Campylobacter jejuni

[NiFe] Hydrogenase—No Urease#

Possesses a membrane-bound [NiFe] uptake-type hydrogenase that oxidizes H2 to generate proton motive force (PMF) for ATP synthesis.^{[1]Role of Nickel in Microbial PathogenesisRobert J. Maier, Stéphane L. Benoit · 2019Open reference 1 ↓}

Hydrogenase is essential for chicken colonization—the primary animal reservoir and food safety concern. hydB deletion mutants show impaired cell division and reduced host cell interaction.

H2 is abundant in the intestinal lumen (produced by fermentative gut microbiota), providing a reliable energy source in the microaerobic environment of the intestinal mucus layer.

C. concisus (a related species) has the highest H2-uptake activity of any pathogenic bacterium characterized to date.

No urease: unlike H. pylori, C. jejuni does not produce urease. It does not colonize the acidic stomach but rather the lower intestinal tract, where acid buffering is unnecessary. This makes C. jejuni a hydrogenase-only nickel (Ni)-dependent pathogen.

Competitive Advantage via H2 Metabolism#

In the microaerobic intestinal mucus niche, H2 oxidation provides a competitive energy advantage over fermentation-only organisms. Hydrogenase activity enables C. jejuni to thrive at the epithelial surface where O2 gradients create favorable conditions for microaerobic H2-dependent respiration.

This nickel-dependent energy metabolism supports the flagellar motility and chemotaxis that are critical for mucosal colonization.

Iron Acquisition#

C. jejuni produces enterobactin receptors (CfrA, CfrB) for siderophore piracy—scavenging iron-loaded siderophores produced by other gut microbes rather than synthesizing its own.

Also acquires iron via ferric enterochelin, hemin, and transferrin/lactoferrin binding proteins. Iron restriction is a major host defense; C. jejuni iron-uptake mutants are severely attenuated.

Clinical Significance#

Leading cause of bacterial gastroenteritis in developed countries. Primarily foodborne (undercooked poultry, unpasteurized milk).^{[1]Role of Nickel in Microbial PathogenesisRobert J. Maier, Stéphane L. Benoit · 2019Open reference 1 ↓}

Causes watery or bloody diarrhea, abdominal pain, fever. Usually self-limiting but can be severe in children and immunocompromised patients.^{[2]Bushman 2025 — The Exploitation of Nutrient Metals by Bacteria for Survival and Infection in the GutSummer D Bushman, Eric P Skaar, N Luisa Hiller · 2025Open reference 2 ↓}

Guillain-Barre syndrome (GBS): C. jejuni infection is the most common antecedent of GBS, an autoimmune peripheral neuropathy. Molecular mimicry between C. jejuni lipooligosaccharide and gangliosides drives the autoimmune response.^{[1]Role of Nickel in Microbial PathogenesisRobert J. Maier, Stéphane L. Benoit · 2019Open reference 1 ↓}

Reactive arthritis: post-infectious joint Metal-Driven Inflammation; related C. fetus has been linked to spondylitis-CKD syndromes demonstrating extraintestinal sequelae of the genus.^{[3]Choi et al. 2016 — Campylobacter fetus subsp. testudinum Spondylitis in CKD PatientHong Sang Choi, Sung Un Shin, Eun Hui Bae et al. · 2016Open reference 3 ↓}

Growing fluoroquinolone resistance complicates treatment of severe cases.