NR AKBM
AU Robinson,M.M.; Hadlow,W.J.; Huff,T.P.; Wells,G.A.H.; Dawson,M.; Marsh,R.F.; Gorham,J.R.
TI Experimental infection of mink with bovine spongiform encephalopathy
QU Journal of General Virology 1994 Sep; 75(9): 2151-5
PT journal article
AB To determine whether the aetiological agent of bovine spongiform encephalopathy (BSE) is pathogenic for mink, standard dark mink were inoculated with coded homogenates of bovine brain from the U.K. Two homogenates were from cows affected with BSE. The third was from a cow that came from a farm with no history of having had BSE or having been fed ruminant-derived, rendered by-products, the proposed vehicle for introduction of the BSE agent. Each homogenate was inoculated intracerebrally into separate groups of mink and a pool of the three was fed to a fourth group. Signs of neurological disease appeared in mink an average of 12 months after intracerebral inoculation and 15 months after feeding. Decreased appetite, lethargy and mild to moderate pelvic limb ataxia were the predominant clinical signs, quite unlike the classic clinical picture of transmissible mink encephalopathy (TME). Microscopic changes in brain sections of most affected mink were those of a scrapie-like spongiform encephalopathy. Vacuolar change in grey matter neuropil was accompanied by prominent astrocytosis. Varying greatly in severity from one mink to another, the degenerative changes occurred in the cerebral cortex, dorsolateral gyri of the frontal lobe, corpus striatum, diencephalon and brainstem. Although resembling TME, the encephalopathy was distinguishable from it by less extensive changes in the cerebral cortex, by more severe changes in the caudal brainstem and by sparing of the hippocampus. The results of this study extend the experimental host range of the BSE agent and demonstrate for the first time the experimental oral infection of mink with a transmissible spongiform encephalopathy agent from a naturally infected ruminant species.
IN Bei Nerzen traten die ersten Symptome 12 Monate nach intrazerebralen Injektionen und 15 Monate nach Verfütterung von Homogenaten BSE-kranker Rinderhirne auf. Robinson et al. fütterten 10 Nerze mit jeweils lediglich 1 Gramm Hirnbrei. Alle Nerze erkrankten. Neun der erkrankten Nerze wurden histopathologisch untersucht und zeigten das typische Zerstörungsbild.
ZR 17
MH Animal; Astrocytes/pathology; Brain/microbiology/*pathology; Brain Stem/pathology; Cattle; Cerebral Cortex/pathology; Corpus Striatum/pathology; Diencephalon/pathology; Encephalopathy, Bovine Spongiform/*pathology/*physiopathology; Female; Frontal Lobe/pathology; Male; *Mink; Neurons/pathology; Prions/isolation & purification/*pathogenicity; Vacuoles/pathology
AD USDA-ARS Animal Disease Research Unit, Pullman, Washington 99164-7030.
SP englisch
PO England
OR Prion-Krankheiten 7