Breeder isolates more often carried plain tet(O) without fluoroquinolone co-resistance, and tetracycline was used sporadically to treat breeder flocks in some years, which may partly explain the difference. The authors also suggest that resistant isolates in breeders may have been introduced sporadically from external sources such as wild birds, where tetracycline-resistant C. jejuni of several sequence types have been reported in Finland.

The study also delivered a molecular curiosity. One broiler isolate, FIXT-145, carried the tet(O) gene yet repeatedly tested phenotypically susceptible to tetracycline, meaning resistance would have been overpredicted from genotype alone. Further analysis revealed a non-synonymous point mutation in tet(O) causing an R623H amino acid change in the encoded tetracycline resistance protein, which the authors hypothesize abolished resistance; they report this as the first description of the mutation and call for future work to confirm it. Separately, more than 90 percent of all isolates carried blaOXA beta-lactamase genes, but phenotypic beta-lactam resistance was not examined, and earlier research shows the gene’s presence does not directly predict resistance, so that finding should be read cautiously.

Context sharpens the significance of the Finnish numbers. In 2022 to 2023, the European Union reported ciprofloxacin resistance of 70.9 percent and tetracycline resistance of 50.7 percent in C. jejuni broiler isolates, against 1.4 percent and 0.0 percent respectively in Finland over the same period. The study has real limitations, which the authors state plainly: both flock types were sampled only at slaughter, one isolate per flock was sequenced, data on epidemiologically linked parent flocks were missing for many broiler flocks, and information on antibiotic treatments and countries of origin was incomplete at the breeder level, so some uncertainty about transmission routes remains. The regional clustering in Ostrobothnia, where animal production is concentrated, points to environmental transmission between farms that slaughterhouse sampling cannot identify, and the authors suggest nearby cattle and fur animal farms as candidates for future investigation. Practically, the findings support genomic surveillance to detect and track emerging resistant clones, stronger on-farm biosecurity, since different broiler houses on the same farm were often contaminated by the same clone, and continued adherence to the all in–all out principle with cleaning and disinfection between flocks, which the study found little evidence of breaching through transmission between consecutive flocks.

Subject of Research: Genomic epidemiology of antimicrobial-resistant Campylobacter jejuni in Finnish broiler and breeder flocks

Article Title: Clonal, regionally clustered spread—rather than vertical transmission—explains surges in fluoroquinolone‑resistant Campylobacter jejuni in Finnish broilers

Article References: Jaakkonen, A., Marte, A., Perko-Mäkelä, P., Nauholz, H., Olkkola, S., & Kivistö, R. (2026). Clonal, regionally clustered spread—rather than vertical transmission—explains surges in fluoroquinolone‑resistant Campylobacter jejuni in Finnish broilers. Acta Veterinaria Scandinavica, 68(1), Article 46. https://doi.org/10.1186/s13028-026-00887-0

Image Credits: AI Generated

DOI: 10.1186/s13028-026-00887-0

Keywords: Campylobacter jejuni, antimicrobial resistance, fluoroquinolone resistance, whole-genome sequencing, broiler production, vertical transmission, clonal spread, Finland, poultry surveillance, cgMLST, ST-206 clonal complex, food safety