Campylobacter

Campylobacter
Campylobacter jejuni
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Epsilonproteobacteria
Order: Campylobacterales
Family: Campylobacteraceae
Genus: Campylobacter
Sebald & Véron, 1963
Species

C. avium
C. butzleri
C. canadensis
C. cinaedi
C. coli
C. concisus
C. corcagiensis
C. cryaerophilus
C. cuniculorum
C. curvus
C. fennelliae
C. fetus
C. gracilis
C. helveticus
C. hominis
C. hyoilei
C. hyointestinalis
C. insulaenigrae
C. jejuni
C. lanienae
C. lari
C. mucosalis
C. mustelae
C. nitrofigilis
C. peloridis
C. pylori
C. rectus
C. showae
C. sputorum
C. subantarcticus
C. upsaliensis
C. ureolyticus
C. volucris

Campylobacter (meaning "curved bacteria") is a genus of Gram-negative, microaerophilic, oxidase-positive, catalase-positive, nonfermentative bacteria.[1] Campylobacter species are typically spiral-shaped and able to move via unipolar or bipolar flagella.[1] Most Campylobacter species are cause for disease and can infect humans and other animals. The bacterium's main reservoir is poultry;[2] humans can contract the disease from contaminated food. Another source of infection is contact with infected animals such as kittens and puppies; most colonized animals -including chickens- develop a lifelong carrier state.[3] At least a dozen species of Campylobacter have been implicated in human disease, with C. jejuni and C. coli being the most common.[4] C. jejuni is now recognized as one of the main causes of bacterial foodborne disease in many developed countries.[4][5] C. jejuni infection can also result in serious bacteremia in individuals with AIDS, while C. lari is a known cause of recurrent diarrhea in children.[3] C. fetus is a cause of spontaneous abortions in cattle and sheep, as well as an opportunistic pathogen in humans.[6]

History

The symptoms of Campylobacter infections were described in 1886 in infants by Theodor Escherich.[7] These infections were named cholera infantum,[7] or summer complaint.[8] The genus was first described in 1963;[9] however, the organism was not isolated until 1972.[7]

Genome and proteome

The genomes of several Campylobacter species have been sequenced.[10] The first Campylobacter genome to be sequenced was C. jejuni, in 2000.[11]

Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence.[12] Nonmotile mutants do not colonize.

Sequence features: Comparative genomic analysis has led to the identification of 15 proteins which are uniquely found in members of the genus Campylobacter and serve as molecular markers for the genus. Eighteen other proteins were also found which were present in all species except C. fetus, which is the deepest-branching Campylobacter species. A conserved insertion has also been identified which is present in all Campylobacter species except C. fetus. Additionally, 28 proteins have been identified present only in C. jejuni and C. coli, indicating a close relationship between these two species. Five other proteins have also been identified which are only found in C. jejuni and serve as molecular markers for the species.[13]

Bacteriophage

The confusing taxonomy of Campylobacter over the past decades make it difficult to identify the earliest reports of Campylobacter bacteriophages. Bacteriophages specific to the species now known as C. coli and C. fetus (previously Vibrio coli and V. fetus), were isolated from cattle and pigs during the 1960s.[14][15][16][17]

Pathogenesis

Main article: Campylobacteriosis

Campylobacteriosis, a gastrointestinal infection caused by Campylobacter, is characterized by inflammatory, sometimes bloody diarrhea or dysentery syndrome, mostly including cramps, fever, and pain.[18][19] The most common routes of transmission are fecal-oral, ingestion of contaminated food or water, and the eating of raw meat. Foods implicated in campylobacteriosis include raw or under-cooked poultry, raw dairy products, and contaminated produce.[20] Campylobacter is sensitive to the stomach's normal production of hydrochloric acid: as a result, the infectious dose is relatively high, and the bacteria rarely cause illness when a person is exposed to less 10,000 organisms.[3] Nevertheless, people taking antacid medication (e. g. people with gastritis or stomach ulcers) are at higher risk of contracting disease from a smaller amount of organisms, since this type of medication inhibits normal gastric acid. The infection is usually self-limiting and, in most cases, symptomatic treatment by liquid and electrolyte replacement is enough in human infections. The use of antibiotics, though, is controversial. Symptoms typically last five to seven days.[20]

The sites of tissue injury include the jejunum, the ileum, and the colon. Most strains of C jejuni produce a toxin (cytolethal distending toxin) that hinders the cells from dividing and activating the immune system. This helps the bacteria to evade the immune system and survive for a limited time in the cells. A cholera-like enterotoxin was once thought to be also made, but this appears not to be the case. The organism produces diffuse, bloody, edematous, and exudative enteritis. Although rarely has the infection been considered a cause of hemolytic uremic syndrome and thrombotic thrombocytopenic purpura, no unequivocal case reports exist. In some cases, a Campylobacter infection can be the underlying cause of Guillain–Barré syndrome. Gastrointestinal perforation is a rare complication of ileal infection.[21]

Campylobacter has also been associated with periodontitis.[18]

Treatment

Diagnosis of the illness is made by testing a specimen of feces.

Epidemiology

Campylobacter infections increased 14% in the United States in 2012 compared to the period from 2006 to 2008. This represents the highest reported number of infections since 2000.[20]

UK

In January 2013, the UK's Food Standards Agency warned that two-thirds of all raw chicken bought from UK shops was contaminated with Campylobacter, affecting an estimated half a million people annually and killing about 100.[25] In June 2014, the Food Standards Agency started a campaign against washing raw chicken, as washing can spread germs by splashing.[26] In May 2015, cumulative results for samples taken from fresh chickens between February 2014 and February 2015 were published as official statistics by the FSA, including results presented by major retailers.

The results for the full year show:

USA

Larger prevalence of Campylobacter (40% or more) has been reported in raw chicken meat in retail stores in the USA.[28] The reported prevalence in retail chicken meat is higher than the reported prevalence by the microbiology performance standard testing collected by the U. S. Department of Agriculture, and the last quarterly progress report on Salmonella and Campylobacter testing of meat and poultry for July–September 2014, published by the Food Safety and Inspection Service of the U. S. Department of Agriculture, shows a low prevalence of Campylobacter spp. in ground chicken meat, but a larger prevalence (20%) in mechanically separated chicken meat (which is sold only for further processing).[29]

Canada

FoodNet Canada conducts surveillance at 3 different sites on behalf of Public Health Agency of Canada. In the 2014 Short Report of FoodNet Canada,[30] they reported:

References

  1. 1 2 Vandamme, Peter; Dewhirst, Floyd E.; Paster, Bruce J.; On, Stephen L.W. (2006). Garrity, George; Brenner, Don J.; Staley, James T.; Krieg, Noel R.; Boone, David R.; DeVos, Paul; Goodfellow, Michael; Rainey, Fred A.; Schleifer, Karl-Heinz, eds. Bergey's Manual of Systematic Bacteriology: Volume Two: The Proteobacteria (Part C) (2nd ed.). Springer Science & Business Media. pp. 1147–1160. ISBN 978-0-387-29298-4.
  2. "Infectious disease Campylobacter clinical Foodborne illnesses | CDC". www.cdc.gov. Retrieved 2016-02-14.
  3. 1 2 3 "Campylobacter Infections: Background, Pathophysiology, Epidemiology".
  4. 1 2 Ryan, Kenneth James; Ray, C. George, eds. (2004). Sherris Medical Microbiology: An Introduction to Infectious Diseases (4th ed.). McGraw Hill. pp. 378–80. ISBN 978-0-8385-8529-0.
  5. Moore, John E.; Corcoran, Deborah; Dooley, James S.G.; Fanning, Séamus; Lucey, Brigid; Matsuda, Motoo; McDowell, David A.; Mégraud, Francis; Millar, B.; O'Mahony, Rebecca; O'Riordan, Lisa; O'Rourke, Michele; Rao, Juluri R.; Rooney, Paul J.; Sails, Andrew; Whyte, Paul (2005). "Campylobacter". Veterinary Research 36 (3): 351–82. doi:10.1051/vetres:2005012. PMID 15845230.
  6. Sauerwein, R. W.; Horrevorts, A. M.; Bisseling, J. (1993). "Septic abortion associated with Campylobacter fetus subspecies fetus infection: Case report and review of the literature". Infection 21 (5): 331–3. doi:10.1007/BF01712458. PMID 8300253.
  7. 1 2 3 Samie, A.; Obi, C.L.; Barrett, L.J.; Powell, S.M.; Guerrant, R.L. (2007). "Prevalence of Campylobacter species, Helicobacter pylori and Arcobacter species in stool samples from the Venda region, Limpopo, South Africa: Studies using molecular diagnostic methods". Journal of Infection 54 (6): 558–66. doi:10.1016/j.jinf.2006.10.047. PMID 17145081.
  8. Condran, Gretchen A.; Murphy, Jennifer (2008). "Defining and Managing Infant Mortality: A Case Study of Philadelphia, 1870-1920". Social Science History 32 (4): 473–513. doi:10.1215/01455532-2008-006.
  9. Debruyne, Lies; Gevers, Dirk; Vandamme, Peter (2008). "Taxonomy of the Family Campylobacteraceae". In Nachamkin, Irving; Szymanski, Christine M.; Blaser, Martin J. Campylobacter (3rd ed.). ASM Press. pp. 3–25. ISBN 978-1-55581-437-3. hdl:1854/LU-680725.
  10. Relman, David A.; Fouts, Derrick E; Mongodin, Emmanuel F; Mandrell, Robert E; Miller, William G; Rasko, David A; Ravel, Jacques; Brinkac, Lauren M; DeBoy, Robert T; Parker, Craig T; Daugherty, Sean C; Dodson, Robert J; Durkin, A. Scott; Madupu, Ramana; Sullivan, Steven A; Shetty, Jyoti U; Ayodeji, Mobolanle A; Shvartsbeyn, Alla; Schatz, Michael C; Badger, Jonathan H; Fraser, Claire M; Nelson, Karen E (2005). "Major Structural Differences and Novel Potential Virulence Mechanisms from the Genomes of Multiple Campylobacter Species". PLoS Biology 3 (1): e15. doi:10.1371/journal.pbio.0030015. PMC 539331. PMID 15660156.
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  20. 1 2 3 "Infections from some foodborne germs increased, while others remained unchanged in 2012". Centers for Disease Control. April 18, 2013. Retrieved April 19, 2013.
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  30. Public Health Agency of Canada, FoodNet Canada

External links

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