Experimental Campylobacter jejuni infection in the chicken: An animal model of axonal Guillain-Barre syndrome

Objective-To develop and characterise an animal model of paralytic neuropathy after Campylobacter jejuni infection. Campylobacter infection precedes development of many cases of Guillain-Barre syndrome and is particularly associated with cases having prominent axonal degeneration. Understanding the pathogenesis of Guillain-Barre syndrome after C jejuni infection has been slowed by the lack of animal models. Methods-A spontaneous paralytic neuropathy is described that developed in chickens from the farms of four patients with Guillain-Barre syndrome. The production of paralytic neuropathy in chickens experimentally fed Campylobacter jejuni isolated from one of these patients is reported. The sciatic nerves of the spontaneously paralysed chickens were examined pathologically in teased fibres, in plastic embedded sections, and by electron microscopy. Two large groups of chickens were then fed cultures of a C jejuni (Penner type O:19) isolated from one of these patients. Results-The chickens with spontaneous paralysis had pathologically noninflammatory neuropathy. Pathology in the sciatic nerves ranged from no detectable changes to severe Wallerian-like degeneration. In the experimentally inoculated groups, an average of 33% of the chickens became paralysed. The median time after inoculation to paralysis was 12 days. The lesions found in the first few days of paralysis included nodal lengthening and paranodal demyelination. In those animals that survived for several days after onset of weakness, the pathology was dominated by extensive Wallerian-Like degeneration. Animals that survived for weeks with no clinically apparent neuropathy had paranodal remyelination in some teased nerve fibres, reflecting earlier paranodal demyelination. Conclusion-Experimental inoculation with C jejuni may provide a new model for understanding some forms of Guillain-Barre syndrome.