Information on various diseases found in dogs is provided through the links below. Descriptions and mode of inheritance, if known, are summarized.
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 your veterinarian about health-related matters. This information provided here is a brief outline only for some of the health issues which may be of concern for the Yorkshire Terrier breed and should not be considered as a complete listing.
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 Yorkies. Allergies can be chronic or seasonal. They can be minor or severe in occurence. They tend to become worse with age. Treatment is much better than in bygone days. Environmental controls, antihistamine treatment, and densitization injections have made huge strides in the last few years.
Glucocorticoids (steroids) 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.
also called: Walrus puppy, Rubber puppy, Water puppy
Usually lethal lymphedema of newborns; huge size (ofter 3 pounds) required c-section to deliver.
Inheritance: Autosomal recessive
Spermtogenci arrest; the sudden onset of sterility in a formerly known fertile male; may be immune-mediated.
Some of the most common ones include:
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 prominent stone type in female dogs of all breeds. Several factors predispose dogs to getting stuvite uroliths:
- Excess struvite crystals in the urine that set the stage for 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 than 7.0) urine from the diet or urease producing bactera 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 the alkaline urine.
This is the second most prevalent type of urolith after Struvite, making up around 30-50% of the uroliths, especially in male dogs of all breeds. 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, Struvite 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 demales. 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 ammonium 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. Dogs with PSS will commonly have abnormalities in the blood sample to give us further clues.
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. 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 minueral that is at the core of the stone.
There are other uroliths that occur, although they are relatively uncommon. They include cystine, silica, calcium phosphate, and miscellaneous minerals.
Inheritance: Considered unknown
Commonly mistaken for Parvovirus, but needs a 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 and 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 a fecal mucus sheath and 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.
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
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.
Shortened, deformed front legs, with a typical downhill stance.
Inheritance: Autosomal recessive
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
Immunoproliferative small intestinal disease. Persistent, nervous diarrhea: may be immune mediated.
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 Toys. 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.
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, bluiah-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 ofter 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 shite 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 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. Pruritis (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 pruritis 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? Weimaraners as a breed are dd, all individuals are dilute, yet the disease is unreported in this breeds. In Dobermans, the dilute individuals comprise only 8-9% of the breed, yet 50-80% of the dilute dogs have CDA. Many individuals are dilutes, the IGCA health survey reported only 71 affected individuals among the approximately 2,200 dogs included in the survey. If half the dogs included in the survey were dilutes, the incidence of CDA in IGs 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 Terrier 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 patter. 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 colors.
Comedo Syndrome ("Schnauzer Bumps")
Crusts on back due to plugged hair follicles, itching.
Cryptochordism (undescended testicles)
Cryptochordism 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 heridtary 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 whould 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.
Cushing's Syndrome is also known as "Hyperadrenocorticism" and is a combination of clinical and chemical abnormalities results 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 cortisone, a natural steroid hormone, by the adrenal glands. It is rare in dogs under five years old. In about 80 percent of 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 malignant and spread, and about half of them are benign and generally tend to stay small.
Glucocorticoids 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 body's 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 bloodstream. It does this by producing a hormone called ACTH that flows through the bloodstream to the adrenal glands. The adrenal glands are very small pockets of specialized cells sitting behind each kidney that are responsible for producing the body's 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 tumors 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 include increased thirst with subsequently increased urine output, an excessive appetite, abdominal distention, 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 steroids 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.
- 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 potbelly
- The dog has a 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 tumors can be surgically removed in a percentage of cases but pituitary surgery would only be attempted in rare cases at very specialized centers.
Distichiasis (Double Eyelashes)
Extra row of eyelashes, usually on lower lid but appearing at times on upper; irritates the cornea causing excessive tearing.
Dry Eye (Keratoconjunctivitis Sicca - KCS, Xeropthalmia)
KCS or "dry eye" 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 section 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 prediposition 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 (i.e., 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.
Abnormal covering of the neural transmitters in the brain/spine; various nervous signs or tremors; may not be progressive and may improve with age.
Multiple cartilage bumps on the bones near joints; if severe can cause lameness.
Renal tubules degenerate, leak sugar, then proteins and slats in urine; leads to complete renal failure.
Inheritance: Autosomal recessive
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
A 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.
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.
Hemorrhagic Gastric Enteritis (HGE)
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 through diarrhea, especially bloody diarrhea.
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 in conjunction with the retention due to cord length of one or both testes. Umbilical or rupture or "outie" - bulging of abdominal contents in sac at umbilicus; common; usually harmless unless very large.
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: Generally the signs gradually worsen, although by two 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
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 stuporous 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.
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, and 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.
- Abnormal loss of coat (often bilateral and symmetrial), 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 hypothryoidism 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 strophy by giving medication improperly.
Idiopathic Tremor Syndrome
see Shaker Dog Syndrome
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, sweeling, and decreased blood flow to the intestines involved.
Intussusceptions generally occur as a secondary problem to some disorder or disease that causes increased intestinal motility 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 intussusceptions 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 - intussusceptions occasionally will resolve on their own and then recur. I have removed one surgically, put the remaining intesting ends back together and watched a new intussusception form right at the same site.
Keratoconjunctivitis Sicca - KCS
see Dry Eye
Fluid filled cysts in kidneys may be with or without symptoms and will lead to renal failure without treatment.
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 terminologym 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 causes 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 diruption 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 beneficial response. If one is not seen, surgical repair should be considered more carefully.
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
see Portal Shunt
no content in the category at this time
Pancreatitis is inflammation of the pancreas, an elongated gland that serves many functions in the process of digestion and metobolism. 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 wil 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 suger levels. The pancreas also has an exocrine gladular function: it makes digestive enzymes that are secreted into the intesting and are critical for the normal digestion of food.
Pancreatitis is a condition where the pancreas becomes inflamed. The time course can be either chrnic (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 pancrease, 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 abcesses - 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 pancretitis 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 will 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.
Diagnosis of pancreatitis can be difficult because no available test is 100% reliable. Two digestive enzymes made in the pancrease can be measured in the blood. Elevations in these enzymes (lipase and amylase) can provide supportive evidence for pancreatitis. The lipase test appears to be the 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 elevation 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 the 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 much 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 fna 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-inflammtory agents don't seem to aid recovery in dogs with pancreatitis.
In severe cases of pancreatitis in dogs, painkillers 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 abcesses 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; chronis pancreatitis): lack of digestive enzymes, gray, greasy feces, chronic weight loss despite huge appetite, insulin producing cells usually remain normal.
Inheritance: Autosomal recessive
Canine parvovirus is an acute, highly contagious disease of dogs that was first described in the early 1970s. The disease is transmitted by oral contact with infected feces. Parvo affects dogs of all ages, but most cases occur in puppies 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 unhealthy and weak for life.
Inheritance: Immune-mediated, environmental factors
Patent Ductus Arteriosus (PDA)
see Heart Defects
Pharyngeal Gag Reflex
see Reverse Sneezing
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 poisonsnare 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 ziploc 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
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.
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 that 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
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 varu slightly.
There are three shunt types: intrahepatic, extrahepatic, or microvascular. The most common is Portosystemic shunt (PSS) which 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 intolerane, 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 signs 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 and 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)
- pushing the head against a solid object
- poor appetite
- increased drinking and urinating
- balance problems
- frequent urinary tract disease or early onset of bladder stones
- If these signs increase after eating, it is a strong supportive sign of a portosystemic shunt.
Most dogs will be diagnosed with portosystemic 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 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 the 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 so, 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 concentrat in a dog with a 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, and 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-hour post meal blood sample 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 is one of the most important methods of establishing a diagnosis of porto-sysyemic shunt, and is currently the only universallu accepted method of confirming a shunt, short of major surgery. Injection of a radiopaque dye into the spleen (Splenoportography) 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 non-surgical diagnosis or 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 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.
Genetic disorders in dogs can spread relatively rapidly if a dog, whether affected or a carrier, is a well-repsected 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 and screening tool.
Inheritance: Unknown, assumed to be polygenetic recessive
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 maturaity. 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 muct carry one copy of the same mutant gene. Both parents could have normal eyesight, but have one gene for normal enzyme production that is dominate over the one 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 one dominant gene and one 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 two 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 one dominant normal enzyme gene and one recessive abnoral 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 come 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 honet disclosire 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 occurence of PRA in the breed.
Until development of the first DNA test, PRA can only be detected by electectroretinography testing. Conclusive diagnosis for Yorkies still requires examination by a canine ophthalmologist. Using special equipment the ophthalmologist 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 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 can can be distinguished in the early stages of development from genetic PRA. When either type of retinal degeration is found in an advanced state (e.g., the retina is 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 informaiton 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: Autosomal recessive
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, it 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 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, and 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.
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 ins't really a health problem, but something that dog owners shold be aware of as it is very common in toy breeds. It is characterized by honking, hacking or 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 when 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 be taking them outside for some fresh air. Or you can plug the nose holes, forcing the dog to breathe through his/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.
Open belly at birth with abdominal organs on outside, usually fatal. Any living should be neutered/spayed for the animal's well being.
see Comedo Syndrome
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 a dilation of the pupils and stiffening of the limbs. The dog may arch its back and paddle its legs. Frequently, the dogs temperature will spike up three to five degrees. Urination of 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 treatment is required, phenobarbitol, dialntin 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
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 a 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, as well as Yorkshire Terriers, Australian Silky Terriers, Poodle, Beagle and Miniature Pinschers.
What does Shaker Dog Syndrome mean to your dog and you?
This disorder usually develops suddently 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 effected; 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. Concious 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 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
If your Yorkie would need surgery or for some other reason need to have anesthetic administered, ask if you vet uses isofluorane. This is one of the safest and most often used anesthetics for the Toy/Terrier breeds.
Inheritance: Immune mediated, environmental factors
see Heart Defects
see Dry Eye