Campylobacter coli

Campylobacter coli is a Gram-negative, microaerophilic, non-endospore-forming, S-shaped bacterial species within genus Campylobacter.[1] In humans, it C. coli can cause campylobacteriosis, a diarrhoeal disease which is the most frequently reported foodborne illness in the European Union.[2] C. coli grows slowly with an optimum temperature of 42 °C. When exposed to air for long periods, they become spherical or coccoid shaped.[3]

Campylobacter coli
Scientific classification
Domain: Bacteria
Phylum: Campylobacterota
Class: "Campylobacteria"
Order: Campylobacterales
Family: Campylobacteraceae
Genus: Campylobacter
Species:
C. coli
Binomial name
Campylobacter coli
(Doyle, 1948) Véron and Chatelain, 1973

History

In the year 1886, Theodor Escherich established that spiral form bacteria were noted in the stool specimen and large intestinal mucous of neonates (an infant less than 4 weeks), and kittens. However, it was not until 1957, as widely spread as the bacteria were, Campylobacter was still not implicated in the human diarrhea. Further to this, in 1973, Campylobacter was proposed as a novel genus. [4]

Pathogenicity and transmission

Campylobacter coli are thought to be mainly transmitted to humans via handling and eating raw or undercooked meat or other contaminated food products, but due to their broad natural reservoir, they can also be transmitted via soil and water.[5] Other known sources of Campylobacter infections include food products, such as unpasteurised milk and contaminated fresh produce. [6] The infectious dose of Campylobacter ranges between 1000–10,000, but even 500–800 colony forming units (CFU) has also been reported to cause disease. The bacteria can also be transmitted to humans via direct contact with infected animals. Usually the incubation time after ingestion ranges between 24–72 hours, but incubation times up to a week have been reported.[7] The adhesion to eukaryotic cells is mediated by several proteins, including the Campylobacter adhesion to fibronectin protein (CadF), which binds specifically to fibronectin in the cell membrane.[8]

Virulence factors

Campylobacteriosis seems to be dependent on several virulence factors involving adhesion, invasion and bacterial motility adherence. Campylobacter secrete a cytolethal distending toxin (CDT), which is an AB toxin composed of three subunits encoded by cdtA, cdtB and cdtC. This toxin has DNase activity, which causes DNA double-strand breaks during the cell cycle G2 phase, leading eventually to cell apoptosis in HeLa and Caco-2 cells.[9]

Survival

Campylobacter are microaerophilic, fastidious organisms that become stressed in aerobic condition, temperature variations, osmotic balances, and starvation . However, in the community of Campylobacter species, C. coli has been discovered to be more aerotolerant than C. jejuni; this explains the increasing survival and transmission of the strains during stressful processing and storage conditions (Karki et al., 2019).

Human infection

Campylobacteriosis is characterized by symptoms including high fever, headache, nausea, abdominal cramps, and diarrhoea, sometimes bloody. Foodborne infections caused by Campylobacter spp. can be diagnosed by isolation of the organism from faeces and identification by growth-dependent tests, immunological assays, or genomic analyses.[10]

Treatment

Campylobacteriosis is often self-limiting infection, which is treated according to the symptoms, for example with electrolyte replacement and rehydration. While extra fluid is required of an infected person for as long as the symptoms lasts, antibiotics such as azithromycin or ciprofloxacin can be used to treat risk groups, including immunocompromised patients.[11] Due to the increased antibiotic usage in both animal agriculture and human populations, Campylobacter spp.  has been reported to be progressively resistant to several antibiotics, including fluoroquinolones and macrolides.[12] Although most patients recover from the infection, severe post-infectious complications such as Guillain-Barré syndrome, a rare autoimmune condition which causes muscle weakness as a result of the immune system damaging the peripheral nervous system, have been linked to campylobacteriosis.[13]

See also

References
  1. Prescott LM, Harley JP, Klein DA (2005). "Campylobacter". Microbiology (6th ed.). pp. 430–433, 500.
  2. "The European Union summary report on trends and sources of zoonoses, zoonotic agents and food-borne outbreaks in 2017". EFSA Journal. 16 (12): e05500. 2018. doi:10.2903/j.efsa.2018.5500.
  3. Public Health Agency of Canada (2011). "Campylobacter coli". www.phac-aspc.gc.ca. Retrieved 22 May 2017.
  4. Véron, M.; Chatelain, R. (1973). "Taxonomic Study of the Genus Campylobacter Sebald and Véron and Designation of the Neotype Strain for the Type Species, Campylobacter fetus (Smith and Taylor) Sebald and Véron". International Journal of Systematic and Evolutionary Microbiology. 23 (2): 122–134. doi:10.1099/00207713-23-2-122. ISSN 1466-5026.
  5. Nilsson A, Johansson C, Skarp A, Kaden R, Engstrand L, Rautelin H (7 December 2017). "Genomic and phenotypic characteristics of Swedish C. jejuni water isolates". PLOS ONE. 12 (12): e0189222. Bibcode:2017PLoSO..1289222N. doi:10.1371/journal.pone.0189222. PMC 5720728. PMID 29216271.
  6. Humphrey, Tom; O'Brien, Sarah; Madsen, Mogens (July 2007). "Campylobacters as zoonotic pathogens: A food production perspective". International Journal of Food Microbiology. 117 (3): 237–257. doi:10.1016/j.ijfoodmicro.2007.01.006. ISSN 0168-1605. PMID 17368847.
  7. Black RE, Levine MM, Clements ML, Hughes TP, Blaser MJ (March 1988). "Experimental Campylobacter jejuni infection in humans". The Journal of Infectious Diseases. 157 (3): 472–479. doi:10.1093/infdis/157.3.472. PMID 3343522.
  8. Monteville MR, Yoon JE, Konkel ME (January 2003). "Maximal adherence and invasion of INT 407 cells by Campylobacter jejuni requires the CadF outer-membrane protein and microfilament reorganization". Microbiology. 149 (Pt 1): 153–65. doi:10.1099/mic.0.25820-0. PMID 12576589.
  9. Whitehouse CA, Balbo PB, Pesci EC, Cottle DL, Mirabito PM, Pickett CL (May 1998). "Campylobacter jejuni cytolethal distending toxin causes a G2-phase cell cycle block". Infection and Immunity. 66 (5): 1934–1940. doi:10.1128/IAI.66.5.1934-1940.1998. PMC 108146. PMID 9573072.
  10. Madigan MM, Martinko J, Bender K, Buckley D, Stahl D (2014). Brock biology of microorganisms (Fourteenth ed.). Boston. ISBN 978-1-292-01831-7. OCLC 880685515.
  11. "Antibiotic Resistance | Campylobacter | CDC". www.cdc.gov. 23 December 2019. Retrieved 15 May 2020.
  12. Schiaffino F, Colston JM, Paredes-Olortegui M, François R, Pisanic N, Burga R, et al. (February 2019). "Campylobacter Species in a Pediatric Cohort Study". Antimicrobial Agents and Chemotherapy. 63 (2). doi:10.1128/AAC.01911-18. PMC 6355604. PMID 30420482.
  13. Zilbauer M, Dorrell N, Wren BW, Bajaj-Elliott M (February 2008). "Campylobacter jejuni-mediated disease pathogenesis: an update". Transactions of the Royal Society of Tropical Medicine and Hygiene. 102 (2): 123–129. doi:10.1016/j.trstmh.2007.09.019. PMID 18023831.

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