Studies on the pathogenesis of<unk>  show that for this organism to cause disease, the susceptibility of the host and the relative virulence of the infecting strain are both important. Infection results from the ingestion of contaminated food or water, and the infective dose can be as low as 800 organisms. To initiate infection, the organism must penetrate the gastrointestinal mucus, which it does using its high motility and spiral shape. The bacteria must then adhere to the gut enterocytes and can then induce diarrhea by toxin release.<unk>  releases several different toxins, mainly enterotoxin and cytotoxins, which vary from strain to strain and correlate with the severity of the enteritis. During infection, levels of all immunoglobulin classes rise. Of these, IgA is the most important because it can cross the gut wall. IgA immobilises organisms, causing them to aggregate and activate complement, and also gives short-term immunity against the infecting strain of organism. The bacteria colonize the small and large intestines, causing inflammatory diarrhea with fever. Stools contain leukocytes and blood. The role of toxins in pathogenesis is unclear.<unk>  antigens that cross-react with one or more neural structures may be responsible for triggering the Guillain–Barré syndrome. Hypoacylated lipopolysaccharide (LPS) from<unk>  induces moderate TLR4-mediated inflammatory response in macrophages and such LPS bioactivity may eventually result in the failure of local and systemic bacterial clearance in patients. At the same time, moderation of anti-bacterial responses may be advantageous for infected patients in clinical practice, since such an attenuated LPS may not be able to induce severe sepsis in susceptible individuals. One of the most important virulence factor of<unk>  are flagella. The flagellar protein FlaA has been proven to be one of the abundant proteins in the cell. Flagella are required for motility, biofilm formation, host cell interactions and host colonization. The production of flagella is energetically costly so the production must be regulated from metabolic standpoint. CsrA is a post-transcriptional regulator that regulates the expression of FlaA by binding to flaA mRNA and is able to repress its translation. CsrA mutant strains have been studied and the mutant strains exhibit dysregulation of 120-150 proteins that are included in motility, host cell adherence, host cell invasion, chemotaxis, oxidative stress resistance, respiration and amino acid and acetate metabolism. Transcriptional and post-transcriptional regulation of flagellar synthesis in<unk>  enables proper biosynthesis of flagella and it is important for pathogenesis of this bacteria. Other important virulence factors of<unk>  are the ability to produce N-linked glycosylation of more than 30 proteins. These proteins are important for the bacteria colonization, adherence and invasion.<unk>  secretes Campylobacter invasive antigens (Cia) which facilitates the motility. The bacteria produces also cytolethal distending toxins that participate in cell cycle control and induction of host cell apoptosis.<unk>  also exploits different adaptation strategies in which the host factors seem to play a role for pathogenesis of this bacteria.
Campylobacter jejuni
Campylobacter upsaliensis
Salmonella
Yersinia enterocolitica
Salmonella enterica subsp. enterica
Escherichia coli O157:H7
Clostridioides difficile 
Enteroaggregative Escherichia coli