Marek's disease virus‐induced transient paralysis in chickens. 3. Differentiation of field cases from classical Marek's disease by central nervous system lesions

Abstract

SUMMARYVasculitis with intramural pseudocyst formation primarily in the cerebellar white matter, but also in nuclei of the medulla, resulted in leakage of IgG and albumin and vacuolation of the neuropil (vasogenic oedema) in brains from chickens with clinical signs of Marek's disease virus (MDV)-induced transient paralysis (TP). Demyelination was absent. Chickens that had recovered from TP had a restored bloodbrain-barrier, indicated by the rarity of vasculitis and vascular intramural pseudocysts in the cerebellum. In addition, the vacuolation and protein leakage were greatly decreased. The minor vacuolation resulted primarily from intramyelinic (cytotoxic) oedema. The small quantity of extravascular protein was being removed by microglial cells and astrocytes. In one chicken which failed to fully recover from TP (TPprolonged) there was neither vasogenic oedema, cytotoxic oedema, nor vasculitis in the cerebellum. The medulla of the TP-prolonged chicken had a severe lymphocytosis, swollen axons, neuronal degeneration, secondary demyelination and some associated serum protein leakage. All TP-affected and TP-recovered chickens, and the TP-prolonged chicken, had perivascular mononuclear cell cuffs within all brain sections. Chickens with classical Marek's disease (MD) generally lacked CNS vacuolation, perivascular mononuclear cell cuffs, vasculitis and serum protein leakage. However, in a few cases of MD with severe perivascular mononuclear cell cuffs, focal demyelinating plaques were seen. These plaques had associated vacuolation, serum protein leakage, axonal spheroids and neuronal degeneration.

In vivo characterisation of two Australian isolates of Marek's disease virus including pathology, viral load and neuropathotyping based on clinical signs

“…Microscopic lesions of the brain of birds clinically affected with progressive paralysis during the early clinical stages of the experiment were characterised primarily by PVC, vasculitis, vacuolation (compatible with oedema) of the cerebrum and cerebellum, and scattered infiltration of lymphoid cells in the neuropil, together with frequent meningitis. These CNS lesions were very similar to those described in previous reports, where it was suggested that vasogenic brain oedema is perhaps the primary lesion resulting in paralysis associated with vv MDV strains.…”

Pathotyping of Australian isolates of Marek's disease virus and association of pathogenicity withmeqgene polymorphism

“…Most chickens were euthanised on ethical grounds prior to terminal coma or death, but death did occur in small numbers of chickens in which intervention was delayed. The syndrome therefore appears not to be the transient paresis/paralysis syndrome induced by MDV (Kornegay et al, 1983;Swayne et al, 1989) but rather the more severe acute paralysis syndrome associated with challenge with highly virulent MDV first detailed by Witter et al (1999). In our experiments the syndrome was associated with increased pathogenicity assessed by subsequent MD gross lesions, and had a significantly higher prevalence in males than females, the converse of the situation observed later in the disease.…”

Marek's disease virus‐induced transient paralysis in chickens. 1. Time course association between clinical signs and histological brain lesions

“…One or more mechanisms may underlie the clinical signs seen in TP. The presence of CNS demyelination is probably not significant since it has been found inconsistently in chickens with TP as well as chickens affected with classical MD (Wight, 1962(Wight, ,1968Swayne et al, 1988b).…”