[3] Due to their diverse natural reservoir, some Campylobacter can also be detected in the air, although not at an epidemiologically significant level.
[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.
Vibrio-like bacteria were also described by Sir John McFadyean and Stockman in 1913 in fetal tissues of aborted sheep.
[17] A single Type VI secretion system (T6SS) cluster was also predicted in approximately one-third of Campylobacter species, grouping into three distinct organisations and harbouring up to five vgrG genes.
[18] The currently accepted taxonomy is based on the List of Prokaryotic names with Standing in Nomenclature (LPSN)[19] and National Center for Biotechnology Information (NCBI)[20] C. canadensis C. lari C. volucris C. armoricus C. peloridis C. novaezeelandiae C. cuniculorum C. avium C. troglodytis C. helveticus C. upsaliensis C. vulpis C. insulaenigrae C. bilis C. hepaticus Campylobacter lari concheus C. ornithocola C. subantarcticus C. jejuni C. estrildidarum C. aviculae C. taeniopygiae C. coli Campylobacter hyointestinalis lawsonii C. lanienae C. magnus C. iguaniorum C. hyointestinalis Campylobacter fetus testudinum C. fetus C. sputorum C. gracilis C. hominis C. blaseri C. geochelonis C. portucalensis C. corcagiensis C. ureolyticus C. rectus C. massiliensis C. showae C. anatolicus C. curvus C. concisus C. pinnipediorum C. mucosalis C. majalis C. suis C. canadensis Inglis et al. 2007 C. insulaenigrae Foster et al. 2004 C. volucris Debruyne et al. 2010 C. peloridis Debruyne et al. 2009
[30] This is characterized by an inflammatory, sometimes bloody diarrhea or dysentery syndrome, mostly including cramps, fever, and pain.
[3][31] The most common routes of transmission are fecal-oral, ingestion of contaminated food or water, and the eating of raw meat.
[31] 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.
[citation needed] 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[32] and thrombotic thrombocytopenic purpura,[33] though no unequivocal case reports exist.
[citation needed] Usually, detection of Campylobacter in humans is done by laboratory culturing a stool sample or swab of the rectum collected by a healthcare provider.
[31] Treatment with antibiotics has only a minor effect on the typical duration of the infection in non-complex cases, and is discouraged except in high-risk patients.
[42] FoodNet Canada has reported that Campylobacter was the most common pathogen found on packaged chicken breast, with nearly half of all samples testing positive.
[43] In Italy, the annual prevalence of Campylobacter infections appears to be relatively stable based on findings from a national survey conducted on more than 5000 isolates.
The survey revealed that the most common species of Campylobacter were C. jejuni, accounting for 83.7% of isolates, followed by C. coli (13.5%) and C. fetus (0.6%).
[45][46][47] In June 2019, an estimated 2,000 residents of Askøy municipality got sick due to the presence of C. jejuni in the water supply.
[31] High prevalence of Campylobacter (40% or more) has been reported in raw chicken meat in regional retail stores in the US, which remained steady from 2005 through 2011.