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Pathogen Page
Campylobacter jejuni
I. General Information
1. NCBI Taxonomy ID:
197
2. Disease:
Campylobacterosis
3. Introduction
Campylobacter jejuni is a small gram-negative, microaerophilic, motile, curved-to-spiral rod that has a single polar flagellum. It can be found in the intestinal tract and oral cavity (Smibert, 1978). C. jejuni is among the most frequent causes of bacterial diarrhea worldwide and an important cause of diarrhea in travellers and deployed military personnel. It is also the infectious agent most often associated with Guillain-Barre syndrome (GBS), a postinfectin polyneuropathy, and is increasingly identified as a cause of bacteremia and a variety of systemic and localized infections in immunocompromised hosts. The bacteria is characterized by a lack of understanding of the basic virulence mechanisms and by its antigenic complexity. The LPS cores of many serotypes have been shown to contain structures which resemble human gangliosides and have been implicated in the development of autoantibodies leading to GBS, although the specific structure or structures which enable a given campylobacter strain to cause GBS are not clear (Lee et al., 1999; Pawelec et al., 2000).
4. Microbial Pathogenesis
Most Campylobacter infections are mild, self-limiting diarrheal illnesses, but severe infections do occur. The primary risk factors associated with Campylobacter infection are consuming and handling foods of animal origins, especially poultry products. In addition to epidemiological evidence, microbiological evidence supports poultry as the primary source of human Campylobacter infection (Nelson et al., 2007). The majority of Campylobacter-associated infections are thought to be sporadic cases of food poisoning; contaminated drinking water, including that from public water supplies, is the vehicle of large Campylobacter-associated outbreaks. Although Campylobacter spp. are widely distributed in the environment, the epidemiology of many cases of Campylobacter-associated infections remains unclear (Abulreesh et al., 2006). After incubation of approximately three days, abrupt cramping pain in the abdomen is followed by diarrhea. The mechanism of diarrhea induction is a complex and multifactorial process. The diarrheal stage lasts a few days. Complications are rare, but infection may be followed by the development of reactive arthritis or GBS.

Flagella-mediated motility has been shown to be necessary for Campylobacter to colonize the intestinal tract, and experimental infections in humans and animals, and in vitro analyses of adherence and invasion in cultured human cells have demonstrated that cell invasiveness is necessary in Campylobacter-induced inflammatory diarrhea. Several bacterial components have been shown to have adhesive properties (LPS, flagella, fimbrial filaments, surface-exposed proteins), and a direct role of toxins including of cytolethal distending toxin (CDT) in disease remains to be demonstrated. Host factors are of importance in the pathogenesis of GBS following a Campylobacter infection. It is now clear that specific bacterial genes are crucial for the induction of anti-ganglioside antibodies (Engberg, 2006).
5. Host Ranges and Animal Models
The primary risk factors associated with Campylobacter infection are consuming and handling foods of animal origins, especially poultry products. In addition to epidemiological evidence, microbiological evidence supports poultry as the primary source of human Campylobacter infection (Nelson et al., 2007).
6. Host Protective Immunity
Anti-flagellar serum antibody titres of the dams did not correlate with protection of their young (Dolby et al., 1986). There was a good correlation between high campylobacter-specific IgG response and bactericidal activity. The degree of protection conferred by vaccinated dams on infant mice against colonization by Campylobacter jejuni depended on the bacterial strain, preparation, and route of administration of the vaccine. In some instances of homologous protection, serum bactericidal titres correlated well with protection. However, boiled C. jejuni vaccine, which was non-protective, also elicited a strong bactericidal antibody response. Conversely, bactericidal activity could not be demonstrated against strains capable of cross-protection. (Abimiku et al., 1989).
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