Submitted to: Avian Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/12/2001
Publication Date: N/A
Interpretive Summary: A disease termed Marek's disease (MD) was differentiated from other chicken diseases about 40 years ago. MD is caused by a virus, termed the Marek's disease virus (MDV), and results in lameness, enlargement of peripheral nerves and development of tumors in visceral organs. Effective MDV vaccines have been developed, and MDV is so prevalent that essentially all commercial chickens in the US and many other countries are vaccinated. Recently a brief abstract described a syndrome termed peripheral neuropathy (PN) where chickens were lame and had enlarged peripheral nerves but lacked tumors in visceral organs. PN is easily misdiagnosed as MD. In this paper we have extensively described PN and shown it is not attributable to MDV, and that MD vaccines do not provide protection against PN. An experimental model was developed for the induction of PN. Criteria to differentially diagnose PN from MD, and strategies for control of PN, are given. The paper provides chicken growers methods to diagnose PN, and poultry breeders ways to reduce the incidence of PN. The experimental model will be useful for further research on the control of this newly defined disease.
Technical Abstract: A clinical neurological syndrome termed peripheral neuropathy (PN) that resembles Marek's disease (MD) occurred at low frequency in a commercial layer strain for several years. Study of chickens from six field cases showed that the PN syndrome could be distinguished pathologically from MD on the basis of several factors including onset as early as 6 weeks, presence of B-type but not A-type lesions in peripheral nerves, and absence of visceral lymphomas. Serotype 1 MD virus (MDV) could not be isolated from blood from any chicken or demonstrated in tissues by histochemistry or polymerase chain reaction assays. Moreover, the syndrome was not prevented by MD vaccination, either in the field or in laboratory trials. PN was induced in 3 to 54% of commercial line chickens inoculated at 1 or 6 days of age with whole blood or buffy coat cells from clinically affected donor chickens. Sonicated cells also induced PN, but plasma was ineffective. Chickens reared in isolators without treatment or vaccinated against MD did not develop PN. However, PN was observed in 9% of 57 B*2/*19 commercial chickens reared in isolators following vaccination against MD, infectious bursal disease, Newcastle disease and infectious bronchitis, suggesting that common vaccines may predispose chickens to PN. The data confirmed a strong influence of the major histocompatibility complex (B-complex) on both naturally-occurring and experimentally-induced PN with the B*19 haplotype conferring susceptibility compared to other alleles.