Campylobacter

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Campylobacter
SEM micrograph of C. fetus
Scientific classification
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Campylobacter

Sebald and Véron 1963
Species

C. coli
C. concisus
C. curvus
C. fetus
C. gracilis
C. helveticus
C. hominis
C. hyointestinalis
C. insulaenigrae
C. jejuni
C. lanienae
C. lari
C. mucosalis
C. rectus
C. showae
C. sputorum
C. upsaliensis

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.[1] 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.[2]

The genomes of several Campylobacter species have been sequenced, providing insights into their mechanisms of pathogenesis.[3]

Pathogenesis

Infection with a Campylobacter species is one of the most common causes of human bacterial gastroenteritis.[4] 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.[5]

Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence.[6] Non-motile mutants do not colonize.

Treatment

Human infections by Campylobacter are usually treated symptomatically by maintaining hydration, and fluid and electrolyte replacement.[1] Erythromycin can be used in children, and tetracycline in adults. Trimethoprim-sulfamethoxazole and ampicillin are ineffective against Campylobacter. Antibiotic treatment has only a marginal benefit (1.32 days) on the duration of symptoms and should not be used routinely.[7]

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).[8]


References

  1. ^ a b c Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. pp. pp. 378–80. ISBN 0838585299. {{cite book}}: |author= has generic name (help); |edition= has extra text (help); |pages= has extra text (help)CS1 maint: multiple names: authors list (link)
  2. ^ Sauerwein R, Bisseling J, Horrevorts A (1993). "Septic abortion associated with Campylobacter fetus subspecies fetus infection: case report and review of the literature". Infection. 21 (5): 331–3. PMID 8300253.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ 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. doi:10.1371/journal.pbio.0030015. PMID 15660156. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: unflagged free DOI (link)
  4. ^ Moore JE; et al. (2005). "Campylobacter". Vet Res. 36 (3): 351–82. PMID 15845230. {{cite journal}}: Explicit use of et al. in: |author= (help)
  5. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ Grant C, Konkel M, Cieplak W, Tompkins L (1993). "Role of flagella in adherence, internalization, and translocation of Campylobacter jejuni in nonpolarized and polarized epithelial cell cultures". Infect Immun. 61 (5): 1764–71. PMID 8478066.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ Ternhag A, Asikainen T, Giesecke J, Ekdahl K (2007). "A meta-analysis on the effects of antibiotic treatment on duration of symptoms caused by infection with Campylobacter species". Clin Infect Dis. 44: 696–700.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ McDermott P, Bodeis S, English L, White D, Walker R, Zhao S, Simjee S, Wagner D (2002). "Ciprofloxacin resistance in Campylobacter jejuni evolves rapidly in chickens treated with fluoroquinolones". J Infect Dis. 185 (6): 837–40. PMID 11920303.{{cite journal}}: CS1 maint: multiple names: authors list (link)

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