Zum Sudden Acquired Retinal Degeneration Syndrome (SARDS) beim Hund

The subject of the study was to investigate the aetiology of SARDS.
Following an initial literature review, patient data and clinical
findings from 39 Patients were collected and analysed. One specific
observation was that one third of all patients comprised Dachshunds
and that 51.3 % of affected animals were female neutered. The
average age of SARDS patients was found to be 8.8 years (range 3
months to 13 years). The ophthalmoscopic appearance of the fundus
of SARDS patients was documented at different stages of the disease
during serial examinations with the help of fundus photography.
This revealed degenerative retinal changes which were found to
progress linear following the onset of SARDS, finally resembling
dogs with severe generalised progressive retinal degeneration. In
the second part of the study, the hypothesis that SARD is an
autoimmune disease, was tested with the help of autoantibody
screening. In a first step, serum from 24 SARDS patients and 14
normal controls were assessed for autoantibodies to the purified
autoantigens S-Antigen and CRALBP with the help of a western blot.
No difference in the incidence of autoantibodies could be found
between SARDS patients and healthy controls while testing the well
known autoantigens S-antigen and CRALBP. In a second step, an
attempt was made to identify new autoantigens by testing the entire
retinal proteom as an autoantigenic source, again using Western
blot techniques. Following the initial detection of a reaction
against a specific protein found almost exclusively in SARDS
patients, it was possible to identify this protein with the help of
mass spectrometry (MALDI/TOF/TOF) as NSE. These findings were
verified by the binding of IgG antibodies to purified NSE in 25% of
the SARDS patients and 0% of the normal control dogs. The results
of this study suggest that an autoimmune aetiology of SARDS
involving autoantibodies against NSE is possible. However, it is
unclear whether these play a causative role in SARDS or whether
they are the result of retinal destruction by another mechanism.
Further investigations into a possible autoimmune aetiology of
SARDS are therefore indicated and the role of NSE as an autoantigen
must be further assessed.