Campylobacter jejuni has long been recognized as a cause of bacterial food-borne illness,
and surprisingly, it remains the most prevalent bacterial food-borne pathogen in the
industrial world to date. Natural reservoirs for this Gram-negative, spiral-shaped
bacterium are wild birds, whose intestines offer a suitable biological niche for the
survival and dissemination of C. jejuni Chickens become colonized shortly after birth
and are the most important source for human infection. In the last decade, effective
intervention strategies to limit infections caused by this elusive pathogen were hindered
mainly because of a paucity in understanding the virulence mechanisms of C. jejuni
and in part, unavailability of an adequate animal model for the disease. However,
recent developments in deciphering molecular mechanisms of virulence of C. jejuni
made it clear that C. jejuni is a unique pathogen, being able to execute N-linked
glycosylation of more than 30 proteins related to colonization, adherence, and invasion.
Moreover, the flagellum is not only depicted to facilitate motility but as well secretion
of Campylobacter invasive antigens (Cia). The only toxin of C. jejuni, the so-called
cytolethal distending toxin (CdtA,B,C), seems to be important for cell cycle control
and induction of host cell apoptosis and has been recognized as a major pathogenicity-associated
factor. In contrast to other diarrhoea-causing bacteria, no other classical virulence
factors have yet been identified in C. jejuni. Instead, host factors seem to play
a major role for pathogenesis of campylobacteriosis of man. Indeed, several lines
of evidence suggest exploitation of different adaptation strategies by this pathogen
depending on its requirement, whether to establish itself in the natural avian reservoir
or during the course of human infection.
(c) 2009 Elsevier GmbH. All rights reserved.