This episode explores two genera of curved Gram-negative rods that occupy distinct niches within the gastrointestinal tract. Drawing from Murray’s Chapter 28, it contrasts Campylobacter - a common cause of inflammatory diarrhoea - with Helicobacter pylori, a master of chronic gastric colonisation.

The narrative begins with Campylobacter jejuni, typically acquired through undercooked poultry or contaminated water. Its motility, invasiveness, and cytotoxin production result in inflammatory diarrhoea often accompanied by fever and abdominal pain. The episode also highlights post-infectious sequelae, particularly Guillain–Barré syndrome, linking microbial surface structures to autoimmune cross-reactivity.

It then transitions to Helicobacter pylori, whose urease production allows survival in the acidic gastric environment. Rather than causing acute diarrhoea, H. pylori establishes long-term colonisation, leading to chronic gastritis, peptic ulcer disease, and increased risk of gastric carcinoma and MALT lymphoma.

Conceptually, this chapter contrasts acute inflammatory invasion with chronic inflammatory persistence. Clinically, it reinforces that bacterial shape, motility, and enzymatic adaptation define anatomical targeting.

Key Takeaways

* Both genera are curved Gram-negative rods

* Campylobacter jejuni causes inflammatory diarrhoea

* Molecular mimicry may lead to Guillain–Barré syndrome

* Helicobacter pylori survives gastric acidity via urease

* Chronic infection is linked to ulcer disease and malignancy

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