This species of microbe is one of the most common causes of food poisoning in Europe and in the US, with the vast majority of cases occurring as isolated events rather than mass outbreaks.

Campylobacter is a helical-shaped, non-spore-forming, Gram-negative, microaerophilic, nonfermenting motile bacterium with a single flagellum at one or both poles,[6] which are also oxidase-positive and grow optimally at 37 to 42 °C.

Seabald and Vernon proposed the genus Campylobacter due to its low levels of guanine and cytosine, non-fermentative metabolism, and microaerophilic growth requirements.

[17] The CDC, USDA and FDA collectively identified C. jejuni as responsible for over 40% of bacterial gastroenteritis found in laboratories as of 1996.

[16] The four main amino acids C. jejuni takes in are serine, aspartate, asparagine, and glutamate, which are listed in order of preference.

[21] Serine is the most important amino acid used for growth, brought into the cell by SdaC transport proteins and further broken down into pyruvate by the SdaA dehydratase.

[22] The conversion of acetyl-CoA to acetate mentioned above has substrate-level phosphorylation take place, giving another form of energy production without the use of microaerophilic respiration.

[23] Unlike almost all other Campylobacter or Helicobacter species, C. jejuni can also accept electrons from sulfite and metabisulfite through its cytochrome c oxidoreductase system.

Enzymes C. jejuni carries to impede the effects of reactive oxygen species include: superoxide dismutase SodB, alkyl hydroxide reductase AhpC, catalase KatA, and thiol peroxidases Tpx and Bcp.

[24] Infection with C. jejuni typically results in enteritis, or inflammation of the small intestine, which is characterized by abdominal pain, voluminous diarrhea (often bloody), fever, and malaise.

Severe (accompanying fevers, blood in stools) or prolonged cases may require erythromycin, azithromycin, ciprofloxacin, or norfloxacin.

[29] The membrane-bound protein Fibronectin is a critical binding site for C. jejuni on the basolateral side of the polarized epithelial cell, facilitating this process.

[29] Once inside the cell, C. jejuni leverages dynein to access the perinuclear space within the Clathrin-Coated Vesicle, avoiding lysosomal digestion for up to 72 hours.

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.

Transcriptional and post-transcriptional regulation of flagellar synthesis in C. jejuni enables proper biosynthesis of flagella and it is important for pathogenesis of this bacteria.

In experimental processes, T cells from an immune response only start to grow in number at the inflammation site from the seventh day after infection.

[29] Campylobacter infections often precede GBS, indicating that molecular mimicry between the bacteria and host nervous tissues may be the underlying cause.

[29] C. jejuni , the most common causative agent of human campylobacteriosis, can survive in the gut for several days but does not establish a long-term infection due to its low replication rate, which is incompatible with a persistent bacterial presence.

[29] The bacteria-induced apoptosis of infected gut cells results in the rapid clearance of the pathogen, which likely contributes to the self-limiting nature of the disease.

Extraintestinal manifestations of campylobacter infection are quite rare and may include meningitis, endocarditis, septic arthritis, osteomyelitis, and neonatal sepsis.

[49] Transient bacteremia in immunocompetent hosts with C. jejuni enteritis may be more common but not detected because the killing action rapidly clears most normal human serotypes, and blood cultures are not routinely performed for patients with acute gastrointestinal illness.

For instance, one major possible complication that C. jejuni can cause is Guillain–Barré syndrome, which induces neuromuscular paralysis in a sizeable percentage of those who suffer from it.

Over time, the paralysis is typically reversible to some extent; nonetheless, about 20% of patients with GBS are left disabled, and around 5% die.

[52] Community based studies done in developing countries show about 60,000 out of every 100,000 children under five years old are affected by campylobacter infections.

[3] Stool cultures are grown at 42 degrees Celsius in an atmosphere of 85% N2, 10% CO2, and 5% O2, as C. jejuni requires these conditions due to being thermophilic and microaerophilic.

[59] Azithromycin usage is increasing due to various drug characteristics, including its once-a-day dosage, tolerability by patients, decreased relation to Infantile hypertrophic pyloric stenosis (IHPS), and less negative symptoms; this is comparative to erythromycin.

Greater selectivity can be gained with an infusion of a cocktail of antibiotics: vancomycin, polymixin-B, trimethoprim, and actidione (Preston's agar),[64] and growth under microaerophilic conditions at 42 °C.

The genome of C. jejuni strain NCTC11168 was published in 2000, revealing 1,641,481 base pairs (30.6% G+C) predicted to encode 1,654 proteins and 54 stable RNA species.

[66] Analysis also predicted the first pathogenicity island in C. jejuni among select strains, harbouring the bacteria's Type VI secretion system and putative cognate effectors.

[69] Natural genetic transformation is a sexual process involving DNA transfer from one bacterium to another through the intervening medium, and the integration of the donor sequence into the recipient genome by homologous recombination.