Brain Lesions in Chickens Experimentally Infected with a Neuroadapted Strain of Mesogenic Newcastle Disease Virus
| Autor: | Yoshiyasu Kobayashi, Muhammad Iqbal Bhaiyat, Chitoshi Itakura, Hiroshi Kida, Muhammad Alimul Islam |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Pathology
medicine.medical_specialty Time Factors Paramyxoviridae Newcastle Disease Newcastle disease virus Quail Newcastle disease Poultry Virus Necrosis Species Specificity Serial passage medicine Animals Gliosis Neurons HN Protein General Veterinary biology Cerebrum Brain biology.organism_classification medicine.disease Virology Astrogliosis medicine.anatomical_structure Spinal Cord nervous system Nerve Degeneration medicine.symptom Chickens Encephalitis |
| Zdroj: | Journal of Veterinary Medical Science. 57:237-244 |
| ISSN: | 1347-7439 0916-7250 |
| Popis: | Neuroadapted Newcastle disease virus (Q10) was selected by tenth serial passage, in the chicken brain of a mesogenic strain (Q0) originally isolated from quails. Specific pathogen-free birds were inoculated intranasally with one of these viruses. At daily intervals for 7 days and then at 10, 14, and 21 days post-inoculation (PI), two birds from each group were killed and samples of the brain were collected for histopathological and virological examination. Q10 caused severe nonsuppurative encephalitis with nervous signs and high mortality. Lesions characterized by neuronal degeneration and necrosis, perivascular lymphocytic infiltration, and focal or diffuse astrogliosis occurred mainly in the parahippocampal cortex, hippocampus, hyperstriatum, neostriatum, subleptomeningeal and periventricular regions of the cerebrum. Spongy changes with neuronal degeneration and axonal spheroids were also observed in the brain stem of a few cases. The amount of virus in the brain reached a peak on day 4 PI and virus could not be recovered from the brain after 6 days PI. In contrast, Q0 caused nonfatal asymptomatic disease and virus could not be isolated from the brain, sections of which showed only minimal inflammatory changes. This difference in the lesions of the brain might be related to neurovirulence and, neuroadaptation by serial passage may occur by increased efficiency of viral replication in neurons. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|