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Issues Information Page

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Collie Nose

Thyroid deficiency

 

This web site is not intended for you to diagnose your Collie's Condition. Always consult with your Animal Care Specialist!

If there is something you do not see here, please E-Mail us at tonyd@ida.net, and we will research it for you.
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FACT

UNDER IDEAL CONDITIONS
OF UNREGULATED BREEDING-

ONE FEMALE DOG AND
HER OFFSPRING CAN
GIVE RISE TO

4,372 PUPS IN 7 YEARS

 

 


 

Bloat, Torsion. Gastric dilatation-volvulus (GDV)

 

Bloat is a serious, life threatening disease in dogs. Bloat is actually two conditions that come under the heading of one syndrome. First there is "simple" bloat or gastric dilatation; second is bloat with twisting of the stomach or gastric dilatation and volvulus. Veterinarians use the abbreviations GD and GDV to describe these clinically. You could think of these as two syndromes in which one becomes the other; gastric dilatation becoming gastric dilatation and volvulus. So the line between the two is not exactly clear.

Normal Stomach
Parts
  • A - Pylorus
  • B - Pyloric Antrum
  • C - Esophagus
  • D - Fundus
  • E - Body
  • F - Omentum

In bloat, due to a number of different and sometimes unknown reasons, the stomach fills up with air and puts pressure on the other organs and diaphragm. Filled with air, the stomach can easily rotate on itself, thus pinching off the blood supply. Once this rotation (volvulus) occurs and the blood supply is cut off, the stomach begins to die and the entire blood supply is disrupted and the animal’s condition begins to deteriorate very rapidly.

The signs of bloat can be subtle at first: restlessness being the most likely first indication of a problem as the distention and pain increases. Drooling, retching or gagging (but not vomiting up stomach contents) will occur and by the time you recognize that your dog's stomach is distended, you have a serious medical emergency on your hands. Now a complex chain of physiologic events begins. The blood return to the heart decreases, cardiac output decreases, and cardiac arrythmias may follow. Toxins build up in the dying stomach lining. The liver, pancreas, and upper small bowel may also be compromised. Shock from low blood pressure and endotoxins rapidly develops. Sometimes the stomach ruptures, leading to peritonitis. You need to seek veterinary care immediately!

Gastric Dilatation with Torsion
Descriptions
  1. Clockwise Torsion of the stomach; the organ is greatly enlarged.
  2. Torsion of the esophagus
  3. Duodenum displaced to the left.
  4. Hemorrhages on the stomach's surface.
  5. The Greater Omnetum covers the Stomach's surface.

The faster the distention and/or twisting can be corrected, the better the dog's chances of survival. Also, these conditions are extremely painful! Even with treatment it is estimated that at least 35% of the dogs with gastric dilatation and volvulus die. Plus treatment can be extremely costly, usually $500 to over $1000.

GDV is a true emergency. If you know or even suspect your dog has bloat, immediately call your veterinarian or emergency service. Do not attempt home treatment, but do take the time to call ahead. While you are transporting the dog, the hospital staff can prepare for your arrival.

Please do not insist on accompanying your dog to the treatment area. Well-meaning owners are an impediment to efficient care. Someone will be out to answer your questions as soon as possible, but for now, have faith in your veterinarian and wait.

The GDV risk ratio of a Great Dane is 41.4 times more likely to develop GDV than a mixed breed dog. It seems the larger the chest cavity of the animal, the greater the risk of GDV. The following chart lists the risk ratio for many of the popular breeds of today.

Breed
GDV Risk Ratio
Risk Rank
Breed
GDV Risk Ratio
Risk Rank
Great Dane
41.4
1
Alaskan Malamute
4.1
14
Saint Bernard
21.8
2
Chesapeake Bay Retriever
3.7
15
Weimaraner
19.3
3
Boxer
3.7
16
Irish Setter
14.2
4
Collie
2.8
17
Gordon Setter
12.3
5
Labrador Retriever
2
18
Standard Poodle
8.8
6
English Springer Spaniel
2
19
Basset Hound
5.9
7
Samoyed
1.6
20
Doberman Pinscher
5.5
8
Dachshund
1.6
21
Old English Sheepdog
4.8
9
Golden Retriever
1.2
22
German Shorthaired Pointer
4.6
10
Rottweiler
1.1
23
Newfoundland
4.4
11
Mixed
1.0
24
German Shepherd
4.2
12
Miniature Poodle
0.3
25
Airedale Terrier
4.1
13
     

Prevention of GDV is preferable to treatment. In susceptible breeds, feed two or three meals daily and discourage rapid eating. Also regulate the amount of water consumed before, during, and after meals. Do not allow exercise for two hours after a meal. As previously mentioned, some owners feel that certain bloodlines are at greater risk and choose to have gastroplexy performed as a prophylactic measure. While the genetics of GDV are not completely worked out, most breeders and veterinarians feel there is some degree of heritability. The incidence is closely correlated to the depth and width of the dog’s chest. Several different genes from the parents determine these traits. If both parents have particularly deep chests then it is highly likely that their offspring will have a deep chest and the resulting problems that may go with it. This is why in particular breeds we see a higher incidence in certain lines, most likely because of that line's particular chest conformation. Therefore, while prophylactic gastroplexy will probably help an individual dog, it makes sense not to breed dogs who are affected or who are close relatives of those suffering from GDV.

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Collie Eye Anomaly (CEA)

 

Collie eye anomaly was first reported in 1953. The original report included a description of a pale area in the retinal along with staphylomas and retinal detachments. CEA is the incomplete development of the eye which is present as early as the 28th day of gestation. The defect involves the sclera, the choroid, the retina, the retinal vasculature, and the optic disc. Clinically, the severity of the anomaly is variable ranging from no apparent visual defect to total blindness. It is found in rough and smooth Collies and all color coats are involved. Most Collies (80 to 90%) with CEA do not demonstrate vision problems. CEA is a simple recessive defect and therefore is expressed in the homozygous state only. Carriers and normals can not be distinguished based on an ophthalmic examination. A number of researchers have attempted to separate the various aspects of the disease, i.e. the choroidal hypoplasia from the ectasia (pits) but were unable to do so. When the disease was first described such a large percentage of the population was affected that a number of simple grading systems were devised to make classifications of individuals easier. In addition, it was the feeling of some people at that time that the severity of the disease might be ameliorated by breeding less afflicted individuals. Certainly this concept has had its place in history of breeding better Collies.

Unfortunately, dogs with minor afflictions can and do produce severely afflicted offsprings. Likewise, blind parents can produce less afflicted offspring. For the purpose of genetic selection, an individual with the mildest affliction is just as bad as a totally blind dog. Because the grading system remains firmly entrenched within the Collie fancy a discussion of the grades and categories is appropriate. Grade 1 - torturous retinal vessels, extremely small areas of choroidal hypoplasia Grade 2 - torturous retinal vessels, substantial areas of choroidal hypoplasia Grade 3 - torturous retinal vessels, substantial areas of choroidal hypoplasia with colobomas (pits) or areas of ectasia in the posterior segment. Grade 4 - all of the above defects with a retinal detachment Grade 5 - all of the above defects with a retinal hemorrhage It is possible for one eye to have a different grade than the other, but if one eye is affected then both eyes in almost all cases are affected. "Go normal" is a term used to describe an affected individual, Grade 1 or Grade 2, in which the area of choroidal hypoplasia fills in so it appears normal at later examinations. These animals act genetically like the affected individuals that they are. They can set a breeding program back years, however. Because the lesion is present in the neonatal puppy, eyes can be checked as early as 5 to 6 weeks of age. For the ease of the examiner and to facilitate a more accurate exam, evaluation at 6 to 8 weeks of age is recommended.

 

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Nasal Solar Dermatitis (Collie Nose)

 

 

Pink Areas at the base of the nose
Side View

Collie Nose is a discoloration of the nose pigment diagnosed as Discoid Lupus Erythematosus. Originally thought to be an allergic reaction to sunlight, the condition is only aggravated by prolonged sun exposure. Though not painful, the lighter colored areas are very sensitive to sunlight and can be sunburned. The dog should be kept out of bright sunlight as much as possible or the affected area should be protected with a sun screen lotion. Though it is known as Collie nose it is not indigenous to the Collie breed as it also appears in the Shetland Sheepdog and any mixed breed farm shepherd type dogs. One Disease know as DM (Dermatomyositis) in it's early stages, has been mistaken for Collie Nose.

 

 

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Double Dilute (DD)

Double Dilute's commonly known as DD's are the result of merle to merle breedings (any two merle dogs, which includes blue merle, sable merle, or merle headed whites). If they carry the merle gene and are bred with another merle they can produce the DD syndrome. A very high percentage of DD collies are born with severe birth defects such as deafness and/or blindness. DD puppies have been known to be born without eyes, just the empty sockets.

The correct term for a "white" puppy from a merle to merle breeding is homozygous merle or double dilute merle. They should not be confused with WHITE Collies (color headed whites). An excellent source of reference on this subject is, The Collie - A Veterinary Reference for the Professional Breeder by Sharon Lynn Vanderlip, D.V.M. Published by Biotechnical Veterinary Consultants, 1984. Look in the color genetics section for this information.

Double dilutes have an absence of pigment in their "white" hairs, while a color headed white dog has pigment in their white hairs.


 

Heart Worm

 

A Heart Worm infested Heart

Heart Worm is a parasite invasion of a proper host's heart. In the larval stage of the worm, the infected host's blood swarms with the Heart Worm microfilariae or larva. A mosquito will ingest the larva along with the host's blood. When the now infected mosquito host bites other animals after the incubation period, viable microfilariae travel from the host mosquito into the bitten animals. If the animal is a proper host, the microfilariae survive. The larva burrows into the dog, and in three to four months the now adult worm travels to the right side of the heart through a vein and await the opportunity to reproduce. Adult heartworms can reach 12 inches in length and can remain in the dog's heart for several years. Female heartworms bear live young -- thousands of them in a day. These young -- the microfilariae -- circulate in the bloodstream for as long as three years, waiting to hitch a ride in a bloodsucking mosquito. The worms thrive in the chambers on the right side of the heart, veins entering the heart, arteries in the lungs, and the liver veins.

Progressive signs of Heart Worm may not manifest for a year. The first sign is a soft cough during exercise which gets worse over time. The dog tires easily, begins to lose weight, could cough up blood, and may even faint when exercised in the later stages of the infection. The dog becomes a couch potato, not wanting to play or exercise. Any form of activity leaves the animal weak and out of breath. If left unchecked, congestive heart failure ensues, and the once-active, outgoing pet is in grave danger.

At one time, the Heart Worm was a Warm Climate pest. But due to the nature of Dog Shows and the traveling exhibitor, Heart Worm now infests animals even into the coldest climates. Heartworm prevention costs money and requires commitment: blood must be drawn to examine for signs of infestation before the preventive drug can be given, and the drug must be administered regularly whether the daily dose or the once-a-month type is chosen. But the effort and the money are well-spent to keep a loved pet from the discomfort and debilitation of the infliction.

But there are dangers in various types of Heartworm Medication for Collies and other herding breeds. Much of the concern over the safety of ivermectin began when this medication was first tested in dogs for toxicity studies. In the initial testing of ivermectin, the drug was tested in Beagles to see at what dose clinical signs of toxicity would develop. Later, these same studies were performed on Collies and it was found that Collies had clinical signs of toxicosis at much lower doses of ivermectin than the Beagles did. The signs of toxicosis seen in clinical trials varied in their severity. Early signs of toxicosis included salivation, dilated pupils, vomiting, tremors, and difficulty walking (ataxia). Severe signs of toxicosis included weakness, inability to stand (recumbency), non-responsiveness, stupor, and coma. In several of these type of studies, there were collies that seemed to react to ivermectin, and other collies that did not react to the ivermectin. It has been suggested that there are collies that are "ivermectin sensitive" and those that are considered to be "ivermectin non-sensitive" based on the results of these studies. Unfortunately, to date, no research has provided us with the ability to differentiate between the ivermectin-sensitive and non-sensitive collies.

Ivermectin is not considered safe for collies by most breeders. Although Merck has recently removed its warning, there are now several cases of toxicity reactions reported from collies given Ivermectin. There have also been numerous reports of sub-clinical toxic reactions from dogs given Heartgard preventative. It is thought that there may be a wider range of sensitivity than indicated by the studies. To be completely safe, Collies should be given either carbamazine Heartworm preventative (daily dose), or the monthly Interceptor Heartworm preventative.

Ascites
Ascites is a fluid build up in the abdomen seen in late stages of Heartworm Disease. If a blood test or the onset of symptoms alert owner and veterinarian to the presence of this devastating parasite, treatment is possible and successful if the disease has not progressed this far. The first step is to evaluate the dog and treat any secondary problems of heart failure or liver or kidney insufficiency so that he can withstand the treatment. The next step is to kill the adult worms -- with an arsenic compound. The drug is administered in two doses each day for two days, followed by several weeks of inactivity to give the dog's system a chance to absorb the dead worms. Exertion can cause the dead worms to dislodge, travel to the lungs, and cause death. Six weeks after the administration of the drug to kill the adult worms, further treatment to kill the microfilariae is needed. The dog is dosed daily for a week , then the blood test is repeated. If microfilariae are still present, the dose can be increased. Follow-up studies should be done in a year.

 

 

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Hip Dysplasia (CHD)

Canine Hip Dysplasia (CHD) is a developmental disorder of the hip that begins with joint laxity and progresses to arthritis over a period of several months to years. It is one of the most common skeletal diseases seen by veterinarians. The condition is very common in large breed dogs, but can be seen in any breed.

Normal Development
Severe Hip Dysplasia
In this X-ray, the Balls of the hips are properly placed within the Hip Sockets. While in this X-ray, the Balls are far removed from the Hip Sockets.

Multiple genes are involved in the inheritance of hip Dysplasia, and many other factors influence its development, including body type, size, growth rate, and nutrition. Overfeeding, and dietary supplementation for maximal growth has been shown to increase the incidence of hip Dysplasia in young, growing, large breed dogs. Conversely the development of hip Dysplasia can be delayed, and its severity diminished when the growth rate of pups is restricted. The diagnosis of hip Dysplasia is based on history, physical examination, and radiographic evaluation

The clinical signs commonly begin between five to eight months of age or after skeletal maturity. Some dogs don't have noticeable problems until eight to ten years of age or older. The onset of signs may appear sudden or gradual. This variability is due to the individual severity of the disease as well as pain tolerance of the pet. Most dogs with CHD are most painful when the hips are extended by pulling the rear legs back behind the body. Palpation of the hips usually reveals joint laxity, although anesthesia may be required to detect it in some cases. Radiographs are necessary to confirm the diagnosis and evaluate the severity of CHD.

Radiographs of animals 24 months of age or older are independently evaluated by three randomly selected, board-certified veterinary radiologists from a pool of 20 to 25 consulting radiologists throughout the USA in private practice and academia. Each radiologist evaluates the animal's hip status considering the breed, sex, and age. There are approximately 9 different anatomic areas of the hip that are evaluated
  1. Craniolateral acetabular rim
  2. Cranial acetabular margin
  3. Femoral head (hip ball)
  4. Fovea capitus (normal flattened area on hip ball)
  5. Acetabular notch
  6. Caudal acetabular rim
  7. Dorsal acetabular margin
  8. Junction of femoral head and neck
  9. Trochanteric fossa

A typical history may include any or all of the following:

In young dogs or in very mild cases, joint laxity may be the only detectable abnormality. Later in the disease arthritic changes are seen. The Orthopedic Foundation of America (OFA) has been the standard for certification of dog's hips as being free of CHD. The radiograph is taken after the dog is 2 years of age and requires the hip extended position. Recently the PennHIP program has emerged as a new scientific method for the early diagnosis of CHD. It measures the passive hip joint laxity or "looseness" of the hip ball in the hip socket under sedation or anesthesia. PennHIP is more reliable and has the advantage of being accurate on puppies as young as 16 weeks of age. Medical management usually consists of exercise restriction, body weight management, and symptomatic pain management with analgesics and anti-inflammatory drugs. A non-weight bearing activity like swimming is the preferred type of exercise since it places minimal stress on the joints. Several surgical options are now available for treating the various stages of hip Dysplasia They include the triple pelvic osteotomy, femoral head and neck excision, and total hip replacement.

The phenotypic evaluation (Grading) of hips done by the Orthopedic Foundation for Animals (OFA) falls into seven different categories. Those categories are Excellent, Good, Fair, Borderline, Mild, Moderate, Severe.

 

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Kennel cough or Bordetella

 

When a dog begins to have a dry or hacking cough, or signs of pneumonia, these could be the warning signs of Kennel Cough or Bordetella. Caused by either the Bordetella bronchiseptica or Canine parainfluenza virus, the infected animal is extremely contagious, and if left untreated the condition can cause death. Symptoms may increase in severity such as;

  1. Coughing spasms
  2. Fever
  3. Thick Nasal Discharge
  4. Loss of Appetite
  5. Depression.

Dogs in stressful situations, such as over crowding in a kennel, are much more susceptible to becoming infected by these pathogens. Other contributors to a dog's susceptibility are temperature and poor nutritional status. Once a dog or puppy has been infected, their immune system may be weakened enough to a point where other diseases may also take hold. The disease will last from 10 to 20 days, but can be treated with standard antibiotics. Even when the disease has run it's course or been treated, the cough may last for weeks after.

 

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Canine Cutaneous (Skin) Immunologic Diseases

 

Demodectic Mange on dog's foreleg

Canine Demodicosis is commonly known as Demodectic Mange which is caused by the Demodex Mite. The mite normally resides in the animals hair follicles in small numbers. There are two types of Demodectic; Localized Demodicosis usually occurs in 3 to 10 month old puppies. It consists of small patches in which well defined scaly areas of hair loss occur around the dog's lips, eyes, and/or forelegs. The second type, Generalized or Pustular Demodectic is more severe and extremely difficult to cure or control. Small patches appear, in which well defined scaly areas of hair loss spread rapidly over large areas of the body. This is accompanied by extreme itching, edema, and bleeding followed by invasion of bacterial infection. Generalized Demodicosis is caused by a hereditary genetic defect in which the 'T'-cell that normally controls the mite is weakened or nonexistent, allowing the mite to multiply in large numbers.

 

 

 

Demodex Mite

The mites usually spend their entire life on a dog. The female mite burrows into the skin and lays eggs several times as she continues burrowing. These tunnels can actually reach the length of several centimeters. After she deposits the eggs, the female mite dies. In 3-8 days the eggs hatch into larvae which have 6 legs. The larvae mature into nymphs which have 8 legs. The nymph then molts into an adult while it is still in the burrow. The adults mate, and the process continues. The entire life cycle requires 2-3 weeks. The mites prefer to live on the dog but will live for several days off of the host in the environment. In cool moist environments they can live for up to 22 days. At normal room temperature in a home they will live from 2 to 6 days. Because of the mite's ability to survive off the host, dogs can become infected without ever coming into direct contact with an infected dog.

 

 

Dermatomyositis, commonly known as DM, is a systemic autoimmune (Although the immune system ordinarily recognizes and destroys infectious organisms and malignant cells, it may become "confused" and damage the host itself.) Disease that targets predominately the skin and muscles, although lung and heart involvement can occur as well. In its most severe form, this disease can lead to death and can cause considerable disability. Also, the development of DM can be the harbinger of the development of internal cancers. It appears that DM in Collies is an "autosomal dominant with variable expression." This means: A. Either sex can inherit the disease. B. Only one parent needs to be a carrier to pass it on to their offspring. C. Afflicted dogs can either show few to no symptoms, or they can show severe symptoms.

If a litter has just one visibly affected puppy then one or both parents are DM carriers. This could mean that at least half of the litter mates will also have the potential for DM even if there are no symptoms. Unfortunately, there are no tests currently to differentiate the non-afflicted Collies, and those that have the disease but show no symptoms of it.

Advanced Dermatomyositis

The first sign of DM is usually a loss of hair on the bridge of the nose or around the eyes. Lesions and scabby,crusty areas generally also develop. The affected areas may at first appear as a "Bad Sunburn", or be mistaken for "Collie Nose". The symptoms can progress to the feet, legs and the tail. Normally, these symptoms are first noticed in an infected dog between 8 and 16 week of age, although there are rare cases of late development appearing in animals 4 - 7 years of age. In Mild cases, the skin symptoms could sometimes fade away and never be seen again. While in the more severe cases the dog will have the lesions for life. Muscle disease may develop along side the skin symptoms. Muscle degeneration is usually first noticed in the areas around the top of the head and jaw. When the disease progresses, general atrophy of the major muscles may develop affecting the neck, shoulder and hip muscles causing sever pain and weakness inhibiting simple movement.

It is impossible to diagnose DM simply by looking at the dog! The visible symptoms described here could be ringworm, Demodectic mange or one of many other skin problems. A biopsy of an active lesion is the only sure way of a positive diagnosis. DM cannot be diagnosed by any other tests or bloodwork. As it is a skin disease, a Dermatologist would be the best choice to determine the disease. Yes, there are Dermatologist for animals. A biopsy could cost around $270. Antibiotics and Pentoxyphylene(a blood thinner) are commonly used to help control this disease.

 

Sarcoptes scabiei

Sarcoptic mange, also known as scabies, is caused by a microscopic mite. The female mite causes the characteristic intense itching as they burrow under the skin to lay their eggs. The eggs hatch in a few days, develop into adults, and begin laying their own eggs in less than three weeks. Dogs with scabies dig and bite at themselves with great ferocity. Their skin reacts with oozing sores, and secondary infection may set in, requiring treatment with an antibiotic in addition to treatment for the mites. Unfortunately, the sarcoptic mange mite can be difficult to find in skin scrapings, and unless the veterinarian parts the hair and carefully examines the bare skin for the characteristic pin-point bite marks, diagnosis is difficult. Furthermore, the presence of a secondary skin infection can hamper the search for the mite bite marks. Telltale signs of sarcoptic mange are crusty ear tips, fierce itching, and hair loss, particularly on the ears, elbows, legs, and face in the early stages. Later on, the hair loss spreads throughout the body. Sarcoptic mange is contagious to canines and humans. If the dogs share sleeping places or if the infected dog sleeps on beds or furniture, everyone will begin scratching. It is not unheard of for the family dog to infest the kids, the kids to infest their playmates, and the playmates to infest their pets and parents with scabies. Fortunately scabies in humans is self-limiting, that is the mite can burrow under the skin and cause itching, but cannot complete its life cycle on humans and dies within a few weeks. Canine skin damaged by sarcoptic mange and secondary skin infections can take weeks or months to recover, depending on the scope of the problems. Frequent medicated baths may be necessary to soothe irritated skin. Mange damage can mimic that caused by other skin conditions, including autoimmune diseases, bacterial infections secondary to flea allergies, and contact dermatitis, making it impossible for the pet owner to diagnose with any success.

 

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Progressive Retinal Atrophy (PRA)

 

PROGRESSIVE RETINAL ATROPHY Progressive retinal atrophy is a collective term used to describe a variety of inherited retinal diseases in dogs. Within this category is a syndrome known as rod-cone Dysplasia or PRA in the Collie. A Dysplasia denotes that malformation process where the designated tissue, in this case the rod and the cones, never form correctly.

Clinically affected animals exhibit night blindness as early as 12 weeks of age and progress to total blindness by one year of age. All affected individuals become totally blind. Changes can be seen in appearance of the retina by 6 months. Late stages are characterized by retinal vascular attenuation, increased tapetal reflectivity, pigment changes in the non-tapetal fundus, and a pale optic disc. Electroretinography changes are evident as early as 10 to 12 weeks of age.

An electroretinogram is the recorded electrical potential changes in the eye over a period of time that results from stimulation by light. The test involves placing a contact lens on the cornea to which a wire has been attached. Two other wires have been attached to the skin around the eye. These wires are then connected to amplifiers and an oscilloscope. A strobe light is then flashed into the eye at various intensities and intervals using a variety of filters.

It is possible to separate the rod and the cone function and differentiate affected puppies from normals prior to the onset of clinical signs. Rod-cone Dysplasia (PRA) is inherited in a simple recessive form. Therefore, homozygous individuals are affected while the normals and carriers appear normal and show no changes in vision or electro-retinographic changes. To date, no test has been devised to detect carriers short of test breeding. Test breeding involves breeding a suspected individual to known afflicted individuals.

Because the disease is expressed in the homozygous form, only the production of affected offspring implicate suspect of the carrier. Statistically, the more normal individuals produced as a result of the test breeding, the greater the assurance the suspect is a normal dog or a non-carrier. At least 6 puppies must be produced to have a 95% level of confidence that the suspect is normal and a non-carrier.

 

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Hypothyroidism or Thyroid deficiency

 

Hypothyroidism or Thyroid deficiency is when the thyroid gland is not working properly; by not producing a normal level of thyroid hormones. The lack of proper thyroid hormone production and secretion results in various physical problems. . This gland produces and secretes two thyroid hormones that are involved in many bodily functions; one such function is the control of the body's basic metabolic rate (oxygen consumption). This condition is usually seen in dogs within the range of 4 to 10 years of age, and in breeds that are medium to large in size. Some of the signs displayed by hyperthyroid dogs are visually apparent, but sometimes the dog may not show any outward signs of the illness. Some of the more common visual signs associated with this disease are:

  1. The dog puts on weight even though he/she is not eating increased amounts of food. When the amount of food is then reduced, he/she doesn't lose the surplus weight.
  2. The dog seeks sources of heat and rarely seems to be comfortable.
  3. The dog doesn't want to exercise, appears uninterested in activity around him/her.
  4. Noticeable changes to the coat and skin such as dryness and hair loss. The loss of hair is commonly seen upon the tail, trunk, thighs and the nose.
  5. The skin may become thickened (common on the face and upon the forehead), and there may be a change in skin color - it becomes darker due to hyperpigmentation.

Other symptoms of hypothyroidism are not visually apparent. Lack of the necessary amounts of thyroid hormones alters the proper function of organ systems. Females that are still intact may experience reproductive problems such as abortion, infertility or failure to cycle. Intact males can also experience infertility.

The only way to find out if the dog is suffering from hypothyroidism must be made through lab tests. It can not be made based only upon the nonspecific signs discussed above. Discovery of below normal levels of thyroid hormone is critical to the diagnosis of this disease.

Providing the dog with thyroid supplementation (through pills) is the only way to help bring the dog back to an improved state of health. This thyroid replacement must continue for the remainder of the dog's life. It is because the thyroid has failed that a supplement must be given. Pills are administered two times each and every day. The vet's instructions must be followed strictly on pill administration; it is so important to continue the therapy even if it appears that the dog is completely cured. He or she only appears cured. Discontinuation of hormone replacement will quickly return the dog to his/her previous untreated and unhealthy condition. The cessation of treatment will also throw off the test results necessary to evaluate the pet's state of health, making dosage reevaluation difficult.

 

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Vaginal Hyperplacia

Though, not common in the Collie Breed, it can occur. Vaginal Hyperplasia is a protrusion of vaginal epithelium during the estrogenic phase of the estrus cycle. To distinguish that from, for instance, vaginal prolapse which occurs following trauma to the pelvic organs or following a difficult birth.

During estrus, vaginal tissues becomes hyperplastic and protrudes through the vulva. The condition results from an exaggeration of the estrogenic response which results in excessive mucosal folding of the vaginal floor just ahead of the urethral papilla in such a manner that tissue protrudes through the vulva labia. Vaginal hyperplasia is most common in large brachycephalic breeds (short nosed breeds) such as Boxers and Bostons, although it does occasionally occur in other large and small breeds.

The hyperplastic tissue will regress at the end of the heat cycle but it will return with the next heat, only more extreme with more tissue protruding each time. And although the tissue may appear healthy it can become necrotic within hours if the tissue dries and/or is self mutilated. It may be necessary to place an Elizabethan collar on the dog to prevent self trauma.

The protruding tissues should be kept clean and moist. It may be necessary to amputate the hyperplastic tissue if it becomes necrotic. Vaginal hyperplasia must be differentiated from tumors which are not associated with estrus cycles. The only true cure is to have the bitch spayed although the problem can sometimes be controlled with the use of hormones to stop the bitch from coming into season (not recommended due to risks from the hormones themselves).

Difficulty results from the trauma that occurs to the tissue once it is outside the body. It very quickly becomes dry and can be infected and ulcerated within a period of twelve hours. Usually the condition occurs on the first estrus cycle and continues to be a problem each time the bitch cycles. On occasion, we may see it again on the 63rd day, whether she is bred or not.

 

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von Willebrand's Disease (vWD)

 

In 1925 Erik von Willebrand, a Finnish physician, recognize vWD in humans. In von Willebrand's Disease, the dog is missing a substance which helps the platelets form clots and stabilizes Factor VIII in the clotting process. This substance is called "von Willebrand's factor". Because of the deficient clotting of blood, dogs with von Willebrand's disease have excessive bleeding upon injury. This would be similar to hemophilia. Certain breeds have a higher incidence of vWD than others. German Shepherds, Doberman Pinschers, Shetland Sheepdogs, Chesapeake Bay Retrievers, German Shorthaired Pointers, Golden Retrievers, Standard Poodles and Scottish Terriers all have a higher than normal incidence, showing that it can be inherited.

vWD Phenotype

Breed
Clear
Carrier
Affected
Doberman
23%
49%
28%
Manchester Terrier
61%
35%
4%
Pembroke Welsh Corgi
55%
39%
6%
Poodle
88%
11%
1%
Collie
90%+
8%
0.1%

 

Even though there is less than 1% affected in the Collie Breed, this does not mean it is a minor issue. The CCofA and The CCofA Foundation support research for this and other alliments that effect the collie breed. They are asking for donations of samples from both know affected and unaffected Collies. For more information, please visit the CCA Foundation web site. The reason for this is to develop an accurate DNA Marker for the Collie as they now have for other Breeds. The blood test in use is very undependable. Test results may be affected by many variables in the patient as well as mistakes made by the lab technician. Blood samples should be sent to a lab familiar with the vWD test, incorrect results will occur if the test procedure is not followed to the letter! It has also been found that there is a smaller variable in the blood test if the animal being tested is under 6 months of age.

Results are influenced by:

  1. Heat cycle
  2. Use of aspirin or non-steroidal anti-inflammatories
  3. Cold environment
  4. Various medications, hormone therapy, pregnancy, nursing, and whelping
  5. Exercise, stress, and emotional behavior
  6. Anything that causes change in blood chemistry or blood loss.

Tests may need to be repeated several times, over several months, before a diagnosis can be confirmed. But, even at that, the results are not 100%.

 

Genetics research demands deep pockets and a well-established infrastructure of support. The development of an accurate test for a specific gene requires several years of gathering data on individual infected animals, working with owners to collect DNA samples, and costs that can run far in excess of $50,000. The main problem is that there needs to be a greater donation of affected animal DNA samples. The smaller the number of DNA sample donations, the longer it will take to find the affected gene.

Another site dedicated to the elimination of Genetic Disease in animals is the Institute for Genetic Disease Control (GDC). This group is a nonprofit organization asking for people to donate information about their animals. They want to create an open registry where both affected and non-affected genealogy can be researched. Other wise, a Genetic Pedigree, thus helping to cure the Genetic Defects that plague animals by allowing a researcher to trace the defective gene..

The greatest health problem that affects any breed is when we, the breeders, showers, and owners, only tell what is right with our dogs and not what is wrong. This will only allow the problems to continue and never be corrected.

 

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