Campylobacter

Campylobacter is a class of rod or spiral-shaped bacteria. Although there are 16 species of Campylobacter, just two types are responsible for most human cases of campylobacter infection: C. jejuni and C. coli.

Infection

Campylobacter infection results in a particularly unpleasant bout of food poisoning, the symptoms being diarrhea (frequently bloody), nausea and/or vomiting, fever, headache, and abdominal and joint pain. Symptoms start within 1 - 7 days of infection and usually last for about a week, although 20% of patients may experience pain and diarrhea for up to 3 weeks. The infection generally clears up on its own.

Occasionally complications may develop - these include hepatitis, pancreatitis, bacteraemia and abortion. On rare occasions patients may be left with reactive arthritis lasting several months, or worse, Guillain-Barré syndrome - a type of paralysis similar to polio, which can be fatal.

Transmission

The disease is usually caught by drinking contaminated water or eating contaminated food. Campylobacter is present in the digestive systems of many domestic animals without causing them any obvious symptoms. It is widespread in household pets and livestock and can easily be passed on through faecal contamination. It used to be quite common to find Campylobacter contamination in milk - garden birds would peck holes through the milk bottle tops as they tried to reach the cream, leaving behind the bacteria which had been on their beaks.

Once in the human digestive system, the bacteria thrive in the semi-anaerobic conditions, invading the gut lining and multiplying rapidly. This causes lesions in the gut wall resulting in blood-stained diarrhea and cramps.

Prevention

Strict standards of food hygiene can virtually eliminate the chances of catching a campylobacter infection.

• Always cook raw meat, especially offal and poultry. Unlike Salmonella, the bacteria do not multiply on food, but Campylobacter infections can still take place upon the ingestion of very low doses of the bacteria
• Keep raw meat away from cooked products during storage and preparation
• Wash fruit and vegetables thoroughly
• Always wash hands after using the toilet, touching animals and before preparing food or drinks
• Never drink water without boiling it first, even if it comes from the clearest, sparkliest mountain stream - a sheep might have pooed in it!
• Avoid ice cubes if you are uncertain of the water source
• Don't drink unpasteurised milk
• Be extra cautious around people or animals suffering from diarrhea

Treatment

As with any form of food poisoning it is essential to maintain fluid levels - dehydration is a killer.

• Drink plenty of liquids. Add 8 tsp of sugar and 1 tsp salt and some orange juice or mashed banana (for potassium) to 1 litre of water to maintain electrolyte balance, or buy Oral Rehydration Salts from the pharmacist. Drink as much and as often as possible - at least 3 litres a day for an adult.
• Antibiotics, often erythromycin, may be prescribed by the doctor. This will kill the bacteria in the gut thus shortening the duration of the illness, and reducing the risk of passing on the infection to others.

Campylobacter infection has always been common in developing countries, where it is often fatal in infants. It is now becoming increasingly problematic in first world nations where it is responsible for more cases of food poisoning per annum than any other bacterium. It is preventable and curable, but high standards of hygiene and cleanliness are of the utmost importance if the prevalence of this disease is to be controlled. Campylobacter is one of the top 10 major diseases threatening public health in the UK, according to the Public Health Laboratory Service, and reported incidences are increasing year by year.

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http://www.who.int/inf-fs/en/fact255.html
http://www.phls.co.uk/
http://www.amm.co.uk/pubs/fa_campy.htm
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C. jejuni virulence Factors

Pertinent virulence factors of Campylobacter jejuni include:

• Motility
• Adhesion
• Production of Toxins
• Invasion

The quest to define the roles of C. jejuni’s (and indeed all Campylobacter) virulence factors has been hindered by the lack of an animal model for the disease. Specific mechanisms and attributes are suspected to differ slightly between strains.

Motility:

As C. jejuni must be flagellated to cause disease, motility is an important virulence factor. The flagella allow the bacterium to escape peristalsis, and by chemotactic means, find and enter the mucous layer that lines the epithelium of the small and large intestine. Once inside the mucous layer, C. jejuni is largely protected from the harsh environment of the lumen and is close enough to the epithelium for adhesions to bind and toxins to reach their cellular targets.

Adhesion:

Adhesion precedes invasion and may increase the local concentration of secreted bacterial products, or perhaps activate a genetic switch that enables transcription of a secretory product. The flagellum has been considered for adhesion, but some studies suggest an ancillary role. Other outer membrane proteins (OMPs) such as OMP 18 and cell binding factor 1 (CBF1) are also likely candidates. OMP 18 is implicated in the formation of a bridge between the cell membrane and the peptidoglycan that helps stabilise the cell wall, whereas CBF1 is thought to be involved in binding to host cells and amino acid transport. Strains that lack the adhesion are avirulent.

Toxins:

One of the earliest proposed mechanisms of Campylobacter pathogenesis was that of toxin production. There has since been numerous studies done, many with conflicting results. Distinct Cholera-like enterotoxin and cytotoxins have been described. Generally, the non-inflammatory, watery diarrhoea in the developing countries is due to the cholera-like enterotoxin, and the bloody mucoid inflammatory diarrhoea and invasion is associated with cytotoxin production.
The pathobiological significance of the Campylobacter jejuni enterotoxin is subject to major debate and conflicting evidence, and until it is cloned and sequenced, it will remain so. However, it is clear that strains lacking the enterotoxin are still fully virulent.
The best-characterised cytotoxin from C. jejuni is the cytolethal-distending toxin, apparently first described by Johnson and Lior (1988). It has recently been shown that CDT causes cells to become arrested in the G2 phase of the cell cycle, leading to cell death.

Invasion:

Bacterial invasion of the lamina propria ultimately results in cellular injury and therefore loss of function, leading to diarrhoea.
Researchers agree both adhesion and bacterial cell protein synthesis are required for internalisation to occur. (At least 14 de-novo proteins are synthesised when bacteria were grown in the presence of cells.) The mechanism, however, is still debated.
It is also clear that an important factor for invasion and progression of disease is that of the host’s immunological response.

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References

J. Cary; J. Linz; D. Bhatnagar, Microbial Foodborne Diseases, Technomic Publishing LTD; Pennsylvania.

Szymanski, C. M., King, M., Haardt, M., and Armstrong, G. D., Campylobacteria jejuni Motility and Invasion in Caco-2 Cells., Infection and Immunity, 63 (1995): 4295-4300

T. M. Wassenaar, M. J. Blaser, Pathophysiology of Campylobacter jejuni Infections of Humans, Microbes And Infection, 1 (1999): 1023-1033