19.3 CASE STUDY

What is the mechanism of pathogenicity of Campylobacter?

Production of adhesins, cytotoxic enzymes and enterotoxins, but factors that regulate adhesion, motility and invasion into intestinal mucosa are poorly defined
The mechanism of pathogenesis of Campylobacter jejuni comprises four main stages: adhesion to intestinal cells, colonization of the digestive tract, invasion of targeted cells, and toxin production
To initiate infection the C. jejuni must penetrate the gastrointestinal mucus, which it does by using its high motility and spiral shape. The bacteria must then adhere to the gut enterocytes and once adhered can then induce diarrhoea by toxin release. C. jejuni releases several different toxins which vary from strain to strain, mainly enterotoxin and cytotoxins, and these correlate with the severity of the enteritis
C. jejuni and C upsalensis have been associated w/ Guillain-Barré syndrome, an autoimmune disorder of the PNS characterized by development of overall weekness over several days. Pathogenesis: antigenic cross-reactivity between the surface lipopolysaccharides of some strains of Campylobacter and peripheral nerve gangliosides

Another immune-related complication is reactive arthritis

Mechanism of Pathogenicity of Campylobacter

Production of adhesins, cytotoxic enzymes, and enterotoxins
Poorly defined factors that regulate adhesion, motility, and invasion into intestinal mucosa

Campylobacter jejuni uses high motility and spiral shape to penetrate gastrointestinal mucus
Adherence to gut enterocytes is necessary for infection

C. jejuni and C. upsalensis linked to Guillain-Barré syndrome
Pathogenesis involves antigenic cross-reactivity between Campylobacter strains and peripheral nerve gangliosides