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Please note that this section
is intended as a source of information only. It is not intended as a substitute
for professional care. Always consult with your Veterinarian about health
related matters. The information provided here is a brief outline only
of some of the health issues which may be of concern for the Yorkshire
Terrier breed and should not be considered as a complete listing.
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A .
ALLERGIES: Allergies can be broken down
into inhalant, contact, or food allergy origins. Flea allergies, grass
allergies, and environmental toxin induced allergies are the most common
causes of skin conditions in Yorkie. Allergies can be chronic or seasonal.
They can be minor or severe in occurrence. They tend to become worse with
age. Treatment is much better than in bygone days. Environmental controls,
antihistamine treatment, and desensitization injections have made huge
strides in the last few years. .
Glucocorticoids (steriods) should
be used only as a last resort due to serious side effects. Diagnosis and
treatment of chronic or severe cases by a Board Licensed Veterinary Dermatologist
is recommended. Inheritance: Unknown .
ANASARCA: Also called WALRUS
PUPPY; RUBBER PUPPY; WATER PUPPY Usually lethal lymphedema of
newborns; huge size (often 3 pounds) requires c-section to deliver. Inheritance: Autosomal Recessive .
AZOSPERMIA Spermtogenci arrest; the sudden
onset of sterility in a formerly known fertile male; may be immune-mediated Inheritance: Unknown .
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B .
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BLADDER STONES: Some of the most common ones
include: STRUVITE This urolith is diagnosed in
almost half the cases of bladder stones. It is also called MAP (Magnesium-Ammonium-Phosphate),
or triple phosphate. It is the predominant stone type in female dogs of
all breeds. Several factors predispose dogs
to getting struvite uroliths: * Excess struvite crystals in
the urine that set the stage for the formation of the urolith. Some breeds
have a genetic predisposition to forming excess amounts of these crystals
in the urine. * Urinary Tract Infection (UTI)-
some bacteria produce a byproduct called urease. Urease will increase the
pH of the urine and promote ammonium in the urine. * The formation of an alkaline
(pH greater that 7.0) urine from the diet or urease producing bacteria
will cause the struvite crystals to precipitate out of solution and begin
the formation of a urolith. *Urine that stays in the bladder
longer than usual gives the struvite crystals further opportunity to precipitate
out of solution and form a urolith. * Struvite uroliths come in
many different shapes and sizes, are radiodense, and form in an alkaline
urine. .
CALCIUM OXALATE This is the second most prevalent
type of urolith after Strive, making up around 30-50% of the uroliths,
especially in male dogs of all species. They come in two versions; the
monohydrate and the dihydrate. Sometimes the two are found together, sometimes
they are found with other uroliths like calcium phosphate, Strive, or ammonia
urate. This is a problem most commonly
in older male dogs. It is suspected that there is a correlation with hormone
changes that occur as a pet ages. The Yorkshire Terrier is prone to these
along with many other breeds. Several predisposing factors
work together to increase the chance of this urolith forming: * Increased calcium in the bloodstream
(hypercalcemia) * Increased calcium in the urine
(hypercalciuria) with no increase in hypercalcemia * Concurrent Cushing's disease * Use of cortisone .
URATE AND AMMONIUM URATE This is a common urolith found
in some breeds around middle age, with males affected much more often than
females. This is because they metabolize protein differently in the liver,
with the end result being uric acid buildup in the urine. They are found
in Yorkshire terriers. There does not seem to be a
connection with a urinary tract infection, and they tend to form in an
acidic urine. .
Urate stones are radiolucent.
If they get large or covered with other minerals they might become radiopaque.
Urate calculi tend to be small and occur as several stones. These stones
usually form in the bladder, and when passed through the urethra, can become
lodged. .
* Ammonium urate uroliths are
sometimes formed in pets with liver disease such as PSS (see liver shunt)
due to improper metabolism of ammonia to urea. This will cause excess uric
acid levels in the bloodstream. The kidneys filter out this excess uric
acid in the production of urine, thus increasing the level of uric acid
in the bladder. The excess ammonia that is in the bloodstream from the
liver problem also builds up in the urine in the bladder. These two compounds
combine to form the ammonium urate bladder stone. .
Dogs with immonium urate bladder
stones might have ammonium urate crystals in their urine and a low specific
gravity (dilute urine). These stones might not be seen on a radiograph
because they are radiolucent. This same radiograph might also show a small
liver, an indication of PSS. This small liver is due to the diverted blood
flow to the liver. Dogs with PSS will commonly have abnormalities in the
blood sample to give us further clues. .
* Compound Uroliths Most bladder stones are caused
predominantly by one type of mineral. The more common ones have been described
above. In a small percent of cases, the bladder stone is caused by a combination
of minerals in similar quantities. These stones are called mixed uroliths.
Some bladder stones consist of a core mineral surrounded by a lesser amount
of a different mineral in a different layer. These are called compound
uroliths. .
Why some minerals form mixed
uroliths and others form compound uroliths is not understood. Compound uroliths form when
the factors that predispose to one type of stone formation have now changed
to factors that favor a different type of stone formation. If a struvite
stone is treated with antibiotics and urinary acidifiers the problem tends
to resolve. The change in urine pH might promote excess calcium in the
urine, resulting in a shell of calcium oxalate formation around the core
struvite stone. The opposite can occur also- a struvite stone can form
over a calcium oxalate stone. .
In general, these stones are
removed surgically and an effort is made to medically prevent the mineral
that is at the core of the stone. Miscellaneous Uroliths There are other uroliths that
occur, although they are relatively uncommon. They include cystine, silica,
calcium phosphate, and miscellaneous minerals. Inheritance considered: Unknown .
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CATARACTS The lens of the eye is clear
and is located behind the pupil. The job of the lens is to focus light
into the retina. When the lens becomes unhealthy, it turns white or opaque.
Cataracts are generally considered a common old age change, but a juvenile
form also occurs. Juvenile cataracts are inherited and are not usually
present at birth, although this condition can present itself at any age-
months to years. Juvenile cataracts affect different areas of the lens
depending upon the breed of dog. They do not always result in the lens
becoming completely opaque. Complete cataracts result in blindness that
can only be corrected by cataract surgery. Yearly CERF examinations are
an important tool in diagnosing this condition. Proper treatment can be
hastened by early diagnosis. Inheritance: Unknown .
CAMPYLOBACTERIOSIS Commonly mistaken for Parvovirus,
but needs different treatment. It's a BACTERIAL imbalance in the digestive
tract. It is a disease that produces acute infectious diarrhea in puppies
and kittens. This is NOT a new form of Parvo. Parvo tests will show a LOW
positive & subsequent tests will continue to show low positives, will
be inconclusive, or will give erratic results. This disease is so similar
to Parvo, that some dogs have tested in the low positive for Parvo. But
they do not have Parvo, and it has been recommended that three parvo tests
are needed to exclude Parvo. .
This disease can be tested for
specifically, so if you have an affected dog that appears to have Parvo,
but in your mind know that, that could not be possible, have them tested
for "Camby". It is important to note that this disease can be transferred
between humans, dogs, cats and other livestock. It starts with fecal mucus
sheath & continues to get progressively softer until it is watery and
contains blood. It then becomes explosive. Vomiting may accompany and may
or may not also contain blood. Feces have a sweet/flowery aroma along with
a "slaughterhouse on a summer day" smell (similar to parvo diarrhea but
with a floral hint). Feces are usually mustard colored. Dogs dehydrate
at an astounding rate. Inheritance: Environmental factors .
CARPAL SUBLUXATION Wrists are congenitally out
of joint; first appears at 3 weeks, the gene is allelic to the gene for
hemophilia A (in the same place on a chromosome) Inheritance: Recessive; sex-linked .
CHONDRODYSPLASIA (Dwarfism) Shortened, deformed front legs,
with a typical downhill stance Inheritance: Autosomal recessive .
COLOR DILUTION ALOPECIA (CDA) Alopecia (hair loss) related
to dilute coat color is a recognized condition in dogs. The currently accepted
medical terminology for this condition is Color Dilution Alopecia (CDA).
The condition may affect any dilutely pigmented dog, regardless of coat
color. This condition was previously known as Blue Balding Syndrome, Blue
Doberman Syndrome, Color Mutant Alopecia, Congenital Alopecia, etc. The
term Color Mutant Alopecia arose because dilutes were at one time mutations
from the deep pigment occurring in wild canines. Dilutes are now a regularly
occurring form of pigmentation in many breeds and have been for hundreds
of years. The term mutation is therefore not applicable to dilute individuals.
References to Doberman Pinschers or blue hair coats arose because the condition
is common in blue individuals of this breed, but it is not limited to either
blue dogs or Dobermans. The term congenital means present at birth, but
CDA affected dogs are born with normal hair coats. .
The dilute (also known as Maltese)
gene also appears in both mice and cats, and interestingly enough, is not
associated with any abnormal coat conditions in those species. Color Dilution
Alopecia (CDA) has been recognized in dilute individuals of many breeds
of dogs including Chow Chows, Dachshunds, Doberman Pinschers, Great Danes,
Irish Setters, Italian Greyhounds, Standard Poodles, Salukis, Whippets,
and Yorkshire Terriers Dilute individuals carry a recessive genotype of
dd and are characterized by blue, bluish-grey, lavender or flesh-colored
noses, lips and eye rims. The coat colors may include blue, fawn, blue-fawn,
bronze, taupe or some variation of these. These dogs are usually easily
distinguished from their deeply (non-dilute) pigmented counterparts. Deeply
pigmented individuals carry a dominant genotype of Dd or DD and have black
or liver noses, lips and eye rims. Coat colors may include black, red,
red-fawn, liver or variations thereof. .
CDA is characterized by loss
of hair from dilutely pigmented areas. Coats are normal at birth, and onset
of hair loss usually begins between six months and three years of age.
Hair loss usually begins along the dorsal midline (middle of the back)
and often spares the head, tail and limbs. The pattern seems to vary from
breed to breed. It has been suggested that darker colored (steel blue)
individuals are less likely to be affected, may be less severely affected
or may start to lose hair later in life than lighter colored dogs. This
suggests that the severity of the disease may be related to the amount
of dilution present. Deeply pigmented or white areas of coat are unaffected.
In blue dogs with tan points (Yorkies and Dobermans) the tan areas retain
a normal appearance. In piebald (white spotted) individuals, the white
areas are unaffected by the hair loss. The hair loss may be total or partial
and any remaining hairs are usually sparse, rough and easily broken or
removed. The skin in the affected areas is usually scaly and may occasionally
develop bacterial infections. Pruritus (itching) is usually absent, unless
a bacterial infection has set in. .
Diagnosis of CDA requires first
ruling out other causes of hair loss. Diagnostic tests should include fungal
cultures, skin scrapings to check for parasitic mites, etc. CDA often closely
resembles endocrine (hormone related) hair loss and the dog should be carefully
examined for any other abnormalities, and tested for normal thyroid function.
Presence of dilute pigment and a characteristic course of disease also
aid in making the diagnosis. Microscopic examination of hairs and\or skin
biopsies can be used to confirm the diagnosis. .
There is no cure for CDA. Treatment
is limited to controlling the scaliness and any associated pruritus with
various shampoos or topical treatments. .
The cause of CDA is not clearly
understood. Microscopic examination of hairs of dilute individuals reveals
that the pigment (melanin) forms large granules (macromelanosomes) which
are rarely found in deeply pigmented hairs. In dilute individuals with
normal appearing coats, these macromelanosomes are not grouped or clumped
and cause no distortion of the cuticle (outer covering) of the hair. Dogs
with CDA have many large groups or clumps of macromelanosomes which tend
to distort the cuticle of the hair. It is hypothesized that this distortion
of the cuticle causes the hairs to break easily, resulting in the short
stubby hairs commonly found in affected individuals. It is further
hypothesized that the rupture of the hair releases byproducts of pigment
formation, which are toxic to the hair follicles. Regrowth of broken hairs
is reduced because of damage to the follicles caused by these toxins. .
Why in some dilute dogs the
macromelanosomes are clumped and in others they are not, is an interesting
question at this time. The relationship between dilute pigment and hair
loss is clear, but why are some dilute individuals unaffected? Weimeraners
as a breed are dd, all individuals are dilute, yet the disease is unreported
in this breed. In Dobermans, the dilute individuals comprise only 8-9%
of the breed, yet 50-80%6 of the dilute dogs have CDA. Many individuals
are dilutes, the IGCA health survey reported only 71 affected individuals
among the approximately 2200 dogs included in the survey. If half the dogs
included in the survey were dilutes, the incidence of CDA in IG's would
be around 7% of the dilute population, as opposed to the 50-80% affected
dilute Dobermans. .
A third allele (dl) which is
associated with CDA has been proposed. While this is a long way from
being proven, it could help explain why some dilute animals are unaffected.
Dogs with a genotype dd would be normal coated dilutes, ddl would be intermediates
(mildly affected?) and dldl would be CDA affected. A genotype of Ddl should
represent deeply pigmented dogs which were carriers of CDA. .
In Yorkshire Terriers it is
known to affect extremeties such as the ears, dorsal nose area. It is also
related to flank alopecia characterized by symmetrical hair loss on each
flank in an equal diameter pattern. There is sometimes a hormonal or seasonal
causation due to a lack of melanomin in these individuals. Inheritance: Unknown but closely
related to the inheritance of the blue gene in coat colours .
COCCIDIOSIS A diarrhea disease caused by
a species of coccidia commonly found in the feces of puppies, and occasionally,
adult dogs. Coccidia are not worms; they are microscopic parasites which
live within cells of the intestinal lining. Because they live in the intestinal
tract and commonly cause diarrhea, they are often confused with worms. Inheritance: Environmental factors .
COLLAPSING TRACHEA Collapsing Trachea is a problem
common to Toy Breeds. The trachea is a long tube that carries air from
the neck to the chest. It is reinforced with rings of cartilage that help
keep it rigid as air moves in and out of the tube. When the cartilage weakens,
the trachea may collapse while the dog is breathing. While many affected
dogs do fine, this isn't the case in all of the Toy's. The round cartilage
rings may flatten, forcing the dog to try to breathe through an extremely
narrow opening. .
The symptoms of the condition---shortness
of breath, coughing, fatigue---usually appear after the age of five, although
they can begin as early as birth. Generally young dogs tolerate collapsing
trachea pretty well until they get older. Inheritance: Unknown but assumed
complex .
COLIFORM ENTERITIS (Immunoproliferative
small intestinal disease) Persistent, nervous diarrhea;
may be immune-mediated Inheritance: Unknown .
COMEDO SYNDROME (Schnauzer bumps) Crusts on back due to plugged
hair follicles, itching. Inheritance: Complex .
CUSHING'S SYNDROME Cushing's Syndromeis also known
as 'Hyperadrenocorticism' and is a combination of clinical and chemical
abnormalities resulting from chronic exposure to excessive amounts of glucocorticoids.
It is a condition that occurs in most species but is most commonly encountered
in the dog and the horse. Cushing's disease is the result of the overproduction
of cortison, an natural steriod hormone, by the adrenal glands. It is rare
in dogs under five years old. In about 80 percent of the dogs the disease
is caused by a lesion in the pituitary gland at the base of the brain that
overstimulates the adrenals, while in about 20 percent of cases one of
the adrenal glands itself will have a tumor that excretes cortisol independent
of what's happening in the body. About half of those tumors are maliganant
and spread, and about half of them are benign and generally tend to stay
small. .
Glucocorticoid have many functions
and are essential for life being responsible or indirectly responsible
for a range of metabolic functions including blood glucose levels, fat
production and distribution, protein metabolism,
inflammation, thirst, counteracting shock, the skin and the immune system.
The list goes on. .
Cushing's Syndrome is a collection
of symptoms caused by an excess of a hormone called cortisol. There are
three main causes of Cushing's Syndrome: a tumor on the pituitary gland;
a tumor on the adrenal gland; or veterinarians who over-prescribe corticosteroids
to treat itching skin. It is, as yet, unknown whether there is an inherited
predisposition to Cushing's Syndrome in Yorkshire Terriers. .
In the base of all our brains
is a small grouping of cells which constitute the pituitary gland. This
gland has many functions and is the 'director' of much of the bodies function.
It gathers information about body hormone levels and then produces its
own regulatory hormones that through 'feedback' mechanisms govern their
production. One of its functions is to govern the level of glucocorticoids
in the blood stream. It does this by producing a hormone called ACTH that
flows through the blood stream to the adrenal glands. The adrenal glands
are very small pockets of specialized cells sitting behind each kidney
that are responsible for producing the bodies glucocorticoid. ACTH stimulates
the production of glucocorticoid in the adrenal gland. .
Excessive production of ACTH
in the pituitary will produce excessive glucocorticoid production. Similarly,
an abnormality in one or both adrenals will cause an overproduction and
both conditions will produce Cushing's Syndrome. The principal cause of
overproduction is due to tumours growing in either the pituitary gland
(usually benign, small and unlikely to cause other symptoms) or the adrenal
gland (50% benign, 50% malignant and spreading to other areas of the body). .
Diagnosis is based on clinical
symptoms and confirmed with selective blood tests. Symptoms are varied
but includes increased thirst with subsequently increased urine output,
an excessive appetite, abdominal distension, often skin changes, with hair
loss on flanks, dandruff, thickened and pigmented skin. The dogs become
weak and lethargic with muscle wastage. Diabetes can be a secondary symptom.
Confirmatory blood tests are many and varied but can be used to produce
a diagnosis and then used to determine where in the body the problem lies. .
The symptoms of Cushing's disease
can also appear if a dog is taking steriods for a medical condition and
ends up with too much in his system. Steroids are found in a lot of creams,
eye ointments and ear ointments, and if you get overzealous with their
administration, that can cause these signs as well. When you stop using
the products, these symptoms will go away. The typical signs of Cushing's
disease are increased thirst and urination, panting, hair loss (usually
on the trunk) and weakness. .
Symptoms: * He is drinking huge amounts
of water and urinating frequently * He is losing coat * His skin is darkening * His muscles are atrophying
and he develops a pot belly. * If your vet finds the following
four symptoms, your Yorkie probably has Cushing's Syndrome: * The dog is drinking copious
amounts of water and urinating frequently. * The dog has an elevated SGPT. * The dog has an elevated alkaline
phophatase level. * The dog's ratio of urinary
cortisol to urinary creatinine is greater than 24 .
Cushing's Syndrome is usually
treated successfully with a drug called Lysodren, newer drugs are 'Vetoryl'
(Trilostane) and Anapryl. Surgery is rarely recommended and radiation therapy,
used in humans, is very expensive and rarely available for dogs. Adrenal
tumours can be surgically removed in a percentage of cases but pituitary
surgery would only be attempted in rare cases at very specialized centers. Inheritance: Unknown assumed
complex .
Cryptorchidism (undescended
testicles) Cryptorchidism is the failure
of one or both of the testicles to descend into the scrotum. Normal descent
is often complete by 6 to 8 weeks of age but may be delayed to as late
as 6 months of age. The undescended testicle may be found within the abdominal
cavity, in the inguinal canal or under the skin next to the penis. The
condition is considered hereditary in most breeds. There is not complete
agreement on the mode of inheritance. Because of the increased incidence
of cancer in retained testicles, cryptorchid dogs should always be neutered.
A neutered cryptorchid dog should have no other expected health risks due
to this condition. Bilateral cryptorchid is sterile, unilateral fertile
but barred from showing. .
Inheritance: Threshold, possible
recessive .
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DISTICHIASIS (Double eyelashes) Extra row of eyelashes, usually
on lower lid but appearing at times on upper; irritates the cornea causes
excessive tearing Inheritance: Unknown .
DRY EYE (ACTUAL NAME: KERATOCONJUNCTIVITIS
SICCA (KCS), xerophthalmia) KCS or "dryeye" is an eye disease
caused by abnormal tear production. The lacrimal glands produce the watery
secretions that make up the bulk of the tears. A deficiency in this secretion
causes KCS in small animals. .
Normal tears are essential for
the health and transparency of the cornea (the surface of the eye). Tears
cleanse and lubricate the cornea, carry nutrients, and play a role in the
control of infection and in healing. Deficient tear production as in KCS
causes chronic irritation of the cornea and conjunctiva. Corneal ulcers
and eventually corneal scarring occur, and blindness can result. .
There is a predisposition to
this condition in some breeds as listed below. KCS can also occur in any
breed as a result of viral infection, inflammation, drug-related toxicity,
or immune-mediated disease. Congenital KCS (ie. the dog is born with the
condition) is rare. It may be one-sided and has been seen in toy breeds
such as the Yorkshire terrier, pug, Pekingese, and Chihuahua. These dogs
have very small or absent tear-producing (lacrimal) glands which leads
to eye damage and potential blindness. Inheritance: Unknown .
DYSMYELINATION Abnormal covering of the neural
transmitters in the brain/spine; various nervous signs or tremors; may
not be progressive and may improve with age Inheritance: Unknown .
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ENCHONDROMATOSIS Multiple cartiliage bumps on
the bones near joints; if sever can cause lameness Inheritance: Unknown .
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FANCONI'S SYNDROME Renal tubules degenerate, leak
suger then proteins and slats in urine; leads to complete renal failure Inheritance: Autosomal recessive .
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GIARDIASIS Caused by a protozoan of the
giardia species. Giardia are one-celled organisms that live in the small
intestines of dogs and cats. Dogs get the infection from drinking water
from streams or other sources contaminated with infective oocysts. Young
dogs can develop diarrhea that may be acute or chronic, intermittent or
persistent, and may be accompanied by weight loss. Inheritance: Environmental factors .
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HEART DEFECTS A variety of heart defects can
occur in every breed of pure-bred dogs. A careful examination of puppies
by a veterinarian at 6 weeks of age is recommended since most congenital
heart problems can be detected this way. .
* Valvular Endocardiosis is
a degenerative change of unknown cause affecting the subendocardial valve
leaflets and chordae tendineae in the middle aged to elderly dog. Smaller
breeds are predisposed. And it is relatively common in Yorkshire Terriers.
Also known as chronic myxomatous valvular heart disease, this disorder
is the most important cause of heart disease in veterinary practice. .
* Cardiomyopathy, is another
heart disease identified with Yorkies and other small toy breeds. .
* Patent Ductus Arteriosus (PDA)
At birth, mammals must adapt from living in a fluid environment (the amniotic
fluid) and acquiring oxygen through the mother's blood, to breathing air
and acquiring oxygen through their own lungs. The ductus arteriosus is
very important in the adaptation process. This is a small communicating
blood vessel between the pulmonary artery (which carries blood to the lungs),
and the aorta (which carries blood to the rest of the body). Before birth,
most of the blood from the fetal heart bypasses the fetal lungs via the
ductus arteriosus. The lungs gradually become functional fairly late in
fetal development. At birth, the blood supply from the mother is of course
cut off, the dog (or other mammal) begins breathing on its own, and blood
flow through the ductus arteriosus decreases dramatically. Within a few
days, the ductus closes off completely. Where the ductus does not close,
the dog is left with a patent ductus arteriosus (PDA). The extent to which
this affects the dog depends on the degree of patency, or opening, of the
ductus. .
Inheritance: complex; polygenic
threshold .
HERNIA Inguinal or rupture Abdominal contents bulge out
under skin most commonly in the groin area of females although some males
are affected. In males it can be inconjunction with the retention due to
cord length of one or both testes. Umbilical or tupture or "outie" Bulging of abdominal contents
in sac at umbilicus; common; usually harmless unless very large. Inheritance: Threshold .
HGE OR HEMORRHAGIC GASTRIC ENTERITIS Particularly dangerous to the
toy and smaller breed dogs. Any kind of bacterial diarrhea can quickly
dehydrate a dog, and the tinies are at greater risk, as they have little
weight to lose before they are dehydrated and need IV rehydration. Your
dog can get infected anywhere. Then it can be from 2-10 days after exposure,
that your dog can come down with this problem. The symptoms start with
vomiting, lethargy, refusing to eat, and progressing to mucous covered
stool, loose stools, severe diarrhea and bloody diarrhea. It is important
to have a culture done first so that you know exactly what bacteria you
are treating, and get them started on antibiotics. DO NOT waste time, especially
with the tiny toy dogs , as they do not have the spare fluids to lose thru
diarrhea, especially bloody diarrhea. Inheritance: Unknown .
HYPOGLYCEMIA (Neonatal or Juvenile
in nature) Hypoglycemia is when the blood
sugar levels (glucose) fall well below normal. Glucose is what the body
uses as fuel and is necessary for the brain tissue and muscles to function.
Hypoglycemia is often seen in toy breeds, and frequently in young toy puppies.
It can cause your puppy to become confused, disoriented, drowsy, have the
shivers, stagger about, collapse, fall into a coma, or have seizures. Typical
signs are listlessness, depression, staggering gait, muscular weakness,
and tremors -- especially of the face. Puppies with a severe drop in the
blood sugar develop seizures or become stuperous and go into a coma. Some
puppies may only exhibit weakness or a wobbly gait, and occasionally a
puppy that seemed just fine is found in a coma. Most of the time
the symptoms can be controlled by eating, or by giving some glucose such
as Karo syrup mixed with water to the puppy. If the puppy is in a
coma, don't try to get it to swallow anything. Dip your finger in Karo
and rub it under the tongue then get to the vet immediately. If not
treated, it can result in death. Inheritance: Unknown .
HYDROCEPHALUS With hydrocephalus there is
an abnormal build-up of cerebrospinal fluid (CSF) in cavities ( the ventricles)
in the brain. The resulting increased pressure on the brain causes the
clinical signs that occur with this condition. .
Hydrocephalus can be primary
(congenital ) - the animal is born with the condition, or secondary - the
condition is acquired later in life due to some disease process that blocks
normal drainage of the CSF. The primary form, discussed here, is seen most
often in brachycephalic (dogs with a shortened head) and toy breeds. .
Puppies with severe hydrocephalus
often die at a very early age due to pressure from the increased fluid
in the brain. In other less severely affected pups, the signs gradually
become apparent over the first few months of life, and in some mild cases
the condition is only diagnosed later in life. .
Symptoms: The types of signs
seen with this condition include unthriftiness (smaller than littermates,
slow to grow), a domed skull (which gradually becomes more pronounced),
abnormal movement behaviors (restlessness, aimless walking), problems with
vision, and seizures. These pups are very slow to learn - it may be extremely
difficult to housetrain them for example. .
Generally the signs gradually
worsen, although by 2 years of age they may stabilize. To minimize brain
damage, the condition must be recognized and appropriate treatment begun
early. However, affected animals will likely always be slow and have a
limited ability to learn. Inheritance: Polygenic; complex .
HYPOTHYROIDISM (Acquired and
Congenital) Hypothyroidism is an underproduction
of hormones by the thyroid gland. It is characterized as an underproduction
of TSH and an iodine deficiency, can be lethal if untreated.. It occurs
in many breeds, including Yorkshire Terriers. Diagnosis is done by a blood
test for complete thyroid activity. Symptoms include poor haircoat, infertility,
lethargy, and cold intolerance. Treatment with synthetic hormones is very
successful in controlling this condition. Blood tests to evaluate dosage
is important on a yearly basis. However Yorkies are in the low precedence
for TGAA testing. .
Symptoms: * Abnormal loss of coat (often
bilateral and symmetrical), poor coat condition, fading of coat color * Chronic skin disorders and
infections, skin allergies, dry or scaling skin * Weight gain * Infertility or reproductive
problems * Fatigue, lethargy * Intolerance of cold .
It is important to determine
the exact cause of your dog's hypothyroidism before embarking on a course
of treatment. Your veterinarian must run a full thyroid panel and have
the blood tested at a laboratory which uses canine thyroid values (suggestion
Michigan State University). Do not be tempted to start thyroid treatment
without proper veterinary supervision. The balance of the endocrine system
is critical to your dog's health and you can cause an otherwise healthy
thyroid gland to atrophy by giving medication improperly. Inheritance: Unclear .
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INTUSSUSCEPTION Intussusception is a problem
with the intestine (bowel), wherein one portion of the bowel slides into
the next, much like the pieces of a telescope. When this occurs, it creates
an obstruction in the bowel, with the walls of the intestines pressing
against one another. This in turn can cause dangerous inflammation, swelling,
and decreased blood flow to the intestines involved. .
Intussusceptions generally occur
as a secondary problem to some disorder or disease that causes increased
intestinal mobility or inflammation. Chronic parasite infestation may be
the most common cause but anything that causes chronic intestinal disease
can lead to an intussusception. There are times when intussuceptions occur
for no apparent reason so it is likely that primary intussusception can
occur. They have been reported following ingestion of foreign bodies, trauma,
ovariohysterectomy surgery, infiltrative or inflammatory bowel diseases
and other conditions that cause intestinal irritability. .
Intussusception can be chronic
sometimes. It can also be a "come and go" problem -- intussuscpetions occasionally
will resolve on their own and then recur. I have removed one surgically,
put the remaining intestinal ends back together and watched a new intussusception
form right at the same site. Inheritance: Unknown .
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K
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KIDNEYS (POLYCYSTIC) Fluid filled cysts in kidneys
may be with or without symptoms and will lead to renal failure without
treatment. Inheritance: Unknown .
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L
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LEGG-PERTHES (LEGG-CALVE-PERTHES
DISEASE or ASEPTIC NECROSIS OF THE FEMORAL HEAD) Legg-Perthe's disease is a degeneration
of the hip joint occurring in young dogs. It is also known as Legg-Calve-Perthe's
Disease, Perthe's disease, Calve-Perthe's disease, or in medical terminology,
avascular necrosis of the femoral head and neck. The former names recognize
the original researchers in the disease as it occurs in humans. .
Most of the time the clinical
signs of this disease occur in 4 to 11 month old dogs and usually consist
of lameness of one leg only. Pain may be mild to very severe. Some dogs
have mild forms of this condition and do not require medical care. In other
dogs, the condition cause sufficient pain and deformity of the hip joint
to require surgical intervention. Atrophy of the muscles of the affected
leg is not uncommon. If this is severe it can slow the recovery period
considerably and may make medical therapy less likely to work. .
Definitive diagnosis is made
by X-rays. As changes to bone occur slowly, X-rays taken early in the course
of the disease may appear normal. Repeating the X-rays in 3 to 4 weeks
will reveal the bony changes. A dog affected with LPD suffers a loss of
blood supply to an area of the femur (thigh bone) known as the neck. Because
the bone loses its blood supply, it dies. As a result of the loss of bone
tissue, the neck of the femur collapses. The neck attaches the head of
the femur to the body of the femur. When the neck collapses, the head of
the femur is moved, and may also become deformed. These changes are readily
apparent in X-rays. The head of the femur is the "ball" which sits in the
"socket" on the pelvis, making up the hip joint. Therefore, changes to
the head result in disruption of function of the hip joint which causes
the pain and lameness. The term "avascular necrosis" means death of tissue
due to lack of blood supply. In most dogs, only one hip is affected, and
males and females are equally affected. .
Treatment of this condition
varies according to the severity of the signs seen. In mild cases, enforced
rest may be sufficient to allow healing of the damaged areas to occur.
In some cases, immobilization of the affected limb using an Ehmer sling
may be beneficial to recovery. Many dogs have advanced cases of this disease
by the time they are examined by a veterinarian and medical treatment is
not likely to work. In these dogs, excision of the femoral head (ball portion
of the hip joint) is often beneficial. Removal of this section of the bone
diminishes painful bony contact in the hip joint. Recovery from this surgery
can be slow with recovery periods of up to one year sometimes occurring
before good use of the affected leg returns. If muscle atrophy is not present
at the time of surgery the recovery time is usually much less. Pain relief
and anti-inflammatory medications may be beneficial. .
There is a stronger tendency
to treat this as a medical condition prior to surgery right now. A general
rule of thumb is to allow non-surgical therapy a month to show a beneficial
response. If one is not seen, surgical repair should be considered more
carefully. .
Treatment of LPD usually consists
of surgery to remove the damaged femoral head and neck (femoral head ostectomy).
Mildly affected animals may recover soundness with only cage rest. Affected
animals will probably always have some gait abnormalities, but make satisfactory
pets after recovering from surgery. .
Prevention of the disease is
only possible through genetic means. Affected animals should not be bred.
Breeding stock should have their hips X-rayed to insure that they are not
affected with mild LPD, the symptoms of which went unnoticed during the
dog's adolescence. Extreme caution should be used when considering breeding
animals that have produced LPD, or have LPD affected littermates. Inheritance: Autosomal recessive .
LUXATED PATELLAE (SLIPPING PATELLA'S) This is a problem in many small
breeds of dogs, including Yorkies . In this disorder, the knee cap slips
out of the trochlear groove. Diagnosis is by X-ray and palpation exam.
The severity of the condition is quite variable. It can occur in one back
leg, or both. Grade 1 cases can be very mild, with minor gaiting anomalies.
Mild cases will do such things as: pick up a leg for a few steps when moving
over irregular ground (gravel or long grass), lope or gallop rather than
trot. They are often straight in the stifle and have no "drive" to their
rear movement. Grade 3 and 4 cases, are less common and do require surgical
correction. This condition does weaken the integrity of the joint, predisposing
to arthritis and traumatic injury. .
The patella or kneecap is usually
located directly in the center of the knee joint. It is held in place by
ligaments and rests in a groove on the femur (thigh bone). The muscle of
the thigh or quadriceps attaches at the top of the kneecap and on the tibia
(calf bone) directly below the groove or trochlea of the femur. Its contraction
causes the knee to extend. In a normal knee, all these structures are well
aligned. The femur is directly above the tibia and when the quadriceps
contracts, the patella glides up the groove. .
Luxation, or dislocation of
the patella, occurs when the tibia is rotated inward or when the lower
portion of the femur is curved, causing a misalignment of the structures
of the knee so that the patella slides out of its groove and moves in toward
the centerline when the knee extends. In a small percentage of the cases,
the luxation is said to be lateral because the patella is dislocated outwards
but this is very uncommon in small breed dogs. Patellar luxation occurs
mostly in toy and small breeds of dogs weighing 10 kg or less such as the
miniature poodle, the Pomeranian and the Yorkshire terrier. A study has
shown that females are 1.5 times more affected than males. .
Causes: In the majority of cases,
patellar luxation is a congenital condition because the abnormalities (weak
ligaments, a too-shallow groove and internal rotation of the tibia) are
present at birth though the actual luxation may appear some time later.
It is thought to be inherited although the exact mode of transmission has
not been determined. In some cases, the condition is acquired through trauma. .
Symptoms: * The symptoms may appear at
weaning or may go undetected at first. * There can be an occasional
rear lameness. * The dog can be seen running
and suddenly yelping in pain, walking on three legs, unable to flex the
stifle. Sometimes, he will make a kind of hop and thus be able to replace
the patella himself. * In other cases, he will show
much pain and will hold the leg up for several days. * In very severe cases, the
animal cannot put weight at all on its hind legs at all and drags himself.
Even if it is very often bilateral, the patellar luxation can occur in
one knee or be worse on one side. .
The diagnosis is made by palpating
and manipulating the knee joint to see if the patella can be luxated manually.
Depending on the laxity, the condition can be classified from Grade 1 (minimal)
to Grade 4 (severe). Radiography is used to document the condition, evaluate
the extent of the changes to the trochlear ridges, see if any osteoarthritis
has developed and evaluate the bone conformation. .
Treatment consists from confined
rest to replacement of the patella. Though surgery is not necessary for
every dog, it is the treatment of choice, especially if it has persistent
lameness. It should be performed early, before osteoarthritis has affected
the joint. This is especially true for luxations graded 2 to 4 as the joints
are easily luxated and remain so until replaced. Many techniques are available
and the method chosen depend on the veterinarian, the severity of the disorder
and the lifestyle of the dog. Conservative treatments such as prednisone
and/or restricted activity doesn't give much benefit and is recommended
mostly for mildly affected or older dogs. For more severe cases, if the
disorder is not corrected by surgery, joint pathology increases with age
as repeated dislocations will damage the cartilage of the patella and lead
to osteoarthritis, making the joint more and more swollen and painful with
poor mobility. The additional strain caused by the misaligned force of
the quadriceps can also increase the rotation of the tibia, thus the severity
of the problem. The condition also predisposes to strained and even torn
and cruciate ligaments. The results after surgery are better if it is performed
before arthritic changes occur and depend on the severity of the condition
. For grades 1, 2, or 3, the dog can usually use its leg in a normal fashion
after 30 days or so. .
Inheritance: Polygenetic with
nutritional and environmental factors .
LIVER SHUNT... click here to
PORTAL
SHUNT .
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P
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PANCREATITIS Pancreatitis is inflammation
of the pancreas, an elongated gland that serves many functions in the process
of digestion and metabolism. When digestive enzymes that normally are excreted
into the intestinal tract are activated in the pancreas instead, they cause
inflammation. Foods high in fat, or a lot of greasy table scraps, tend
to trigger pancreatitis. This is a serious, potentially
life-threatening disease. Mortality is upwards of 20 to 25 percent. Affected
animals will have severe abdominal pain, loss of appetite, lethargy, depression,
vomiting and diarrhea. Dehydration is also a danger. .
The Role of the Pancreas The pancreas is a glandular
organ located near the liver and duodenum. It has two different types of
glandular functions. The first is its endocrine function: it makes insulin,
which is a very important hormone in the control of metabolism and blood
sugar levels. The pancreas also has an exocrine glandular function: it
makes digestive enzymes that are secreted into the intestine and are critical
for the normal digestion of food. .
Pancreatitis is a condition
where the pancreas becomes inflamed. The time course can be either chronic
(slow and smoldering over weeks to months) or acute (rapid in onset). Inflammation
can be particularly severe in the pancreas because the organ contains digestive
enzymes. These powerful enzymes are normally stored in an inactive state
and are only activated when released into the intestine. This is necessary
or the pancreas might "digest itself." In cases of severe inflammation,
the digestive enzymes can be activated within the pancreas, which only
worsens the swelling and inflammation. Sometimes the swelling in an inflamed
pancreas can become so severe as to obstruct the outflow of bile coming
via the bile duct, which passes near the pancreas on its way from the liver
to the duodenum. .
In chronic pancreatitis, scar
tissue (fibrosis) develops. This interferes with the normal function of
the pancreas. .
The Causes of Pancreatitis Pancreatitis can occur in dogs,
cats or humans. In humans, it can be a complication of alcoholism. Humans
are prone to abscesses — bacterial infections of the pancreas — while bacteria
are rarely involved in cases of pancreatitis in cats and dogs. If you want
to learn more about pancreatitis in humans, several links are provided
at the end of this article. Very little is known about the
causes of pancreatitis in dogs and cats. The disease appears to be more
common in dogs. There is some evidence, at least in dogs, that certain
cases are brought on by dietary indiscretion, especially by eating foods
that are very high in fat. Also, dogs with other serious illnesses such
as diabetes, Cushing's disease and cancer, or dogs that are recovering
from surgery, are at higher risk for pancreatitis than are dogs that are
otherwise healthy. .
Symptoms: * Dogs with acute pancreatitis
usually have vomiting and often have abdominal pain. Often dogs will stop
eating and seem quite sick. Dogs with severe, acute pancreatitis are at
risk for dehydration and associated complications (blood clotting abnormalities,
kidney failure, fluid buildup around the lungs, diabetes). They require
hospitalization for IV fluids and sometimes intensive care. .
* The signs of chronic pancreatitis
are more subtle and may be difficult to detect. Sometimes intermittent
vomiting, diarrhea or signs of vague abdominal pain will be reported. It
appears that many times the disease progresses without detection. In some
cases, either diabetes (due to lack of ability to make insulin because
of pancreatic damage) or pancreatic exocrine insufficiency (inability to
make enough digestive enzymes)may eventually result. .
Diagnosis of pancreatitis can
be difficult because no available test is 100% reliable. Two digestive
enzymes made in the pancreas can be measured in the blood. Elevations in
these enzymes (lipase and amylase) can provide supportive evidence for
pancreatitis. The lipase test appears to the be better of the two, but
it is not always available on the routine chemistry panel. Veterinarians
may add it as a special test when dogs are presented for evaluation of
vomiting. Some dogs with pancreatitis do not have elevations in lipase
and amylase so when these blood values are normal, it does not exclude
the diagnosis of pancreatitis. .
There is a relatively new test
called TLI (trypsin-like immunoreactivity) that appears to show promise
in the diagnosis of acute pancreatitis, at least in cats. The TLI seems
to be more reliably elevated than is lipase. The current problem with the
test is turn-around time. It is performed at only a limited number of labs
and the samples have to be shipped, often out of state, so it may take
one to two weeks for results. This hampers its diagnostic usefulness. Ultrasound can be helpful in
the diagnosis of pancreatitis. However, ultrasound of pancreas is technically
difficult. Abnormalities are not always seen, even when acute pancreatitis
is present. .
There is no specific treatment
for pancreatitis. At present, the treatment is predominantly supportive
allowing time for the inflammation to subside while preventing complications. In dogs, most cases of acute
pancreatitis will resolve in a few days, with complete rest of the GI tract.
Dogs must be maintained NPO (this stands for "nothing per os," which means
that no food or water can be given by mouth). When nothing is taken by
mouth, the stimulus for pancreatic secretion abates, which allows the inflammation
to subside. When the enzymes (lipase and amylase) have fallen to normal
or nearly normal then water and a very low fat diet is instituted. To prevent
dehydration during the period of complete bowel rest, dogs must be given
fluid therapy; usually fluids are given intravenously. This is why patients
with pancreatitis are generally hospitalized. Steroids and other anti-inflammatory
agents don't seem to aid recovery in dogs with pancreatitis. .
In severe cases of pancreatitis
in dogs, pain killers may be needed. Also, plasma transfusions may benefit
some patients. It is thought the certain proteins in plasma can bind the
damaging pancreatic enzymes being released from the damaged pancreas. Surgery is generally not indicated
except when abscesses or cysts are present. Even with treatment, some cases
of pancreatitis may be fatal. .
Reduced fats are indicated as
assisting in preventing recurrence during the convalescent phase of pancreatitis
in dogs, and probably in cats. For dogs it is critical to avoid invasions
of the garbage can because dietary indiscretion seems to underly many cases. There is some anecdotal evidence
that dietary supplementation with pancreatic enzymes may help in prevention
of recurrence or treatment of chronic pancreatitis. Although this seems
to be a harmless therapy, there is no experimental evidence to support
its use. .
*Pancreatic Hypoplasia (pancreatic
atrophy; chronic pancreatitis) Lack of digerstive enzymes;
gray, greasy feces, chronic weight loss despite huge appetite, insulin
producing cells usually remain normal Inheritance: Autosomal recessive .
PARVOVIRUS Canine parvovirus is an acute,
highly contagious disease of dogs that was first described in the early
1970's. The disease is transmitted by oral contact with infected feces.
Parvo affects dogs of all ages, but most cases occur in pupies 6 to 20
weeks of age. Parvovirus is characterized by severe, bloody diarrhea and
vomiting, high fever and lethargy. The diarrhea is particularly foul smelling
and is sometimes yellow in color. Parvo can also attack a dog's heart causing
congestive heart failure. This complication can occur months or years after
an apparent recovery from the intestinal form of the disease. Puppies who
survive parvo infection usually remain somewhat un-healthy and weak for
life. Inheritance: Immune mediated,
enviromental factors .
POISON What To Do For A Poisoned Animal Before You Call the ASPCA Animal
Poison Control Center If you suspect that your pet
has been exposed to a poison, it is important not to panic. While rapid
response is important, panicking generally interferes with the process
of helping your animal. .
Take 30 to 60 seconds to safely
collect and have at hand the material involved. This may be of great benefit
to the Center professionals as they determine exactly what poison or poisons
are involved. In the event that you need to take your animal to your local
veterinarian, be sure to take with you any product container. Also bring
any material your pet may have vomited or chewed, collected in a zip-lock
bag. .
If your animal is seizuring,
losing consciousness, unconscious or having difficulty breathing, you should
contact your veterinarian immediately. Most veterinarians are familiar
with the consulting services of the Center. Depending on your particular
situation, your local veterinarian may want to contact the Center personally
while you bring your pet to the animal hospital. .
Call the ASPCA Animal Poison
Control Center 888-4ANI-HELP (888-426-4435) .
There is a $45 consultation
fee for this service. A credit card number may be required. When you call the Center, be
ready to provide: * Your name, address and telephone
number * Information concerning the
exposure (the amount of agent, the time since exposure, etc.). For various
reasons, it is important to know exactly what poison the animal was exposed
to. [If the agent is part of the Animal Product Safety Service, the consultation
is at no cost to the caller.] * The species, breed, age, sex,
weight and number of animals involved * The agent your animal(s) has
been exposed to, if known * The problems your animal(s)
is experiencing. .
Be Prepared Your animal may become poisoned
in spite of your best efforts to prevent it. Because of this, you should
be prepared. .
Your animal companions regularly
should be seen by a local veterinarian to maintain overall health. You
should know the veterinarian's procedures for emergency situations, especially
ones that occur after usual business hours. You should keep the telephone
numbers for the veterinarian, the Animal Poison Control Center, and a local
emergency veterinary service in a convenient location. * You may benefit by keeping
a pet safety kit on hand for emergencies. Such a kit should contain: * A fresh bottle of hydrogen
peroxide 3% (USP) * Can of soft dog or cat food,
as appropriate * Turkey baster, bulb syringe
or large medicine syringe * Saline eye solution to flush
out eye contaminants * Artificial tear gel to lubricate
eyes after flushing * Mild grease-cutting dishwashing
liquid in order to bathe an animal after skin contamination * Rubber gloves to prevent you
from being exposed while you bathe the animal * Forceps to remove stingers * Muzzle to keep the animal
from hurting you while it is excited or in pain * Pet carrier to help carry
the animal to your local veterinarian Inheritance: Environmental Factors .
PROGRESSIVE RETINAL ATROPHY
(PRA) Progressive Retinal Atrophy
(PRA), is an incurable hereditary eye disease which, as the name implies,
progressively attacks and destroys the retina of the eye, causing blindness.
The retina is essential to eyesight, for it is here that a visual image
is formed before being transmitted via the optic nerve to the brain. A
defect in an enzyme causes a chemical compound to form that kills the cells
in the retina. .
PRA begins with night blindness,
followed by gradual loss of day vision and, eventually, total sightlessness.
In some affected breeds, vision loss is observed in puppies, and the dogs
may become blind before or soon after maturity. In other breeds, the disease
can go undetected until the dog is several years old and has passed the
PRA gene to subsequent generations of puppies. Like retinitis pigmentosa
in humans, canine PRA is not one disease but a group of related ones. All
are characterized by malformation or degeneration of the retinal visual
cells. .
Most forms of PRA are caused
by different, autosomal recessive gene defects. This means that for offspring
to be affected, both parents must carry one copy of the same mutant gene.
Both parents could have normal eyesight,but have 1 gene for normal enzyme
production that is dominate over the 1 recessive gene for the abnormal
enzyme defect. In this case the parents would be considered carriers. When
a carrier is bred to another dog with 1 dominant normal gene and 1 recessive
abnormal enzyme defect gene (i.e., another carrier), 25% of the offspring
will be afflicted with PRA, 50% will be carriers like their parents, and
25% will possess the normal 2 dominant correct enzyme genes. If a dog afflicted
with PRA is bred to another dog who is neither afflicted nor a carrier,
then all the offspring from that breeding will be carriers (possessing
1 dominant normal enzyme gene and 1 recessive abnormal enzyme gene). All
of these offspring are then capable of producing PRA if they are bred to
another carrier or a PRA afflicted dog. .
In some cases, breeders have
resorted to producing "test litters" as a means of identifying and removing
all carriers and affected dogs from their lines. The disease afflicts an
estimated 80 breeds of dogs worldwide. While PRA is not widespread among
Yorkshire Terriers, it can, and does, occur in Yorkies and should not be
ignored in breeding or selecting a puppy. .
Research has achieved some success
in developing a test for the defective gene in other breeds such as the
Mastiff and Irish Setter. Carriers of the mutant gene for one type of PRA
in Irish Setters can be detected with a new blood test developed at the
Cornell College of Veterinary Medicine. The unequivocal DNA blood test
for rod-cone dysplasia-1 (rcd-1) in Irish Setters gives researchers hope
that similar tests for other affected breeds will produce equally promising
results. .
Meanwhile, the best recourse
available to Yorkie breeders and buyers alike is regular eye checks by
qualified veterinarians, and honest disclosure of the problem when diagnosed.
Until the method of detecting the defective gene in Yorkies is available,
buyers and breeders alike must depend upon vigilance and careful research
of pedigrees to reduce the occurrence of PRA in the breed. .
Until development of the first
DNA test, PRA can only be detected by electro- retinography testing. Conclusive
diagnosis for Yorkie still requires examination by a canine ophthalmologist.
Using special equipment the opthamologist will examine your dog's eyes
for a thinning of the retina, which causes the dog's eyes to be hyper-reflective.
They may also observe a paleness of the optic disk and a reduction of blood
vessels in the eyes. This test, which is available at regional veterinary
centers, identifies only dogs affected by PRA - not the clinically normal
animals that carry one copy of the defective gene. Thus, a carrier can
still be unknowingly used in breeding. Responsible breeders will supply
information on the eyes of their dogs in the form of one or more of the
following: eye examination reports (preferably from veterinary ophthalmologists),
electroretinogram (ERGs), and examination forms for the Canine Eye Registry
Foundation (CERF). .
Since the various forms of PRA
are progressive it is important that repetitive checks of a dog's eye health
are obtained as they age, potentially as old as 6 to 7 years (PRA has been
observed in Yorkies (a long lived breed) as old as 9 years), or prior to
breeding. Although some Yorkies have been diagnosed as young as 12 months,
a single eye check at a young age (e.g., 2 or 3 years old) does not ensure
a dog is not afflicted. Often, the symptoms of the disease can go un-noticed
by owners until it has progressed significantly. Since the disease advances
slowly, an afflicted dog can adapt by depending more heavily on his sense
of smell and hearing. Often an afflicted dog can cope very well until total
blindness occurs. It is not unusual for owners of afflicted dogs to be
unaware of the problem until an eye examination is obtained. .
Not all retinal degeneration
is caused by genetic PRA. non-PRA retinal degeneration does exist and can
be distinguished in the early stages of development from genetic PRA. When
either type of retinal degeneration is found in an advanced state (e.g.,
the retina in nearly totally degenerated) it is not possible to distinguish
between the two types by eye examination. This is further reasoning for
routine and periodic eye examinations. Also, because the determination
of PRA can be subjective and have significant consequences, a second opinion
would be a good idea. .
If the CERF information is obtained
for dogs 6 years old or older and for 3 generations on both sides of the
pedigree, then that is even better. However, be aware that a CERF will
not guarantee the lack of a problem, and likewise, not having a CERF does
not indicate the presence of PRA. Some breeders have their dog's eyes checked
and never register the results with the CERF. Inheritance: Automsomal recessive .
PORTAL SHUNT (LIVER SHUNT) This condition is often referred
to as a "liver shunt" but the current favored term appears to be portosystemic
shunt. These have also been referred to by more exact terms since there
are specific types of shunts that vary slightly. .
There are three shunt types:
intrahepatic, extrahepatic, or microvascular. The most common is Portosystemic
shunt (PSS) occurs in many dog breeds the Yorkshire Terrier is one. It
is an abnormal flow of blood between the liver and the body. Since the
liver is responsible for detoxifying the body, metabolizing nutrients and
eliminating drugs, the blood bypassing the liver can cause indications
of a possible PSS which might include, but are not limited to, neurobehavioral
abnormalities, anorexia, hypoglycemia, intermittent gastrointestinal symptoms,
urinary tract problems, drug intolerance, unthriftiness and stunted growth. .
Signs of PSS usually appear
before two years of age, but later onset has been recorded. If an animal
has a confirmed PSS, corrective surgery can be helpful in the long-term
management of these animals. Dietary manipulation is also important in
maintaining PSS animals. Mode of inheritance has not been established. .
Symptoms: Most shunts cause recognizable
by the time a dog is a young adult but once in a while one is diagnosed
at a later time in life. Since the severity of the condition can vary widely
depending on how much blood flow is diverted past the liver it is possible
for a lot of variation in clinical signs & time of onset for the signs
to occur. Often, this condition is recognized after a puppy fails to grow,
making an early diagnosis pretty common. Signs of portosystemic shunts
include: * poor weight gain * sensitivity to sedatives (especially
diazepam) * depression * pushing the head against a
solid object * seizures * weakness * salivation * vomiting * poor appetite * increased drinking and urinating * balance problems * frequent urinary tract disease
or early onset of bladder stones. * If these signs increase dramatically
after eating, it is a strong supportive sign of a portosystemic shunt. .
Most dogs will be diagnosed
with port-systemic shunts under one year of age, but dogs as old as eight
have been diagnosed with the condition. Animals are usually stunted, thin,
depressed, have trouble gaining weight, and are usually characterized by
the owners as chronic "poor doers". In most affected dogs there will be
some degree of behavioral signs ranging from listlessness, apathy, or depression
to more severe signs of circling, head pressing, stupor, drooling, blindness,
or convulsions, some leading to coma. .
These behavioral changes are
due to an accumulation of toxins (especially ammonia) that affect the brain
causing a condition called Hepatic Encephalopathy. These toxins are most
abundant in the blood stream following the dog eating, especially a high
protein meal, and may remain high for hours afterward. Not all dogs with
the shunt will show this meal associated behavioral change, but in 25%
of the affected dogs that do, the diagnosis becomes clearer. A high percent
of affected animals show an intolerance to anesthetics or tranquilizers,
and will show increased recovery times following use of these products.
Even anti-convulsants used to control seizures may be potentially dangerous
if allowed to concentrate in a dog with functional shunt. .
Approximately 75% of affected
individuals will show digestive system symptoms including poor appetite,
ascites, vomiting, drooling, diarrhea, or occasionally deranged appetite
(eating paper, etc.). Urinary system symptoms may include increased thirst
and urination, & in a majority of porto-systemic shunt cases, there
will be crystals or stones formed in the urinary tract. These crystals
will be either uric acid or ammonium urate (ammonium biurate or thorn-apple
crystals.). There can be bladder stones formed or crystals may be noted
on the hair around the prepuce or vulva. .
* In virtually all porto-systemic
shunts there will be a significant rise in the bile acid levels over normal.
The use of bile acids in screening clinically normal dogs for liver shunts
is not currently being advised due to the variation of normal bile acid
levels in Yorkshire Terriers, and other breeds as well. .
* Routine performed serum chemistries
are fairly nonspecific toward confirming the diagnosis of porto-systemic
shunts, but there may be a decreased total protein (primarily albumin),
decreased blood glucose, decreased cholesterol, and decreased blood urea
nitrogen (BUN). The uric acid levels may be elevated in a significant number
of affected individuals. Acid levels are extremely important in the diagnostic
screening of symptomatic potential shunts. Fasting and 2-hr. post meal
blood samples are evaluated for bile acid levels. .
* Liver function testing with
Bromosulfaphthalein (BSP) or ammonia tolerance testing are sensitive and
reliable if performed correctly. These tests measure the liver's ability
to excrete/detoxify known agents, and thus measure liver function accurately. .
* Radiography. Radiography is
one of the most important methods of establishing a diagnosis of porto
systemic shunt, and is currently the only universally accepted method of
confirming a shunt, short of major surgery. Injection of a radiopaque dye
into the spleen (Splenoportograpy) will show the shunt on radiographs and
allow accurate assessment for surgical correction. .
* Nuclear Medicine. The placement
of a radiopharmaceutical agent (radioisotope) specific for the liver into
the colon for absorption through the mucosa has been gaining favor because
of its noninvasive diagnostic value. This procedure requires expensive
equipment and the diagnosis is based on the distribution of the radionuclide
in the lung or heart compared to that in the liver. This procedure also
does not identify the exact location of the shunt for surgical correction
if required. .
* Until recently, ultrasound
was fairly unreliable for nonsurgical diagnosis of porto-systemic shunts.
With the advent of Color Flow Ultrasound, there is the potential for diagnosis
of this condition on non-anesthetized animals. At the present time, this
technology appears to be the diagnostic procedure of choice. If currently
undertaken research confirms its value, Color Doppler Ultrasound will soon
be the preferred screening and diagnostic tool. At the present time, Hepatic
Porto-Systemic shunts are considered to be UNQUESTIONABLY genetic by some
of the leading canine experts, but the mode has not been identified at
the present time; research is being conducted at Michigan State University
to identify this pattern (See the Yorkshire Terrier Foundation page and
the Joint Research Project between the YTCA Foundation and the CTCA Foundation). .
Genetic disorders in dogs can
spread relatively rapidly if a dog, whether affected or a carrier, is a
well-respected animal in either conformation or ability, and is used extensively
for breeding. This is especially true in the case of the male that can
produce hundreds of offspring during his breeding life. If the cause of
such a condition can be discovered, then a working strategy can be implemented
to control and eliminate the disorder. The Yorkshire Terrier Club of America
Foundation, Inc. is currently funding research into both the genetic nature
of the problem and into the use of Color Flow Doppler Ultrasound as a diagnostic
& screening tool. Inheritance: Unknown, assumed
to be polygentic recessive .
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REVERSE SNEEZING (PHARYNGEAL
GAG REFLEX) This is a dramatic, rapid inhalation
and exhalation of air through the nasopharynx. Dogs may do this when they
have a mild irritation at the back of their throat. Often confused with
seizuring or gasping for air, it is usually a harmless event. Reverse sneezing isn't really
a health problem, but something that dog owners should be aware of as it
is very common in toy breeds. It is characterized by honking, hacking or
a snorting sounds. It usually happens when a dog is excited or can sometimes
happen after drinking, eating, running around, or while pulling on the
leash. The dog will usually extend his/her neck while gasping inwards with
a distinctive snorting sound, it is reverse sneezing. Usually by gently rubbing the
throat of your dog, the spasms will stop after they swallow a couple of
times and that's the end of it. Other dogs respond well by taking them
outside for some fresh air. Or you can plug the nose holes forcing the
dog to breathe through her mouth and that will usually stop an episode
as well. Reverse sneezing is a harmless
condition and medical attention is not necessary. It is important to not
confuse reverse sneezing with a collapsing trachea. Inheritance: Unknown .
RETINAL DYSPLASIA The retina is the light sensitive
portion of the eye (like the film in a camera), and dysplasia is an abnormality
of development. Sounds pretty simple, and in the extreme case, it is. If
the retina fails to develop properly in its entirety the dog is blind at
birth, will never see, is easily diagnosed, and decisions can be taken
rationally and early. With the other major inherited ocular diseases -
progressive retinal atrophy and cataract - the decisions are much more
clear and the outcomes much more predictable. Not necessarily so with retinal
dysplasia, in which the diagnosis may be less certain, the visual outcome
much more variable, and the variations of the disease much more numerous. .
There is one type of retinal
dysplasia first described in England and Sweden in the early seventies
affecting another breed. The retinal dysplasia was complete, the retinas
detached from their normal position, and the affected pups blind at birth.
The inheritance pattern was quickly determined to be a simple recessive
trait without any complicating factors. Test breeding failed to reveal
any significant abnormalities other than those of the eye, and all decisions
were essentially "no brainers." Both sire and dam were carriers of the
trait and should not be used for breeding, the affected pups should be
put down, the unaffected pups were probably carriers (two chances out of
three) and shouldn't be used as reproductive stock. The disease was much
like that seen and described well in other unrelated breeds, the Yorkshire
Terrier, the Sealyham Terrier and the Bedlington Terrier. .
This type of retinal dysplasia
is completely different genetically than the one described in Europe, and
goes under the general name "Retinal and Vitreal Dysplasia with Skeletal
Abnormalities (Dwarfism with Retinal Dysplasia)." In this type of retinal
dysplasia in various breeds there are three different eye types (phenotypes),
and two different skeletal types that can accompany the eye types. The
investigators found puppies with normal eyes, puppies with localized retinal
dysplasia (retinal folds) and puppies with total retinal detachment (total
retinal dysplasia). The two skeletal phenotypes were (simply) affected
and normal. Most of the skeletally affected breeds have complete retinal
dysplasia, retinal detachment, and an abnormal vitreous body (the gel-like
portion of the eye). A few also have a peculiar pattern of pigment in the
cornea and varying degrees of cataract (opacity) of the lens. Some dogs
with skeletal abnormalities have multiple small retinal folds, without
having a complete blinding retinal detachment. Some researchers believe
that the occurrence of multiple retinal folds is a lesser manifestation
of the more severe retinal disorder. .
Visual difficulties in severely
affected pups become visible at eight weeks or before, and both visual
deficiencies and skeletal abnormalities become more noticeable as the pups
grow. The skeletal abnormalities include retarded growth of the front legs
and bowing out at the elbows with deformation of the carpus. The hind limbs
are straighter than normal, which causes difficulty in rising from the
sitting position. There is also retarded growth in the tibia, elbow hypoplasia
or dysplasia, hip dysplasia, and delayed development of growth plates of
the bones. These severely affected dogs tend to have larger than normal
eyes. .
Researchers did breeding experiments,
outcrossing severely affected (both skeletally and ocularly) as well as
crossingpurebred and outcrossed (including to control Beagles) breeds having
various degrees of the syndrome. Crosses of dogs with severe ocular abnormalities
and abnormal skeletons to normal dogs produced dogs with mild ocular abnormalities
and no skeletal deformities. Crosses of dogs with clinically normal skeletons
and mild ocular abnormalities to similarly affected dogs produced five
types of dog: those without either skeletal or ocular abnormalities, those
with normal skeletons and mild ocular abnormalities, those with abnormal
skeletons and mild ocular abnormalities, those with abnormal skeletons
and severe ocular abnormalities, and those with abnormal skeletons and
no ocular abnormalities. Similar results happened by crossing dogs with
skeletal abnormalities and severe ocular abnormalities with dogs with no
skeletal abnormalities and mild ocular abnormalities. Crossing dogs with
both skeletal abnormalities and severe ocular abnormalities to similarly
affected dogs resulted in dogs with skeletal abnormalities and either severe
or mild ocular abnormalities. The breeding results from crossing either
purebred Labrador Retrievers or by outcrossing to beagles were similar.
The breeding experiments indicate that the tendency to develop ocular and
skeletal defects are inherited together. .
Because of the possibility that
dogs with multiple skeletal as well as severe ocular abnormalities may
be produced by breeding two mildly affected dogs, the ACVO (American College
of Veterinary Ophthalmologists) Genetics Committee advises breeders not
to breed affected stock, and CERF (Canine Eye Research Foundation) certificates
are not issued for affected animals. Ophthalmoscopically, retinal
folds vary somewhat. They can be dots, lines, or branches of various shapes.
Dogs with more severe folds ("geographic") almost invariably also have
a severe disturbance of the vitreous humor. When Drs. Nelson and MacMillan
reexamined some two year old dogs that had been minimally affected with
retinal folds as pups, they found that in some dogs the retinal folds seen
previously had disappeared (this happened in Collies and Cocker Spaniels),
and that a dog previously diagnosed as having retinal folds now appeared
normal. This experience has been shared by others and makes control of
the disease more complex. So it is necessary to have young pups checked
(ophthalmoscopically) in order to detect the presence of minor dysplasia
before it disappears. The best time is eight to ten weeks. Apparently normal
older dogs may in fact be affected animals; in some only the presence of
an abnormal vitreous humor may reveal the condition. But what of those dogs affected
with retinal folds? The ACVO Genetics Committee advises that dogs with
extensive retinal folds ("geographic") "are associated with vision impairment."
Drs. Nelson and MacMillan, suggests that the practical effect of the presence
of retinal folds ("geographic" or simple) varies and is not predictable. .
Dogs with retinal folds and
vitreous abnormalities are likely to make acceptable pets, but they do
have a risk of developing retinal detachment, which may be treatable in
the early stages. Therefore ophthalmologic examinations should be performed
repeatedly in affected pet animals for at least three years. Inheritance: Autosomal recessive .
REVERSE REAR LEGS Born with abnormal joints in
rear legs Inheritance: Unknown .
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SCHISTOSOMA REFLEXUS Open belly at birth with abdominal
organs on outside, usually fatal any living should be neutered/spayed for
the animals well being. Inheritance: Unknown .
SEIZURES AND EPILEPSY Seizures may be caused by a
number of conditions, including low blood sugar, brain tumor, heat stroke,
poison, nutritional deficiency and distemper. Classic or idiopathic (meaning
"of unknown cause") epilepsy is characterized by recurrent seizures with
no active underlying disease process occurring in the brain. This form
of epilepsy is not usually seen until a dog is mature, usually between
three and five years of age. .
In a typical seizure, the dog
will salivate excessively. There is usually dilation of the pupils and
stiffening of the limbs. The dog may arch its back and paddle its legs.
Frequently, the dog's temperature will spike up three to five degrees.
Urination or defecation may accompany or follow the episode. Seizures usually
last only a minute or two, but severely affected dogs may have longer and
more frequent episodes. Dogs who have infrequent seizures do not require
treatment. When treatmen is required, phenobarbitol, dilantin and primidone
are frequently used. .
Epilepsy can usually be controlled
by medication. Specific diagnosis of the cause of seizure symptoms is critical
to successful treatment. Seizures can start early in life or be sudden
onset in adult dogs of varying age. There are a myriad of reasons for a
dog to suffer seizures. Seizure episodes that occur over an extended period
of time are likely to be genetic in origin. Inheritance: Causative dependent .
SURGICAL ANESTHETIC If your Yorkie would need surgery
or for some other reason need to have anesthetic administered ask if your
vet uses isoflurane. This is the one of the safest and most often used
anesthetic's for the Toy/Terrier Breeds. Inheritance: Immune mediated,
environmental factors .
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SHAKER DOG SYNDROME (related
terms: "little white shakers" syndrome, idiopathic tremor syndrome, acquired
tremor in young adult dogs) .
Dogs that have this disease
are subject to tremors that affect their entire body. Stress, handling,
and excitement seem to worsen the condition. Occasionally, other neurological
abnormalities are seen in association with this condition such as head
tilts, limb weakness and seizures. .
What is shaker dog syndrome? This disorder develops suddenly
in young adult, primarily small white dogs, causing a diffuse tremor of
the entire body. The cause is unknown although there is speculation that
there may be a generalized neurotransmitter deficiency due to an autoimmune
reaction. .
What breeds are affected by
shaker dog syndrome? For many breeds and many disorders,
the studies to determine the mode of inheritance or the frequency in the
breed have not been carried out, or are inconclusive. We have listed breeds
for which there is a consensus among those investigating in this field
and among veterinary practitioners, that the condition is significant in
this breed. .
This syndrome is seen in small
breed, mostly white dogs especially the Maltese, and West Highland white
terrier White Shaker Dog Syndrome most commonly is seen in such breeds
as West Highland White Terriers, Maltese, Yorkshire Terriers, Australian
Silky Terriers,Poodle, Beagle and Miniature Pinschers. .
What does shaker dog syndrome
mean to your dog & you? This disorder usually develops
suddenly in young adult dogs (6 months to 3 years of age). The signs become
progressively worse over 1 to 3 days and then remain the same until treatment
is begun. There is an all-over tremor that can range from mild to so severe
that the dog may have difficulty walking. This is called an intention tremor,
meaning that it is worse when the animal is excited or trys to perform
a specific action (such as eat, walk towards an object, etc). The tremor
decreases or disappears when the dog is relaxed or at rest. Commonly there
are rapid, random eye movements as well. .
The condition is not painful
and your dog's personality is unaffected. Treatment is generally effective;
some dogs require medication for life to control the tremors. .
How is shaker dog syndrome diagnosed? Your veterinarian will diagnose
this condition based on the clinical signs and the fact that tests for
other possible causes of these signs show no abnormalities. For the veterinarian: Intention
tremors may be mild to severe, affecting all 4 limbs and the head. There
is mild to moderate hypermetria and occasionally a head tilt. Conscious
proprioception, spinal and higher reflexes, cranial nerves, personality
and voluntary motor functions are unaffected. Para- or tetraparesis may
occur. .
How is shaker dog syndrome treated? Most dogs recover completely
with early treatment with corticosteroids and/or benzodiazepines. Your
veterinarian will start your dog at a relatively high dose which is gradually
decreased over several weeks. Clinical signs usually begin to improve within
a few days of starting treatment, but If treatment is stopped too early
the signs usually return. Some dogs may have to remain on a low dosage
on alternate days for life, so as to remain free of signs of the disorder. Inheritance mode: unknown .
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Please note that this section
is intended as a source of information only. It is not intended as a substitute
for professional care. Always consult with your Veterinarian about health
related matters. The information provided here is a brief outline only
of some of the health issues which may be of concern for the Yorkshire
Terrier breed and should not be considered as a complete listing. .
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