C. jejuni virulence Factors

Pertinent virulence factors of Campylobacter jejuni include:

The quest to define the roles of C. jejuni’s (and indeed all Campylobacter) virulence factors has been hindered by the lack of an animal model for the disease. Specific mechanisms and attributes are suspected to differ slightly between strains.


As C. jejuni must be flagellated to cause disease, motility is an important virulence factor. The flagella allow the bacterium to escape peristalsis, and by chemotactic means, find and enter the mucous layer that lines the epithelium of the small and large intestine. Once inside the mucous layer, C. jejuni is largely protected from the harsh environment of the lumen and is close enough to the epithelium for adhesions to bind and toxins to reach their cellular targets.


Adhesion precedes invasion and may increase the local concentration of secreted bacterial products, or perhaps activate a genetic switch that enables transcription of a secretory product. The flagellum has been considered for adhesion, but some studies suggest an ancillary role. Other outer membrane proteins (OMPs) such as OMP 18 and cell binding factor 1 (CBF1) are also likely candidates. OMP 18 is implicated in the formation of a bridge between the cell membrane and the peptidoglycan that helps stabilise the cell wall, whereas CBF1 is thought to be involved in binding to host cells and amino acid transport. Strains that lack the adhesion are avirulent.


One of the earliest proposed mechanisms of Campylobacter pathogenesis was that of toxin production. There has since been numerous studies done, many with conflicting results. Distinct Cholera-like enterotoxin and cytotoxins have been described. Generally, the non-inflammatory, watery diarrhoea in the developing countries is due to the cholera-like enterotoxin, and the bloody mucoid inflammatory diarrhoea and invasion is associated with cytotoxin production.
The pathobiological significance of the Campylobacter jejuni enterotoxin is subject to major debate and conflicting evidence, and until it is cloned and sequenced, it will remain so. However, it is clear that strains lacking the enterotoxin are still fully virulent.
The best-characterised cytotoxin from C. jejuni is the cytolethal-distending toxin, apparently first described by Johnson and Lior (1988). It has recently been shown that CDT causes cells to become arrested in the G2 phase of the cell cycle, leading to cell death.


Bacterial invasion of the lamina propria ultimately results in cellular injury and therefore loss of function, leading to diarrhoea.
Researchers agree both adhesion and bacterial cell protein synthesis are required for internalisation to occur. (At least 14 de-novo proteins are synthesised when bacteria were grown in the presence of cells.) The mechanism, however, is still debated.
It is also clear that an important factor for invasion and progression of disease is that of the host’s immunological response.


J. Cary; J. Linz; D. Bhatnagar, Microbial Foodborne Diseases, Technomic Publishing LTD; Pennsylvania.

Szymanski, C. M., King, M., Haardt, M., and Armstrong, G. D., Campylobacteria jejuni Motility and Invasion in Caco-2 Cells., Infection and Immunity, 63 (1995): 4295-4300

T. M. Wassenaar, M. J. Blaser, Pathophysiology of Campylobacter jejuni Infections of Humans, Microbes And Infection, 1 (1999): 1023-1033