WE TEST!



WE TEST FOR: 
ALL GARLIND RIDGE COLLIES ARE TESTED FOR THE FOLLOWIING PRIOR TO BEING BRED!!! 

CEA

PRA

OFA Cardiac 

Degenerative Myelopathy

MDR1

HIP DYSPLASIA 

DMS risk assessment Dermatomyositis (DMS) is an autoimmune disease that causes lesions on the bony prominences (face, tail tip, and feet)





We test our collies for CEA-We only produce puppies that do not have CEA

Collie Eye Anomaly / Choroidal Hypoplasia (CEA) Test

For: Australian Shepherd (including Miniature and Toy varieties), Bearded Collie, Border Collie, Boykin Spaniels, Hokkaido dog, Lancashire Heeler, Miniature American Shepherd, Nova Scotia Duck Tolling Retrievers, Rough Collie, Shetland Sheepdog, Silken Windhound, Smooth Collie and Whippet, Longhair

Collies share Collie Eye Anomaly (CEA) with several other breeds – it’s not just a problem for collies. CEA is more technically known as Choroidal Hypoplasia (CH). It is a recessively inherited eye disorder that causes abnormal development of the choroid - an important layer of tissue under the retina of the eye. This disease is seen most frequently in U.S. collies, but also worldwide in Rough and Smooth Collies, Border Collies, Australian Shepherds, Lancashire Heelers, and Shetland Sheepdogs. Since the choroid layer does not develop normally from the start, the primary abnormality can be diagnosed at a very young age. Regrettably, there is no treatment or cure for CEA.

Photo: Border CollieThe symptoms and signs – the clinical phenotype – can vary greatly among affected dogs within one breed, between parent and offspring and even within a litter. This creates a difficult situation for the breeder. Learning about the genetic cause and the course of the disease will help you understand how to manage it better and eventually avoid it altogether with genetic testing.

The primary problem is choroidal hypoplasia (CH). There is under-development (hypoplasia) of the eye tissue layer called the choroid. The choroid appears pale and thin, almost transparent, and the blood vessels of the choroid can easily be recognized in those “thin” areas. The ophthalmologist, looking at the back of the eye (the fundus) with an ophthalmoscope, typically will see an area of choroidal thinning that appears like a “window” to the underlying vessels and sclera.

sheltie MILD disease: Mild disease is very common in U.S. collies and is present in the other breeds named above. It is easily recognizable on careful ophthalmologic examination as early as 5 to 8 weeks of age. The lesion appears as an area lateral (temporal) to the optic disc with reduction or absence of pigment so that the underlying vessels of the choroid are seen. The choroidal vessels may be reduced in number and of abnormal shape. The underlying white sclera might also be visible. Once the retina changes to its adult color around 3 months of age, the normal pigment sometimes masks the changes in the choroid (so-called “go normal” – read more below). In mildly affected dogs, choroidal thinning is the only detectable abnormality and the dog retains normal vision throughout life. However, dogs with mild disease can produce severely affected offspring.

(The eye anomaly “merle” can be confused with choroidal hypoplasia, primarily in dogs from merle to merle breeding and whose coat color is whiter than their littermates. Although both conditions are inherited, can occur in the same breed and exhibit a range of fundus anomalies, there are sufficient dissimilarities for the ophthalmologist to make the distinction.)

SEVERE disease: In severely affected dogs, approximately 25% of dogs with CEA/CH, there are related problems with the health of the eye that can result in serious vision loss in some cases. Colobomas are seen at and near the optic nerve head as outpouchings or “pits” in the eye tissue layers. Colobomas can lead to secondary complications such as partial or complete retinal detachments and/or growth of new but abnormal blood vessels with hemorrhage – bleeding inside the eye. This happens in 5-10% of dogs with CEA/CH, generally by 2 years of age, and can affect either one or both eyes. Complications of severe disease can lead to vision loss, although this disorder only rarely threatens total blindness.

CEA/CH is not progressive in the usual sense. The essential features, choroidal hypoplasia and coloboma, are congenital – the abnormalities develop as the eye develops. These features are also stationary once ocular development is complete around 8-12 weeks of life. Retinal detachments and/or aberrant vessel formation can be congenital or develop later, in general only in eyes with colobomas.

Based on research done jointly by scientists at Cornell University and at The Fred Hutchinson Cancer Research Center, BOTH the mild and severe forms of CEA/CH disease now are proven to result from the exact same gene and mutation in ALL of the affected breeds named above. This disease gene is located on canine chromosome number 37 and the disease-causing mutation has been identified. The mutation acts like a RECESSIVE mutation. That means, both parents of an affected dog must have at least one copy of the mutation and both parents must have passed a copy of the mutation to the offspring. The affected dog is HOMOZYGOUS RECESSIVE – that is, both copies of the gene are mutant. ALL dogs that are homozygous recessive affected will show at least the mild form of the disease. ALL affected dogs, regardless of the actual severity of the lesions, are homozygous for the same mutant gene.

(A dog with one mutant copy and one normal copy of the CEA/CH gene is a carrier – is heterozygous. A dog with two copies of the normal CEA/CH gene is homozygous normal.)

The frequency of CEA/CH disease varies among breeds and by country of origin. The U.S. registration organization, CERF, reported the incidence in the U.S. of choroidal hypoplasia, optic disc/nerve coloboma and retinal detachment among several affected breeds over the period of 1991 to 1999. (Comparable data from other countries isn’t available to us yet.)

Frequencies Based on CERF Eye Exams in the U.S. from 1991 to 1999
 Choroidal
Hypoplasia
ColobomaRetinal
Detachment
Collie - Rough & Smooth66.7%8.75%1.88%
Border Collie2.12%0.57%0.06%
Shetland Sheepdog0.39%0.79%0.05%
Australian Shepherd0.22%0.27%0.13%

The frequency of the CEA/CH gene mutation in U.S. Rough and Smooth Collies appears to be extremely high. In general, the frequency of affecteds in Rough and Smooth Collies is well over 50%, and in some populations has been observed to be as high as 85-90% of dogs examined. Of the remaining, most are carriers. The frequency of the CEA/CH gene mutation in European Shetland Sheepdogs appears to be significantly higher than in the U.S.

The OptiGen genetic test for CEA/CH provides a powerful management tool for the breeder. This genetic test can distinguish all three genetic states – normal, carrier and affected. With this information, the breeder can plan matings that avoid producing any affected dogs by always selecting one parent that is normal. The other parent can be normal, carrier or even affected, and no affected dogs will result. (See table at the end.) This breeding recommendation is a big step forward, especially for breeds and countries where frequency of CEA/CH is much lower. Earlier advice cautioned against breeding affected dogs, their parents, their offspring or their siblings (unless eye exams before 3 months of age demonstrate the sib is unaffected).

Understandably, genetic testing will be a difficult tool to use for some breeders of “standard” collies (i.e., Rough, Smooth, Show, Standard) where the disease is very common. In some circumstances, genetically normal – homozygous normal – collies could be difficult to find and it may not be practical for the breeder to plan matings that include one normal dog. And, it may not be reasonable to expect complete avoidance of CEA/CH in one generation. All the same, genetic testing is a sure-fire tool to move toward elimination of the disease. To start, breeding a carrier to a carrier will produce an average of 25% normals, 50% carriers and 25% affecteds. With genetic testing at each subsequent generation, and with a goal of breeding normal by carrier or normal by affected, the frequency of disease will drop and frequency of normals will increase without loss of other desirable traits valued in collies.

Breeders should pay attention to protecting the genetic diversity of breeds that have very high frequencies of an inherited disease. In the case of CEA/CH, the genetic test can be viewed as an adjunct to traditional strategies for avoiding severe cases of CEA. Over the last 30 years, many animals have been examined and those with only mild CEA (no colobomas or detachments) have been selected for breeding. The result is the percentage of collies affected with choroidal hypoplasia remains high, but the severe grades of the disease (colobomas and retinal detachments) have decreased due to this conscientious breeding.

Even though the ideal recommendation is to breed genetically normals, preservation of other desirable physical traits might override the ideal in the short-term. Reduction or even elimination of the CEA/CH mutant gene can be viewed as a longer-term goal. You should consult with your breed club for further breeding recommendations.

You might ask: if the mild form and the severe form of CEA/CH disease are caused by the exact same genetic mutation, why do some dogs have only mild disease while others have severe disease? Is the severity due to diet, activity, or other insults like infections or trauma? So far, there are no clues that non-genetic factors are responsible. Instead, there are probably other independently acting “modifier” genes that influence CEA/CH gene expression. If that is so, eventually these modifier genes will be detected, although the chore will be difficult. Possibly, by choosing mildly affected dogs and avoiding severely affecteds in a breeding program, breeders have concentrated positive influencing independent modifier genes in their line. The CEA/CH gene frequency may not have changed, but the disease may be partially suppressed as long as the modifying genes are carried along. This is a risky approach, since the identity of those influencing genes – indeed even their number and action – is a complete unknown.

You might also ask: is it true that early choroidal hypoplasia can “go normal,” that is, reverse to a normal appearance? There are occasional reports of puppies, found to be affected as early as 5 weeks of age, that appear to “go normal” when re-examined some months later. The abnormal features seem to disappear or lessen due to pigment changes and masking of the thin choroid areas. (However, if a dog had a coloboma, this will remain – it is a permanent lesion.) The majority of dogs that “go normal” are homozygous for the CEA/CH mutation, especially if they “go normal” slowly or incompletely. A small minority, however, are heterozygous carriers that tend to “go normal” at a very young age. Regardless, the genetic status of such dogs was and remains constant during their lifetime, so these dogs can pass the mutant disease gene to their offspring. Testing will help you identify the genetic status of dogs that have an ambiguous clinical diagnosis.

The CEA/CH genetic test provides the life-long genetic status of a dog for this disease. In conjunction with genetic testing, an eye exam by a veterinary ophthalmologist is recommended before 8-9 weeks of age, with annual eye exams thereafter. The eye exam will give you information about mild versus severe CEA/CH disease among affected dogs. Annual eye exams are always recommended for all dogs of all breeds. Clinical exams detect a wide variety of eye problems, both genetic and non-genetic.

Expected Results of Breeding Strategies for Inherited Recessive Diseases
Parent 1 
Genotype
Parent 2     Genotype
NormalCarrierAffected
NormalAll = Normal1/2 = Normal 
1/2 = Carriers
All = Carriers
Carrier1/2 = Normal
1/2 = Carriers
1/4 = Normal 
1/2 = Carriers 
1/4 = Affected
1/2 = Carriers
1/2 = Affected
AffectedAll = Carriers1/2 = Carriers
1/2 = Affected
All = Affected
The table shows the desirable breedings (gray-shaded boxes) which have at least one parent that is Normal by the OptiGen CEA/CH test. All other breedings are at risk of producing pups affected with CEA/CH.

Limits to All Genetic Testing

There are basic limits for any and all DNA genetic tests. Whether a test is mutation-based or marker-based, it identifies only the specific mutation being tested or the association between a specific marker set and the disease. For example, a mutation test detects one specific mutation in one specific gene. If there are several different mutations or several different genes that can cause the same condition, one must discover and then test for each mutation and each gene. Likewise, a marker test uses one marker or set of markers to define a specific condition. If the condition is associated with several different marker combinations, one must discover and then test for each marker combination. It can be difficult or even impossible to know how many mutations or how many marker sets exist in all the members of a specific breed. As more and more dogs are tested, previously unknown variations may come to light.

In the case of CEA/CH, the OptiGen genetic test for the listed breeds is a mutation-based test.

Resources for this article: Acland, G., Retinal Disorders in Border Collies.http://www.dogstuff.info/retinal_disorders_in_border_collies_acland.html.
Acland, G., Aguirre, G., Personal Communications.
A.C.V.O. Genetics Committee, “Ocular Disorders Presumed to be Inherited in Purebred Dogs.” 1999 Edition.
Riis, R., “Inherited Eye Anomalies of Australian Shepherds, Collies, and Shetland Sheepdogs.” In: Small Animal Ophthalmology Secrets, Chapter 38, Hanley & Belfus, Inc., 2002.
Lowe JK, Kukekova AV, Kirkness EF, Langlois MC, Aguirre GD, Acland GM, Ostrander EA. Linkage Mapping of the Primary Disease Locus for Collie Eye Anomaly. Genomics 2003 Jul;82(1):86-95.

How you can participate

The CEA/CH test is done on a small sample of blood obtained by your veterinarian. This allows the lowest risk of contamination of the sample and added assurance of a match of the sample with the identified dog.

Read and print the instructions on the Ship Sample page. Then fill out the Test Request Form. On-line submission of the Test Request Form lets you be sure accurate information and correct spellings are put in the database. When you've completed one Form, a second Test Request Form for another dog or for a litter is easy and saves you time.

Special recognition is due to the ABCA - American Border Collie Association for financial support of the research and to other concerned groups and individuals in the community for their participation in the development of this test. The research leading to this discovery was undertaken by scientists at the James A. Baker Institute for Animal Health at Cornell University's College of Veterinary Medicine in Ithaca, New York, and at The Fred Hutchinson Center for Cancer Research in Seattle, Washington. The patent-pending technology underlying this test is under exclusive license to OptiGen from Cornell Research Foundation, Inc. 



We test our collies for PRA-All of our puppies are PRA Non carriers

TEST for rod-cone dysplasia type 2 (rcd2) in Collies 


rcd2 Background of Disease:  “Collie PRA”, or rod-cone dysplasia type 2 (rcd2), is a form of retinal degeneration that has been a health concern in rough and smooth collies for decades.  In this disease, an abnormal development (dysplasia) of the rods and cones (the light sensitive cells in the eye) leads to an early onset of night blindness that is typically apparent by the time pups are 6 weeks of age. In most cases, the rcd2-Affected dog is completely blind by the time it is 1 year old.

 

rcd2 Mutation Identified:  After many years of study at Cornell University by scientists in the laboratory of Drs. Greg Acland and Gus Aguirre, the mutation causing rcd2 was identified and a manuscript describing the finding has been submitted for publication (Kukekova, Goldstein et al., 2008).  This work was supported prior to 2006  by the Morris Animal Foundation and also by continued contributions of the Collie Health Foundation. The rcd2 DNA test (patent pending) is able to identify with complete accuracy whether a dog has no copy (is Normal), has 1 copy (is a Carrier) or has 2 copies of the mutation (is Affected).

 

Inheritance of rcd2:  Collie breeders and researchers knew for many years that Collie PRA/rcd2 is inherited in an autosomal recessive manner.  In order for disease to occur, two copies of the mutation must be present.  Carriers do not show disease but are able to pass the disease on to offspring. The table below shows the predicted outcome of different matings when the rcd2 status of each parent is known. It should be kept in mind that these predictions are statistical in nature. A Carrier will pass the mutation on to half of its offspring on average .  The larger the population that one examines, the more closely the predicted outcome will fit the actual outcome.  A single litter of pups (a small population) produced by a Carrier parent can show quite a variation from the expected results.

Expected results for breeding strategies using the OptiGen rcd2 test

Parent 1

Status

Parent 2 Status

Normal/Clear

Carrier

Affected

Normal/Clear

All = Normal/Clear

1/2 = Normal/Clear

1/2 = Carrier

All = Carrier

Carrier

1/2 = Normal/Clear

1/2 = Carrier

1/4 = Normal/Clear

1/2 = Carrier

1/4 = Affected

1/2 = Carrier

1/2 = Affected

Affected

All = Carrier

1/2 = Carrier

1/2 = Affected

All = Affected


OptiGen DNA Test for rcd2/Collie PRA:  A patent for rcd2 is pending and owned by Cornell University which granted OptiGen permanent and exclusive licensing rights to make the test immediately available to the public.  The rcd2 DNA test will identify dogs as being Normal, Carrier, or Affected with rcd2.  The rcd2 DNA test requires special techniques compared to the other DNA tests that OptiGen offers so it  typically takes 1-2 weeks longer to obtain rcd2 test results.  Blood samples, cheek swabs or semen samples are all acceptable sources of DNA for the rcd2 test.

Benefits & Limits to All Genetic Testing: Many Collie breeders already make use of OptiGen’s services to test their dogs for Collie Eye Anomaly (CEA), and so they are aware of the great advantage that genetic testing offers. With informed breeding practices, breeders can immediately avoid producing dogs that are affected with specific diseases. Since genetic testing can be done at any age, each dog’s genetic status can be known even before clinical disease signs are recognized. Over several generations of selection away from the disease gene, breeders can eliminate a disease gene completely from their line.

BUT, there are basic limits for all genetic tests. Any DNA test is only able to identify a specific change in DNA (e.g. a mutation) that is being tested. For example, the rcd2DNA test detects one specific mutation in the rcd2 gene and the CEA test detects a specific mutation in a different gene.  Both mutations cause eye diseases but the DNA tests can only detect the specific type of mutation for which it is designed.  The rcd2test will not identify any other forms of PRA that may occur.  At this point we are not aware of other forms of PRA that occur in the collie but many breeds do have multiple types of PRA to contend with and this is a possibility in any breed.

Ordering the rcd2 Test: The rcd2 test is done on a small sample of blood obtained by your veterinarian or on a cheek swab or semen sample. Please read the paragraphs below, and then read "Instructions and Information" to learn about ordering a test, shipping a sample and prices. 

Collies already tested for CEA by OptiGen: OptiGen may be able to do the rcd2 test on samples that previously were sent for another test (e.g. for CEA testing or Long Term Storage). OptiGen retained many frozen samples that were previously submitted, and these may be available for rcd2 testing. We hope this will help owners to obtain the newrcd2 test more easily. You may order the rcd2 test online on a stored sample. If the frozen sample is still available at OptiGen we will run the test on that. If an insufficient frozen sample remains to run the rcd2 test, we will contact you to request a new sample. Link to "Order Test” and complete the order form as usual. Be sure to indicate that this dog's sample is already at OptiGen by selecting "Blood sample is already at OptiGen under a long-term storage agreement." Mark this choice even if you did not specifically pay for Long-Term Storage.



Multiple Tests for Collies  not tested previously by OptiGen: There is a discounted price for ordering multiple tests on one sample (rcd2 and CEA). See the price list for current pricing. 

Note: A manuscript describing the rcd2 mutation and its physiological significance has been submitted (Kukekova et al.). A patent for these tests is pending and owned by Cornell University which has granted OptiGen permanent and exclusive rights to make the test immediately available to the public.



Hip Dysplasia

All Garlind Ridge Collies are Xrayed for Hip Dysplasia prior to breeding. If they are not rated by the OFFA as good or excellent, they do not join our breeding program! 

THE DYSPLASTIC HIP JOINT

Severe Hip DysplasiaHip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.

The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases.

No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.


At Garlind Ridge  WE DO NOT PRODUCE MDR1 Mutant/Mutant puppies! 

Multidrug Sensitivity in Dogs

Many herding breed dogs have a genetic predisposition to adverse drug reactions involving over a dozen different drugs. The most serious adverse drug reactions involve several antiparasitic agents (ivermectin, milbemycin and related drugs), the antidiarrheal agent loperamide (Imodium), and several anticancer drugs (vincristine, doxorubicin, others). These drug sensitivities result from a mutation in the multidrug resistance gene (MDR1 gene). At Washington State University's College of Veterinary Medicine you can test your dog for multidrug sensitivity and prevent serious adverse drug reactions. We can work with your dog’s veterinarian to find appropriate drug doses or alternative drugs for your dog based on results of MDR1 testing.

The Partnership for Preventive Healthcare, is an initiative jointly sponsored by the American Animal Hospital Association and the American Veterinary Medical Association. Together the two associations offer a set of Canine and Feline Preventive Healthcare Guidelines. One of the important recommendations is that dog owners use genetic testing—like the MDR1 test —as part of an overall healthcare plan for their pets.

Breeds affected by the MDR1 mutation (frequency %)

BreedApproximate Frequency
Australian Shepherd50%
Australian Shepherd, Mini50%
Border Collie< 5%
Collie70 %
English Shepherd15 %
German Shepherd10 %
Herding Breed Cross10 %
Long-haired Whippet65 %
McNab30 %
Mixed Breed5 %
Old English Sheepdog5 %
Shetland Sheepdog15 %
Silken Windhound30 %



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We test for Degenerative Mylopathy
At least one collie non carrier for Degenerative myelopathy is in every breeding at Garlind Ridge 

Degenerative Myelopathy - Disease Basics

 

What is Degenerative Myelopathy?

Degenerative myelopathy is a progressive disease of the spinal cord in older dogs. The disease has an insidious onset typically between 8 and 14 years of age. It begins with a loss of coordination (ataxia) in the hind limbs. The affected dog will wobble when walking, knuckle over or drag the feet. This can first occur in one hind limb and then affect the other. As the disease progresses, the limbs become weak and the dog begins to buckle and has difficulty standing. The weakness gets progressively worse until the dog is unable to walk. The clinical course can range from 6 months to 1 year before dogs become paraplegic. If signs progress for a longer period of time, loss of urinary and fecal continence may occur and eventually weakness will develop in the front limbs. Another key feature of DM is that it is not a painful disease.

 


Affected brain
Degenerative myelopathy is a devastating disease causing progressive paralysis in a large number of dog breeds. New research has identified a gene that is associated with a major increase in risk of the disease.

What causes Degenerative Myelopathy?

Degenerative myelopathy begins with the spinal cord in the thoracic (chest) region. If we look under the microscope at that area of the cord from a dog that has died from DM, we see degeneration of the white matter of the spinal cord. The white matter contains fibers that transmit movement commands from the brain to the limbs and sensory information from the limbs to the brain.

DM vs Normal

In the section of a spinal cord from a dog who has died of DM (Left), the degeneration is seen as a loss of the blue color at the edges (arrows) compared with the spinal cord from a normal dog which is blue througout (Right).

This degeneration consists of both demyelination (stripping away the insulation of these fibers) and axonal loss (loss of the actual fibers), and interferes with the communication between the brain and limbs. Recent research has identified a mutation in a gene that confers a greatly increased risk of developing the disease.

How is degenerative myelopathy clinically diagnosed?

Degenerative myelopathy is a diagnosis of elimination. We look for other causes of the weakness using diagnostic tests like myelography and MRI. When we have ruled them out, we end up with a presumptive diagnosis of DM. The only way to confirm the diagnosis is to examine the spinal cord under the microscope when a necropsy (autopsy) is performed. There are degenerative changes in the spinal cord characteristic for DM and not typical for some other spinal cord disease.

What else can look like degenerative myelopathy?

Any disease that affects the dog’s spinal cord can cause similar signs of loss of coordination and weakness. Since many of these diseases can be treated effectively, it is important to pursue the necessary tests to be sure that the dog doesn’t have one of these diseases. The most common cause of hind limb weakness is herniated intervertebral disks. The disks are shock absorbers between the vertebrae in the back. When herniated, they can cause pressure on the spinal cord and weakness or paralysis. Short-legged, long back dogs are prone to slipped disks. A herniated disk can usually be detected with X-rays of the spine and myelogram or by using more advanced imaging such as CT scan or MRI. Other diseases we should consider include tumors, cysts, infections, injuries and stroke. Similar diagnostic procedures will help to diagnose most of these diseases. If necessary, your veterinarian can refer you to a board certified neurologist who can aid in diagnosing degenerative myelopathy. A directory to a neurologist near you can be found at American College of Veterinary Internal Medicine website under the "Find a Specialist Near You" link.

How do we treat degenerative myelopathy?

There are no treatments that have been clearly shown to stop or slow progression of DM. Although there are a number of approaches that have been tried or recommended on the internet, no scientific evidence exists that they work. The outlook for a dog with DM is still grave. The discovery of a gene that identifies dogs at risk for developing degenerative myelopathy could pave the way for therapeutic trials to prevent the disease from developing. Meanwhile, the quality of life of an affected dog can be improved by measures such as good nursing care, physical rehabilitation, pressure sore prevention, monitoring for urinary infections, and ways to increase mobility through use of harnesses and carts. 


What we can expect in breeding regarding the DNA results for Degenerative myleopathy. 

dm-chart

Dermatomyositis Risk Assessment

What is dermatomyositis?

Dermatomyositis (DMS) is an autoimmune disease that causes lesions on the bony prominences (face, tail tip, and feet). Lesions are characterized by crusting, scaling, redness, and hair loss. In severe cases, the lesions may progress to muscles and affect a dog's gait and ability to eat and drink. Steroids, Pentoxifylline (Trental), and vitamin E may help manage lesions; however, even after lesions heal there may be long term changes to the skin, such as darkened or mottled pigmentation, and permanent hair loss. Onset of DMS may occur at any age, and lesions can come and go throughout a dog's lifetime.

What causes dermatomyositis?

DMS results from a combination of environmental and genetic factors. The initial outbreak of lesions often occurs after exposure to a stressor, such as a virus, vaccinations, or a traumatic experience. The fact that DMS occurs primarily in Collies and Shetland sheepdogs and not equally across all breeds indicates an underlying genetic component.

 

Dermatomyositis research at Clemson University

In order to determine the genetic factors contributing to the development of DMS, we undertook a genome-wide association study (GWAS) in both Collies and Shelties. We identified three regions of the genome (loci) that are associated with DMS. Each region harbors a genetic change (allele) that is associated with DMS. Certain combinations of alleles at these three loci cause an increased risk for development of DMS, while other combinations are rarely observed in affected dogs.



AND we screen our collies for more than 150 inherited diseases and traits commonly found in dogs

https://www.caninehealthcheck.com/results/targets/

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