Campylobacter

Campylobacter (from Greek campylo = curved) refers to a genus of bacteria, gram-negative rods with a spiral or S-shaped form. More than 30 species have been identified to date in the genus Camphylobacter, of which Campylobacter jejuni and Campylobacter coli are the most important human pathogenic species (Bolton DJ 2015). Both germs are closely related to each other. They are diagnosed collectively as C. jejuni for practicality. They are derived from Other species that are predominantly animal pathogens e.g. Campylobacter lari, Campylobacter fetus can also rarely cause disease in humans.

The most important human pathogenic species of the genus Campylobacter:

• C. coli (pigs and birds): Enteritis pathogen, reactive Guillain-Barré syndrome.
• C. jeuni (numerous mammals and birds): Enteritis pathogen, reactive Guillain-Barré syndrome
• C. lari (gulls): Enteritis pathogen
• C. fetus: (sheep and cattle): numerous organ infections associated with immune deficiency and bacteremia

Campylobacter species are almost ubiquitously distributed in nature. They colonize a wide range of animals as enteric commensals. These include wild animals (e.g. wild birds), farm animals (e.g. poultry, cattle and pigs) and pets (e.g. dogs and cats). The pathogens can survive for some time in the environment or in food, especially at low ambient temperatures, but cannot replicate outside the host organism, e.g. in food.

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Infections caused by bacteria of the Campylobacter genus are widespread worldwide. In Central Europe, the illnesses occur more frequently during the warm season. Children < 5 years of age and young adults between 20 and 29 years of age are particularly frequently affected by the disease in Germany. Camphylobacter infections. Campylobacter enteritis (travellers' diarrhoea) is the most frequent bacterial notifiable disease in Germany, with 60,000 - 70,000 reported cases per year (80 - 90 cases per 100,000 inhabitants) (RKI reports).

Many mechanisms are involved in the spread of campylobacter, including pathogenicity, biofilm formation, and antibiotic resistance (García-Sánchez L et al. 2018).

Camphylobacter jejuni produces a heat-labile enterotoxin, which can be considered to play a pathogenetic role in disease symptoms.
Certain lipopolysaccharides in the outer membrane of the pathogen cause a cross-reaction due to similar structural features (antigenic/molecular mimicry) of the gangliosides of the patient's peripheral nerve. This postinfectious inflammation manifests as a Guillain-Barré syndrome. 30% of all cases of Guillain-Barré disease occur after infection with Campylobacter infections.

Other rare sequelae of Campylobacter infection may include reactive arthritis. Irritable bowel syndrome and chronic inflammatory bowel diseases are also discussed.

Campylobacter infections in humans are predominantly foodborne (García-Sánchez L et al. (2018). Poultry meat, especially chicken meat, has been identified as the most important source of infection for sporadic Campylobacter enteritis (especially C. jejuni). Disease outbreaks in Germany are repeatedly caused by the consumption of unpasteurised milk (raw milk), but also of raw or insufficiently heated meat.

Other causes of outbreaks have been described as infections via contaminated drinking water or contact with pets, e.g. puppies. Infections from bathing in contaminated surface water also occur.

Contamination of food and water occurs primarily through excretions from animals colonized with Campylobacter.

Poultry meat may become contaminated during the slaughter process via the intestinal contents of the animals. Fresh retail chicken meat is often contaminated with Campylobacter. Direct human-to-human transmission plays a minor role. However, because of the low disease-causing infectious dose of ≥500 germs, it is possible, especially in young children. Infection with C. fetus is a special case.

Intrauterine or perinatal mother-to-child transmission is possible, which can lead to abortion, sepsis or meningitis.

Incubation period: Usually 2-5 days, in individual cases 1-10 days. Many infections are asymptomatic. A symptomatic infection usually presents as acute enteritis, which cannot be distinguished from enteritis of other etiologies without further diagnostics. Prodromal symptoms of fever (38-40°C), headache, myalgias, arthralgias, and lassitude are often present 12-24 hours before the onset of enteritic symptoms. The most common symptoms are diarrhea, abdominal pain or cramps, fever, and lassitude. The diarrhea can be mushy to massively watery, and not infrequently bloody (Hof H et al. 2019).

Course: The disease usually lasts up to a week, sometimes longer. The rare protracted or chronic courses usually affect resistance-compromised and immunocompromised individuals.

Duration of infectiousness: Patients are infectious as long as pathogens are excreted in the stool. The mean duration of excretion is 2-4 weeks. In young children and immunocompromised persons, e.g. AIDS patients, long-term excretion is to be expected.

Confirmation of the diagnosis by detection of the pathogen is usually carried out by cultivation from stool that is as fresh as possible (without further pre-enrichment via blood-containing selective media in a Campylobacter gas atmosphere at 42°C; thermophilic pathogens). The transport time of the sample is a relevant factor due to the sensitivity of the pathogens to temperature fluctuations. In principle, the aim should be to obtain samples for pathogen diagnostics at the stage of acute symptoms and to send them to the laboratory as soon as possible. The detection of C. jejuni and C. coli can also be performed by antigen detection in stool using enzyme-linked immunosorbent assay (ELISA) or by nucleic acid detection (PCR) . A cultural detection should additionally be aimed at in order to enable resistance testing, if necessary. It is foreseeable that genome sequencing(Whole Genome Sequencing, WGS) - initially in special laboratories - will also become increasingly established here for epidemiological questions.

Other bacterial (e.g. salmonella, shigella, yersinia, enterotoxic E. coli, enterohaemorrhagic E. coli, Clostridium difficile), viral (e.g. noroviruses, adenoviruses, rotaviruses) and parasitic diarrhoeal pathogens (e.g. amoebae, giardia) should be considered for differential diagnosis. Other non-infectious causes, such as chronic inflammatory bowel diseases and irritable bowel syndrome, should also be included in the diagnostic calculation in the absence of pathogen detection or persistence of symptoms.

As a rule, the disease is self-limiting. Symptomatic therapy with volume and electrolyte substitution is sufficient in almost all cases.

According to the recommendations of the S2k guideline "Gastrointestinal infections and Whipple's disease" (2015), antibiotic therapy should not be administered if clinical symptoms have already improved by the time microbiological evidence is obtained. In severe disease, lack of clinical improvement or immunosuppression, antimicrobial therapy (considering resistance testing) should be performed with azithromycin (1st choice) or ciprofloxacin (alternative). However, the decision to treat must be made on an individual basis.

Therapy with erythromycin is no longer considered the agent of choice due to the spectrum of side effects. Cephalosporins show insufficient activity against Campylobacter and are therefore not suitable for therapy. Antibiotic therapy should be carried out depending on the results of resistance testing, as it is not uncommon for resistance to these substances to be present.

Camphylobacter enteritis is notifiable according to the Infection Protection Act.

1. Bolton DJ (2015) Campylobacter virulence and survival factors. Food Microbiol 48:99-108.

2. Fitzgerald C (2015) Campylobacter. Clin Lab Med 35:289-298.

3. García-Sánchez L et al (2018) Campylobacter in the food chain. Adv Food Nutr Res 86:215-252.

4. Hof H et al (2019) Campylobacter. In: Hof H, Schlüter D, Dörries R, eds Dual series medical microbiology. 7th, completely revised and expanded edition. Stuttgart: Thieme p 450-451