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The genus Campylobacter, (meaning ‘twisted bacteria’) first discovered in 1963[1], describes Gram-negative, spiral, microaerophilic bacteria. Motile, with either uni- or bi-polar flagella, the organisms have a characteristic spiral/corkscrew appearance (see photo) and are oxidase-positive.[2] Campylobacter jejuni is now recognized as one of the main causes of bacterial foodborne disease in many developed countries.[3] At least a dozen species of Campylobacter have been implicated in human disease, with C. jejuni and C. coli the most common.[2] C. fetus is a cause of spontaneous abortions in cattle and sheep, as well as it is an opportunisitic pathogen in humans.[4]
The genomes of several Campylobacter species have been sequenced, providing insights into their mechanisms of pathogenesis.[5] The first Campylobacter genome to be sequenced was C. jejuni, in 2000.[6]
Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence. [7] Non-motile mutants do not colonize.
Campylobacteriosis is an infection by campylobacter.[8] The common routes of transmission are fecal-oral, person-to-person sexual contact, ingestion of contaminated food or water, and the eating of raw meat. It produces an inflammatory, sometimes bloody, diarrhea, periodontitis[9] or dysentery syndrome, mostly including cramps, fever and pain. The infection is usually self-limiting and in most cases, symptomatic treatment by reposition of liquid and electrolyte replacement is enough in human infections. The use of antibiotics, on the other hand, is controversial.
The exact cause of campylobacteriosis has not been clarified yet, but seem to involve multiple mechanisms. One mechanism is invasion into epithelial cells of the gut, which is generally low, but damages these cells. The sites of tissue injury include the jejunum, the ileum, and the colon.
Most strains of C jejuni produce a toxin (cytodistending toxin) that hinders the cells to divide and activate the immune system. This helps the bacteria to evade immune system and survive for a limited time in the cells. For a while, it was thought that also a cholera-like enterotoxin was made, but this appeared to be not the case. The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with hemolytic uremic syndrome and thrombotic thrombocytopenic purpura through a poorly understood mechanism.
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