Many breeders will tell you
not to worry about Cerf test or even go so far as to say their vets
said not to worry about it (no vet worth his salt would tell that lie).
Let me tell this on myself. Many years ago I would have been one of
those breeders to say we’ve never had a problem – I’ve had this
bloodline for years and nothing has happened. I had champion toy
poodle age 15 – her daughter also a champion age 8 and her recently
finished champion son sired by another champion who was a little over 2
years old when we first were persuaded to get Cerf test done. Long
story short he flunked and we were advised he would probably be blind
by 5 years old. I said but mom is fine! So is grandma! Must be the
sire’s fault! Further discussion with the Ophthalmologist led to
some interesting insight. Yes mom bumped into things at night – so do
I. Night blindness was a symptom – not as overt as being blind but… her
daytime navigation was fine. All dogs since have been tested and will
continue to be. We have even taken in the retired dogs as we had kept
pups and they are fine also. Of course that poodle bloodline and a few
that have tested positive for PRA since are not part of the breeding
program. On a side note – a number of breeders have acquired our
dogs to improve and diversify their bloodlines. While this is a
good thing it is not a ‘fix all’ to not testing their own stock and
certainly not to having those pups tested as they become of age to
breed. PRA may not show up in the younger dog. (See below breed
based info). Both parents should be tested. Any stock kept for
breeding should be tested. As should the dog be tested periodically
through out its breeding life if not into old age for information on
the bloodline and especially if pups have been kept from that dog for
breeding purposes.
Why we test our older dogs
including those of retirement age:
Progressive retinal atrophy (PRA) is the name for a group of
devastating eye diseases that can lead to complete blindness in dogs.
PRA has been identified in numerous breeds and can occur in mixed breed
dogs as well. Recently there has been much research into these
inherited eye diseases to better characterize them in terms of pattern
of inheritance, age of onset, and location of the causal gene mutation
in the different breeds that are affected. Researchers at the Jams A.
Baker Institute have identified six separately- inherited forms of PRA
in dogs. In one of these, rod cone dysplasia 1 (rcd1) of Irish setters,
the gene mutation has been identified. * At this time 02/05 there is
not a reliable marker identified for the poodle or cocker spaniel. PRA
is an inherited simple autosomal recessive in most breeds. In 1988, it
was found that PRA in Cockers, Poodles and Labradors was the result of
a mutation at the same gene locus in all these breeds.
PRA is a disease of the retina which is located inside the back of the
eye,which contains specialized cells - photoreceptors that absorb the
light focused on them by the eye’s lens, which then convert the light
via a series of chemical reactions into electrical nerve signals. The
nerve signals from the retina are passed by the optic nerve to the
brain where they become ‘sight’. The retinal photoreceptors are
specialized into rods, for vision in dim light (night vision), and
cones for vision in bright light (day and color vision). PRA usually
affects the rods initially - then cones in later stages of the disease.
The human equivalent is termed retinitis pigmentosa.
Early in the disease, affected dogs are night blind, lacking the
ability to focus their vision in dim light followed by their daytime
vision failing. As their vision deteriorates, affected dogs will adapt
to their handicap as long as their environment remains constant, and
they are not faced with situations requiring excellent vision. At the
same time the pupils of their eyes become increasingly dilated, in an
attempt to gather more light, causing a noticeable "shine" to their
eyes; and the lens of their eyes may become cloudy, or opaque,
resulting in a cataract.
Age of onset and the rate of progression of the disease varies by
breed. Some breeds, notably including the Collie, Irish Setter,
Norwegian Elkhound and the Miniature Schnauzer, have early onset forms.
In these breeds the disease results from abnormal or arrested
development of the photoreceptors—the visual cells in their retina, and
affects pups very early in life. In other breeds, including the
Miniature Poodle, the English and American Cocker Spaniel PRA is much
later in onset. Affected dogs in these breeds appear normal when young,
but develop PRA as adults.
Diagnosis is normally made by ophthalmoscopic examination requiring
dilatation of the dog’s pupil with eyedrops. Generalized all forms of
PRA have the same sequence of ophthalmoscopic changes. increased
reflectivity (shininess) of the fundus, reduction in the diameter and
branching pattern of the retina’s blood vessels and shrinking of the
optic nerve head.These changes occur in all forms of PRA, but at
different times in the different breed-specific forms. Usually by the
time the affected dog has these changes there is already significant
evidence of loss of vision.
The normal
retina showing prominent blood vessels.
A
mid-stage PRA retina. the vascular structure notably reduced.
For more detailed info on the Cerf program and part
ofhttp://www.vmdb.org/cerf.html (Phots from CERF and
used with permission)
There are ongoing investigations
attempting to identify the gene mutation in other types of PRA.
Progressive rod-cone degeneration (prcd) is the most widespread form of
PRA and affects many breeds including poodles, American and English
cocker spaniels. This form of PRA is particularly devastating because
it is a late-onset disease. This means that the rods and cones (the
visual cells in the retina) develop normally and then later (at about 1
year of life) degenerate. Prcd starts with night blindness and
progresses to total blindness at 3 to 5 years of age. The late onset of
clinical signs in prcd is particularly devastating to breeding programs
because many dogs have already been bred prior to the onset of
symptoms. Thus the development of a genetic test for this disease which
could determine both affected and carrier animals would be particularly
useful.
