Campylobacter

Campylobacter species generally appear as curved or comma-shaped rods, and are able to move via unipolar or bipolar flagella.[1] They generally survive in environments with low oxygen. When exposed to atmospheric oxygen, C. jejuni is able to change into a coccal form [8] They are positive by the oxidase test and catalase test. Campylobacter spp. are nonfermentative,[1] and are best cultured at 42 °C.[8]

Survival at room temperature is poor, but they can survive for a short time at refrigeration temperatures – up to 15 times longer at 2 °C than at 20 °C. The bacterium dies out slowly at freezing temperatures and is heat sensitive: the cells are destroyed at temperatures above 48 °C.[9]

The symptoms of Campylobacter infection were described in 1886 in infants by Theodor Escherich.[10] These infections were named cholera infantum,[10] or summer complaint.[11] The species was first isolated by Sir John McFadyean, of the Royal Veterinary College in London, in 1906.[12]

The genus was further defined in 1963.[13]

The genomes of several Campylobacter species have been sequenced, beginning with C. jejuni in 2000.[14][15] These genome studies have identified molecular markers specific to members of Campylobacter. Additionally, several markers were found in all Campylobacter species except for C. fetus, the most distantly related species. Many markers were also found which were conserved only between C. jejuni and C. coli, indicating a close relationship between these two species.[16]

Similar studies have investigated the genes responsible for motility in Campylobacter species. All Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence.[17]

The number of known quinolone-resistant strains is growing. Evidence suggests this is caused by an overuse of this class of antibiotics in animal agriculture.[8]

The confusing taxonomy of Campylobacter over the past decades makes identifying the earliest reports of Campylobacter bacteriophages difficult. Bacteriophages specific to the species now known as C. coli and C. fetus (previously Vibrio coli and V. fetus), were first isolated from cattle and pigs during the 1960s, and Campylobacter bacteriophage therapy is an ongoing area of research in the age of bacterial antibiotic resistance.[18][19][20][21]

Campylobacter can cause a gastrointestinal infection called campylobacteriosis. The incubation period is 24–72 hours after infection.[22] This is characterized by an inflammatory, sometimes bloody diarrhea or dysentery syndrome, mostly including cramps, fever, and pain.[23][24] 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 under-cooked poultry, raw dairy products, and contaminated produce.[25] Campylobacter is sensitive to the stomach's normal production of hydrochloric acid: as a result, the infectious dose is relatively high, and the bacteria rarely cause illness when a person is exposed to less than 10,000 organisms.[3] Nevertheless, people taking antacid medication (e. g. people with gastritis or stomach ulcers) are at higher risk of contracting disease from a smaller number of organisms, since this type of medication neutralizes normal gastric acid.

In humans, the sites of tissue injury include the jejunum, the ileum, and the colon. Most strains of C jejuni produce cytolethal distending toxin, which inhibits cell division and impedes activation of the immune system. This helps the bacteria to evade the immune system and survive for a limited time inside intestinal cells. A cholera-like enterotoxin was also, at one time, believed to be produced, but this appears not to be the case. The organism produces diffuse, bloody, edematous, and exudative enteritis. Campylobacter has, on rare occasions, been blamed for hemolytic uremic syndrome and thrombotic thrombocytopenic purpura, though 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.[26]

Campylobacter has also been associated with periodontitis.[23]

The infection is usually self-limiting and, in most cases, symptomatic treatment by liquid and electrolyte replacement is sufficient to treat human infections. Symptoms typically last 5–7 days.[25] Treatment with antibiotics has little effect, and is discouraged except in high-risk patients.[27] Diagnosis of campylobacteriosis is made by testing a fecal specimen. Standard treatment in high-risk cases is azithromycin, a macrolide antibiotic, especially for Campylobacter infections in children,[28] although other antibiotics, such as quinolones, tetracycline and other macrolides are sometimes used to treat gastrointestinal Campylobacter infections in adults.[29] In case of systemic infection, other bactericidal antibiotics are used, such as ampicillin, amoxicillin/clavulanic acid, or aminoglycosides. Fluoroquinolone antibiotics, such as ciprofloxacin or levofloxacin, may no longer be effective in some cases, due to resistance.[30] In addition to antibiotics, dehydrated children may require intravenous fluid treatment in a hospital.

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