Campylobacter

Campylobacter spp. generally appear as curved or comma-shaped rods, and are able to move via unipolar or bipolar flagella.[1] They grow best between 37–42 °C in a microaerophilic environment.[11] When exposed to atmospheric oxygen, C. jejuni is able to change into a coccal form.[12] Most species of Campylobacter are positive by the oxidase test and catalase test and are able to reduce nitrate. The number of known quinolone-resistant Campylobacter strains is growing. It is suggested that this is caused by the overuse of quinolone antibiotics in animal agriculture.[12]

Theodor Escherich was the first to describe in 1886 what are known today as Campylobacters in the stool samples of infants, who perished from a disease he named "cholera infantum".[13] In the following years until the end of the century, a number of publications appeared, describing the occurrence of such "spirilla" in cases of "cholera-like" and "dysenteric" disease. These organisms were mainly found in the colon or associated with mucous in diarrhoeal stool specimens. Vibrio-like bacteria were also described by Sir John McFadyean and Stockman in 1913 in fetal tissues of aborted sheep.[14] For several years Campylobacters were continuously referred to as ‘‘Vibrio-like organisms’’, until 1963 when Sebald and Veron gave the name "Campylobacter" to the genus based on their shape and microaerophilic growth requirement and after showing significant biological differences with Vibrio species.[13]

The genomes of several Campylobacter species have been sequenced, beginning with C. jejuni in 2000.[15][16] These genome studies have identified molecular markers specific to members of Campylobacter {{Citation needed}}. Campylobacter ssp. genomes are rather small compared to those of other gastrointestinal pathogens, with sizes ranging between 1.60 and 1.90 Mbp.[17] A characteristic of most Campylobacter genomes is the presence of hypervariable regions, which can differ greatly between different strains.[16]

Studies have investigated the genes responsible for motility in Campylobacter species. Some Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence.[18]

The confusing taxonomy of Campylobacter over the past decades makes identifying the earliest reports of Campylobacter bacteriophages difficult {{Citation needed}}. 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.[19][20][21][22]

Campylobacter can cause a gastrointestinal infection, campylobacteriosis. The incubation period is 24–72 hours after infection.[23] This is characterized by an inflammatory, sometimes bloody diarrhea or dysentery syndrome, mostly including cramps, fever, and pain.[4][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.[6] 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 {{Citation needed}}. 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 {{Citation needed}}. Campylobacter has, on rare occasions, been suggested to cause hemolytic uremic syndrome and thrombotic thrombocytopenic purpura, though no unequivocal case reports exist {{Citation needed}}. 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.[4]

Campylobacter testing needs to be done to manage the risk of foodborne Campylobacter and reducing the level of foodborne Campoboteriosis, to protect people and to determine if a person is infected with Campylobacter.

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.[30] 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,[31] although other antibiotics, such as quinolones, tetracycline and other macrolides are sometimes used to treat gastrointestinal Campylobacter infections in adults.[32] 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.[33] 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