Abstract
The central nervous system lesions in encephalitozoonosis were studied in 11 naturally infected blue foxes. Immunohistochemical staining was employed in the demonstration of the parasites and identification of host cells. Consistent findings in acute to subacute stages included granulomatous meningoencephalomyelitis and vasculitis, with arterial lesions similar to polyarteritis nodosa. Chronic stages were dominated by arteriosclerosis, perivascular mononuclear infiltrations and gliosis, with less prominent granulomatous reaction. Parasites were almost constantly observed in association with active lesions both in vessels and nervous tissue. Parasitophorous vacuoles (PV) occurred in endothelial cells and in the medial layer of arteries. Neurons, including even their processes, were widely parasitized, a fact that may account for the brain being an important target organ. PV also occurred in ependymal cells of the choroid plexus and occasionally in macrophages. A great number of parasites was demonstrated in phagolysosomes of macrophages, a fact that probably reflects a relative resistance to digestion, and may consequently contribute to the development of the prominent granulomatous reaction. It was concluded that the brain lesions, except in chronic stages of mild infections, seem to be pathognomonic for encephalitozoonosis in the blue fox.
Keywords: Encephalitozoon cuniculi, central nervous system, pathomorphological changes, immunohistochemistry.
Sammendrag
De patoanatomiske forandringer i sentralnervesystemet ved encephalitozoonose hos 11 naturlig infiserte blårever beskrives. Immunoperoxidaseteknikk ble benyttet til påvisning av parasittene og til identifisering av vertsceller. I alle tilfeller med akutte og subakutte forandringer påvistes en grånulomatøs meningoencefalomyelitt og vaskulitt, med arterieforandringer som tilsvarte polyarteritis nodosa. I de kroniske stadier var forandringene dominert av arteriosklerose, perivaskulære mononukleære infiltrater, gliose og moderat granulomatøs reaksjon. Parasitter ble nesten alltid påvist i forbindelse med aktive betennelsesprosesser både i kar og hjernevev. Parasitofore vakuoler (PV) opptrådte i endotelceller i alle typer av kar og i tunica media i arterier. Parasittene viste stor affinitet til neuroner og fantes til og med i deres utløpere, noe som kan forklare at hjerneforandringene er så framtredende ved encephalitozoonose hos blårev. PV påvistes også i ependymceller i plexus choroideus og noen ganger i makrofager. Et stort antall parasitter forekom i fagolysosomer i makrofager. Dette kan tyde på at de er forholdsvis resistente mot nedbryting, noe som kan være grunnlag for utvikling av granulomatøs betennelse. Det konkluderes med at bortsett fra i kroniske stadier ved mild infeksjon, antas hjerneforandringene å være patognomoniske for encephalitozoonose hos blårev.
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