Tick-Borne Encephalitis Virus (TBEV) Infection in Two Horses

Abstract

A final diagnosis in a horse with clinical signs of encephalopathy can be challenging despite the use of extensive diagnostics. Clinical signs are often not pathognomonic and need to be interpreted in combination with (specific) laboratory results and epidemiological data of the geographical region of the origin of the case(s). Here we describe the diagnostic pathway of tick-borne encephalitis virus infection in two horses using established molecular diagnostic methods and a novel in situ hybridization technique to differentiate between regionally important/emerging diseases for central Europe: (i) hepatoencephalopathy, (ii) Borna disease virus, and (iii) West Nile virus infections.

Keywords: Borna disease virus (BoDV); West Nile virus (WNV); clinical case; encephalopathy; in situ hybridization.

Figure 1

(panels A–E): Brain changes of TBEV-infected 15-year-old haflinger gelding. (A,B): Histological changes comprise multifocal lymphohistiocytic infiltration and microgliosis (arrows) scattered throughout grey matter of cortices (A) and nuclei (B). The infiltrates are occasionally associated with nerve cell degeneration (frames) and neuronophagia (not shown) indicating cytopathic activity of the virus. (C–E): Viral RNA has been visualized using RNA Scope^® technology in infected HeLa cells (A: small arrows), used as the positive control, and in affected brains (D,E). At this stage of infection, the yield of viral RNA flags up in individual pyramidal (D: frame) and granule neurons (E: frame) only, even distant from other tissue changes such as lymphocytic perivascular infiltrates (Barrow). Cort: cortex; SCWM: subcortical white matter. Stains/chromagens: (A,B): haematoxilin-eosin; (C–E): haematoxilin (blue)/AEC (red).