Campylobacter

Campylobacter (meaning 'twisted bacteria') is a genus of bacteria that are Gram-negative, spiral, and microaerophilic. Motile, with either unipolar or bipolar flagella, the organisms have a characteristic spiral/corkscrew appearance (see photo) and are oxidase-positive.^[1] Campylobacter jejuni is now recognized as one of the main causes of bacterial foodborne disease in many developed countries.^[2] At least a dozen species of Campylobacter have been implicated in human disease, with C. jejuni and C. coli the most common.^[1] C. fetus is a cause of spontaneous abortions in cattle and sheep, as well as an opportunistic pathogen in humans.^[3]

Genome

The genomes of several Campylobacter species have been sequenced, providing insights into their mechanisms of pathogenesis.^[4] The first Campylobacter genome to be sequenced was C. jejuni, in 2000.^[5]

Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence.^[6] Nonmotile mutants do not colonize.

Pathogenesis

Campylobacteriosis is an infection by Campylobacter.^[7] The common routes of transmission are fecal-oral, ingestion of contaminated food or water, and the eating of raw meat. It produces an inflammatory, sometimes bloody, diarrhea, periodontitis^[8] or dysentery syndrome, mostly including cramps, fever and pain. The infection is usually self-limiting and in most cases, symptomatic treatment by reposition of liquid and electrolyte replacement is enough in human infections. The use of antibiotics, on the other hand, is controversial. Symptoms typically last for five to seven days.

Cause

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. It was thought previously that a cholera-like enterotoxin was also made, but this appears not to be the case. The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with hemolytic uremic syndrome and thrombotic thrombocytopenic purpura through a poorly understood mechanism. Gastrointestinal perforation is a rare complication of ileal infection ^[9]

Treatment

Diagnosis of the illness is made by testing a specimen of faeces (bowel motion).

• Quinolone antibiotics, as Cipro or Levaquin, are effective therapy for Campylobacter enteritis, shortening the clinical course by days, with a rapid improvement in patient well being
• Dehydrated children may require intravenous (by vein) fluid treatment in a hospital.
• The illness is contagious, and children must be kept at home until they have been clear of symptoms for at least two days
• Good hygiene is important to avoid contracting the illness or spreading it to others.
• Intestinal perforation is very rare; increased abdominal pain and collapse require immediate medical attention.

History

The symptoms of Campylobacter infections were described in 1886 in infants by Theodor Escherich.^[10] These infections were named cholera infantum,^[10] or summer complaint.^[11] The genus was first discovered in 1963;^[12] however, the organism was not isolated until 1972.^[10]

See also

• Periodontitis

References

External links

• Campylobacter genomes and related information at PATRIC, a Bioinformatics Resource Center funded by NIAID
• Campylobacter info from the CDC