Abstract

Campylobacter jejuni is one of the most common causes of foodborne diseases worldwide. There are few reports on Campylobacter strains isolated from Latin-American countries. Here, 140 C. jejuni strains isolated from cloacal and transport boxes swabs, water from chiller tanks, and broiler carcasses of five poultry companies in Southern Brazil were identified using phenotypic and genotypic methods. Polymerase chain reaction (PCR) was used to analyze eight C. jejuni virulence markers: flaA, cadF, and invasion-associated (iam) genes, cdtABC operon (associated with the cytolethal distending toxin), and plasmidial virB11 and wlaN genes were present in 78.5%, 77.8%, 0%, 74.2%, 22.1%, and 10.7% of samples, respectively. There were 25 different virulence profiles: 1 (cdtA, cdtB, cdtC, flaA, and cadF), 2 (cdtA, cdtB, cdtC, flaA, cadF, and virB11), and 3 (cdtA, cdtB, cdtC, flaA, cadF, and wlaN) were the most common (> 60% of strains). We provide insight into factors related to the occurrence of this pathogen and their epidemiology.

Highlights

  • Campylobacter jejuni is one of the most common causes of foodborne diseases worldwide

  • There are 17 species and six subspecies assigned to the genus Campylobacter, of which the most frequently reported to cause human diseases are C. jejuni and C. coli[3]

  • Out of a total of 140 screened samples, all of them were confirmed as having Campylobacter jejuni species

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Summary

Introduction

Campylobacter jejuni is one of the most common causes of foodborne diseases worldwide. Despite its public health importance, virulence factors and mechanisms of C. jejuni pathogenesis remain poorly studied in Latin-American c­ ountries[13], especially regarding their occurrence among poultry companies and the different sources of isolation throughout the slaughtering process. The majority of virulence factors are associated with motility, chemotaxis, adhesion and colonization of intestinal epithelial cells, invasion and translocation capabilities, production of toxins and secreted proteins, and other mechanisms essential for bacterial ­survival[14,15]. Other pathogenic mechanisms, such as the production of enterotoxins and cytotoxins, and the ability to adhere and invade epithelial cells, have been proposed to play a role in ­enteritis[16,17]. The cdtA and cdtC gene products are two subunits responsible for toxin binding to the cell membrane and for the delivery of the cdtB gene product (CdtB), which is the enzymatically active ­subunit[14]

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