Campylobacter
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 SEM micrograph of C. fetus
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C. coli |
Campylobacter is a genus of Gram-negative bacteria. Motile, with either uni- or bi-polar flagella, the organisms have a somewhat curved, rod-like appearance, and are oxidase-positive. At least a dozen species of Campylobacter have been implicated in human disease, with C. jejuni and C. coli the most common.[1] C. fetus is a cause of spontaneous abortions in cattle and sheep, as well as an opportunisitic pathogen in humans.
The genomes of several Campylobacter species have been sequenced, providing insights into their mechanisms of pathogenesis.[2]
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[edit] Pathogenesis
Infection with a Campylobacter species is one of the most common causes of human bacterial gastroenteritis.[3] In the United States, 15 out of every 100,000 people are diagnosed with campylobacteriosis every year, and with many cases going unreported, up to 0.5% of the general population may unknowingly harbor Campylobacter in their gut annually. Diarrhea, cramps, abdominal pain, and fever develop within 2–5 days of pathogenic Campylobacter infection, and in most people, the illness lasts for 7–10 days. Infection can sometimes be fatal, and some (less than 1 in 1000 cases) individuals develop Guillain-Barré syndrome, in which the nerves that join the spinal cord and brain to the rest of the body are damaged, sometimes permanently.
Campylobacteriosis is usually caused by C. jejuni, a spiral-shaped bacterium normally found in cattle, swine, and birds, where it is non-pathogenic. But the illness can also be caused by C. coli (also found in cattle, swine, and birds) C. upsaliensis (found in cats and dogs) and C. lari (present in seabirds in particular). Disease-causing bacteria generally get into people via contaminated food, often undercooked or poorly handled poultry, although contact with contaminated drinking water, livestock, or household pets can also cause disease.[4]
Campylobacters contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to the campy virulence. Non-motile mutants do not colonize.
[edit] Treatment
Human infections by Campylobacter are usually treated symptomatically by maintaining hydration, and fluid and electrolyte replacement. Erythromycin can be used in children, and tetracycline in adults. tremethoprim-sulfamethoxazole and ampicillin are ineffective against Campylobacter.
Poultry infections were treated by enrofloxacin and sarafloxacin, many times by mass administration to flocks for single instances of infection. According to the FDA study banning this practice, this generally did not eliminate all Campylobacter bacteria, and promoted populations of bacteria resistant to fluoroquinolone drugs (like the human drug ciprofloxacin)[citation needed].
[edit] References
- ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill. ISBN 0-8385-8529-9.
- ^ Fouts DE et al. (2005). "Major structural differences and novel potential virulence mechanisms from the genomes of multiple Campylobacter species". PLoS Biol 3 (1): e15. PubMed DOI:10.1371/journal.pbio.0030015.
- ^ Moore JE, et al. (2005). "Campylobacter". Vet Res 36 (3): 351-82. PMID 15845230.
- ^ Saenz Y, Zarazaga M, Lantero M, Gastanares MJ, Baquero F, Torres C (2000). "Antibiotic resistance in Campylobacter strains isolated from animals, foods, and humans in Spain in 1997-1998". Antimicrob Agents Chemother 44 (2): 267-71. PMID 10639348 fulltext.
