Jump to content

Campylobacter: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
→Pathogenesis: supply requested medrs and rewrite/relocate sentence accordingly
→Pathogenesis: + hidden note re meddate
Line 71: Line 71:
{{Main article|Campylobacteriosis}}
{{Main article|Campylobacteriosis}}


''Campylobacter'' can cause a gastrointestinal infection called campylobacteriosis. This is characterized by inflammatory, sometimes bloody [[diarrhea]] or [[dysentery]] syndrome, mostly including cramps, fever, and pain.<ref name=cazp>{{cite journal |last1=Humphrey |first1=Tom |last2=O'Brien |first2=Sarah |last3=Madsen |first3=Mogens |title=Campylobacters as zoonotic pathogens: A food production perspective |journal=International Journal of Food Microbiology |volume=117 |issue=3 |pages=237–57 |year=2007 |pmid=17368847 |doi=10.1016/j.ijfoodmicro.2007.01.006 }}</ref><ref>{{cite press release |title=Infections from some foodborne germs increased, while others remained unchanged in 2012 |publisher=CDC |date=April 18, 2013 |url=http://www.cdc.gov/media/releases/2013/p0418-foodborne-germs.html |accessdate=October 22, 2015}}</ref> 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.<ref name="CDC41813" /> ''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.<ref name=":0" /> Nevertheless, people taking [[Antacid|antacid medication]] (e. g. people with [[gastritis]] or [[Peptic ulcer|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. Symptoms typically last five to seven days.<ref name="CDC41813" /> Treatment with antibiotics has little effect and is discouraged except in high-risk patients.<ref>{{cite journal | vauthors=Ternhag A, Asikainen T, Giesecke J, Ekdahl K | title=A meta-analysis on the effects of antibiotic treatment on duration of symptoms caused by infection with Campylobacter species | journal=Clin Infect Dis | year=2007 | volume=44 | pages=696&ndash;700 | doi=10.1086/509924 | pmid=17278062 | issue=5}}</ref>
''Campylobacter'' can cause a gastrointestinal infection called campylobacteriosis. This is characterized by inflammatory, sometimes bloody [[diarrhea]] or [[dysentery]] syndrome, mostly including cramps, fever, and pain.<ref name=cazp>{{cite journal |last1=Humphrey |first1=Tom |last2=O'Brien |first2=Sarah |last3=Madsen |first3=Mogens |title=Campylobacters as zoonotic pathogens: A food production perspective |journal=International Journal of Food Microbiology |volume=117 |issue=3 |pages=237–57 |year=2007 |pmid=17368847 |doi=10.1016/j.ijfoodmicro.2007.01.006 }}</ref><ref>{{cite press release |title=Infections from some foodborne germs increased, while others remained unchanged in 2012 |publisher=CDC |date=April 18, 2013 |url=http://www.cdc.gov/media/releases/2013/p0418-foodborne-germs.html |accessdate=October 22, 2015}}</ref> 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.<ref name="CDC41813" /> ''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.<ref name=":0" /> Nevertheless, people taking [[Antacid|antacid medication]] (e. g. people with [[gastritis]] or [[Peptic ulcer|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. Symptoms typically last five to seven days.<ref name="CDC41813" /> Treatment with antibiotics has little effect and is discouraged except in high-risk patients.<ref>{{cite journal | vauthors=Ternhag A, Asikainen T, Giesecke J, Ekdahl K | title=A meta-analysis on the effects of antibiotic treatment on duration of symptoms caused by infection with Campylobacter species | journal=Clin Infect Dis | year=2007 | volume=44 | pages=696&ndash;700 | doi=10.1086/509924 | pmid=17278062 | issue=5}}</ref> <!-- as of November 2016, most recent 'ideal' MEDRS - not a controversial/fast-moving issue -->


The sites of tissue injury include the [[jejunum]], the [[ileum]], and the [[Colon (anatomy)|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.<ref>{{cite journal |last1=Jassim |first1=S.S. |last2=Malik |first2=A. |last3=Aldridge |first3=A. |title=Small bowel perforation: an unusual cause |journal=Grand Rounds |volume=11 |issue=1 |year=2011 |pages=17–9 |doi=10.1102/1470-5206.2011.0006}}</ref>
The sites of tissue injury include the [[jejunum]], the [[ileum]], and the [[Colon (anatomy)|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.<ref>{{cite journal |last1=Jassim |first1=S.S. |last2=Malik |first2=A. |last3=Aldridge |first3=A. |title=Small bowel perforation: an unusual cause |journal=Grand Rounds |volume=11 |issue=1 |year=2011 |pages=17–9 |doi=10.1102/1470-5206.2011.0006}}</ref>

Revision as of 15:13, 17 November 2016

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 bacteria.[1] Campylobacter typically appear comma or s-shaped and motile.[1]

Most Campylobacter species can cause disease and can infect humans and other animals. The bacterium's main reservoir is poultry;[2] humans can contract the disease from eating food contaminated with Campylobacter species. Another source of infection is contact with infected animals, which often carry Campylobacter asymptomatically.[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 spread to the blood 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]

Description

Campylobacter generally appear curved or comma-shaped, and are able to move via unipolar or bipolar flagella.[1] They generally survive in environments with low oxygen. They are positive by the oxidase test and catalase test. Campylobacter are nonfermentative.[1]

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]

Genetics

The genomes of several Campylobacter species have been sequenced, beginning with C. jejuni in 2000.[10][11] These genome studies have identified molecular markers specific to members of Campylobacter. Additionally, several markers were found in all Campylobacter species except for C. fetus, the most distantly-related species. Many markers were also found which were conserved only between C. jejuni and C. coli, indicating a close relationship between these two species.[12]


Similar studies have investigated the genes responsible for motility in Campylobacter species. All Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence.[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

Campylobacter can cause a gastrointestinal infection called campylobacteriosis. This 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. Symptoms typically last five to seven days.[20] Treatment with antibiotics has little effect and is discouraged except in high-risk patients.[21]

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.[22]

Campylobacter has also been associated with periodontitis.[18]

Treatment

Diagnosis of campylobacteriosis is made by testing a specimen of feces. Standard treatment is azithromycin, a macrolide antibiotic, especially for Campylobacter infections in children,[23] although other antibiotics, such as macrolides, quinolones, and tetracycline are sometimes used to treat gastrointestinal Campylobacter infections in adults.[24] In case of systemic infections, other bactericidal antibiotics are used, such as ampicillin, amoxicillin/clavulanic acid, or aminoglycosides. Fluoroquinolone antibiotics, such as ciprofloxacin or levofloxacin, may no longer be effective in some cases due to resistance.[25] In addition to antibiotics, dehydrated children may require intravenous fluid treatment in a hospital.

Epidemiology

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.[26] In June 2014, the Food Standards Agency started a campaign against washing raw chicken, as washing can spread germs by splashing.[27] In May 2015, cumulative results for samples taken from fresh chickens between February 2014 and February 2015 were published by the FSA and showed 73% of chickens tested positive for the presence of Campylobacter.[28]

USA

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]

High prevalence of Campylobacter (40% or more) has been reported in raw chicken meat in retail stores in the USA.[29] 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).[30]

Canada

FoodNet Canada has reported that Campylobacter was the most common pathogen found on packaged chicken breast, with nearly half of all samples testing positive. Additionally, Campylobacter and Salmonella were the most common causes of gastrointestinal illness in Canada[31]

New Zealand

In August 2016, an estimated 4,000+ residents of Havelock North, a town with 13,000 or so residents, had gastric illness after the water supply was thought to be contaminated by Campylobacter.[32][33]

References

  1. ^ a b c d 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. ^ a b c "Campylobacter Infections: Background, Pathophysiology, Epidemiology". {{cite journal}}: Cite journal requires |journal= (help)
  4. ^ a b 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. ^ a b c 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. (eds.). Campylobacter (3rd ed.). ASM Press. pp. 3–25. ISBN 978-1-55581-437-3. hdl:1854/LU-680725. {{cite book}}: External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help); Unknown parameter |editor3link= ignored (|editor-link3= suggested) (help)
  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.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  11. ^ Parkhill, J.; Wren, B. W.; Mungall, K.; Ketley, J. M.; Churcher, C.; Basham, D.; Chillingworth, T.; Davies, R. M.; Feltwell, T.; Holroyd, S.; Jagels, K.; Karlyshev, A. V.; Moule, S.; Pallen, M. J.; Penn, C. W.; Quail, M. A.; Rajandream, M-A.; Rutherford, K. M.; van Vliet, A. H. M.; Whitehead, S.; Barrell, B. G. (2000). "The genome sequence of the food-borne pathogen Campylobacter jejuni reveals hypervariable sequences". Nature. 403 (6770): 665–8. doi:10.1038/35001088. PMID 10688204.
  12. ^ Gupta, Radhey S (2006). "Molecular signatures (unique proteins and conserved indels) that are specific for the epsilon proteobacteria (Campylobacterales)". BMC Genomics. 7: 167. doi:10.1186/1471-2164-7-167. PMC 1557499. PMID 16817973.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  13. ^ Grant, Christopher C. R.; Konkel, Michael E.; Cieplak, Witold; Tompkins, Lucy S. (1993). "Role of flagella in adherence, internalization, and translocation of Campylobacter jejuni in nonpolarized and polarized epithelial cell cultures". Infection and Immunity. 61 (5): 1764–71. PMC 280763. PMID 8478066.
  14. ^ Firehammer, BD; Border, M (1968). "Isolation of temperate bacteriophages from Vibrio fetus". American Journal of Veterinary Research. 29 (11): 2229–35. PMID 5693467.
  15. ^ Fletcher, R. D. (1965). "Activity and morphology of Vibrio coli phage". American Journal of Veterinary Research. 26 (111): 361–4.
  16. ^ Fletcher, R. D.; Bertschinger, H. U. (2010). "A Method of Isolation ofVibrio colifrom Swine Fecal Material by Selective Filtration". Zentralblatt für Veterinarmedizin. Reihe B. 11 (6): 469–74. doi:10.1111/j.1439-0450.1964.tb01075.x.
  17. ^ Connerton, P.L.; Timms, A.R.; Connerton, I.F. (2011). "Campylobacter bacteriophages and bacteriophage therapy". Journal of Applied Microbiology. 111 (2): 255–65. doi:10.1111/j.1365-2672.2011.05012.x. PMID 21447013.
  18. ^ a b Humphrey, Tom; O'Brien, Sarah; Madsen, Mogens (2007). "Campylobacters as zoonotic pathogens: A food production perspective". International Journal of Food Microbiology. 117 (3): 237–57. doi:10.1016/j.ijfoodmicro.2007.01.006. PMID 17368847.
  19. ^ "Infections from some foodborne germs increased, while others remained unchanged in 2012" (Press release). CDC. April 18, 2013. Retrieved October 22, 2015.
  20. ^ a b c "Infections from some foodborne germs increased, while others remained unchanged in 2012". Centers for Disease Control. April 18, 2013. Retrieved April 19, 2013.
  21. ^ 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 (5): 696–700. doi:10.1086/509924. PMID 17278062.
  22. ^ Jassim, S.S.; Malik, A.; Aldridge, A. (2011). "Small bowel perforation: an unusual cause". Grand Rounds. 11 (1): 17–9. doi:10.1102/1470-5206.2011.0006.
  23. ^ Vukelic, Dalibor; Trkulja, Vladimir; Salkovic-Petrisic, Melita (2010). "Single Oral Dose of Azithromycin Versus 5 Days of Oral Erythromycin or No Antibiotic in Treatment of Campylobacter Enterocolitis in Children: A Prospective Randomized Assessor-Blind Study". Journal of Pediatric Gastroenterology and Nutrition. 50 (4): 404–10. doi:10.1097/MPG.0b013e3181a87104. PMID 19881393.
  24. ^ Gendrel, D.; Cohen, R. (2008). "Diarrhées bactériennes et antibiotiques : les recommandations européennes". Archives de Pédiatrie (in French). 15 (Suppl 2): S93–6. doi:10.1016/S0929-693X(08)74223-4. PMID 19000862. {{cite journal}}: Unknown parameter |trans_title= ignored (|trans-title= suggested) (help)
  25. ^ Lehtopolku, M.; Nakari, U.-M.; Kotilainen, P.; Huovinen, P.; Siitonen, A.; Hakanen, A. J. (2010). "Antimicrobial Susceptibilities of Multidrug-Resistant Campylobacter jejuni and C. coli Strains: In Vitro Activities of 20 Antimicrobial Agents". Antimicrobial Agents and Chemotherapy. 54 (3): 1232–6. doi:10.1128/AAC.00898-09. PMC 2825995. PMID 20038624.
  26. ^ "FSA warns that chicken bacteria could be next meat scandal". The Telegraph. January 23, 2013.
  27. ^ "Don't wash raw chicken". Food Standards Agency.
  28. ^ "Campylobacter survey: cumulative results from the full 12 months (Q1 – Q4)" (Press release). Food Standards Agency. May 28, 2015. Retrieved October 23, 2015.
  29. ^ Williams, Aretha; Oyarzabal, Omar A (2012). "Prevalence of Campylobacter spp. in skinless, boneless retail broiler meat from 2005 through 2011 in Alabama, USA". BMC Microbiology. 12: 184. doi:10.1186/1471-2180-12-184. PMC 3490988. PMID 22920043.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  30. ^ Food Safety and Inspection Service (April 24, 2015). "Quarterly Progress Report on Salmonella and Campylobacter: Testing of Selected Raw Meat and Poultry Products: Preliminary Results, July 2014 to September 2014". United States Department of Agriculture.
  31. ^ "FoodNet Canada 2014 Short Report". Public Health Agency of Canada, FoodNet Canada. Retrieved 3 October 2016.
  32. ^ "Woman died in Havelock North gastro outbreak". Stuff. 19 August 2016.
  33. ^ "Govt rejects call for Hawke's Bay water emergency declaration". Radio New Zealand. 19 August 2016.
Retrieved from "https://en.wikipedia.org/enwiki/w/index.php?title=Campylobacter&oldid=750045983"