Characterization and experimental reproduction of peripheral neuropathy inWhite Leghorn chickens

A clinical neurological syndrome termed peripheral neuropathy (PN) that res embles Marek's disease (MD) occurred at low frequency in a commercial layer strain for several years. Study of chickens from six field cases showed th at the PN syndrome could be distinguished pathologically from MD on the bas is of several factors, including onset as early as 6 weeks, presence of B-t ype but not A-type lesions in peripheral nerves, and absence of visceral ly mphomas. Serotype 1 MD virus could not be isolated from blood from any chic ken or demonstrated in tissues by histochemistry or polymerase chain reacti on assays. Moreover, the syndrome was not prevented by MD vaccination, eith er in the field or in laboratory trials. PN was induced in 3 to 54% of comm ercial line chickens inoculated at 1 or 6 days of age with whole blood or b uffy coat cells from clinically affected donor chickens. Sonicated cells al so induced PN, but plasma was ineffective. Chickens did not develop PN if r eared in isolators without cellular transfer or when vaccinated solely agai nst MD. However, PN was observed in 9% of 57 B*2/*19 commercial chickens re ared in isolators following vaccination against MD, infectious bursal disea se, Newcastle disease and infectious bronchitis, suggesting that common vac cines may predispose chickens to PN. The data confirmed a strong influence of the major histocompatibility complex (B-complex) on both naturally occur ring and experimentally induced PN with the B*19 haplotype conferring susce ptibility compared with other alleles. It is postulated that PN may represe nt an autoimmune reaction to nerve tissue that may result from response to a combination of common vaccines. These studies confirmed that PN is distin ct from MD, provided criteria for its differential diagnosis, identified st rategies for its control, and established a model for its experimental indu ction.