Foodborne campylobacteriosis

May 2017

Campylobacters occur widely as part of the intestinal flora of many warm-blooded animals and birds, particularly cattle and poultry, and can be carried in animals that are used for food production and in domestic pets, including cats and dogs. In addition, the bacteria can also occur in untreated water and raw milk. In The UK and Europe Campylobacter is the most commonly reported bacterial cause of intestinal infection and is considered to be one of the leading global causes of human gastroenteritis. Evidence indicates that the most important risk factors for food-borne infection are consumption of undercooked poultry (particularly chicken) and other meat, unpasteurised milk and food that has been cross-contaminated.


In 1886 Theodor Escherich observed non-culturable spiral form bacteria in stool samples from children with diarrhoea and subsequently in kittens. Campylobacter was identified for the first time in 1906 when two British veterinarians reported the presence of “large numbers of a peculiar organism” in the uterine mucus of a pregnant sheep; following this in 1913 McFaydean and Stockman identified Campylobacter in fetal tissue of aborted sheep. The isolation of Campylobacter from blood samples of children with diarrhoea was described by King in 1957(1). Sebald and Véron first proposed the genus Campylobacter in 1963, distinguishing them from Vibrio spp(2), and then in 1972 clinical microbiologists in Belgium isolated Campylobacter from stool samples of patient’s with diarrhoea(3).

The development of selective growth media in the 1970’s permitted more laboratories to test stool specimens for Campylobacter, and the species emerged as an important human pathogen.

What is Campylobacter?

Campylobacters are the most frequently reported bacterial cause of human diarrhoeal disease in countries where surveillance of infection has been implemented. Campylobacter species are a leading cause of zoonotic enteric infections in many developed countries, commonly affecting infants and children; making Campylobacter a medically and socio-economically important human pathogen. C. jejuni is responsible in developed countries for approximately 90—95% of diagnosed campylobacter infections, although other species including C. coli, C. lariC. upsaliensis may also cause infection. In developing countries C. hyointestinalis may be responsible for a larger percentage of infections.

Within the last 20 years, the reported incident rate of Campylobacter infections has increased in many countries; the increase in reports may be due in part to increased awareness, improved laboratory diagnosis and surveillance. Under-reporting of Campylobacter infections is believed in to be an issue in many countries with a reporting structure, with incidence rates only reflecting the number of laboratory-confirmed cases. Documented outbreaks of Campylobacter infections are rare, with most reported cases being sporadic or as part of small, family-related outbreaks(4,5,6).

Campylobacters, especially Campylobacter jejuni, frequently colonise the mucosal layer of the intestinal tract of poultry, other birds and animals. Levels of Campylobacters in the intestines of infected poultry can be particularly high, up to 1010 CFU per g of faeces; during times of stress on farm the bacteria can be excreted in large numbers and during slaughter and processing the poultry carcasses can become contaminated with low numbers of campylobacters released from the intestinal tract during evisceration. A survey of chicken on retail sale in the UK showed that 63.1% of chicken skin and 5.5% of outer packaging was contaminated with Campylobacter(7).


Two genera, Campylobacter and Arcobacter form the family Campylobacteraceae, which occur primarily as commensals in humans and domestic animals. The genus Campylobacter generally contains small (0.2–0.8 μm × 0.5–5 μm) Gram-negative, slender spirally curved rods, which form an “S” or a “V” shape when two or more bacterial cells are grouped together. The majority of the species have a corkscrew-like motion by means of a single polar unsheathed flagellum at one or both ends of the cell(8).

C. jejuni has been isolated from cattle, sheep, goats, dogs and cats. In contract C. coli is predominantly found in pigs although has also been isolated from poultry, cattle and sheep.

Campylobacter jejuni hydrolyses hippurate, and indoxyl acetate and reduces nitrate. Most strains are resistant to cephalothin with resistance to fluoroquinolones becoming an increasing concern as this is a category of antibiotics normally used to treat animal and human illness.

Characteristic spiral, or corkscrew, shape of C. jejuni cells and related structures (from United States Department of Agriculture, Agricultural Research Service)

Growth and survival

Campylobacter spp. typically grows at 37°C, but not below 32°C. The high optimum growth temperature of 42°C of C. jejuni and C. coli distinguishes them from most other Campylobacter spp. While it is therefore not likely that Campylobacter will multiply during processing, refrigerated transport and storage, the organism can survive these steps and therefore follow the refrigerated supply chain. Campylobacter sppmay persist for prolonged periods in chilled and frozen products. A decrease at 4°C in the concentration and viability of cells has been recorded after several weeks but the cells can respire, generate ATP, and move towards more favourable environments. Persistence in frozen poultry may be several months, with the largest log reduction during initial freezing. Oxidative stress has been shown to contribute to the freeze-thaw induced killing of Campylobacter. Research has shown that on chilled raw chicken and pork skin, C. jejuni and C. coli can survive for several weeks.

While most Campylobacter species are microaerophilic, optimally growing in low oxygen or microaerophilic environment such as an atmosphere of 5% oxygen, 10% carbon dioxide and 85% nitrogen, a few species can grow under strictly aerobic or anaerobic conditions. The microaerophilic species appear to have an inherent sensitivity towards oxygen and its reduction products, with a requirement for cellular defences to survive during exposure to air. Because of this the survival of Campylobacter outside the host intestine is poor and replication does not readily occur outside of the organism. C.jejuni may be able to adapt to differing hosts and niches and survive environmental atmospheric oxygen conditions(13).

The organism is sensitive to heat, drying and acidic conditions (pH of less than 4.9 with optimal growth at pH 6.5 to 7.5) and salinity. Campylobacter is sensitive to salt concentrations above 1.5%; both C. jejuni and C. coli are sensitive to heat and do not survive cooking or pasteurisation temperatures with D-values of 0.21–2.25 minutes at 55–60°C. Research has shown that C. jejuni can mount adaptive responses to both acidic and aerobic conditions, and there is increasing recognition that Campylobacter is more resistant to stress than had initially been thought. The organism is relatively sensitive to osmotic stress; however evidence shows that the organism can be recovered from dry surfaces 24 hours after contamination albeit in low numbers. (14).

An important factor in the persistence of the organisms is their tendency to become attached to or entrapped in the skin surface and this may also limit the removal of Campylobacter during carcass washing. This tendency seems to offer a degree of protection from environmental stresses to the organism encountered during heating, chilling and exposure to chlorinated water.

Campylobacter appears unable to multiply in the processing plant, as the minimum growth temperature is 32-35°C and the optimum is 37-42°C. Growth outside the intestine requires a reduced concentration of atmospheric oxygen and preferably 10% carbon dioxide. C.jejuni may survive at 4ºC in low oxygen, moist foods for 2-4 weeks.

Under unfavourable growth conditions, such as osmotic stress, Campylobacter converts from the typical spiral shape to a coccoid form, possibly via a ‘doughnut’ shape as the cells curl during the transition from rod to coccoid shape. This form is non-motile despite maintaining the presence of flagella and is likely to be a non-viable degenerate cell form which is undergoing an autolytic process of cellular degradation with a possible role in biofilm formation(9,10). Research has shown that Campylobacter species can survive cleaning and disinfection steps in poultry processing environments and survive for at least 21 days(11). 

Reservoirs and sources

The gastrointestinal tracts of birds (particularly poultry), cattle, rodents and domestic pets are typical reservoirs of infection for Campylobacter. C. jejuni grows best at the body temperature of a bird, and seems to be well adapted to birds, which carry it without becoming ill. Flies are a vehicle for this organism through transmission from fecal sources to broiler chickens(18); some wild birds including the European Blackbird may be a persistent source of Campylobacter(19).

As already discussed, poultry can have a high bacterial load, and occupational exposure when processing poultry in abattoirs may be implicated in some cases. While not usually spread from person to person, this can happen if the infected person is producing a large volume of diarrhoea and personal hygiene is poor.

For consumers the primary reservoir is typically undercooked meat (especially poultry), or cross contamination - undercooking of poultry / meat and using the same equipment and utensils for raw poultry and then vegetables or other raw or lightly cooked products. A considerable proportion of raw chicken on sale in the UK are contaminated with a high level of Campylobacters(7). Barbecued meat, bottled mineral water, unpasteurised milk, bird-pecked milk on doorsteps and untreated water are all vehicles of Campylobacter. Young children acquire the infection through contact with poultry packages in shopping carts and cases have been reported from contact with stools of an ill dog or cat.

Other risk factors that have been identified are acquiring an infection during travelling, contact with pets and farm animals, and recreational activities (sand from beaches, surface waters, rivers and lakes) in nature via sewage and from the faeces of wild animals and birds.


Infectivity and symptoms

The main route of infectivity is generally foodborne, with a low infectious dose (500 or less cells) for Campylobacter dependent upon a number of factors which may be strain specific, including the virulence of the strain, the vehicle with which it is ingested and the susceptibility of the individual, although the organism does not multiply in food. The most common symptoms of campylobacter infection include diarrhoea (from profuse and watery to bloody and dysenteric), abdominal pain which can mimic acute appendicitis, fever, headache and nausea, with vomiting being uncommon. Symptoms usually start 2–5 days after infection, although can be 1-11 days after infection, lasting for 3–6 days although mild relapses do occur and the organism may continue for up to 2 to 3 weeks(11).

The elderly, children, and individuals with immuno-compromised illnesses are most at risk; due to contaminated aerosols new workers at slaughterhouses also have an increased risk. Young adults (15-25 years old) appear to be either more frequently exposed or more susceptible to Campylobacter than other age groups. The reason is unknown but males appear to have a higher incident rate of infections than females.

Specific treatment is not usually necessary, except to replace electrolytes and water lost through diarrhoea. Antimicrobials may be needed to treat invasive cases and the carrier state. Severe complications, such as reactive arthritis, Guillain-Barré syndrome (GBS) (demyelinating disorder of the peripheral nervous system resulting in weakness of the limbs, weakness of the respiratory muscles and loss of reflexes and Miller Fischer Syndrome (thought to be a variant of GBS) may follow Campylobacter infection.

Few deaths are related to Campylobacter infections and these deaths typically occur among the at-risk populations of infants, elderly and immuno-suppressed individuals.

A vital part of the pathogenesis of Campylobacter mediated gastroenteritis is the penetration of the intestinal mucosaAfter adhering to the intestinal cell lining the bacterium becomes internalised within the cells, reflecting the virulent mechanism by which the organism gains access to sub-mucosal tissue causing damage and inflammation leading to gastroenteritis (13). Campylobacter adhere to cell membranes and are internalized into cytoplasmic vacuoles, providing the asaccharolytic, slow growing organism a suitable intracellular niche where microbial competition is either less or absent and Campylobacter can process metabolites from other microbes.


During each year the reported number of cases of Campylobacter regularly changes, with a consistent increase in the late spring and early summer with a gradual reduction during the summer and autumn months.

Studies have shown an increase in the level of Campylyobacter during late spring and summer, particularly in children under 5. This correlates with an increase in Campylobacter bacterial load in broiler chicken flocks and raw poultry in retail.

The changes in cases since 1989 have been broadly similar for most regions in the UK with an increase between 1987 and 2001. Some of the change between 1989 and 2008 may reflect improvements in the diagnosis and reporting over this period.

Cases and Outbreaks

Outbreaks are infrequent but large outbreaks from raw and inadequately pasteurised milk and contaminated water supplies have been reported, with campylobacter increasing since 2009; campylobacter is now the most frequently implicated causative agent causing 24% of all reported outbreaks(11).

Campylobacter cases increased in England and Wales from 1989 to 2000, declined in numbers between 2000 and 2004 and have risen again since 2004(9). Most campylobacter outbreaks were associated with consumption of undercooked poultry liver pâté or parfait from food service establishments, with the remainder from residential or institutional setting s (11). In 2016 there was a 17% decrease in the number of laboratory reports reported by UK surveillance bodies.

Rate of Campylobacter infections by country per 100,000 populations for quarters 1-3, 2007-2016

 General outbreaks of Campylobacter are rare, with 0.4% of outbreaks from 1995-1995 being recognized as due to Campylobacters(7).



Raw poultry handling and the consumption of poultry products have typically been identified as important risk factors, accounting for a variable percentage of cases, along with cross contamination of Campylobacter from raw chicken to prepared food.

Other food-related risk factors that have repeatedly been identified include consumption of other meat types, undercooked or barbecued meat, raw seafood, drinking untreated surface water, contaminated cucumbers or unpasteurised milk or dairy products. Eating meat cooked outside the home (at restaurants) has also been identified as a risk factor in the United States of America and New Zealand.

While campylobacter does not multiply within food, the bacteria rapidly attach to a surface when exposed to air and encase themselves in a sticky biofilm. Cells can be shed from the biofilm and potentially enter the food chain. This provides an example of campylobacter’s ability to sense and respond quickly to stresses in its environment and may have an impact on how Campylobacter infections are spread (15).

Isolation of Campylobacter

Due to the different growth requirements of different Campylobacter species, detection and isolation of Campylobacter from foods and food-animal matrices is dependent on the types of media, isolation methods and laboratory method used. Primary isolation of this organism usually requires the use of selective filtration, non-selective media and incubation at 37°C.

The various species do not ferment or oxidise sugars and are sensitive to hydrogen peroxide and superoxide anions produced in media. To increase the aerotolerance of the organisms and neutralise the toxic products of oxygen various oxygen scavengers can be added to enrichment broths and selective agars including superoxide dismutase, catalase, lysed blood, FBP (0.025% each of ferrous sulphate, sodium metabisulphite and sodium pyruvate) or CFP (0.4% charcoal, 0.025% ferrous sulphate and 0.025% sodium pyruvate). Oxygen sensitivity is dependent on the growth media, so results obtained in one substrate do not necessarily translate to others.

Alternative and rapid methods have been developed for the detection and confirmation of the presence of Campylobacter spp. with examples including fluorescence in situ hybridization, latex agglutination and a physical enrichment method (filtration) that permits the separation of Campylobacter from other organisms present in the food matrix. Polymerase chain reaction (PCR) reaction tests can be very effective and this method has been combined with some success with immuno-separation giving the ability to detect Campylobacter in detecting low numbers in about 6 hours8.

Good Industry Practice


  • Maintenance and pest proofing (including fly screens)– it is important that buildings are of sound construction and well maintained to prevent access by wild birds, insects and to deter rodents
  • Chlorination of the water supply (2ppm) or in-line UV treatment
  • Biosecurity and intervention measures including hygiene practices to prevent introduction by farm staff from external sources such as dedicated clothing and footwear
  • Cleaning and disinfection of barns and houses between flocks
  • Restricted access of cats and dogs to poultry flocks
  • Limit ‘thinning’ of flocks as it may introduce campylobacter through staff, crates and modules and also cause stress, resulting in increased susceptibility to colonisation –or carry out thinning in association with crate washing that will reduce microbial load and biosecurity measures
  • Wash crate surfaces and lorry decks in a manner that will reduce campylobacter load e.g, warm/hot water, suitable detergents, and or/disinfectants at correct usage levels between journeys – including wheels on lorries
  • High levels of stockmanship and staff training on flock infection
  • Simple modification of the diet, e.g. addition of organic acids or probiotics, has shown a potential influence upon Campylobacter levels with no net adverse effects on the health, welfare or productivity of the animal

Animal transport

  • Animal welfare handling practices to reduce stress

Slaughter and processing

  • HACCP and up to date GMP practices
  • Segregation of Campylobacter-positive flocks from negative flocks for poultry (using rapid testing protocols) at the slaughter house, and slaughtering of the positive flocks
  • Withdrawal of feed for at least 12 hours before slaughter


  • Moving carcasses against the flow of incoming water (counter-flow), so that they meet the cleanest water at the carcass-exit end
  • High flow rates of water with adequate agitation
  • Optimum scalding temperature to minimise levels of Campylobacter
  • Use of approved chemicals e.g. pH regulators.
  • Using several successive tanks operated in the same way, to provide a dilution effect
  • Empty and clean tanks at end of a processing period (at least twice daily)
  • Hygiene measures applied to reused/recycled water


  • Minimise rupture of exposed intestines and prevent the spread of faecal bacteria such as Campylobacter, which occur in relatively high numbers particularly in the intestines of positive birds
  • Careful siting of evisceration machinery to prevent microbial attachment and cross contamination
  • Strategic washing of carcasses at points close to sites of contamination, in order to avoid microbial attachment
  • Spraying of contact surfaces with chlorinated water where legislation allows
  • Use of automatic transfer of carcasses from the slaughter line to the evisceration line and, where possible, on to the chilling line.


  • High-pressure washers may remove significant numbers of microbial contaminants from both the inner and outer surfaces of the carcass. The extent to which contamination is reduced at this stage depends upon the frequency and degree of washing at earlier stages but may have little effect on cells attached to carcass surfaces


  • Super-chlorination of water used in chilling is of value in controlling cross-contamination via the water itself, although is thought to have little further effect on microbial contamination of carcasses
  • Processing aids including free chlorine, organic acids and other antioxidants added to potable, chilled water or recirculated water
  • Storage at -20°C for 31 days
  • Crust freezing for skinless boneless through continuous carbon dioxide belt freezing


  • Use of GMP’s to prevent cross contamination from workers, tools and equipment.
  • Risk management to differentiate between campylobacters from the carcass exterior and campylobacters in the faeces that leaks during processing.
  • Pasteurisation of milk
  • Treatment of municipal water supplies
  • Consumer education/cooking instructions

[1] Microbial update Campylobacter: International Food Hygiene— Volume 21 Number 2 Pages 12-13

[2] International Journal of Systematic and Evolutionary Microbiology doi: 10.1099/ijs.0.64109-0 IJSEM May 2006 vol. 56 no. 5 937-945

[3] Altedruse SF, Stern NJ, Fields PI, Swerdlow DL. Campylobacter jejuni—An Emerging Foodborne Pathogen.Emerg Infect Dis [serial on the Internet]. 1999, Feb

[4] [date cited].Available from 

[5] Hilpi Rautelin. Campylobacter, The Lancet Infectious Diseases, Volume 8, Issue 11, Page 673



[8] FSA Project FS102121 Year 2 Report A microbiological survey of Campylobacter contamination in fresh whole UK-produced chilled chickens at retail sale. 2017. Frieda Jorgensen, Andre Charlett, Eve Arnold, Craig Swift, Bob Madden and Nicola C Elviss Public Health England.

[9] Silva J, Leite D, Fernandes M, Mena C, Gibbs PA and Teixeira P (2011) Campylobacter spp. as a foodborne pathogen: a review. Front. Microbio. 2:200. doi: 10.3389/fmicb.2011.00200

[10] Eur J Microbiol Immunol (Bp). 2012 Mar; 2(1): 41–49. Published online  2012 Accessed: Mar 2017. DOI:  10.1556/EuJMI.2.2012.1.7 PMCID: PMC3933989. Putative mechanisms and biological role of coccoid form formation in Campylobacter jejuni. N. Ikeda and A. V. Karlyshev                      

[11] Autolytic process (J Clin Microbiol. 1983 August; 18(2): 420–421. PMCID: PMC270816 Electron microscopy of the coccoid form of Campylobacter jejuni. G E BuckK A Parshall, and C P Davis )

[12] Food Microbiol. 2017 Aug;65:185-192. doi: 10.1016/ Epub 2017 Feb 24. Campylobacter jejuni survival in a poultry processing plant environment. García-Sánchez LMelero BJaime IHänninen MLRossi MRovira J.

[13] Front Microbiol. 2016 Dec 26;7:2117. doi: .3389/fmicb.2016.02117. eCollection 2016. The Campylobacter jejuni Oxidative Stress Regulator RrpB Is Associated with a Genomic Hypervariable Region and Altered Oxidative Stress Resistance. Gundogdu Oda Silva DTMohammad BElmi AWren BWvan Vliet AHDorrell N.


[15] [

[16] (S.P. Bhavsar, B.P. Kapadnis: Virulence factors of Campylobacter. The Internet Journal of Microbiology. 2007 Volume 3 Number 2. DOI: 10.5580/62b)

[17] [11] [12] 

[18] J Food Prot. 2003 Sep;66(9):1587-94. Survival and persistence of Campylobacter and Salmonella species under various organic loads on food contact surfaces. De Cesare A 

[19] Sheldon BWSmith KS , Jaykus LA.

[20] Epidemiol Infect. 2016 Nov;144(15):3326-3334. Epub 2016 Aug 15. A role for flies (Diptera) in the transmission of Campylobacter to broilers? Royden AWedley AMerga JYRushton SHald BHumphrey TWilliams NJ.

[21] Environ Microbiol Rep. 2015 Oct;7(5):782-8. doi: 10.1111/1758-2229.12314. Epub 2015 Sep 8.Wild bird-associated Campylobacter jejuni isolates are a consistent source of human disease, in Oxfordshire, United Kingdom. Cody AJMcCarthy NDBray JEWimalarathna HMColles FMJansen van Rensburg MJDingle KEWaldenström JMaiden MC.

[22] FSA Project FS102121 Year 2 Report A microbiological survey of Campylobacter contamination in fresh whole UK-produced chilled chickens at retail sale. 2017. Frieda Jorgensen, Andre Charlett, Eve Arnold, Craig Swift, Bob Madden and Nicola C Elviss Public Health England.



The Institute of Food Science & Technology has authorised the publication of this statement, prepared and updated by Julie Ashmore, peer reviewed by professional members of the IFST and approved by the IFST Scientific Committee

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