Abstract

BackgroundCampylobacter 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.ResultsWe 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.ConclusionsThis 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.

Highlights

  • Campylobacter colonise the gastrointestinal tract of warm-blooded animals and are major enteropathogens in humans

  • Campylobacter coli in the PubMLST/Campylobacter database To better understand the contribution of C. coli to Campylobacter infection and bacteraemia, the number of C. jejuni and C. coli isolates from human and animal sources were retrieved from PubMLST (Additional file 1: Table S1)

  • When looking at the human blood and stool isolates separately, there was a clear difference in the distribution, where C. coli accounted for 25.9% of blood isolates, but only 8.9% of the stool isolates (Fig. 1a)

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Summary

Introduction

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 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. Campylobacter colonise the gastrointestinal tract of warm-blooded animals, such as poultry and wild birds, ruminants, pigs, cats and dogs but rarely cause any symptoms in animal hosts. Campylobacter coli is less common than C. jejuni as a human pathogen and seems to account for about 10% of the total number of Campylobacter infections [9]. C. coli isolates cluster into three clades [10,11,12], where those of clade 1 are mainly clinical and animal isolates, including the clonal complexes of ST828CC and ST1150CC [13], whereas clade 2 and clade 3 lack clonal complex structure and mainly contain isolates of environmental origin [10, 12]

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