Welcome to the Health Tests Available page...                           

Below we have listed the Health Tests and Schemes available to you if you elect to make an informed choice to use them.

Once you have read the information below you can click on the link at the end of the page to find out when to health test.

BVA/KC EYE SCHEME *

The BVA/KC Eye Scheme offers breeders the possibility of eye testing to screen for inherited eye disease in certain breeds. By screening breeding stock for these diseases, breeders can use the information to eliminate or reduce the frequency of eye disease being passed on to puppies. Although any breed can be examined for eye disease, currently only the results of those breeds that appear on Schedule A of the Eye Scheme are sent to the Kennel Club for inclusion on computer records and printing in the Breed Records Supplement. In general, the best age for eye testing is before a dog has reached one year old and thereafter on an annual basis. However, in some breeds, it is necessary to test them as young puppies (usually between six and twelve weeks of age) and so details of litter screening are also included in the literature although results of litter screening are not published.

Although any breed can be examined for eye disease, currently only the results of those breeds that appear on Schedule A of the Eye Scheme are sent to the Kennel Club for inclusion on computer records and printing in the Breed Records Supplement.

 

There is a list available, from either the BVA or the Kennel Club, of appointed eye panellists who can issue certificates under the scheme and owners can make an appointment with one of the panellists directly or through their own veterinary surgeon. Often, breed clubs will arrange for a BVA panellist to attend their shows. This allows many dogs to be examined on one occasion and may save time and money.


 

PRA *

Progressive retinal atrophy (PRA) is an inherited condition that is seen in a number of different dog breeds and affects the rod and cone cells that make up the dog’s retina. In all the breeds that have been investigated in sufficient detail, the mode of inheritance has turned out to be a single recessive gene.

Different breeds of dogs actually suffer from different forms of PRA, but the end result is the same; the rod and cone cells eventually die and the affected dogs become totally blind. Owners of affected dogs usually first notice a loss of night vision, especially when the affected dog is in unusual surroundings; the condition eventually progresses to produce a loss of vision under all light conditions. There is as yet no known cure for PRA.

There are broadly two different types of PRA in the dog: rod/cone dysplasia and rod/cone degeneration. Breeds like the Irish Setter and the Miniature Long-haired Dachshund suffer from rod/cone dysplasia. In this case the rod and cone cells develop abnormally and begin to degenerate even before they are fully mature, leading to a very early age of onset in affected dogs, usually within the first few months of life. In breeds that suffer from rod/cone degeneration, like the Labrador, the Golden Retriever and the Cocker Spaniel, the rod and cone cells develop normally and only begin to degenerate later in life leading to a much later age of onset of the disease, usually anywhere from 3 to 4 years of age onwards.

GLAUCOMA  - GONIOSCOPY *                                     

Glaucoma is defined as an increase in pressure within the eye. The increased pressure is the result of a buildup of the intraocular fluid which is known as aqueous humor. In a healthy animal, aqueous humor primarily drains out through a circular filter at the junction of the clear cornea and white sclera, called the iridocorneal angle. Animals with glaucoma have an abnormality in the filter which obstructs outflow, resulting in a buildup of fluid within the eye. An analogy would be a kitchen sink - if the drain is open and the water is running, the sink is operating normally. However, the drain becomes clogged for some reason and the water continues to flow, then the sink fills up with water and overflows!

There are various causes of a defective filter. Dogs of some breeds are often born with abnormal filters and are therefore prone to getting inherited (genetic or primary) glaucoma in both eyes. Other breeds have a genetic predisposition to developing displaced (luxated) lenses, which block the filters, obstructing the flow of fluid. In both dogs and cats, the filters can be clogged with inflammatory cells if inflammation inside the eye (uveitis) occurs. Intraocular tumors can also lead to glaucoma.

 

prcd - PRA *

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.

Unfortunately, at this time there is no treatment or cure for PRA.

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.

 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).

TO FIND OUT MORE VISIT
www.optigen.com

 To see the test results visit

http://www.thekennelclub.org.uk/item/1969

FN - Familial Nephropathy *

Familial Nephropathy (FN) is a recessively inherited renal disease that has been recognized in the English Cocker for more than 50 years .  FN is a form of "hereditary nephritis"  which refers to a group of glomerular diseases that are linked to genetic collagen defects. 

Onset of renal failure due to FN typically occurs between six and 24 months of age . Clinical signs may include polydipsia (drinks more), polyuria (urinates more), weight loss, lack of appetite, vomiting, or diarrhea.  These symptoms are commonly associated with any type of renal failure.


Structure/Function

    The kidney is an organ made up of hundreds of thousands of tiny structures called nephrons.  Each nephron consists of a glomerulus and a tubule.  Blood flowing through the kidney is filtered by the glomerulus, with the fluid that is filtered out of the blood subsequently passing down the length of the tubule.  Cells that line the inner surface of the tubule process the fluid as it flows along, reabsorbing certain components of the fluid and excreting others. The fluid leaving the tubule at the end of this process is urine, which is a combination of water and waste products.
 
Dogs affected with FN have a genetic defect within the glomerulus.  This defective glomerulus lacks a certain type of collagen that helps to hold the structure of the filter together.  As a result of this collagen defect, a chain reaction of events takes place. Once the glomerulus begins to loose its ability to function properly, blood proteins leak through the defective filter into the urine.  The glomerular abnormality also leads to subsequent tubular damage, and the chain of events eventually destroys the entire nephron.  Nephrons that are severely damaged or destroyed can’t be replaced.

Since the kidney serves as the main waste-disposal system in the body, it is a master at compensation.   When one nephron dies, another takes over its work.  Over the course of time and with continual compensation the number of functioning nephrons is greatly reduced.  Once at least 75 percent of the nephron population is destroyed, end-stage renal failure occurs.  Since the disease is gradual and progressive, affected dogs do not appear sick until very late in the course of disease.

In the Beginning...

English Cockers affected with FN are born with normally developed kidneys.  Because they lack a certain type of collagen, however, the kidneys begin to deteriorate while the dogs are just a few months old.  As   glomerular damage evolves, the kidneys will first allow protein (proteinuria) to escape into the urine.  Generally, while proteinuria persists, the pup’s growth rate will slow down.  Once the pup begins to spill protein into the urine, the ability of the kidneys to ‘concentrate’ the urine will also diminish.  Finally, as a result of progressive nephron damage, the ability of the kidneys to excrete waste products (eg, urea and creatinine) will become impaired. As excretion of waste products by the kidneys progressively diminishes, the severity of renal failure will gradually worsen.

Sequence of Events
 
The sequence of events is always the same, but the rate of disease progression varies for reasons that are not fully understood .  As a result, it is difficult to give a specific age when to expect various stages of the disease to take place.  "For example, onset of proteinuria was at 5 to 8 months of age in 3 dogs in which it was carefully studied.  Because we can’t be sure that these 3 dogs are representative of all FN-affected dogs, we are uncertain what age to say is the oldest an FN-affected dog can be when  it first has proteinuria.  Nonetheless, we suspect that all, or almost all, dogs with FN will have proteinuria before a year of age.  The age range for occurrence of renal failure is 6 months to 2 years"

Clinical Signs


One way to identify a pup that might have FN is through observation.  Breeders and owners can watch the voiding patterns of young dogs.  Make it a point to regularly check the color of the urine.  The first morning release (assuming water hasn’t been available during the night) is probably best.  There should be good yellow color (well concentrated).  A youngster that lacks the ability to pass concentrated urine repeatedly should be taken to a veterinarian for a complete urinalysis.  A test called a "specific gravity (SG)" should be performed as well as an analysis for protein (proteinuria).  Usually, protein can be checked by using a color-coded plastic strip (Bili-Labstix).  This strip is merely dipped into a urine specimen and the plastic strip changes color and is checked against a chart on the side of the bottle the strips come in.  This strip will test for several things other than protein.  A pup with a low specific gravity and  excess protein (++) in the urine should be tested using a more specific test.  This test, a ‘protein-creatinine ratio,’ will provide a better estimate of the amount of protein in the urine.  A complete urinalysis should also be done to identify other urinary problems that may be present.  A positive dip-stick for protein does not necessarily indicate that the dog has renal disease or will develop FN.  It’s merely an indication that a more thorough evaluation is needed.  Not all young-age renal failure in this breed is FN; however, the symptoms are the same.

End Stage

 
Once it is established that a young dog is consistently passing dilute urine with protein, serum chemistry tests should be performed.  Such tests will only show significant elevations in specific areas once 75% of both kidneys are destroyed.  Elevations in BUN (blood urea nitrogen), creatinine, and inorganic phosphorus suggest kidney disease.  These findings coupled with a low urine specific gravity and proteinuria signal end-stage renal disease.
 
When the serum chemistry tests show "abnormally high levels of urea (BUN), creatinine, and other non-protein nitrogenous substances, a laboratory term called Azotemia is used to identify these specific abnormal levels ."
   
Generally, once the BUN reaches approximately 120 mg/dl, the dog only has a few weeks before critical illness sets in.  When these animals become critically ill, they will not eat.  If they do eat, they usually vomit.  They may go for two or three days without food, loosing more weight.  They will drink a tremendous amount of water and urinate even more.  Sometimes there will be an ammonia odor from the mouth.  Since the dog sleeps on the ear leathers, this ammonia odor may be apparent on the ear furnishings.  The dog will become very weak, and may tremble as if it’s cold.  They loose the ability to regulate their body temperature.  Since the kidney’s are no longer able to filter the body’s waste products, and regulate many important functions essential for life, the animal is essentially poisoning itself with its own waste products.

Perhaps one of the most frequent questions asked by owners with a young dog in failure is how will they know when it’s time to say good-bye.  Despite being in the critical stage of renal failure, these youngsters can always manage to wag their tail and greet family members, not with the usual exuberance, but the effort is there until the end.  When the time comes to say good-bye you’ll know…

Those that have lost a dog to FN will tell you the loss is more profound with this disease process than any other they’ve experienced.  It’s something no one wants to experience. 
 
To have your cocker tested for FN please contact Antagene on the link below

 

http://www.antagene.com

To see the test results so far visit

http://www.thekennelclub.org.uk/item/1970

HIP DYSPLAYSIA (HD) *

Hip dysplasia (HD) is a genetically transmitted condition, but environmental factors may influence the final score achieved. The score does not therefore absolutely reflect the potential for transmission of HD of an individual animal but should be regarded only as an indicator of possible transmission of the condition. For the Scheme to be meaningful and successful it is important that a film from EVERY dog radiographed be submitted for scoring, whether or not the animal is required for breeding and whatever the state of the hips, in order to provide the widest possible information for use by a geneticist.

The Scheme
The main purposes of the scheme are the examination of radiographs of hips of dogs for hip dysplasia and the issue of a certificate in respect of that examination. The examination is conducted by the evaluation of a radiograph for any anatomical and pathological changes indicative of hip dysplasia and a score is recorded. This score, and its relation to the Breed Mean Score, is intended to assist dog breeders in their selection of breeding stock. Breeders wishing to reduce the risk of HD should select their breeding stock (both dogs and bitches) only from animals with hip scores WELL BELOW the Breed Mean Score. Many clinically sound dogs may have high HD scores and should not therefore be used for breeding. The scheme does not cover any other hereditary or clinical defects which may need to be considered when choosing suitable breeding stock.

To learn more about HD please click on the link below.

 
To find out when to health test for all the above conditions click below