NR ATQC
AU Mestre-Frances,N.; El Mathari,B.; Crozet,C.A.; Pascal,V.; Rouland,S.; Lehmann,S.L.; Picaud,S.; Berge-Lefranc,J.L.; Verdier,J.M.
TI Adaptation of the Bovine Spongiform Encephalopathy to the Primate Microcebus murinus by Oral Route.
QU International Conference - Prion 2005: Between fundamentals and society's needs - 19.10.-21.10.2005, Congress Center Düsseldorf - Poster Session: Pathogenesis PATH-39
PT Konferenz-Poster
AB
Experimental transmission of BSE through oral route to mice or to non-human primates such as Cynomolgus macaca have been reported in several studies. Here, we report on the investigation of oral transmission of BSE to a small non-human primate, the lesser-mouse lemur (Microcebus murinus). Seven microcebes were contaminated by bovine brain or bovine-adapted macaca brain. Only the three microcebes that received BSE-macaca brain develop a neurological disease after long incubation periods (44 months). The duration of clinical stage was 2 months. The symptoms begin by nervousness evolving rapidly to agressivity, visual troubles, imbalance then incoordination of movements, myoclonic jerks and later on, the microcebes became ataxic, turning round on itself.
The spongiform extent was related with the duration of illness. It ranged from small discrete vacuoles randomly dispersed throughout the neuropil to large confluent cystic spaces traversed by thin septae. Spongiform changes were most pronounced in the thalamus, the basal ganglia, the hypothalamus and the brainstem. The neocortex was relatively spared by spongiosis: small sparse vacuoles were seen in the frontal and occipital lobes whereas the hippocampus showed larger vacuoles. Spongiform changes were accompanied by important astrocytic gliosis.
Proteinase K resistant-prion protein was detected by western blot as well as immunocytochemistry. PrPres accumulation was observed in all the microcebes presenting clinical signs. The prion immunostaining was more intense in thalamus, basal ganglia and brainstem. Focal deposits or plaques were seen in the cortex. In the cerebellum, some plaques were evidenced in the molecular layer.
In conclusion, BSE agent does not seem to be directly pathogenic to microcebe by oral route, but necessitates an adaptation of the strain to macaca.
IN Die Autoren fütterten 4 Mausmakis (Microcebus murinus) mit BSE-infektiösem Rinderhirnhomogenat und 3 weitere Mausmakis mit Hirnhomogenat BSE-infizierter Makaken. Mit Inkubationszeiten von 44 Monaten erkrankten bisher nur die 3 mit Makakenhirn inokulierten Mausmakis. Bei diesen dauerte die klinische Phase 2 Monate. Die Autoren beschreiben ausführlich ihre klinischen und pathologischen Befunde und meinen aus ihren 4 noch lebenden Versuchstieren schließen zu können, dass BSE nicht oral auf Mausmakis übertragbar sei.
AD N.Mestre-Frances, B.El Mathari, V.Pascal, S.Rouland, J.M.Verdier, INSERM U710-EPHE-University Montpellier 2, France; C.Crozet, S.Lehmann, CNRS UPR1142, IGH, Montpellier, France; S.Picaud, INSERM U592, Paris, France; J.L.Berge-Lefranc, EA1784-IFR PMSE 112, University Aix -Marseille, France
SP englisch
PO Deutschland