Entropion:
This is where the eyelid rolls in towards the
eye, rubbing against the cornea and irritating this sensitive structure. Watery
eyes, infection, even a corneal ulcer, can occur. Surgical correction is
required. Dogs with this condition should not be bred, as a genetic component is
suspected. ·
Hypothyroidism
The thyroid glands secrete a hormone which
controls the basic metabolic rate of the entire body. Inadequate hormone levels
reset the body to function at a lower metabolic level. In that case, dogs fatten
easily on a normal diet, become sluggish, and are easily chilled. Hair changes
are most noticeable and include loss of hair from the flanks and back, increased
pigmentation of the skin, scaling and seborrhea (an abnormality in the
production of skin cells.) Secondary bacterial infection of the skin is common.
The ears may also be affected, filling with thick, yellow greasy material which
may predispose the dog to ear infections. Blood tests will determine the level
of thyroid function and administration of thyroid hormone can treat the
condition. ·
Familial Shar-Pei Fever
Familial Shar-Pei fever also known as "Swollen Hock Syndrome" (SHS)
typically may include the following symptoms: Swelling of the hock joint and
sometimes other joints can be affected. Reluctance to move. Sometimes a swollen
painful muzzle. Abdominal pain, vomiting, diarrhea, and shallow breathing.
"Familial Shar-Pei Fever (FSF) is an episodic fever disorder. Shar-Pei with
this disorder have one or more bouts of unexplained fever, usually 103-107
degrees but rare cases may go higher. Fevers usually start when they are less
then 18 months old but sometimes the first attack is not until they are adults.
Fever episodes usually become less frequent with age. Fevers last 24-36 hours in
most cases without treatment". The disorder is "thought to result from
an inability to regulate the immune system. Dogs suffering from this disorder
are at risk of dying from a related disorder, amyloidosis.
Demodectic
Mange
The mite, Demodex canis, starts off as small
dry areas on the head, chest, and legs of the Shar-Pei. Because the dog
scratches to relieve the intense itching, the skin becomes red and raw with a
leathery look about it. Check with your veterinarian for prescribed medication,
shampoos, and other appropriate treatment. ·
Seborrhea
Severe rancid body odor
which comes from raw, scaly, bloody skin. Could be caused by hypothyroidism,
yeast infections, and or food allergies. This situation should be immediately
discussed with a veterinarian and the appropriate shampoos and medication can
effectively treat this condition.
Malocclusion
Overbites
This can occur
due to the misplacement of the incisors causing an overcrowding. Extraction at a
young age can prevent the adult canines from cutting into the hard palate.
Tight
Lip
This is where the excess flesh from the lower
lip covers the teeth making it difficult for the Shar-Pei to chew. This excess
flesh also traps food and is usually associated with an overbite. ·
Nose
Steno tic makes These dogs snore because of
excess flesh. If the dog is unable to pass air with ease, surgery to the alar
folds of the nostril may be necessary. An "elongated soft palate" is
likely to be the cause of "respiratory distress."
Carpal
Laxity
This is a weakness is the carpal ligaments
which causes instability and bowing forward in young puppies. Decrease the
protein level and exercise on a non-slippery surface. In severe cases soft wraps
will be in order. · Patellar LuxationIs where the knee cap slips out of its
socket. Any Shar-Pei with this condition should not be bred.
Hip
Dysplasia A
dysplastic dog has an abnormal hip joint
where the femur and acetabulum are misaligned. This can range in severity from
mild (controllable) pain to dogs in such agony they must be put down. Make sure
the parents of any puppy you consider has been cleared of Hip Dysplasia through
the Orthopedic Foundation for Animals. ·
Megaesophagus
Megaesophagus and or diaphragmatic hernias may
not be detected until the dog is much older when they will appear underweight or
emaciated with a history of vomiting. This is a developmental defect possibly a
delayed maturation of the esophageal neuromuscular system. Mild cases in young
dogs can improve with careful feeding." ·
Coetaneous Mucinosis
"Mucin is the substance in the Shar-Pei
skin that causes all the wrinkling. It is clear and stringy and acts like glue
in fight wounds." Some Shar-Pei have an excess of Mucin causing it to form
clear bubbles on the skin that may rupture and ooze. May be associated with
possible allergies and can be treated by a alternate day steroid therapy. ·
Torsion/Bloat Being one of many deep chest breeds, bloat can occur in Shar-Pei.
Can also be caused by the way you roll your dog. Although similar to colic in
horses, "bloat and torsion occur when the stomach swells with gas and then
twists and cuts off its blood supply. Without timely surgical intervention the
condition is fatal". The dog must see a veterinarian as soon as possible.
·
Chronic Inflammatory
Bowel Disease Often complicated by food
allergies and or Chronic stress diarrhea. Usually responds to a strict
hypoallergenic diet. · Allergies Some Shar-Pei can be susceptible to allergies
caused by food, grass, plants (indoor and outdoor), flea-bite dermatitis an
allergy-based condition where the dog develops an itchy rash in reaction to flea
saliva after being bitten. Try to keep the dog's living quarters and play area
as flea-free as possible. Other allergies are "Inhalant allergies"
that causes the dog to lick his/her paws, scratch, and rub its muzzle.
"Eliminating the allergy's cause, using the correct type of shampoo and
administering antihistamines or cortisone are common forms of treatment".
Amyloidosis
Amyloidosis is the deposition of
an abnormal substance called amyloidal in the tissues of the body. These amyloidal
deposits are composed of protein fibrils formed by the polymerization of protein
subunits forming a specific pattern called the beta-pleated sheet.
The specific biophysical arrangement of this
sheet gives the amyloidal deposits their unique staining and optical properties.
Due to this structure amyloidal is insoluble and can be thought of as
"wax". It is also important to realize that amyloidosis is not a
single disease, but can be the end point of many diseases. The structure of amyloidal
also is responsible for the characteristic green color after staining
with Congo red. In Shar-Pei amyloidosis is a reactive amyloidosis.
This form of systemic amyloidosis usually occurs with chronic inflammatory
diseases and is characterized by the presence of amyloidal protein AA. Amyloidal
protein AA is derived from an acute phase protein called serum amyloidal A protein
(SAA) produced by the liver. There are many other acute phase proteins produced
by the liver which have important roles in the inflammatory process and in
tissue repair after injury. It is important to understand that amyloidal protein
AA is a normal protein and that it's production is a normal response to tissue
injury and inflammation. It is also important to realize that many diseases,
traumatic injuries, cancer disorders, stresses, etc. can stimulate the
production of the acute phase proteins. There appears to be a balance between
the production of SAA and the degradation and excretion of SAA from the body. It
is not known whether the development of amyloidosis in the Shar-Pei is due to
prolonged excessive SAA production by the liver which overwhelms the degradation
mechanisms or a defect in the degradation process itself, or a combination of
both. We do know that Familial Shar-Pei Fever is an inflammatory process which
does stimulate the synthesis and release of acute phase proteins from the liver.
That this occurs can be surmised from the changes seen on the hem gram and
biochemical profiles of Shar-Pei during, or shortly after, an FSF episode. It
certainly appears that the cause of amyloidosis in Shar-Pei has a genetic basis.
Reactive amyloidosis results in extra cellular deposition of amyloidal protein in
tissues. This means the "waxy" amyloidal is surrounding the cells and
slowly crushes them as well as interfering with nutrition of the cells. These
cells die and the structures they make up are replaced by fibrous, nonfunctional
scar tissue. There are species differences as to which tissues amyloidal will
accumulate in. In dogs, the kidney is the primary organ involved with the spleen
and liver affected less often. The kidney is especially vulnerable due to its
decreased ability to replace damaged cells and ultimately, when a certain number
of cells have been irreparably damaged, kidney failure with its accompanying
clinical signs develops. Once amyloidal is deposited in the tissues it appears
that nothing can remove it. Why does amyloidosis have so many different
clinical presentations? Why does it occur in some Shar-Pei at 2 years of age and
in others at 10 years of age? Why do some Shar-Pei develop amyloidosis and
others don't? Why is it a genetic disease in Shar-Pei? There are many questions
which have no answers at this time. I think several theories are plausible to
explain the variations we see: The underlying basis of amyloidosis in
Shar-Pei is Familial Shar-Pei Fever (FSF). It is quite possible that FSF has
variable age of onset and variable degrees of severity in terms of the
inflammatory disease it causes. This may result in a variable rate of
progression in the development of amyloidosis in different individuals. For
example, the response of the liver to FSF and the synthesis and release of the
acute phase proteins, especially SAA, may be more acute in some dogs resulting
in a more rapid deposition of amyloidal. In other individuals, the response to FSF
may be more chromic and result in slower deposition of amyloidal. In effect, there
may be milder forms and more severe forms of the same disease. The exact
mechanism of amyloidal deposition may be different in different individuals. There
may be other effects of FSF on the body which are additive with the amyloidosis.
As an example, we know Shar-Pei are more susceptible to disseminated intra vascular
coagulation (internal blood clotting) during an episode of FSF and
blood clots in the kidneys may cause more kidney damage than just amyloidal deposition itself. Some dogs may have other disease processes going on which can
be additive with the effects of amyloidosis. These are just some ideas on
why we see different presentations of the same disease. One fact remains - any amyloidal
deposits found in a Shar-Pei have to be regarded as related to FSF and
genetic until proven otherwise. It really doesn't matter whether a little or a
large amount of amyloidal is found. Another point to keep in mind is that the
mechanisms initiating amyloidal deposition are normal protective responses seen in
any breed of dog. It appears in our breed that the mechanisms, which regulate
the inflammatory response, don't work properly allowing this normal response to
go out of control and cause disease.
Always consult a Shar-Pei knowledgeable
veterinarian for proper treatment and care.
