Helping Cockapoo’s in their hour of need

Health Testing

Within the gene pool that affects Cockapoo breeding there are some known genetic diseases that can cause serious illness later in life that will not be apparent as puppies. The Cockapoo Club of GB is promoting health testing awareness and following procedures to minimise the occurrence of the diseases now and in future Cockapoos in this country. The chart below lists the diseases which can affect the original breeds used to produce the first (F1) cross, and which could consequently be carried by later generations of Cockapoos.  Further information about each disease can be found in the chart below.  Whilst the Cockapoo Club of GB has a minimum health testing standard in order to register litters, we value all test results and therefore add them all to our database.

Looking ahead to the later generations of breeding Cockapoo to Cockapoo, F2, F3 etc we can predict that  specific diseases that can affect each breed could become a problem: Phosphofructokinase (PFK) for the American Cocker and FN – Familial Nephropathy for both the English Show and Working Cockers. 

For example to breed a cocker to a poodle, displays that the poodle who does not carry either of these diseases, therefore takes the place of a CLEAR parent.  However to breed a F2+ generation Cockapoos where both parents carry American Cocker genes or where both parents carry English Show or Working Cocker genes reintroduces the possibility that there could be carriers or worse, affected genes in both parents. Hence we have put in place the new mandatory testing as show in the diagram above to protect any later generation Cockapoos being registered with the CCGB, from these terrible diseases.


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. Laboklin or 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.


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.

DNA testing laboratories: in UK/FRANCE Antagene, UK/GERMANY Laboklin, and in USA OptiGen


Glaucoma is caused by increased pressure build up within the eye. Cells inside the eye produce a clear fluid (“aqueous humor”) that maintains the shape and architecture of the eye, whilst nourishing the tissues inside the eye. The balance of fluid production with subsequent drainage is responsible for maintaining a normal pressure homeostasis within the eye. With glaucoma, the drain becomes clogged or stymied, but the eye keeps producing fluid. As a result, the pressure in the eye increases. The increased pressure in the eye can actually cause the eye to stretch and enlarge, whilst destroying delicate structures within the eye. The British Veterinary Association (BVA) have a scheme for specialist Canine Opthalomogist, who do a manual examination of the eye to test the inherited eye disease status. 

Glaucoma is classified as either primary or secondary. Primary glaucoma is a genetically inherited condition. It is prevalent in many breeds, most notably Labrador Retrievers, Basset Hounds, American Cocker Spaniels, Chow Chows, Shar Peis, and the Spitz type breed of dogs (Huskies, Elkhounds, etc). It usually presents with just one affected eye, but in the majority of cases will affect the other eye leading to complete blindness.  

Secondary glaucoma occurs when other eye diseases lead to decreased intraoccular fluid drainage. Common causes of secondary glaucoma are inflammation within the eye (uveitis), cataracts, cancer of the eye, chronic retinal detachment and luxation of the lens.

It is very important to determine whether the patient is affected by primary or secondary glaucoma, as the treatment needed and the prognosis for vision is different for each type.

Hip Dysplasia

Hip dysplasia (HD) is a common inherited orthopaedic problem of dogs and a wide number of other mammals. ‘Dysplasia’ means abnormal growth – in this case it means abnormal development of the structures that make up the hip joint, which leads to subsequent joint deformity. The developmental changes appear first and because they are related to growth, they are termed primary changes. Subsequently these changes may lead to excessive wear and tear. The secondary changes may be referred to as (osteo)arthritis (OA), (osteo)arthrosis or degenerative joint disease (DJD).

Later, one or both hip joints may become mechanically defective. At this stage the joint(s) may be painful and cause lameness. In extreme cases the dog may find movement very difficult and may suffer considerably.

It was in the light of this knowledge that the British Veterinary Association (BVA) and the Kennel Club (KC) developed a scheme some 40 years ago to assess the degree of hip deformity of dogs using radiography. To date radiographs (X-rays) from more than 250,000 dogs have been assessed providing a standardised reflection of the HD status of those dogs that have been examined. This information is primarily of use for breeders. Currently 126 breeds are surveyed by the scheme in the UK.

Structure and function

The hip joints of land animals and even some birds are remarkably similar. Overall the design has withstood the test of time and is probably close to anatomical perfection. When athletic activity is required, the normal hip is an ideal means of transferring power from the muscles to drive the body forwards with maximum strength and speed. It is the close relationship of the femoral head (ball) and acetabulum (socket) which enables rapid changes of direction. The entire hip joint is a unit comprising the bony structures contained within a joint capsule and supported by ligaments, tendons and muscles together with all their blood vessels and nerves. The large joint surfaces are lubricated by synovial fluid. The viscosity (oiliness) of this fluid ensures smooth pain free joint movement. It is not surprising that any variation from this ideal can have severe consequences.

Developmental demands

It is argued that dogs are not born with hip joints already affected by dysplasia (unlike humans) but that any faults in development will tend to escalate with time, particularly during the rapid growth phase from about 14 to 26 weeks of age. However, changes begin as the very young puppy starts to become active and continues until the puppy is skeletally mature.

The hip is a ‘ball-and- socket’ joint, the ball being the head of the thigh bone or femur, and the socket being part of the pelvis called the acetabulum. In good hips the femoral head is smoothly rounded and fits tightly and deeply into the acetabulum. The outlines of the bone are clear since there is no secondary osteoarthrosis. 

Wear and tear of the deformed joint results in varying amounts of inflammation and degeneration which lead to more deformity. This progressive deformation is sometimes referred to as remodelling. Some dogs may treble their size and body weight in just three months of adolescence so it is not surprising that there are many critical factors for the puppy at this stage. All the essential nutritional requirements for skeletal growth must be available in the right proportions and at the right time. The environment within which the dog is raised, including the type and intensity of exercise, growth rate and body weight are significant influences. However, inheritance is a major factor and this is something which we are able to influence by the selection of breeding animals.


As HD can include joint looseness (laxity), inflammation, pain, new bone formation and bone erosion, it may cause a range of observable signs from normal to minor changes in gait (in the mildly affected cases) to obvious lameness, stiffness after rest and exercise intolerance and pain. As some individuals and breeds may be more stoical than others there is no way of estimating the severity of HD in any dog by observation alone. A veterinary surgeon’s physical examination will provide a more reliable assessment by revealing limitation of joint movement, muscle wasting and pain in the joint(s). Usually a dog with HD does not demonstrate discomfort by yelping, as pain is likely to be dull and continuous rather than sharp and acute. The dog may, though, groan whilst resting or getting up.

Radiography is the only means of determining the presence or absence of HD. This is an X-ray examination to look at the relative shape and positions of the femoral head and acetabulum and the presence and degree of any secondary changes.


It is known that two factors determine whether HD will occur, and if so, how bad it will be. These are hereditary and ‘environmental’ factors. ‘Hereditary’ relates to the genetic code passed to the offspring by both parents. Environmental factors are all the outside influences which alter and shape the growth and functions of the bones, cartilage, ligaments, tendons and muscles of the body, for example the over exercising, jumping or excessively exuberant play of developing puppies up to one year old. In simple terms the genetic code is rather like an architect’s plan (genotype), whilst the environment is like the builder and his materials (phenotype).

In HD the architect has made some errors but the builders have a great influence on how things finally look and function.

The BVA/KC HD Scheme

All radiographs submitted to the BVA/KC Hip Dysplasia Scheme are ‘scored’. The hip score is the sum of the points accrued for each of nine radiographic features in each hip joint. The lower the score the less the degree of HD present. The minimum (best) score for each hip is zero and the maximum (worst) is 53, giving a range for the total score of 0 to 106.

Sires (fathers) to be bred from should ideally be ones whose progeny (offspring) have achieved consistently low scores. The same selection procedure should be used for bitches for breeding, since the use of animals with greater than ideal scores will increase the risk of producing offspring with higher scores.

Failure to use the scoring system may give disappointing results but can also be potentially costly in terms of compromised breeding plans. It may lead to litigation, besides raising important animal welfare issues. For the hip scoring scheme to be meaningful and successful it is important that all potential breeding dogs are radiographed and that all radiographs taken under the scheme are submitted for scoring, whatever the apparent state of the hips. In addition, scoring of progeny, even if not intended for breeding, will provide much useful data for genetic analysis. This will ensure that the information gathered is as relevant as possible. It is only by this means that proper conclusions may be drawn by the scheme’s statisticians, geneticists and veterinary advisers.

For further information please visit

Breed mean score

The breed mean score is calculated from all the scores recorded for a given breed (both high and low) and reflects the overall HD status for the dogs scored in that breed. At the time the radiograph and certificate are returned to the submitting veterinary surgeon, a copy of the sheet giving current breed mean scores will be enclosed so that the veterinary surgeon may best advise his/her client regarding the dog’s suitability for breeding. All breeders wishing to control HD should breed only from animals with hip scores well below the breed mean score. The suggested mean score for Cockapoos is 12/13.

Getting a dog’s hips scored

Owners should contact their veterinary surgeon and arrange an appointment for their dog to be radiographed (X-rayed). The radiographs must be taken under anaesthesia or heavy sedation which means that the dog may have to be left for a short time at the veterinary practice. Hip radiographs can be taken at the same time as those for the BVA/KC Elbow Dysplasia Scheme. When taking the dog for its radiographs owners should remember the following:

● The dog must be at least one year old, but there is no upper age limit. 
● The dog must be permanently and uniquely identified by way of a microchip or tattoo. 
● The dog’s KC registration certificate and any related transfer certificates must be available so that the appropriate details can be printed on the radiographs
   (microchip/tattoo numbers will also be printed on the radiographs).
● The owner will be asked to sign the declaration (first part) of the certificate, to verify the details are correct and grant permission for the use of the results.

Once the radiographs have been taken, the veterinary surgeon must fill out the appropriate section of the certificate and submit both the radiographs and the certificate and the current fee to the BVA.

The results and the radiographs are normally returned to the veterinary surgeon within three weeks with a certificate for the owner and a copy for the veterinary surgeon. Once a score has been given for a dog, the radiograph cannot be re-submitted. However, owners have the right to an appeal, which takes the form of a re-appraisal of the original radiographs. A letter of appeal must be made within 45 days of the date of the original certificate. The whole process from initial appointment to receiving the scores is handled through the submitting veterinary surgeon.

Please note that Permanent Identifications (microchip/tattoo) have been a requirement from January 2010.

There is a reduced fee when radiographs of the same dog are submitted simultaneously to the CHS for the Hip and Elbow Dysplasia Schemes.

For current fees and further information please contact:

CHS, 7 Mansfield Street, London, W1G 9NQ.   Tel 020 7908 6380   Email    Web

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.

Affected breed: English Show or Working Cocker Spaniel

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 lose 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. When 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.

DNA testing laboratories: in UK/FRANCE Antagene and UK/GERMANY Laboklin

Phosphofructokinase (PFK)

Phosphofructokinase (PFK) is an enzyme that is crucial for production of energy from sugar sources in all cells of the body, especially red blood cells and muscle cells. Lack of this enzyme causes a range of effects: weakness and muscle cramps, discolored urine, anemia and jaundice. In American Cocker Spaniels, this disease is inherited as an autosomal recessive condition.

Affected  breed: American Cocker Spaniel

Study of the PFK gene in normal and affected dogs revealed the specific mutation causing this disease. A DNA-based genetic test uses this information to identify dogs that are either affected, a carrier or normal.

DNA testing laboratories: in UK Laboklin and in USA OptiGen

Retinal Dysplasia

Most cases of retinal dysplasia in dogs are hereditary. It can involve one or both retinas. Retinal dysplasia can be focal, multifocal, geographic, or accompanied by retinal detachment. Focal and multifocal retinal dysplasia appears as streaks and dots in the central retina. Geographic retinal dysplasia appears as an irregular or horseshoe-shaped area of mixed hyper or hyporeflectivity in the central retina. Retinal detachment occurs with complete retinal dysplasia, and is accompanied by blindness in that eye. Cataracts or glaucoma can also occur secondary to retinal dysplasia. Other causes of retinal dysplasia in dogs include infection with canine adenovirus or canine herpesvirus, or radiation of the eye in newborns. An OptiGen DNA test is available.

Commonly affected breed

American Cocker Spaniel – focal or multifocal.


Dogs that have a mild form of retinal dysplasia may show no symptoms of the disease. In dogs with more severe cases of RD, the symptoms may include not wanting to walk into dark areas (such as hallways), bumping into things and obvious visual impairment.


In some dogs, retinal dysplasia may be an inherited condition. Other causes of RD in dogs may include prenatal infections such as the herpesvirus. The herpesvirus can cause severe inflammation in the eye and retinal dysplasia may develop later in life. Parvovirus, trauma, exposure to toxins and exposure to radiation can all cause retinal dysplasia in dogs.

Von Willebrand disease Type 1 (vWD 1)

Von Willebrand disease (vWD) is probably the most common inherited bleeding disorder in dogs. It is caused by lack of von Willebrand factor which is a protein that plays a key role in the blood clotting process resulting in prolonged bleeding. The disorder occurs in varying degrees of severity ranging from trivial bleeding to excessive life threatening haemorrhages.

Affected breed: Poodle

Symptoms include spontaneous bleeding from the nose, gum and other mucous membranes. Excessive bleeding occurs after an injury, trauma or a surgery. Often dogs don’t show clinical signs until something starts the bleeding, such as nail trimming, teething, spaying, sterilizing, tail docking, cropping or other causes. Bleeding also occurs internally in the stomach, intestines, urinary tracts, the genitals and / or into the joints.Type I von Willebrand’s disease is considered relatively mild when compared to Type II in Scotch Terriers and Shetland Sheep Dogs and Type III in the German Wirehaired pointer, Type II and Type III are much more severe than type I.

DNA testing laboratories: in UK/GERMANY Laboklin