Campylobacter

Campylobacter
Campylobacter jejuni
Scientific classification
Kingdom:	Bacteria
Phylum:	Proteobacteria
Class:	Epsilonproteobacteria
Order:	Campylobacterales
Family:	Campylobacteraceae
Genus:	Campylobacter Sebald and Véron 1963
Species
C. avium C. butzleri C. canadensis C. cinaedi C. coli C. concisus C. corcagiensis C. cryaerophilus C. cuniculorum C. curvus C. fennelliae C. fetus C. gracilis C. helveticus C. hominis C. hyoilei C. hyointestinalis C. insulaenigrae C. jejuni C. lanienae C. lari C. mucosalis C. mustelae C. nitrofigilis C. peloridis C. pylori C. rectus C. showae C. sputorum C. subantarcticus C. upsaliensis C. ureolyticus C. volucris

Campylobacter (meaning "curved bacteria") is a genus of Gram-negative, microaerophilic, oxidase-positive, nonfermentative bacteria.^[1] Campylobacter species are typically spiral-shaped and able to move via unipolar or bipolar flagella.^[1] Most Campylobacter species are pathogenic and can infect humans and other animals. At least a dozen species of Campylobacter have been implicated in human disease, with C. jejuni and C. coli the most common.^[2] C. jejuni is now recognized as one of the main causes of bacterial foodborne disease in many developed countries.^[2][3] C. fetus is a cause of spontaneous abortions in cattle and sheep, as well as an opportunistic pathogen in humans.^[4]

History

The symptoms of Campylobacter infections were described in 1886 in infants by Theodor Escherich.^[5] These infections were named cholera infantum,^[5] or summer complaint.^[6] The genus was first described in 1963;^[7] however, the organism was not isolated until 1972.^[5]

Genome and proteome

The genomes of several Campylobacter species have been sequenced.^[8] The first Campylobacter genome to be sequenced was C. jejuni, in 2000.^[9]

Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence.^[10] Nonmotile mutants do not colonize.

Sequence features: Comparative genomic analysis has led to the identification of 15 proteins which are uniquely found in members of the genus Campylobacter and serve as molecular markers for the genus. Eighteen other proteins were also found which were present in all species except C. fetus, which is the deepest-branching Campylobacter species. A conserved insertion has also been identified which is present in all Campylobacter species except C. fetus. Additionally, 28 proteins have been identified present only in C. jejuni and C. coli, indicating a close relationship between these two species. Five other proteins have also been identified which are only found in C. jejuni and serve as molecular markers for the species.^[11]

Bacteriophage

The confusing taxonomy of Campylobacter over the past decades make it difficult to identify the earliest reports of Campylobacter bacteriophages. Bacteriophages specific to the species now known as C. coli and C. fetus (previously Vibrio coli and V. fetus), were isolated from cattle and pigs during the 1960s.^{[12][13][14][15]}

Pathogenesis

Campylobacteriosis, a gastrointestinal infection caused by Campylobacter, is characterized by inflammatory, sometimes bloody diarrhea or dysentery syndrome, mostly including cramps, fever, and pain.^[16][17] The most common routes of transmission are fecal-oral, ingestion of contaminated food or water, and the eating of raw meat. Foods implicated in campylobacteriosis include raw or undercooked poultry, raw dairy products, and contaminated produce.^[18] The infection is usually self-limiting and in most cases, symptomatic treatment by liquid and electrolyte replacement is enough in human infections. The use of antibiotics, though, is controversial. Symptoms typically last five to seven days.^[18]

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. A cholera-like enterotoxin was once thought to be also made, but this appears not to be the case. The organism produces diffuse, bloody, edematous, and exudative enteritis. Although rarely has the infection been considered a cause of hemolytic uremic syndrome and thrombotic thrombocytopenic purpura, no unequivocal case reports exist. In some cases, a Campylobacter infection can be the underlying cause of Guillain–Barré syndrome. Gastrointestinal perforation is a rare complication of ileal infection.^[19]

Campylobacter has also been associated with periodontitis.^[16]

Treatment

Diagnosis of the illness is made by testing a specimen of faeces.

• Standard treatment is now azithromycin. Quinolone antibiotics such as ciprofloxacin or levofloxacin are no longer as effective due to resistance.
• Dehydrated children may require intravenous 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.

Epidemiology

Campylobacter infections increased 14% in the United States in 2012 compared to the period from 2006 to 2008. This represents the highest reported number of infections since 2000.^[18]

In January 2013, the UK's Food Standards Agency warned that two-thirds of all raw chicken bought from UK shops was contaminated with Campylobacter, affecting an estimated half a million people annually and killing about 100.^[20] In June 2014, the Food Standards Agency started a campaign against washing raw chicken, as washing can spread germs by splashing.^[21]

References

External links

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