Campylobacter spp. are Gram-negative, spiral, thermophilic, motile bacteria, which require microaerophilic environment for growth. They have restricted carbohydrate catabolism, but have well-developed mechanism of acquiring micronutrients instead. A common problem, especially in developing countries, is campylobacteriosis, mostly caused by Campylobacter jejuni. The major reason of this disease is the increasing resistance of these bacteria to commonly used antibiotics. The most frequent source of infection is poorly cooked poultry meat. Despite numerous cases of campylobacteriosis, its pathogenesis is not fully understood. However, the role of bacterial motility, adhesion, ability to invade hosts intestinal epithelial cells and secretion of toxins have been found significant. In addition to developing gastrointestinal infections, C. jejuni is firmly established as a causative agent of Guillain-Barré Syndrome, which is an autoimmune-mediated demyelinating polyneuropathy of peripheral nerves. Molecular mimicry between bacterial surface structures and hosts gangliosides is responsible for the development of this disease. The serious local and systemic consequences of C. jejuni infections are the reason for monitoring the microbial purity of food, especially meat and drinking water, for C. jejuni contamination necessitating also new approaches to contamination prevention or minimization.
1. Introduction. 2. Colonization and transmission pathways for Campylobacter spp. 3. The pathogenesis of Campylobacter spp. 3.1. Virulence factors. 4. Systemic consequences of Campylobacter spp. infections in humans. 4.1. Role of C. jejuni infection in demyelination of peripheral nerves. 4.2. Antigenic mimicry between host gangliozydes and C. jejuni. 4.3. Role of cytokines in the development of GBS. 4.4. The strategy in Guillain-Barré Syndrome therapy. 5. Summary
