Basic Facts About SA
This is the text of a handout provided at the seminar sponsored
by the Poodle Club of America Foundation in June of 1992.
(Updated July 2000.)
Sebaceous adenitis with hyperkeratosis - SA for short - is
a hereditary skin disease. It shows up in Standard Poodles,
and has been reported in Miniature Poodles and Toy Poodles.
At least 33 other breeds as well as mixed breeds have been
identified with SA.
This disease has been around since at least the 1960s, and
carriers of the disease have been tracked to dogs in the 1950s.
The disease affects all colors of Standard Poodles in roughly
the same proportion as their coat colors make up the population.
While SA may be an autoimmune disease, it is recessive in
its mode of inheritance, requiring defective genes from both
sire and dam. Currently it appears to be a simple autosomal
recessive, meaning it is transmitted by a single gene from
each parent and not sex linked. Such genetically produced
diseases cannot be cured, but they can be treated and can
be bred away from.
SA was first described in the veterinary literature in 1987.
In 1991, after several years of study, it was estimated that
7 percent of Standard Poodles were affected by SA and 38 percent
were carriers of the SA gene. By mid-1992, the calculations
based on nearly 1000 biopsied dogs indicate 9 percent affected
and 42 percent carriers. The conclusion is the disease is
increasing.
Most veterinarians have not seen SA in their clinical practice.
For this reason, expensive bills can be run up experimenting
with treatments that don't work as the dog's health deteriorates
and it looks progressively more moth-eaten. However, effective
treatment is relatively inexpensive once any secondary infection
is controlled. SA dogs can live happy lives without pain and
suffering.
How is SA Diagnosed?
SA begins to show up any time between 18 months to 9 years
of age in clinically affected dogs. Visible symptoms include
thickening skin, scales, excessive production of dandruff
(hyperkeratosis), patchy hair loss, and often secondary infections
accompanied by a musty odor. At present, 4 percent of Standard
Poodles are showing these symptoms, and another 5 percent
are showing no visible symptoms. This latter group is subclinically
affected, and may or may not become clinically affected. Both
clinically affected and subclinically affected dogs are carriers
and produce offspring that are at least carriers themselves.
Early signs of SA reported by owners include sensitive feet
reported by groomers at clipping time, difficulty clipping
the face, excessive dandruff on the muzzle or other areas,
and secondary skin infections. SA dogs do not itch, unless
they have secondary skin infections. For further information please visit www.offa.org and click on Sebaceous Adenitis.
What's the Treatment for SA?
SA affected dogs are sometimes placed on thyroid medication
without any determination of their thyroid level. This is
because hair loss can be a symptom of thyroid deficiency,
and the medication is cheaper than the test for thyroid level.
However, thyroid medication will have NO effect on SA, and
may postpone prompt treatment to prevent or clear up secondary
infection.
The suggested treatment is to treat secondary infection immediately
with antibiotics. Then use baby oil baths to remove the scales.
Although the baby oil can be used directly, many people have
mixed the baby oil and water in a spray bottle. Shake well
and spray the baby oil mixture on the dog, rubbing it in to
thoroughly saturate the skin. Let the dog soak for one hour
while standing in the tub. The baby oil is thought to expand
and mechanically loosen the scales. After an hour, shampoo
the dog with Palmolive dish washing detergent.
The rinse water will run gray with loosened hyperkeratosis
scales. Be careful not to get any detergent in the eyes of
the dog. It will take several rounds of shampooing with Palmolive
liquid to cut the oil. The more hair, the more rounds. Then
shampoo with any good dog shampoo to eliminate any traces
of detergent. How many shampoos will it take to see improvement?
Most dogs show immediate improvement in their skin. Most Poodles
treated with baby oil begin to grow hair at a normal rate,
but this may take 5 or 6 months of regular oilings. Many owners
report a baby oil soak once very 3 or 4 weeks is sufficient
to maintain the dog when the secondary infection has been
controlled. Some users also spray their dogs every few days
with propylene glycol to keep the skin soft.
Owners of one dog developed a comprehensive treatment using
a variety of Redken Laboratories cosmetology products. This
is described in the Spring 1992 issue of Progress in SA Research.
Significant hair growth has been reported from these treatments
in most cases, and owners are able to discontinue expensive
medications and supplements without ill effect. There is no
question that clinically affected SA dogs require more maintenance
than unaffected dogs, although the initial effort generally
yields good results within a few months.
How Can I Reduce SA Risk?
Two factors make SA a risky disease: late onset, and the subclinical
(non-visible) state. Some dogs have already been bred before
any symptoms of the disease are apparent, and subclinically
affected dogs may never show visible symptoms of SA. In combination,
this means the incidence of SA has been increasing and will
continue to increase unless breeders and owners breed away
from SA. For further information please visit www.offa.org and click on Sebaceous Adenitis.
How can breeders find "safe" breeding stock?
The
owner wishing to breed a dog submits the names of candidate
dogs to GDC for a relatives report. The fee is $10 per inquiry.
Information in the database if processed by the GDC computer
and compiled into a report on the SA phenotype and genotype
information on file. Calculations of probabilities are listed,
permitting the owner to make an intelligent assessment of
alternatives. The strategy is to breed to low risk vs. high
risk dogs.
How reliable is the information in the registry? First, the
open registry contains information about dogs with a genetic
history of SA, as well as those that test normal at this time.
Unlike closed registries that provide information only on
normal animals, the breeder receives a more comprehensive
vies of the data. The European open registry model has thus
reduced the incidence of hip dysplasia, while the closed registry
model has not significantly reduced hip dysplasia. Second,
the more dogs registered, the more reliable are the data.
Can We Rid the Breed of SA?
Time will tell. A recessive Malamute disease open registry
was set up, and seven years later was discontinued because
the disease had virtually disappeared. We do not know how
long it will take to eliminate the risk of SA, but if most
breeders cooperate, it should be accomplished within a decade.
Additional research is being conducted to see if skin lipid
levels can be measured to provide early warning of SA. In
the long range, mapping of the canine genome may reveal the
location of the gene responsible for SA. The success of this
research may be many years away, but it could lead to a blood
test screen for SA and other hereditary diseases. In the meantime,
our best hope is to breed away from SA by wise selective breeding.
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