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Background   Campylobacter  colonise the gastrointestinal tract of warm-blooded animals and are major enteropathogens in humans.  C. coli  is less common than  C. jejuni  and accounts for about 10% of the total number of  Campylobacter  infections although the two species seem to share many virulence determinants.  Campylobacter  bacteraemia is rare, estimated to occur in less than 1% of the infections, and the exact mechanisms regulating the progression of the infection from the gastrointestinal tract to the blood stream are unclear. Here, we looked at the contribution of  C. coli  to  Campylobacter  infections and further compared various virulence traits in  C. coli  clade 1 blood and stool isolates.    Results  We assessed the numbers of  C. jejuni  and  C. coli  among typed isolates in the PubMLST database and found that  C. coli  accounted for 25.9% of blood isolates, but only 8.9% of the stool isolates. Phylogenetic analysis of 128  C. coli  clade 1 whole genome sequences deposited to NCBI revealed no specific clustering of the human blood, stool or animal isolates. Of the six  C. coli  isolates chosen for phenotypic analyses, stool isolates adhered significantly better to human HT-29 colon cancer cells than the blood isolates, while there was no difference in induced IL-8 levels between the isolates. Furthermore, the stool isolates had two- to fourfold higher RNA expression levels of the  flpA ,  ciaB, iamA  and  cdt  virulence genes than the blood isolates. Finally, we looked at the gene structure of the  cdtA, B  and  C  toxin genes and found numerous nucleotide additions and deletions disrupting the open reading frames. In contrast to 58% isolates of animal origin, only 38% and 32% of human blood and stool isolates, respectively, had all three  cdt  genes intact, a prerequisite to produce functional toxins.    Conclusions  This study reveals interesting differences between  C. coli  clade 1 isolates of human and animal origin on one hand, and also between human blood and stool isolates, on the other. The results suggest that  C. coli  might downregulate and/or inactivate various virulence determinants as the isolates pass from the animal host to the human gastrointestinal tract and enter the human blood stream.    Electronic supplementary material  The online version of this article (10.1186/s13099-019-0322-9) contains supplementary material, which is available to authorized users.

Differences in virulence gene expression between human blood and stool Campylobacter coli clade 1 ST828CC isolates