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 neu ropathy after Campylobacter jejuni infection. Campylobacter infection precedes development of many cases of Guillain-Barre syndrome and is p articularly associated with cases having prominent axonal degeneration . Understanding the pathogenesis of Guillain-Barre syndrome after C je juni infection has been slowed by the lack of animal models. Methods-A spontaneous paralytic neuropathy is described that developed in chick ens from the farms of four patients with Guillain-Barre syndrome. The production of paralytic neuropathy in chickens experimentally fed Camp ylobacter jejuni isolated from one of these patients is reported. The sciatic nerves of the spontaneously paralysed chickens were examined p athologically in teased fibres, in plastic embedded sections, and by e lectron microscopy. Two large groups of chickens were then fed culture s of a C jejuni (Penner type O:19) isolated from one of these patients . Results-The chickens with spontaneous paralysis had pathologically n oninflammatory neuropathy. Pathology in the sciatic nerves ranged from no detectable changes to severe Wallerian-like degeneration. In the e xperimentally inoculated groups, an average of 33% of the chickens bec ame paralysed. The median time after inoculation to paralysis was 12 d ays. The lesions found in the first few days of paralysis included nod al lengthening and paranodal demyelination. In those animals that surv ived for several days after onset of weakness, the pathology was domin ated by extensive Wallerian-Like degeneration. Animals that survived f or weeks with no clinically apparent neuropathy had paranodal remyelin ation in some teased nerve fibres, reflecting earlier paranodal demyel ination. Conclusion-Experimental inoculation with C jejuni may provide a new model for understanding some forms of Guillain-Barre syndrome.