Temperament & Health concerns should be the top priority for breeders.
Below are some of the health topics we feel potential owners should educate themselves about. A brief summary of our encounters (or lack there of) with these can be found by clicking on each heading.
Health concerns should be the top priority for breeders. Below are some of the issues we feel potential owners should educate themselves about. A brief summary of our encounters (or lack there of) with these issues can be found under each heading.
by Scott A. Krick D.V.M.
Reprinted from Delaware Valley Golden Retriever Rescue Golden Opportunities newsletter (DVGRR, Sinking Spring, PA)
Perhaps no other topic relating to Golden Retrievers has generated so much discussion, misunderstanding, information, dis-information, hurt feelings and gossip as that of a dog’s hip status. There are many reasons for this. Foremost is the inescapable fact that the breed has many representatives who harbor “bad hips.” Another reason is that there is a tremendous amount of misunderstanding on exactly what constitutes “bad” (or “good”) hips. Also, hip problems have been heavily emphasized during breeding and purchasing considerations. If nothing else, I hope to leave you with a clearer understanding of what all the fuss is about. The hip (coxofemoral) joint of the dog is a “ball and socket” joint. The head of the femur (“ball”) is seated in the acetabulum (“socket”) of the pelvis. Although many factors will affect the function of this joint, perhaps the most widely accepted indicator of the joint’s status is its laxity (looseness of the ball and socket joint). Consequently, most methods of evaluating this joint focus on the degree of laxity.
Dysplasia is a “catch all” term used to describe a hip joint in which some or all of the signs associated with joint instability are present radiographically. Many factors can contribute to “hip dysplasia.” For the most part, dysplasia is an inherited instability of the joint. This instability can be compounded by environmental factors such as injury to the joint and by dietary factors such as pushing rapid growth in puppies. It is my opinion that if a dog is predisposed to joint instability, you can aggravate the condition by overfeeding high protein diets and by excessive exercise, but you cannot create problems if the dog is not already genetically predisposed. Conversely if the dog is genetically predisposed it would be wise to encourage slow growth by switching to adult food at six months of age, not using high protein foods and by discouraging excessive stress on the hip joint during exercise.
Most people find it surprising that physical examination of the hips by a veterinarian is, itself, not a very reliable way to evaluate the hip joint status. There are several reasons why this is true. Perhaps the greatest reason is that there is a substantial amount of muscle mass surrounding the hip, making palpation of the joint itself virtually impossible. Another significant factor is that pain associated with degenerative joint disease will vary considerably among individuals, making assessment based on resentment of manipulation very subjective. This is not to say, however, that physical examination and observation are useless.
A thorough history and examination often reveal that the dog experiences difficulty when rising from a lying position. Many dogs exhibit reluctance to jump up or to climb stairs (actions that place greater weight and stress on the hip joints). Some dogs show a “bunny-hopping’ gait in which they run using both back legs together. While this can also be normal, it commonly suggests that the dog is unconsciously “sharing” the weight between the legs rather than using them alternately. Some individuals show marked lameness (limping). A veterinarian may also note atrophy (loss of muscle mass) of the thigh muscles suggesting that the dog is not using the limb as athletically as usual. This is not specific to the hip joint, but may support a diagnosis of hip joint problems. Additionally, a dog who resents full extension of the rear limbs may be experiencing degenerative problems with its hips. The final complicating factor is that hip joint pain is often episodic. The dog may be physically “normal” some or most of the time, and therefore may appear to be normal on physical examination even in the presence of substantial degenerative changes.
The most widely used methods of evaluating the hips are the OFA and the PennHip technique. Both rely on radiography (x-rays) of the hip joint to assess its conformation and stability. OFA evaluation is performed entirely through subjective interpretation of observation, while PennHip evaluation relies on actual measurements of laxity. As you are probably aware, there is a great deal of controversy as to which of the methods of evaluation is better. I personally feel that the PennHip method is much more accurate, repeatable and predictive of future degenerative joint disease. Using its information and recommendations, it is possible to actually improve hip status in succeeding generations through selective breeding. The arguments against it most frequently arise from individuals who are apparently afraid to find out the truth about their dog(s) or breeding lines, because rarely are there legitimate reasons for distrusting the results.
Once a diagnosis of hip dysplasia is made, there are several options for the dog and owner. In “mild” cases, no treatments may be indicated. One of the “nutriceuticals” (products used in treatment which are not considered drugs) such as Glycoflex, Inflammex, glucosamine sulfate, chondroitin sulfate or Cosequin may be recommended. This class of products is claimed to increase joint fluid viscosity and provide nourishment for the joint surfaces. Until recently no controlled studies had been done to document the effectiveness of the nutriceuticals. A study of a similar injectable product (Adequan) suggested marked improvement in the joints of dogs treated versus the untreated control group. I have been very impressed with the effects of Glycoflex in particular in reducing or alleviating the symptoms of discomfort associated with joint problems. Another option available is the use of non-steroidal-antiinflammatory drugs. This category of medication includes aspirin, phenylbutazone, Rimadyl, Etogesic, Arquel and other drugs. While they may give relief from the symptoms of joint pain, they do not improve the joint in any way. A third choice is steroids such as prednisolone and methylprednisolone. Steroids are, for me, the drug of last resort for joint pain. Like the non-steroidals, these drugs do nothing to improve the joint. They are strictly used to reduce inflammation. Long term use of either steroidals or non-steroidals may actually contribute to degeneration of the joint. I have found that the neutriceutical products may decrease or eliminate the need for other classes of medications in many cases.
Another consideration for the treatment of dysplasia involves surgical intervention. There are several procedures used to restore some or all of the function of the joint. Total hip replacement is the “gold standard” by which other procedures are measured. Like in humans, a new metal alloy “ball” and an acrylic “socket” are installed to replace the damaged one(s). Success rates are high in the 90 percentile for nearly perfect return to function. Many surgeons have found that replacement of only one affected hip often returns the dog to soundness even if initially both legs are affected, so rarely does the other hip require replacement. This is appealing since the surgery costs in the $1,800 to $ 3,000 price range. Pectinectomy involves cutting the tendons attachment of the “groin” muscle known as the Pectineus. This relieves the immediate tension on the hip joint and tends to diminish pain. Unfortunately, this procedure is often only a temporary solution to the chronic problem. This procedure has become less frequently used because of this fact.
The other commonly used surgical options included the Triple Pelvic Osteotomy (TPO) and the Femoral Head and neck Excision (FHO). The TPO involves cutting the supports for the “socket” and realigning it so as to reduce stress on the hip joint. The FHO involves completely removing the femoral head (“ball’), allowing the gluteal muscles to support the weight of the rear leg and thus avoiding any bone on bone contact. Both techniques can restore good to excellent function to the dog, depending on the underlying problem and the dog’s age and weight.
Ideally, it is best to avoid the problem altogether. The only way to do that is to screen all potential breeding animals and breed only dogs of “better” hip conformation, so as to eliminate affected animals from the breeding population. Until a concerted effort is made to accomplish this, however, the tragedy of hip dysplasia will remain a common occurrence.
The above is written by Scott A. Krick D.V.M.
Hip problems will be around for a long time since only a % of the problem is genetics. How do you prevent hip problems? Here are a few do’s and don’ts.
- Do feed quality food for his size and breed.(Goldens are a medium to large breed)
- Do give him vitamins like Ester C and vitamin E for his coat.
- Do keep him SLIM! I can’t say this enough.
- Do give him joint supplements.(Glucosamine in dog food is in such small amounts as to not be effective. See below * for advice.)
- Do provide him with plenty of exercise.
- Do provide him with a bed to sleep on.(Cold floors can promote arthritis)
- Do not keep him in a crate day and night. (Once he’s house broken give him room)
- Do not make him slide on slippery floors, ice or wet grass.
- Do not allow him to jump or climb big stairs until he’s done growing.
- Do not keep him in cold damp places.
- Do not make him swim in cold water.
- Do not neuter or spay too young. Dogs lose much of their muscle mass when neutered. If you spay during the rapid growth time of his life, the muscles mass he needs to keep things together will be affected.Castration at an early age will cause the dog to become overly tall, as the growth plates in the long bones will not close at the appropriate time; additionally, the dog will lack breadth of chest. The combination of these two factors sets the stage for your dog to have painful orthopedic problems. An early age means below 1 year in small and medium sized dogs, and below 2 to 2.5 years in large breeds. I would put goldens somewhat between the two, so spay the girls at 11 months and the boys between 18 to 24 months.
*Human grade Glucomsamine Sulfatensodium free 500 MG (give 2 a day with food) These are sold at your local pharmacy or Costco in capsules. Glucosamine will reduce joint pain in senior dogs and help promote healthy cartilage growth in growing pups specially those large, fast growing, males.
***To date (2015) while our sampling is extremely small, as we do not require owners who have a dog from us to have x-rays taken and submitted for grading, we have had one dog fail a hip clearance. As with many other conditions I believe it’s not a matter of if it will happen but rather when. Each litter we produce we take great strides to ensure we are stacking the odds in our favour of producing dogs that will not be effected by Hip abnormalities. Even while taking every precaution, these issues can still show up in litters that have no history of hip problems in their pedigree.
Elbow soundness is extremely important, more so in large breed dogs. Abnormal elbows can range from unnoticeable, to uncomfortable to crippling.
Elbow Dysplaysia is a developmental abnormality in the elbow joint that that can affect large breed dogs, including Golden Retrievers. The disease has been diagnosed in dogs ranging in age from three and a half months to three years with six months the most frequently reported age of diagnosis.
Elbow Dysplaysia is caused by a failure of the bones involving the elbows of one or both forelegs to unite and move properly, or by bone fragments within the joint.
Fragments of bones or cartilage in the elbow joint are abrasive, causing severe irritation which results in pain and impairment of the dog’s movement. Signs of the disease vary from slight lameness to refusal to bear weight on the affected limb. The elbow will be thrown out of place as the dog walks or runs and the dog will hold its elbow away from the chest. Severely affected dogs stand with bowed elbow and have swollen joint with increased joint fluid. The lameness generally is gradual in appearance, intermittent in nature, and may become more pronounced after exercise. Affected dogs resent forced movement of the elbow joint, and another frequent complaint is lack of drive in gaiting and loss of stamina.
Diagnosis of the condition is by x-ray. Surgical removal of the bone fragments will relieve the pain and discomfort, but since the process is degenerative, it may not be halted. . All aspects of this condition will produce generative joint disease over a period of time. Permanent or recurring lameness in the front legs may be the result.
Elbow Dysplaysia is thought to be inherited, and thus prevention is the most important way to deal with the disease. Concerned breeders try to eliminate the disease from their line dogs by maintaining accurate records and by not mating dysplastic dogs. In 1990, the OFA established a registry for dogs free of elbow dysplaysia, in addition to their registration of dogs free of hip dysplaysia.
***To date (2015) while our sampling is extremely small, as we do not require owners who have a dog from us to have x-rays taken and submitted for grading, we have not yet had a dog fail an elbow clearance. As with many other conditions I believe it’s not a matter of if it will happen but rather when. Each litter we produce we take great strides to ensure we are stacking the odds in our favour of producing dogs that will not be effected by Elbow abnormalities. Even while taking every precaution, these issues can still show up in litters that have no history of elbow problems in their pedigree.
Pigmentary Uveitis (PU) is a disease of the eye, it seems to be found at around age 8, but there are many cases found much earlier (2) and some much later. Early in the disease process inflammation in the eye is usually very subtle and may go unnoticed, assuming it’s allergies etc. Symptoms of Pigmentary Uveitis (PU) include, but aren’t limited to, squinting, increased tearing or discharge, redness, photophobia (light sensitivity) and cloudiness of the eye or eyes.
Pigmentary Uveitis (PU) is a chronic concern that will require long term treatment. In many cases inflammation is mild and controllable with medication, but many affected dogs will eventually develop glaucoma. Glaucoma, which is painful and blinding, has been found to develop in almost half of the Golden Retrievers diagnosed with Pigmentary Uveitis.
Pigmentary Uveitis (PU) is a serious disease, as breeders we urge all Golden Retriever owners to obtain yearly eye examinations by a board certified Ophthalmologist, for the life of your pet. Should you have any difficulty in locating an Ophthalmologist in your area please contact us, and we will assist you in locating one.
We encourage everyone to read the information on Pigmentary Uveitis located on the GRCA Website.
**To date (2015) Pigmentary Uveitis (PU) has not affected our dogs, yet. I am a firm believer it’s not a matter of if Pigmentary Uveitis (PU) affects a breeders breeding program, but rather when. All of our dogs are checked yearly by a board certified Ophthalmologist. We strongly urge all owners to have their dogs checked yearly.
Cancer is an ugly word that no one wants to hear. There are many forms of cancer that can strike a dog, some rarer (prostate, uterine etc.) and some are more common (lymphoma, hemangiosarcoma etc.). According to some articles, 1 in every 3 dogs will get cancer (that’s dogs, not just Golden Retrievers). By those stats we can see cancer is a very real concern. Equally as concerning, cancer knows no age, it can strike a dog at 16 years of age or at 2.
Lymphoma is one of the most common cancers seen in dogs. Although there are breeds that appear to be at increased risk for this disease, lymphoma can affect any dog of any breed at any age. It accounts for 10-20% of all cancers in dogs.
Lymphoma (lymphosarcoma or non-Hodgkin’s lymphoma) is a malignant cancer that involves the lymphoid system. In a healthy dog, the lymphoid system is an important part of the body’s immune system defense against infectious agents such as viruses and bacteria. Lymphoid tissue normally is found in many different parts of the body including lymph nodes, liver, spleen, gastrointestinal tract and skin. Lymphosarcoma is classified according to the location in the body in which the cancer begins.
- Multicentric form occurs in the lymph nodes.
- Gastrointestinal form occurs in the stomach, intestines, liver and lymph nodes in the abdomen.
- Mediastinal form occurs in the mediastinum, in front of the heart in an organ called the thymus.
Hence this form of lymphosarcoma sometimes is called thymic lymphoma.
- Cutaneous form occurs in the skin.
- Acute lymphoblastic leukemia occurs when the disease starts in the bone marrow.
- Miscellaneous forms of lymphosarcoma are less common and include thoseÂ that begin in the
nervous system, nasal cavity or kidneys.
Hemangiosarcoma in dogs is an aggressive, malignant tumor of blood vessel cells. With the exception of the skin form of hemangiosarcoma, a diagnosis of hemangiosarcoma is serious. Because these tumors start in blood vessels, they are frequently filled with blood and when a blood-filled tumor ruptures, it can cause problems with internal or external bleeding.
Hemangiosarcoma can theoretically arise from any tissue where there are blood vessels, which is essentially anywhere in the body, but usually appear in the skin, soft tissue, spleen or liver with the most common site being the spleen. They are highly metastatic and will frequently spread to the brain, but also to the lungs, spleen, heart, kidneys, skeletal muscle and bone. This type of cancer in dogs is typically classified as dermal, subcutaneous or hypodermal, and visceral.
Mast Cell Tumors
Mast cells are specialized cells that are normally found throughout the body and help animals respond to inflammation and allergies. Mast cells can release several biologically active chemicals when stimulated which include histamine, heparin, seratonin, prostaglandins and proteolytic enzymes. Although these chemicals are vital to normal bodily function, especially immune response, they can be very damaging to the body when released in chronic excess.
Mast cell tumors (MCTs) (also referred to as histiocytic mastocytoma, mast cell sarcoma, mastocystosis (when there is systemic involvement)) are cancerous proliferations of mast cells that can spread throughout the body. The most significant danger from mast cell tumors arises from the secondary damage caused by the release of chemicals that they produce: gastric ulcers, internal bleeding, and a range of allergic manifestations. These tumors are the most frequently recognized malignant or potentially malignant neoplasms of dogs. MCTs may be seen in dogs of any age, but the average age is 8-10 years. There is no way to definitively identify MCTs without a biopsy and pathology report. It can be difficult not only to recognize mast cell tumors but to predict their course. They may be relatively innocent or aggressively malignant.
These tumors may develop anywhere on the body surface as well as in internal organs, but the limbs, especially the posterior upper thigh, ventral abdomen, and thorax are the most common sites. Location on mucocutaneous junctions or on the ventral surface of the body is associated with a more aggressive behavior. Many breeds appear to be predisposed, especially boxers, pugs, Rhodesian ridgebacks, and Boston terriers. The tumors vary significantly in size, shape, appearance and texture, but most commonly, they appear as raised, nodular masses that may be soft or solid which usually have dark granules in them. The granules contain substances which, when released, cause swelling, itching, and redness. Infrequently, when a large number of granules discharge their chemical contents into the bloodstream resulting in vomiting, stomach ulcers, shock and even death.
Osteosarcoma (OSA) accounts for only approximately 5% of all canine tumors, but is by far the most common boneÂ tumor of the dog. It is a malignant tumor of the bone and can develop in any bone, but most often occurs in bones bordering the shoulder, wrist and knee. Osteosarcoma of the limbs is called appendicular osteosarcoma and accounts for 75-85% of the cases of bone cancer. However, these tumors can also affect the axial skeleton (cranium, spinal column, ribs).
Osteosarcoma develops deep within the bone and becomes progressively more painful as it grows outward and the bone is destroyed from the inside out. Lameness may occur suddenly or start intermittently and progress over several weeks. Obvious swelling becomes evident as the tumor grows and normal bone is replaced by tumorous bone.
Tumorous bone is not as strong as a healthy bone and can break with minor injury. This type of broken bone is called a pathologic fracture. Pathologic fractures will not heal, therefore it is critical to diagnose and start treatment for osteosarcoma before this occurs.
Osteosarcoma usually occurs in middle aged or elderly large and giant breed dogs but can occur in a dog of any age with larger breeds tending to develop tumors at younger ages.
Highly aggressive and metastatic in nature, over 90% of all clinically significant osteosarcomas have already micrometastasized by the time of diagnosis. Most metastasis happens via menatogenous spread to the lungs and other bones, but lymph node metastases have been reported.
**To date (2015) there have been two dogs of our breeding who have been affected by what we consider early Cancer (diagnosed prior to 9 years of age). A 6 year old with lymphoma who passed away due to a pulmonary embolism (it is suggested due to the cancer), and a 5 year old with hemangiosarcoma who passed away.
Golden Retrievers with Ichthyosis develop white scales on the skin soon after birth. The scales may persist through the animal’s life, however many affected dogs remain asymptomatic their entire lives. This condition is of no discomfort to a dog, nor does it cause any ‘smell’ or secondary issues (despite what some articles may state).
***To date (2015) we have tested 6 dogs for Ichthyosis. Of these dogs tested 2 have tested Clear, and 4 tested as Carriers.
There appears to be three types of PRA in Golden Retrievers, prcd-PRA, PRA1, and an unidentified third type.
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. If your dog is affected, you may find it helpful to read about other owners’ experiences living with blind dogs. (suggested links:www.eyevet.org and www.blinddogs.com)
A research team at the Animal Health Trust in the UK and the Swedish University in Upsaala have recently identified a mutation, GR_PRA1, that causes Progressive Retinal Atrophy (PRA) in the golden retriever. OptiGen had previously identified another form of PRA caused by the prcd mutation in this breed. With the aid of the new GR_PRA1 DNA test, the cause of the majority of PRA cases in the golden retriever can now be explained. Unfortunately, there are still a few cases of PRA in the golden retriever that are not caused by either of the known mutations. These cases will continue to be a subject of ongoing PRA research. If you know of any PRA-affected golden retrievers, please encourage the owners to contact OptiGen to learn about our Free PRA Testing/Research program : (http://www.optigen.com/opt9_research.html)
Current statistics on the incidence of GR_PRA1 indicate that the disease is primarily of concern in European lines of golden retriever however we have confirmed that GR_PRA1 is the cause of some of the PRA-affected in golden retrievers that have been sent to OptiGen for research from Canada and the USA. OptiGen will be happy to provide the Golden Retriever Club health committees with regular updates of the statistics on the incidence of PRA, both prcd and GR_PRA1, as more dogs are tested.
Similar but completely unrelated to prcd, GR_PRA1 is inherited in an autosomal recessive manner. This means that GR_PRA1 disease will occur only if two copies of the mutation are present; carriers of one copy of the mutation do not show disease. By ensuring that at least one parent is Normal/Clear of GR_PRA1 then no GR_PRA1 affected offspring will be produced in a mating.Â See the chart below for expected breeding outcomes when the GR_PRA1 status (Genotype) has been determined by DNA testing.
***To date (2015) we have tested 8 dogs for PRA via DNA testing, 8 for prcd-PRA, 7 for PRA1 and 7 for PRA2. Of these dogs tested we have 6 dogs tested Clear and 2 tested as a Carrier for the prcd-PRA Mutation, 7 have tested Clear for PRA1 & PRA2.
There are two forms of Epilepsy, Primary and Secondary. Primary Epilepsy includes dogs with idiopathic, genetic, inherited, or true epilepsy, there is no concrete cause for the seizures. Secondary Epilepsy refers to dogs who’s seizures cause can be determined (toxins, brain tumor, etc.). There are many different treatments available to help control seizures in dogs, based on your pets history and health status your vet may discuss one or several with you (even in combination).
Primary epilepsy: also known as idiopathic, genetic, inherited, or true epilepsy. There are no positive diagnostic findings that will substantiate the diagnosis. It is a case of ruling out every other possibility. The first seizure in a dog with primary epilepsy usually occurs between the ages of 6 months and 5 years. (Oliver, Seizures). However, a diagnosis of primary epilepsy is not proof of a genetic defect; only careful breeding studies could prove that. The breed, the age, and the history may suggest a genetic basis for primary epilepsy if there is a familial history of seizures.
Secondary epilepsy refers to seizures for which a cause can be determined, and there are many. In dogs less than one year of age, the most commonly-found causes of seizures can be broken down into the following classes: degenerative (storage diseases); developmental (hydrocephalus); toxic (lead, arsenic, organophosphates, chlorinated hydrocarbons, strychnine, tetanus); infectious (distemper, encephalitis, and others); metabolic (such as transient hypoglycemia, enzyme deficiency, liver or kidney failure); nutritional (thiamine, parasitism); and traumatic (acute injury). In dogs 1-3 years of age, a genetic factor is most highly suspected. In dogs 4 years of age and older, seizures are commonly found in the metabolic (hypoglycemia, cardiovascular arrhythmia, hypocalcemia, cirrhosis) and neoplastic (brain tumor) classes. (Oliver, Seizure). Dr. Jean Dodds has mentioned that seizures are also associated with hypothyroidism, which is a familial (inherited) autoimmune disease of purebred dogs.
Read more about canine epilepsy here.
**To date (2015) there has been one dog of our breeding diagnosed, at age 6, with idiopathic epilepsy which was being treated with Potassium Bromide. This course of treatment reduced the seizures (which last on average 30-60 seconds) to one every 6-9+ months.
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.
**To date (2015) there has been 3 of our dogs tested, all 3 have been tested Clear of DM. It should be noted, currently there is an extremely small number of Golden Retrievers that have been DNA tested for DM (according to OFA as of July 2015 only 183 Golden Retrievers have been tested, of these 3% are carriers and 2% are considered at risk of developing the disease).