Before adopting a new companion please research health issues.  When searching for the perfect companion you want to consider one with a long lived, healthy, prosperous life!  

 

Hip Dysplasia HD:

• Hip Dysplasia HD:  Hip Dysplasia is among the most studied and the most frustrating diseases in veterinary medicine. 
• Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis it can eventually produce, leading to pain and debilitation.

GRADES GIVEN BY OFA: 

• EXCELLENT HIP JOINT CONFORMATION***

Superior hip joint conformation as compared with other individuals of the same breed and age.

• GOOD HIP JOINT CONFORMATION ***

Well formed hip joint conformation as compared with other individuals of the same breed and age.

• FAIR HIP JOINT CONFORMATION ***

Minor irregularities of hip joint conformation as compared with other individuals of the same breed and age.

• THERE ARE THREE PASSING GRADES:  Excellent, Fair, and Good.

These all receive a number and certificate.

·         THERE ARE FOUR FAILING GRADES:  Borderline, Mild, Moderate, & Severe Hip Dysplasia.

The Borderline grade is usually given with a note from OFA asking you to re-x-ray the dog and re-submit those x-rays in "X" number of months. This is because (as outlined above) borderline does not receive a certificate and it is because the dog is deemed to have: "marginal hip joint conformation of INDETERMINATE status with respect to hip dysplasia at this time". So.....the dog is not passed, but failed because the hip conformation is unable to be determined. When the owners resubmit new x-rays they will either be given a Pass or Fail rating. Note: If a dog fails OFA or gets a low passing Grade the owners can resubmit x-rays over & over to try and get the dog to pass. The X-rays are graded "as compared with other individuals of the same breed and age." However if the x-rays are sent in on a dog at 24 months and the dog is rated Good and the owner resubmits at 36 months and the dog is rated Fair the lower rating will be recorded and listed for the dog.

How Hips are Graded

The phenotypic evaluation of hips done by the Orthopedic Foundation for Animals falls into seven different categories. Those categories are Excellent, Good, Fair, Borderline, Mild, Moderate, Severe. Below is an in depth at each of these classifications and what they mean.
     Once each of the radiologists classifies the hip into one of the 7 phenotypes below, the final hip grade is decided by a consensus of the 3 independent outside evaluations. Examples would be:

1. Two radiologist reported excellent, one good--the final grade would be excellent
2. One radiologist reported excellent, one good, one fair--the final grade would be good
3. One radiologist reported fair, two radiologists reported mild--the final grade would be mild

     The hip grades of excellent, good and fair are within normal limits and are given OFA numbers. This information is accepted by AKC on dogs with permanent identification (tattoo, microchip) and is in the public domain. Radiographs of borderline, mild, moderate and severely dysplastic hip grades are reviewed by the OFA radiologist and a radiographic report is generated documenting the abnormal radiographic findings. Unless the owner has chosen the open database, dysplastic hip grades are closed to public information.

Excellent: this classification is assigned for superior conformation in comparison to other animals of the same age and breed. There is a deep seated hip ball (femoral head) which fits tightly into a well-formed hip socket (acetabulum) with minimal joint space. There is almost complete coverage of the hip socket over the hip ball.

Good: slightly less than superior but a well-formed congruent hip joint is visualized. The hip ball fits well into the hip socket and good coverage is present.

Fair: Assigned where minor irregularities in the hip joint exist. The hip joint is wider than a good hip phenotype. This is due to the hip ball slightly slipping out of the hip socket causing a minor degree of joint incongruency (called subluxation).

There may also be slight inward deviation of the weight-bearing surface of the hip socket (dorsal acetabular rim) causing the hip socket to appear slightly shallow (Figure 4). This can be a normal finding in some breeds however, such as the Chinese Shar Pei, Chow Chow, and Poodle.

Borderline: there is no clear cut consensus between the radiologists to place the hip into a given category of normal or dysplastic. There is usually more incongruency present than what occurs in the minor amount found in a fair but there are no arthritic changes present that definitively diagnose the hip joint being dysplastic. There also may be a bony projection present on any of the areas of the hip anatomy illustrated above that can not accurately be assessed as being an abnormal arthritic change or as a normal anatomic variant for that individual dog. To increase the accuracy of a correct diagnosis, it is recommended to repeat the radiographs at a later date (usually 6 months). This allows the radiologist to compare the initial film with the most recent film over a given time period and assess for progressive arthritic changes that would be expected if the dog was truly dysplastic. Most dogs with this grade (over 50%) show no interval change in hip conformation over time and receive a normal hip rating; usually a fair hip phenotype.

Mild Canine Hip Dysplasia: there is significant subluxation present where the hip ball is partially out of the hip socket causing an incongruent increased joint space. The hip socket is usually shallow only partially covering the hip ball. There are usually no arthritic changes present with this classification and if the dog is young (24 to 30 months of age), there is an option to resubmit an x-ray when the dog is older so it can be re-evaluated a second time. Most dogs will remain dysplastic showing progression of the disease with early arthritic changes. There are a few dogs however, that show improved hip conformation with increasing age. Since HD is a chronic, progressive disease, the older the dog, the more accurate the diagnosis of HD (or lack of HD). At 2 years of age, the reliability for a radiographic diagnosis of HD is 95% and as the dog ages, the reliability steadily increases. Radiographs should definitely be resubmitted if they were taken during times of known environmental effects such as physical inactivity and high estrogen levels during or around the time of a heat cycle which could lead to a "false" diagnosis of mild hip dysplasia.

Moderate Canine Hip Dysplasia: there is significant subluxation present where the hip ball is barely seated into a shallow hip socket causing joint incongruency. There are secondary arthritic bone changes usually along the femoral neck and head (termed remodeling), acetabular rim changes (termed osteophytes or bone spurs) and various degrees of trabecular bone pattern changes called sclerosis. Once arthritis is reported, there is only continued progression of arthritis over time.

Severe HD: assigned where radiographic evidence of marked dysplasia exists. There is significant subluxation present where the hip ball is partly or completely out of a shallow hip socket. Like moderate HD, there are also large amounts of secondary arthritic bone changes along the femoral neck and head, acetabular rim changes and large amounts of abnormal bone pattern changes.

 

   We take great pride with our Excellent Hips!  All of our collies  are OFA certified passing hip grades and free from Hip Dysplasia!

 

Collie eye anomaly (CEA):

It is an inherited disorder of the choroid structure of the eye.

It is also known as:

• choroidal hypoplasia (CH)
• collie scleral ectasia syndrome
• optic nerve/disc coloboma

Since the choroid layer does not develop normally from the start, the primary abnormality can be diagnosed at a very young age typically between 5 - 12 weeks.

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.

Cure: None

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.

MILD disease: Mild disease is very common in U.S. collies and is present in the other breeds. 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.

Expected Results of Breeding Strategies for Inherited Recessive Diseases
Parent 1 Genotype	Parent 2     Genotype
	Normal	Carrier	Affected
Normal	All = Normal	1/2 = Normal 1/2 = Carriers	All = Carriers
Carrier	1/2 = Normal 1/2 = Carriers	1/4 = Normal 1/2 = Carriers 1/4 = Affected	1/2 = Carriers 1/2 = Affected
Affected	All = Carriers	1/2 = 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.

Source:Optigen

   We do not produce any puppies with Collie Eye Anomaly!

 

PRA:

PRA genetic testing is done by Optigen.  They developed the tests and hold patents on them, making Optigen the only place in the U. S . to have them done. Here is a brief synapses of each test and the link to Optigen for more information, test questions, and forms and fees for testing.

The genetic disorder, prcd-PRA , causes cells in the retina at the back of the eye to degenerate and die, even though the cells seem to  develop normally early in life. The “rod” cells operate in low light levels and are the first to lose normal function. Night blindness results. Then the “cone” cells gradually lose their normal function in full light situations. Most affected dogs will eventually be blind. Typically, the clinical disease is recognized first in early adolescence or early adulthood. Since age at onset of disease varies among breeds, you should read specific information for your dog. Diagnosis of retinal disease can be difficult. Conditions that seem to be prcd-PRA might instead be another disease and might not be inherited. OptiGen’s genetic test assists in making the diagnosis. It’s important to remember that not all retinal disease is PRA and not all PRA is the prcd form of PRA. Annual eye exams by a veterinary ophthalmologist will build a history of eye health that will help to diagnose disease.

Inheritance

Prcd-PRA is inherited as a recessive trait. This means a disease gene must be inherited from each parent in order to cause disease in an offspring. Parents were either “carrier” or affected. A carrier has one disease gene and one normal gene, and is termed “heterozygous” for the disease. A normal dog has no disease gene and is termed “homozygous normal” – both copies of the gene are the same. And a dog with two disease genes is termed “homozygous affected” – both copies of the gene are abnormal.

It’s been proven that all breeds being tested for prcd-PRA have the same disease caused by the same mutated gene. This is so, even though the disease might develop at different ages or with differing severity from one breed to another.

Although prcd-PRA is inherited, it can be avoided in future generations by testing dogs before breeding. Identification of dogs that do not carry disease genes is the key. These “clear” dogs can be bred to any mate – even to a prcd-affected dog which may be a desirable breeding prospect for other reasons. The chance of producing affected pups from such breedings depends on the certainty of test results. Again, you’ll find the specific information on certainty of test results for your dog by linking to breed specific information.

The Genetic Test

The OptiGen prcd test is done on a small sample of blood from the dog. The test analyzes the specific DNA mutation causing prcd-PRA. The OptiGen test detects the mutant, abnormal gene copy and the normal gene copy. The result of the test is a genotype and allows separation of dogs into three groups: Normal/Clear (homozygous normal), Carrier (heterozygous) and Affected (homozygous mutant).

Possible results using the OptiGen prcd test
Genotype	Risk Group	Significance For Breeding	Risk of prcd Disease
Homozygous Normal	Normal/Clear	Can be bred to any dog, extremely low risk of producing affecteds	Extremely low
Heterozygous	Carrier	Should be bred only to Normal/ Clear to remove risk of producing affecteds	Extremely low
Homozygous Mutant	Affected	Should be bred only to Normal/ Clear to remove risk of producing affecteds	Very high

The prcd-PRA 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. 

RD/OSD

Retinal Dysplasia/OSD Background of Disease: Retinal Dysplasia-retinal folds (RD) is a common clinical observation in many dog breeds. Since many retinal folds are benign and of unknown heritability, veterinary ophthalmologists will often advise that breeding dogs with RD is an acceptable option.

OptiGen is approaching ACVO, CERF and other organizations involved with genetic eye registries to develop a system by which a dog once diagnosed as clinically “affected” for retinal-dysplasia-folds can be ‘recertified’ if it tests clear for the RD/OSD mutation using the OptiGen DNA test.

   PRA does not exist in our bloodlines!

 

Drug Reactions in Collies:

It is now widely accepted that the Collie breeds (Rough Collies, Smooth Collies, and Border Collies) appear to be hypersensitive to certain toxins (natural or drug-induced) and are more prone to stress-related problems. The problem first came to light in 1983 when several Collies died from Ivermectin poisoning and, since then, the veterinary profession has accepted this drug should never be given to Collies. More recently a Rough Collie died from eating horse feces (Ivermectin is used for worming horses and any excess drug passes out with their feces). Researchers have since found that approximately 60% of Rough and Smooth Collies appear to be susceptible not only to Ivermectin, but to a wide range of other drug substances. The MDR1 (multi-drug resistant) gene is responsible for ensuring the body's natural P-glycoprotein functions normally by protecting the body from both environmental toxins and administered toxins e.g. drugs, and acting as a transport mechanism moving substances from cell to cell. P-glycoprotein are normally extensively distributed in the blood-brain and blood-testes barriers as well as major organs such as the liver, kidneys, intestines and placenta. When they are present in the intestinal tract three things normally occur - the substance may be metabolized; it may enter the circulatory system; or it may be passed out of the large intestine with the feces. In MDR1-affected dogs the function of the P-glycoprotein is compromised so toxins may leak into the major organs. If these compounds leak across the blood-brain barrier, they enter the central nervous system causing toxic reactions such as excessive salivation, Ataxia, blindness, coma, respiratory problems or even death. Because of the lack of the P-glycoprotein transporter in the body, an MDR1-affected dog also tends to have a deficiency of Cortisol (a steroid hormone produced by the Adrenal glands). Cortisol is responsible for stress management and the maintenance of an efficient immune system, and a deficiency can therefore lead to stress-related problems such as colitis or inflammatory bowel disease.  An MDR1 Normal dog (+/+) receives a healthy MDR1 gene from each of its parents and can therefore only pass on healthy genes to its offspring. Such animals do not exhibit drug toxicity. A ‘Carrier' (+/-) is a dog that has received a normal MDR1 gene from one of its parents, and a defective gene from the other parent. An Affected dog (-/-) receives a defective MDR1 gene from both its parents, so such dogs will display toxic reactions to a wide range of drug compounds (see list below).  If you have an MDR1-affected Collie (-/-) you could be in a position to save its life by providing your veterinary surgeon with a copy of its MDR1 Certificate and the list of drug compounds that your Collie should never be given. Of those vets who have already been asked to put MDR1 test results onto a Collie's records, all have been aware of the Ivermectin problem but have had no idea about the broad spectrum of drug compounds that can severely threaten an MDR1-affected dog. Please note there are usually alternative, safe drugs your Collie could be given instead. The table here shows three classes of drug compounds: Class A includes substances that have been proven to pass through the blood-brain barrier in MDR1-affected dogs and cause problems; Class B lists substances which have shown interactions in animal tests, whereas Class C substances can be given without problems, even to affected dogs:

Class A DO NOT USE in dogs with MDR1 defect. An affected dog (-/-) carries two MDR1 gene mutations, having received one from each of its parents. It will also  pass on a mutant MDR1 gene to its offspring. MDR1-affected dogs are likely to experience drug toxicity following normal doses of the drugs listed here: Anti-Parasitic drugs:  Ivermectine substances: Diapec®, Ecomectin®, Equimax®,Eqvalan®, Ivomec®, Noromectin®, Paramectin®, Qualimec®, Sumex® & Virbamec® Doramectine substances: Dectomax® Moxidectine substances: Cydectin® & Equest® Loperamide substances (anti-diarrhoea): Immodium® Metronidazole (Flagyl ® - general antibiotic   Class B Toxic reactions have been known to occur so only use under the close supervision of your vet Cancer treatments (Cytostatics): Vinblastine, Doxorubicine, Paclitaxel, Docetaxel, Methotrexat & Vincristine Glucocortisoids (steroids commonly used to treat auto-immune diseases): Dexamethason Immuno-suppressants: Cyclosporine A Heart glycosides: Digoxine & Methyldigoxine Antiarrhythmics (heart problems): Verapamil, Diltiazem & Chinidine Pain control: Morphine & Butorphenol Anti-emetics (sickness/vomiting): Ondansetron,  Domperidon andMetoclopramide Antibiotics: Sparfloxacin, Grepafloxicin & Erythromycin Antihistamines: Ebastin Tranquillisers & pre-anaesthetic agents: Aceptomazine (ACP) & Butorphenol Other drugs: Etoposide, Mitoxantrone, Ondanestron, Paclitaxel, Rifampicin   Class C Can be used safely providing the correct dosage is given. Stronghold®, Advocate® & Milbemax® can be used only in the recommended application and dosage. The importance of knowing your Collie's MDR1 status cannot be over-emphasized, as you never know when he or she may require surgery and/or drug treatment. If your dog is known to be affected (-/-), you will at least be in a position to inform your vet of the dangers of certain drugs, by printing off the information above. The test is carried out using simple cheek swabs, which you can easily do yourself. The DNA sample collected identifies genetic normal, affected and carrier animals.  References: Veterinary Clinical Pharmacology Laboratory, Washington State University,

   

MDR1 Breeding Guidelines

This chart provides guidelines for consideration when owners are contemplating breeding dogs that may be affected by the MDR1 mutation.  While it is ideal to use only "Normal/Normal" breeding pairs, one must always consider other genetic factors in addition to the MDR1 gene.  Because the MDR1 gene is present in such a large percentage of Collies and Australian Shepherds, it may be necessary to breed "Normal/Mutant" dogs in order to maintain a large enough pool of good breeding stock.   By using thoughtful breeding strategies including these guidelines, future generations of dogs will have a substantial decrease in the frequency of the mutant MDR1 gene.  

MDR1 Breeding Pair Combinations and Outcomes

	Normal/Normal Male	Normal/Mutant* Male	Mutant/Mutant Male
Normal/Normal Female	100% Normal/Normal puppies	Normal/Normal and/or Normal/Mutant puppies	100% Normal/Mutant puppies
Normal/Mutant* Female	Normal/Normal and/or Normal/Mutant puppies	Any combination of puppies	Normal/Mutant and/or Mutant/Mutant puppies
Mutant/Mutant Female	100% Normal/Mutant puppies	Normal/Mutant and/or Mutant/Mutant puppies	100% Mutant/Mutant puppies