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each disease. In this study, we included 15 dogs

with proven neoplasia and 15 dogs with

inflammatory meningoencephalitis, which were

then compared to normal dogs.

There were statistical differences between

diseased and normal dogs. Differences were

also noted between neoplasia

versus

inflammation. The concentration of

N-

acetylaspartate is lower in neoplasia than in

meningoencephalitis, whilst the concentration

of choline is higher in neoplasia than in

meningoencephalitis.

In Fig. 4 is a typical short echo time

magnetic resonance spectra of a dog with

granulomatous meningoencephalitis. In this

type of meningoencephalitis, the presence of

lactate is common due to hypoxia. Choline is

slightly elevated, whilst

N-

acetylaspartate is

moderately reduced.

A follow-up

1

H MRS of four dogs with

meningoencephalitis showed recovery of

N-

acetylaspartate to normal values, correlated

with the clinical improvement. This proves that

the reduction of

N-

acetylaspartate in

meningoencephalitis may be due to neural

dysfunction, rather than neural death.

Interestingly, in ten out of 15 patients with

meningoencephalitis, taurine was found; this

metabolite was only found in one neoplasia.

Potentially, taurine may serve as a metabolic

marker for patients with meningoencephalitis.

Future projects involving tumours and

meningoencephalitis are the investigation of the

response after treatment.

Tick-borne encephalitis

This investigation focused on the brain

metabolite abnormalities in dogs infected with

tick-borne encephalitis (TBE). Central European

TBE is an infection caused by a

Flavivirus.

It is

transmitted by tick bites (

Ixodes ricinus)

to

various species, including humans, dogs,

horses, sheep and goats; the disease is

endemic in 27 European countries. TBE virus is

a neurotropic RNA virus which causes a

non-suppurative encephalomyelitis in dogs,

characterised by widespread neurophagia and

gliosis throughout the grey matter of the central

nervous system, but mainly involving the

brainstem, cerebellum and ventral horn of the

spinal cord.

Ines Carrera, Dr med vet Dip ECVDI

Henning Richter, Dr med vet

Patrick Kircher, Prof Dr med vet Dipl ECVDI

Head CABMM: Professor Dr Brigitte von Rechenberg

University of Zürich

B R OW S E

www.cabmm.uzh.ch

H O R I Z O N

2 0 2 0

www.horizon2020projects.com

H O R I Z O N 2 0 2 0 P R O J E C T S : P O R TA L

I S S U E S E V E N

107

M E D I C A L T E C H N O L O G Y & R E S E A R C H

Diagnosis of TBE in dogs is very challenging. During the first viremic

phase of the disease, the virus can only be isolated from the blood or

from cerebrospinal fluid (CSF) by reverse-transcriptase-polymerase chain

reaction. During the second phase, when neurological signs become

clinically evident and humoral immune response starts, the virus clears

up from the blood and CSF and cannot be detected anymore.

MRI has been described in both people and dogs. The MRI changes are

very characteristic, showing bilateral symmetrical lesions of the thalamus,

hippocampus and grey matter ventral horn of the spinal cord. However,

MRI may be negative in some patients, even with evident clinical signs.

We are investigating the metabolic changes in dogs with confirmed TBE,

especially those in which there are no evident morphological lesions.

When compared to normal dogs, patients with TBE show a marked

decrease in

N-

acetylaspartate concentration and higher myo-inositol.

These findings may help to detect brain abnormalities at a metabolic

level, even though conventional MRI is normal.

Fig. 4 Typical short

echo time magnetic

resonance spectra of a

dog with

granulomatous

meningoencephalitis