Submitted to: Avian Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 26, 2010
Publication Date: April 15, 2011
Repository URL: http://handle.nal.usda.gov/10113/60750
Citation: Ecco, R., Susta, L., Afonso, C.L., Miller, P.J., Brown, C.C. 2011. Neurological lesions in chickens experimentally infected with virulent Newcastle disease virus isolates. Avian Pathology. 40(2):145-152. Interpretive Summary: Newcastle disease virus (NDV) has five pathotypes. That is, there are different clinical presentations seen when poultry is infected with NDV. They are velogenic viscerotropic, velogenic neurotropic, mesogenic, and lentogenic. The velogenic cause the most disease. The viscerotropic usually have more hemorrhagic lesions with some nervous signs. The neurotropic usually have only nervous signs. While, many NDV strains have been examined over the years, this paper examines viruses from each of the pathotypes using archived tissue samples. Specifically, the goal was to characterize neurologic lesions using markers that identified specific lymphoctyes, T-cells and astrocytes. In this study, only the lentogens were not able to invade the central nervous system and cause lesions. The underlying mechanism in all cases seems to be infection of neurons leading to neuronal death, and subsequent inflammatory response. The primary component of the inflammatory lesions are T lymphocytes, and astrocytes activated by NDV, which gets worse over time. In addition, there may be some involvement of blood vessels that increases the severity of the lesions.
Technical Abstract: Distribution, character, and severity of lesions were evaluated in tissues from the central nervous system of chickens inoculated with 10 different Newcastle disease virus (NDV) isolates: CA 1083, Korea 97-147, Australia (all velogenic viscerotropic); Texas GB and Turkey North Dakota (both velogenic neurotropic), Nevada cormorant, Anhinga and Roakin (all mesogenic), and B1 and QV4 (lentogenic). Tissues for this study included archived formalin-fixed, paraffin-embedded brain (all strains) plus spinal cord (two strains). Encephalitis was observed in all velogenic viscerotropic and velogenic neurotropic, and some mesogenic strains. In general, the encephalitic lesions began at 5 days post-infection (dpi) with more severe lesions occurring around 10 dpi. In this time point, especially in the gray matter of the brain, cerebellum and spinal cord there were neuronal necrosis, neuronal phagocytosis, and clusters of cells with microglial morphology. Axonal degeneration and demyelination were also observed. Immunohistochemistry for viral nucleoprotein confirmed the presence of virus. In the areas of encephalomyelitis, immunohistochemistry (IHC) for CD3 revealed that many of the inflammatory cells were T lymphocytes. IHC using an antibody for glial fibrillar acid protein (GFAP) showed reactive astrogliosis, which was most pronounced at the later time points.