Monday, July 6, 2009

Health Testing for Thyroid Issues in Mastiffs

What is the purpose of testing for thyroid problems in our dogs? As breeders, it is essential that we identify those dogs that are phenotypically normal for our breeding programs and to gather data on the genetic disease autoimmune thyroiditis. Since autoimmune thyroiditis is considered genetic, it is important that we screen and eliminate affected dogs from our breeding programs.

Hypothyroidism is the most common endocrine disorder in dogs and almost 80% of these cases result from autoimmune thyroiditis. Although thyroid dysfuction is the most frequently recognized endocrine disorder, it is often difficult to make a definitive diagonosis.

Think of your thyroid as the" gas pedal' to your dog's body--it regulates the metabolism of all body cellular functions, thus reduced thyroid levels can manifest in a wide range of clinical signs. Since many of these clinical signs minic other causes, recognizing thyroid disease can be problematic.

Here are some common Clinical Signs of Canine Hypothyroidism:

Alterations in Cellular Metabolism
weakness / stiffness / laryngeal paralysis / facial paralysis / tragic expression / knuckling or dragging feet / muscle wasting / megaesophagus / head tilt / drooping eyelids.

Neuromuscular Problems

lethargy / mental dullness / exercise intolerance / neurologic signs polyneuropathy / seizures / weight gain / cold intolerance / mood swings hyperexcitability-- this can also include unexplained sudden aggression) / stunted growth / chronic infections.

Dermatologic Diseases
dry, scaly skin and dandruff / coarse, dull coat / bilateral symmetrical hair loss / rat tail, puppy coat / hyperpigmentation / seborrhea or greasy skin pyoderma or skin infections / myxedema / chronic offensive skin odor.

Reproductive Disorders
infertility of either sex / lack of libido / testicular atrophy / hypospermia aspermia / prolonged interestrus interval / absence of heat cycles / silent heats / pseudopregnancy / weak, dying or stillborn pups.

Cardiac Abnormalities
slow heart rate (bradycardia) / cardiac arrhythmias / cardiomyopathys/ Gastrointestinal Disorders constipation / diarrhea / vomiting.

Hematological Disorders
bleeding / bone marrow failure / low red blood cells / low white blood cells / low platelets.

Ocular (Eye) Diseases
corneal lipid deposits / corneal ulceration / uveitis Keratococonjunctivitis / sicca or dry eye / infections of eyelid glands (Meibomian gland).

Other Associated Disorders
lgA deficiency / loss of smell (dysosmia) / loss of taste / glycosuria / chronic active hepatitis / other endocrinopathies adrenal, pancreatic, parathyroid.

How do you test for thyroid problems?

Each dog tested is to examined by an attending veterinarian and have a serum sample sent to an OFA approved laboratory for testing as per theOFA guidelines. The laboratory will process the blood result and send it to OFA. OFa will then issue a certifiaction based on the lab result. Some breeders will screen their dog each year with a simple blood test and not do a new OFA certification.

I do screenings at 1 year of age, 2 years of age, before each breeding, and I submit an OFA test between 3 and 5 years of age. A dog may be "clear" at 2, 3 or even 4 years of age and then develop thyroditis at a later age. All stud dogs should have a yearly screening for as long as they stand at stud. All bitches should have a screening test done before any breeding. This is my personal practice and one I recommend to others who breed.

OFA will issue A breed database number to all dogs found to be normal at 12 months of age. Ages will be used in the certification process since the classification can change as the dog ages and the autoimmune disease progresses. OFA recommends that reexaminations occur at ages 2,3,4,6, and 8 years.

An evaluation of dogs under 12 months of age can be performed for private use of the owner, but it should be noted that few dogs are already positive at that age. For this reason, OFA will not issue a certification.

All data, whether normal or abnormal is to be submitted for purposes of completeness. There is no OFA fee for entering an abnormal evaluation of the thyroid into the data bank. Information on results determined to be positive or equivocal will not be made public (you can not find it listed on the OFA site) without explicit written permission of the owner.

What are the Thyroid Abnormalities that you test to find?

Thyroid abnormalities fall into several categories—two types will be defined by the registry. They are: Autoimmune Thyroiditis and Idiopathically Reduced Thyroid Function. Autoimme thyroiditis is known to be heritable

FYI--Sometimes a result maybe called"Equivocal"--that simply means is is neither negative or positve--it's undertermined. For those dogs with laboratory results that are questionable, therefore not definitive, it is recommended that the test the repeated in three to six months.

Autoimmune thyroiditis is the most common cause of primary hypothyroidism in dogs. The disease has variable onset, but tends to clinically manifest itself at 2 to 5 years of age. Dogs may be clinically normal for years, only to become hypothyroid at a later date. The marker for autoimmune thyroiditis, thyroglobulin autoantibody formation, usually occurs prior to the occurrence of clinical signs. Therefore, periodic retesting is recommended.

The majority of dogs that develop autoantibodies have them by 3 to 4 years of age. Development of autoantibodies to any time in the dog’s life is an indication that the dog, most likely, has the genetic form of the disease. Using today's technology only a small fraction of false positive tests occur.

As a result of the variable onset of the presence of autoantibodies, periodic testing will be necessary. Dogs that are negative at 1 year of age may become positive at 6 years of age. Dogs should be tested every year or two in order to be certain they have not developed the condition. Since the majority of affected dogs will have autoantibodies by 4 years of age, annual testing for the first 4 years is recommended. After that, testing every other year should suffice.

Unfortunately, a negative at any one time will not guarantee that the dog will not develop thyroiditis.

The registry data can be used by breeders in determining which dogs are best for their breeding program. Knowing the status of the dog and the status of the dogs lineage, breeders and genetic counselors can decide which matings are most appropriate for reducing the incidence of autoimmune thyroiditis in the offspring.

Please note that dogs should not receive any type of thyroid supplementation for 3 months prior to thyroid testing.

When I look at the results, how do I know what is "normal"?

The method for classifying the thyroid status will be accomplished using state-of-the-art assay methodology. I.E--we look at the blood result!

First, let's familiarize ourselves with the different "test" used and their indications for our use in evaluating our breeding dogs for thyroid problems.

(A.) Free T4 (FT4)—this procedure is considered to be the "gold standard" for assessment of thyroid's production and cellular availability of thyroxine. FT4 concentration is expected to be decreased in dogs with thyroid dysfunction due to autoimmune thyroiditis.

(B.) Canine thyroid simulating hormone (cTSH)—this procedure helps determine the site of the lesion in cases of hypothyroidism. In autoimmune thyroiditis the lesion is at the level of the thyroid gland and the pituitary gland functions normally. The cTSH concentration is expected to be abnormally elevated in dogs with thyroid atrophy from autoimmune thyroiditis.

(C.) Thyroglobulin Autoantibodies (TgAA)—this procedure is an indication for the presence of the autoimmune process in the dog’s thyroid.

How do the results translate into the OFA Certification?


FT4 within normal range
cTSH within normal range
TgAA is negative

Positive autoimmune thyroiditis

FT4 less than normal range
cTSH greater than normal range
TgAA is positive

Positive compensative autoimmune thyroiditis

FT4 is within normal range
cTSH is greater than or equal to normal range
TgAA is positive

Idiopathically reduced thyroid function

FT4 is less than normal range
cTSH greater than normal range
TgAA is negative

All other results are considered equivocal and will require a retesting after 6 months for a certification.

My information source for this entry is the OFA site.

Please direct any questions to me at Thank you. Catie C. Arney

Health Testing for Eye Problems in Mastiffs

For the purpose of a health testing discussion, I will not try and discuss all possible eye disorders that a Mastiff have inherit. I will discuss the process (test) we have for testing: the CERF exam along with the PRA and CMR DNA testing.

In this entry, I will only discuss the PRA (Progressive Rential Atrophy) and the CMR (Canine Multi-Focal Retinopathy) diseases since they are the only eye diseases that we can currently DNA test for in Mastiffs.

Please note, that a CERF exam may also show other "genetic eye diseases"--i.e. Entropion, "cherry eye", Cataracts, Glaucoma, etc.- disorders that we DO NOT have DNA tests for at present in Mastiffs--so a CERF exam is essential to rule out genetic eye disorders.

Below is a labeled diagram of the canine eye. In the later discussions, you can use it as reference.

What is a CERF (Canine Eye Registration Foundation) Examination?

The Canine Eye Registration Foundation (CERF) was established in 1974 to track heritable eye diseases in purebred dogs. A database is maintained through registered purebred dogs examined by board certified veterinary ophthalmologists (Diplomates of the ACVO -- American College of Veterinary Ophthalmologists).

This database helps breeders and ophthalmologists monitor eye diseases. A CERF exam is basically the same exam you would get if you went to an ophthalmologist. A dog can be registered by CERFonce it has been examined by an ACVO diplomate and found to be unaffected by a major heritable eye disease.
CERF examinations are performed annually. The ophthalmologist fills out a computerized form and gives a copy to the owner. This copy can be sent to CERF by the owner (if the dog has been found to be unaffected, as previously described) along with the registration fee to receive a CERF registration number, which can be used by the owner for show purposes, breeding, and AKC pedigrees.
This registration is good for one year and it must be renewed annually by examination, to maintain an up-to-date CERF number. Since many ocular diseases do not appear until later in a dog's life, such as progressive retinal atrophy and some forms of cataract, it is suggested that an annual examinations be done to rule out heritable disease which occurs as a dog ages.

In an effort to educate the public, CERF also publishes a quarterly newsletter about eye diseases in dogs. It contains current information about the frequency and heritability of eye diseases in dogs, and gives tips for healthy breeding practices. This publication is a great source of inform,ation for dog owners and breeders.

The goal of CERF is to identify those conditions that should be selected away from when breeding. To simplify, dogs with bad hips should not be bred, and dogs with inherited cataracts and certain other eye diseases are not suitable for breeding either. Other problems result from facial conformation considered desirable by breeders. For example, breeding for prominent eyes and facial folds in Mastiffs might lead to corneal irritation, scarring, and eventual blindness.

CERF works with the ACVO genetics committee to determine ocular conditions that are identified with certain breeds. A book is available that lists all the known ocular disorders of dogs: Ocular Disorders Presumed to be Inherited in Purebred Dogs. It is updated as new information becomes available, and can be ordered from CERF.

What is Progressive Retinal Atrophy (PRA) in Dogs?

This is a genetic, inherited disease of the retina (the "film" in the camera), which occurs in both eyes simultaneously. The disease is nonpainful, and there is no cure for it. The eyes are genetically programmed to go blind. PRA occurs in most breeds of dogs and can occur in mixed breeds also.
It is recessively inherited in all breeds studied, with the following exceptions: PRA is dominantly inherited in Old English Mastiffs and Bullmastiffs, and PRA is sex-linked and found primarily in male dogs in the Siberian Husky and Samoyed breeds. In other words, for a Mastiff to inherit and manifest PRA, it must inherit a copy of the gene from only one parent.

Clinical signs vary from the dog first becoming night blind in the early stage of PRA (not able to see in low light surroundings) to the entire visual field in all light levels becoming affected, which is advanced PRA. The pupils are usually dilated, and owners often notice a "glow" and increased "eye shine" from the eyes.
All dogs with PRA will eventually develop blindness from advanced PRA, and this time frame until the dog is blind varies considerably from dog to dog, but usually takes at least 6 months from the time of diagnosis, and can rarely take years until the dog is completely blind.

Although no treatment for PRA, nor is it possible to stop the disease. A nutritional antioxidant supplementation for retinal health may help slow the deterioration of the retina in some dogs to "buy some time" before the blindness inevitably happens. Holostic Animal Eye Care experts believe that in many of these PRA patients, specific oral antioxidant nutritional therapy can delay the progression of blindness.
However, Blindness can not be avoided in any PRA patients. If oral antioxidants were used, they would be continued until complete vision loss occurred.

What Should I do if I suspect My Mastiff has PRA?

As with any serious eye disorder, have your dog examined by a board certified veterinary ophthalmologist to determine if this disease is indeed present. Your local Vet can refer you to the closest Canine opthalomigy specialist fo an ophthalmic examination.
Dogs with PRA should not be bred, and the breeder that you received your dog from should be notified that the dog is affected, so the breeder can alter their breeding program in future.
It is important to understand that dogs with PRA are happy dogs. Their eyes don't hurt, and they adjust very well to their slow loss of vision. In fact, if a dog were destined to become blind and you could pick the disease, it would be PRA, as the vision loss is slow and nonpainful, and the dog is given much time to adjust to its vision loss.

It is important to realize that it is OK to grieve about your pet's vision loss, but you must not put your sad feelings in your dog's head--they aren't really there! Your dog is not suffering. They adjust well to their vision loss, and it is by far hardest to deal with on the owner's side.
Your dog's job description has not changed. Your blind dog is happy as long as its routine is stable. From your dog's point of view, life continues to be great-- you are there as always, and they just need to use their other keen senses a bit more to get the same information they used to view. Keep household furniture in its place, and consider purchasing the book "Living With Blind Dogs" by Caroline Levin. It is the only book of this subject matter, and is beneficial in helping owners and their affected pets adjust to the vision loss. It is suggested that you purchase a pet medical alert tags that reads, "I Have Poor Vision" or "I Am Blind" along with your address and contact info. Blind dogs have been known to wander away from home and be unable to find their way home.

Dogs with PRA can develop cataracts late in the disease process. Cataract surgery would never be done, as it would not help the dog to see. However, cataracts can cause pain and damage to the eye, and if the eyes look very cloudy to you, please call your opthomoligist vet for a reexamination as soon as possible.

In the 1990's when PRA began to appear in Mastiffs, the MCOA along with the American Kennel Club Canine Health Fund help to set up and conduct a study which lead to the development of a DNA test for PRA. We now have a blood test available to determine if dogs are likely affected with PRA, are likely carriers for PRA, or are not likely carrying the PRA gene. Always ask a breeder if their dogs have had the DNA test for PRA.

In the table below, you can see how this disease is inherited:

For more information about this test, go to The Optigen website- (

What is Canine Multi-focal Retinopathy (CMR)?
CMR is a recently identified recessively inherited eye disease known so far to affect the Mastiffs (English, Bullmastiff, French mastiff or Dogue de Bordeaux), Great Pyrenees and Coton de Tulear. Early clinical studies in 1998 by Dr. Bruce Grahn at the University of Saskatchewan, Canada, first described CMR in the Great Pyrenees.

This condition was observed in each of the named breeds at an ophthalmologist’s exam that included numerous distinct (i.e. multi-focal), roughly circular patches of elevated retina with accumulation of material that produces gray-tan-pink colored lesions. These lesions, looking somewhat like blisters, often vary in location and size, although typically they are present in both eyes of the affected dog. Occassionally, Discrete areas of tapetal hyper-reflectivity might also be seen.

The disease generally develops in young dogs before 4 months and might progress slowly, might even appear to heal, or might even appear and then go away again. Some lesions disappear with no remaining sign, while some lesions leave a wrinkled area – a fold. Some leave the lasting lesion of a blister formation. Most dogs exhibit no noticeable problem with vision despite their abnormal appearing retinas.
And in almost all cases, CMR does not progress significantly over time. The disease seems to have a consistent pattern among the breeds identified so far, although lesions in the Coton de Tulear are often more serious and seem to remain longer than in some of the other CMR-affected breeds. In rare severe cases, the clinical diagnosis could be confused with progressive retinal atrophy (PRA). The full range of clinical symptoms will learned as more dogs are tested for their genetic status.

The clinical presentation and pathology of CMR closely resembles lesions of “Best vitelliform dystrophy”, a human disease with variable clinical expression but usually with serious affects on central vision. Identification of the gene mutation responsible for CMR was based on these similarities. A mutation in the human VMD2 gene – Vitelliform Macular Dystrophy 2 Gene – causes dominantly inherited human Best Disease. Analysis of the canine version of the VMD2 gene indicates that mutations in it cause CMR as a recessively inherited canine condition. The normal form of the VMD2 gene produces a protein named “bestrophin”. The bestrophin protein assembles, in the cells of the retinal pigment epithelium, in a group of four or five units that form a pore through which chloride ions pass.

Our current understanding is that CMR in Mastiffs is inherited in an autosomal recessive pattern. This means the gene mutation responsible for CMR is located on an autosome (that is, a chromosome that is not a sex chromosome) and CMR disease results when the gene mutation is passed to the offspring by both the mother and the father.
(It should be noted that the human disease that mirrors CMR in dogs is an autosomal dominant disease with incomplete penetrance. This means that sometimes, but not always, only one copy of the disease gene needs to be present in order for the disease to be observed clinically.)
At this point CMR in dogs is NOT considered to be an autosomal dominant disease however as more animals are characterized genetically with the DNA CMR test, it is possible that we will find a similar form of inheritance as is seen in humans.
There is complete concordance of the mutation with the disease among affected dogs in the Mastiffs, Great Pyrenees and Coton de Tulear. However, retinal dysplasia described in other breeds, for example in Labradors, Samoyeds or English Springer Spaniels, is very distinct in comparison to CMR and these conditions are not caused by the CMR mutation.

Due to the abnormal appearance of the CMR-affected retina, CERF, ACVO, ECVO and other ophthalmologist’s eye exam reports typically record these multi-focal lesions as “retinal dysplasia” or “retinal folds”, to denote a defect in formation of the retina. Such findings might disqualify the dog from breeding. Presently CERF doesn’t list CMR as a specific condition, but does fail a dog for “retinal dysplasia/retinopathy – folds, detached.”

The genetic test for CMR is valuable for identifying Mastiffs affected and those which are carriers. Given the exact genetic diagnosis, a breeder can identify carriers and breed only to "clear" dog--thus no "affected" puppies will be produced. Puppy buyers who purchase a "carrier" puppy can be assured that there probably will be no vision loss due to this condition. By using the DNA CMR test and eliminating Carriers and affected dogs from our breeding programs, future cases of the condition can be prevented.
In the table below, one can see how breeding affected and carrier dogs produced this disease.

For further information, go to the Optigen website, (Http://

Health Testing for Cardiac Problems in Mastiffs

Thankfully, we do not have a wide spread incidence of cardiac problems within the Mastiff breed. However, as the Mastiff breed continues to rise in popularity and the overall numbers of puppies produced each year continues to increase; It stands to reason that we could see an "increase" in Cardiac problems.

How do you test for Cardiac disease in a dog?

As breeders, it is essential that we screen and clear all dogs for any cardiac problems before breeding. Most Mastiff breeders obtain a cardiac certification through OFA.

An OFA Cardiac certification consist of a simple 15 minute exam by a trained Vet--preferrably one who is Board certification by the American College of Veterinary Internal Medicine, Specialty of Cardiology . This certification is considered by the American Veterinary Medical Association as the benchmark of clinical proficiency for veterinarians in clinical cardiology, and examination by a Diplomate of this specialty board is recommended. Please note, that other veterinarians may be able to perform these examinations, provided they have received advanced training in the subspecialty of congenital heart disease.

The clinical cardiac examination should be conducted in a systematic manner. The arterial and venous pulses, mucous membranes, and precordium should be evaluated. Heart rate should be obtained. Cardiac auscultation (listen to the heart) should be performed in a quiet, distraction-free environment. The animal should be standing and restrained, but sedative drugs should be avoided. Panting must be controlled and if necessary, the dog should be given time to rest and acclimate to the environment. The clinician should able to identify the cardiac valve areas for auscultation. The examiner should gradually move the stethoscope across all valve areas and also should auscultate over the subaortic area, ascending aorta, pulmonary artery, and the left craniodorsal cardiac base. Following examination of the left precordium, the right precordium should be examined in the same manner.

If the examiner detects an abnormaility (i.e. Murmmer) upon asculation--a recommendation will be made for an echocardigram to be done in order to "clear" the dog. When the dog is cleared and an OFA number is issued, A notation will also be listed on the OFA report noting that the exam included an echocardigram.

How does a Breeder use an OFA Caridac Exam?

A careful clinical examination that emphasizes cardiac auscultation is the most expedient and cost-effective method for identifying Congenital Heart Disease (CHD) in dogs. While there are exceptions, virtually all common congenital heart defects are associated with the presence of a cardiac murmur. Consequently, it is recommended that cardiac auscultation be the primary screening method for initial identification of CHD and the initial classification of dogs. Murmurs related to CHD may at times be difficult to distinguish from normal, innocent (also called physiologic or functional) murmurs. Innocent cardiac murmurs are believed to the related to normal blood flow in the circulation. Innocent murmurs are most common in young, growing animals. The prevalence of innocent heart murmurs in mature dogs (especially in athletic dogs) is undetermined. A common clinical problem is the distinction between innocent murmurs and murmurs arising from CHD and may require an echocardiogram to diagonse.

If you hear a murmur, what other tests can you do?

Definitive diagnosis of CHD usually involves one or more of the following methods:

(1). Echocardiography with Doppler studies,

(2). Cardiac catheterization with angiocardiography, or

(3). Post-mortem examination of the heart (necropsy) after a dog dies.

Other methods of cardiac evaluation, including electrocardiography and thoracic radiography, are useful in evaluating individuals with CHD, but are not sufficiently sensitive nor specific to reliably identify or exclude the presence of CHD.

The noninvasive method of echocardiography with Doppler is the preferred method for establishing a definitive diagnosis in dogs when CHD is suspected the clinical or screening examination. Echocardiography is an inappropriate screening tool for the identification of congenital heart disease and should be performed only when the results of clinical examinations suggest a definite or potential cardiovascular abnormality.

Two-dimensional echocardiography provides an anatomic image of the heart and blood vessels. While moderate to severe cardiovascular malformations can generally be recognized by two-dimensional echocardiography, mild defects (which are often of great concern to breeders of dogs) may not be identifiable by this method alone.

Doppler studies, including pulsed-wave and continuous wave spectral Doppler, and two-dimensional color Doppler demonstrate the direction and velocity of blood flow in the heart and blood vessels. Abnormal patterns of blood flow are best recognized by Doppler studies. Results of Doppler studies can be combined with those of the two-dimensional echocardiogram in assessing the severity of CHD.

Color Doppler echocardiography is used to evaluate relatively large areas of blood flow and is beneficial in the overall assessment of the dog with suspected CHD. Turbulence maps employed in color Doppler imaging are useful for identifying high velocity or disturbed blood flow but are not sufficiently specific (or uniform among manufacturers) to quantify blood velocity. It is emphasized that quantitation of suspected blood flow abnormalities is essential and can only be accomplished with pulsed or continuous wave Doppler studies. Pulsed wave and continuous wave Doppler examinations provide a display of blood velocity spectra in a graphical format and are the methods of choice for assessing blood flow patterns and blood flow velocity in discrete anatomic areas.

Cardiac catheterization is an invasive method for identification of CHD that is considered very reliable for the diagnosis of CHD. Cardiac catheterization should be performed by a cardiologist, usually requires general anesthesia, carries a small but definite procedural risk, and is generally more costly than noninvasive studies. While cardiac catheterization with angiocardiography is considered one of the standards for the diagnosis CHD, this method has been supplanted by echocardiography with Doppler for routine evaluation of suspected CHD.

Necropsy examination of the heart should be done in any breeding dog that dies or is euthanized The hearts of puppies and dogs known to have cardiac murmurs should always be examined following the death of the animal. A post mortem examination of the heart is best done by a cardiologist or pathologist with experience in evaluating CHD. While it is obvious that necropsy cannot be used as a screening method, the information provided by this examination can be useful in guiding breeders and in establishing the modes of inheritance of CHD.

Can you miss a Cardiac realted problem with these tests?

Of course you can. Limitations exist for each of the methods of evaluation we have discussed. Any of the above tests may be associated with false positive and false negative diagnoses. It must be recognized that some cases of CHD fall below the threshold of diagnosis. In other cases, a definitive diagnosis may not be possible with currently available technology and knowledge.

These limitations can be minimized by considering the following general guidelines:

(1). The results to the examinations described above are most reliable when performed by an experienced individual with advanced training an experience in cardiovascular diagnosis.

(2). Echocardiography with Doppler, cardiac catheterization, and post-mortem examination of the heart for CHD requires advanced training in cardiovascular diagnostic methods and the pathology and pathophysiology of CHD.

(3). Examinations performed in mature dogs are most likely to be definitive. This is especially true when considering mild congenital heart defects. Innocent heart murmurs are less common in mature animals than in puppies are less likely to be a source of confusion. Furthermore, the murmurs associated with some mild congenital malformations become more obvious after a dog has reached maturity. While it is quite reasonable to perform preliminary evaluations and provide provisional certification to puppies and young dogs between 8 weeks and 1 year of age, final certification, prior to breeding, should be obtained in mature dogs at 12 months of age or older.

(4). Examination conditions must be appropriate for recognition of subtle cardiac malformations. Identification of soft cardiac murmurs is impeded by extraneous noise or by poorly restrained, anxious, or panting dogs.

(5). A standardized cardiac clinical examination must be performed according to a predetermined and clearly communicated protocol. Physical examination and cardiac auscultation should be used as the initial method of cardiac evaluation. If the clinical (as indicated above).

(6). Examiners who perform echocardiography with Doppler must use appropriate ultrasound equipment, transducers, and techniques. Such individuals should have advanced training in noninvasive cardiac diagnosis and should follow diagnostic standards established by their hospital and by the veterinary scientific community, including standards published by the American College of Veterinary Internal Medicine, specialty of Cardiology (J Vet Internal Med 1993;7:247-252).


From January 1974 to December 2008, a total of 1,810 Mastiff have had Cardiac OFA exams completed. The Mastiff ranks 31st of all breeds examined in the occurrance of heart/Cardiac disease. Thankfully, 99.2% are normal with only 0.4% affect by CHD; the remaining 0.4% had equivocal results.

Hopefully, as more breeders utilize the OFA cardiac exam to clear their dogs before breeding, we can continue to improve the cardiac health of our breed.

Please refer any comments or questions to me at Thank you. Catie Arney Kiokee Mastiffs

Health Testing-Patella problems in Mastiffs-Patella Luxation?

Any breed can have problems with the patellas. OFA offers a Certification for patellas after the age of 12 months which requires a Hands on exam by a vet. No x-rays or sedation is needed. The information below can be found on the OFA site at

What is Patellar Luxation?

The patella, or kneecap, is part of the stifle joint (knee). In patellar luxation, the kneecap luxates, or pops out of place, either in a medial or lateral position. Bilateral involvement is most common, but unilateral is not uncommon. Animals can be affected by the time they are 8 weeks of age.

The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can be seen to twist laterally as weight is placed on the limb.

Patellar Luxation Categories

Patellar luxations fall into several categories:

(1). Medial Luxation in Toy, Miniature, and Large Breeds-which includes Mastiffs
(2). Lateral luxation; toy and miniature breeds-excludes Mastiffs
(3). Lateral luxation; large and giant breeds-the most common type found in Mastiffs.
(4). Luxation resulting from trauma- various breeds, of no importance to the certification process.

Numbers 1, 2 and 3 are either known to be heritable or strongly suspected.

Medial Luxation in Toy, Miniature, and Large Breeds-Although the luxation may not be present at birth, the anatomical deformities that cause these luxations are present at that time and are responsible for subsequent recurrent patellar luxation.

Patellar luxation should be considered an inherited disease.

What are the signs of Patella Luxation?

The Clinical Signs of patella luxation can be easily identified with an exam often as early as 8 weeks of age. A good Breeder will have all puppies health certified by a Vet before placement and this simple exam should be done at that time.

There are some very distinct clinical signs of patella Luxation that a vet may look for dependeding upon the age of the puppy/dog. Three classes of patients are identifiable:

Neonates and older puppies- often show clinical signs of abnormal hind-leg carriage and function from the time they start walking; these present grades 3 and 4 generally.

Young to mature animals -with grade 2 to 3 luxations usually have exhibited abnormal or intermittently abnormal gaits all their lives but are presented when the problem symptomatically worsens.

Older animals-with grade 1 and 2 luxations may exhibit sudden signs of lameness because of further breakdown of soft tissues as result of minor trauma or because of worsening of degenerative joint disease pain.

Signs vary dramatically with the degree of luxation. In grades 1 and 2, lameness is evident only when the patella is in the luxated position. The leg is carried with the stifle joint flexed but may be touched to the ground every third or fourth step at fast gaits. Grade 3 and 4 animals exhibit a crouching, bowlegged stance (genu varum) with the feet turned inward and with most of the weight transferred to the front legs.

Permanent luxation renders the quadriceps ineffective in extending the stifle. Extension of the stifle will allow reduction of the luxation in grades 1 and 2. Pain is present in some cases, especially when chondromalacia of the patella and femoral condyle is present. Most animals; however, seem to show little irritation upon palpation.

Lateral Luxation in Toy and Miniature Breeds
Lateral luxation in small breeds is most often seen late in the animal's life, from 5 to 8 years of age. The heritability is unknown. Skeletal abnormalities are relatively minor in this syndrome, which seems to represent a breakdown in soft tissue in response to, as yet, obscure skeletal derangement. Thus, most lateral luxations are grades 1 and 2, and the bony changes are similar, but opposite, to those described for medial luxation. The dog has more functional disability with lateral luxation than with medial luxation.

Clinical Signs -In mature animals, signs may develop rapidly and may be associated with minor trauma or strenuous activity. A knock-knee or genu valgum stance, sometimes described as seal-like, is characteristic.

Sudden bilateral luxation may render the animal unable to stand and so simulate neurological disease. Physical examination is as described for medial luxation.

Lateral Luxation in Large and Giant Breeds

Also called genu valgum, this condition is usually seen in the large and giant breeds. A genetic pattern has been noted, with Great Danes, St. Bernards, and Irish Wolfhounds being the most commonly affected. Components of hip dysplasia, such as coxa valga (increased angle of inclination of the femoral neck) and increased anteversion of the femoral neck, are related to lateral patellar luxation. These deformities cause internal rotation of the femur with lateral torsion and valgus deformity of the distal femur, which displaces the quadriceps mechanism and patella laterally.

Clinical Signs Bilateral involvement is most common. Animals appear to be affected by the time they are 5 to 6 months of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can often be seen to twist laterally as weight is placed on the limb.

Who do you diagnose Patellar Luxation ?

The dog is examined awake (chemical restraint is not recommended) and classified by the attending veterinarian according to the application and general information instructions. The veterinarian then completes the application form indicating the the results of the dog's patella evaluation.

The application and fee can then be mailed to OFA. The attending veterinarian and owner is encouraged to submit all evaluations, whether normal or abnormal, for the purpose of completeness of data. There is no OFA fee for entering an abnormal evaluation of the patella in the data bank.

A breed database number will be issued to all dogs found to be normal at 12 months of age or older. The breed database number will contain the age at evaluation and it is recommended that dogs be periodically reexamined as some luxations will not be evident until later in life.

Preliminary Evaluations

Evaluation of dogs under 12 months of age is encouraged if the owner desires to breed at this age. The most opportune time to gather breeding data is at 6-8 weeks of age prior to the puppy's release to the new owner.

How does OFA Grade Patellar Luxation?

The Patellar Luxation Database is for dogs 12 months and over. Examinations performed on dogs less than 12 months will be treated as Consultations and no OFA breed numbers will be assigned.

A method of classifying the degree of luxation and bony deformity is useful for diagnosis, and can be applied to either medial or lateral luxations by reversing the medial-lateral directional references. The position of the patella can easily be palpated starting at the tibial tubercle and working proximal along the patellar ligament to the patella.

Grade 1

Manually the patella easily luxates at full extension of the stifle joint, but returns to the trochlea when released. No crepitation is apparent. The medial, or very occasionally, lateral deviation of the tibial crest (with lateral luxation of the patella) is only minimal, and there is very slight rotation of the tibia. Flexion and extension of the stifle is in a straight line with no abduction of the hock.

Grade 2

There is frequent patellar luxation, which, in some cases, becomes more or less permanent. The limb is sometimes carried, although weight bearing routinely occurs with the stifle remaining slightly flexed. Especially under anesthesia it is often possible to reduce the luxation by manually turning the tibia laterally, but the patella reluxates with ease when manual tension of the joint is released. As much as 30 degrees of medial tibial torsion and a slight medial deviation of the tibial crest may exist. When the patella is resting medially the hock is slightly abducted. If the condition is bilateral, more weight is thrown onto the forelimbs.

Many dogs with this grade live with the condition reasonably well for many years, but the constant luxation of the patella over the medial trochlear ridge of the trochlea causes erosion of the articulating surface of the patella and also the proximal area of the medial lip. This results in crepitation becoming apparent when the patella is luxated manually.

Grade 3

The patella is permanently luxated with torsion of the tibia and deviation of the tibial crest of between 30 degrees and 50 degrees from the cranial/caudal plane. Although the luxation is not intermittent, many animals use the limb with the stifle held in a semi flexed position. The trochlea is very shallow or even flattened.

Grade 4

The tibia is medially twisted and the tibial crest may show further deviation medially with the result that it lies 50 degrees to 90 degrees from the cranial/caudal plane. The patella is permanently luxated. The patella lies just above the medial condyle and a space can be palpated between the patellar ligament and the distal end of the femur. The trochlea is absent or even convex. The limb is carried, or the animal moves in a crouched position, with the limb flexed.


If one reviews the statisical data collectedby OFA, Mastiffs only have a 0.3% of patella luxation occurance. However, it is not a health screening done frequently by most breeders. Hips and elbows are the most common OFA exam for Mastiffs.

IMO-since the certification process only involves an exam and does not require any sedation, I feel all dogs should have this health screening before breeding. Of course, that's just my opinion.

Please feel free to contact me with any questions or comments at Thank you. Catie C. Arney

Health testing--What is elbow dysplasia?

Well, have you recovered from learning about Hip dysplasia? Elbow dysplasia should be slightly easier to discuss since currently we only use one method for evaluation--OFA. The following information is condensed from the OFA site. For further information, please refer to .

Elbow dysplasia is a general term used to identify an inherited polygenic disease in the elbow of dogs. Three specific etiologies make up this disease and they can occur independently or in conjunction with one another. These etiologies include:

(1) Pathology involving the medial coronoid of the ulna (FCP)

(2) Osteochondritis of the medial humeral condyle in the elbow joint (OCD)

(3) Ununited anconeal process (UAP)

Studies have shown the inherited polygenic traits causing these etiologies are independent of one another. The most common Clinical sign an owner may see in their dog is lameness which may remain subtle for long periods of time. No one can predict at what age lameness will occur in a dog due to a large number of genetic and environmental factors such as degree of severity of changes, rate of weight gain, amount of exercise, etc.

Since Subtle changes may occur over time, it often taks a vet exam to note any excessive inward deviation of the paw which raises the outside of the paw so that it receives less weight and distributes more mechanical weight on the outside (lateral) aspect of the elbow joint away from the lesions located on the inside of the joint and affects the appearence of lameness in the gait. Range of motion in the elbow is also decreased. One may notice a stiffness in the front legs as the dog gets up and down.

What Does Elbow Dysplasia look like?

The most sensitive view used to diagnose secondary degenerative changes in the elbow joint is an extreme flexed medio-lateral view of the elbow (Figure 1) which is required by the OFA and recommended by the International Elbow Working Group. The veterinary radiologists are most interested in the appearance of the anconeal process of the ulna.

When there is instability of the elbow joint due to elbow dysplasia, one of the most sensitive radiographic findings is new bone proliferation (osteophytes) on the anconeal process of the ulna (Figure 2) associated with secondary developmental degenerative joint disease.

Sometimes the associated Bone proliferation can be very subtle to visualize in some dogs and may require the use of a special light source (hot light) rather than a traditional view box to diagnose it. Other arthritic findings such as sclerosis in the area of the trochlear notch of the ulna and bone spurs at joint edges are also reported and wwould be mostlikely seen in advanced cases.

If fragmentation of the medial coronoid only involves the cartilage, it may not be seen radiographically but occasionally if the bone is also fragmented, it can be visualized as a separate calcific opacity superimposed over the radius (Figures 3 and 4).

Evaluating and Grading the Elbow

For elbow evaluations, there are no grades for a radiographically normal elbow. Normal is normal. The only grades involved are for abnormal elbows with radiographic changes associated with secondary degenerative joint disease.

Like the hip certification, the OFA will not certify a normal elbow until the dog is 2 years of age. The OFA also accepts preliminary elbow radiographs. To date, there are no long term studies for preliminary elbow examinations like there are for hips, however, preliminary screening for elbows along with hips can also provide valuable information to the breeder.

Grade I Elbow Dysplasia-Minimal bone change along anconeal process of ulna (less than 3mm).

Grade II Elbow Dysplasia-Additional bone proliferation along anconeal process (3-5 mm) and subchondral bone changes (trochlear notch sclerosis).

Grade III Elbow Dysplasia- Well developed degenerative joint disease with bone proliferation along anconeal process being greater than than 5 mm.

Some breeders believe that Grade I elbows are within the “normal” range, much like Fair hips are considered to be within the normal range. What is the OFA’s position on this?

The OFA’s distinction between normal and abnormal elbows is actually more clearly defined than are the differences between fair and borderline hips. Elbows are diagnosed as dysplastic when evidence of Degenerative Joint Disease (DJD) is present as evidenced by osteophytes or sclerosis. Thus, DJD is a "symptom" of ED.

It is not a gradual continuum from normal to abnormal, in which minor differences might be interpreted as normal by one reader and abnormal by another. The degree of DJD present is the determining factor in the grade of dysplasia.

The term “degenerative joint disease” is often misunderstood and misinterpreted. “Degenerative” is defined as some distinct change from a normal state to a diseased state. It does not imply a continuing process in which the disease will progress and worsen continuously over time, and it is incorrect to assume that a dog with Grade I ED will eventually develop Grade II or III ED.

It is also important to understand that DJD is a finding which aids in the diagnosis of elbow dysplasia, but the DJD itself is the secondary result of one or more of three distinct "causes" of ED(listed above) that make up the generalized description of elbow dysplasia.

My dog has never limped. How can it have elbow dysplasia?

The radiographic evidence of ED, the presence of secondary DJD, and the clinical presentation do not correlate directly. Grondalen did a study and reported on a population of 207 Rottweilers affected with ED and 141 were not lame. Yet 68% of the non-lame dogs had DJD of the elbow.

Another ED study by Read reported on serial radiographic (x-rays) and physical examination of 55 Rottweilers at 6 and 12 months of age. At 6 months of age the majority of lame dogs did not have radiographic evidence of ED; however, by 12 months of age the radiographic changes were apparent. But the majority of dogs remained sound.

Like hip dysplasia, many dogs affected with Grade I ED do not exhibit lameness; and like hip dysplasia, breeders cannot depend on using clinical signs to diagnose the disease. Dogs with minimal pathology involving the medial coronoid process may not always present clinical lameness, as the DJD and fibrosis of soft tissues may actually help to stabilize the joint. It is very likely that using lameness as a guideline to accept the diagnosis of ED would permit an increased incidence of disease genes to proliferate in the breeding population.

My Vet says my dog has Elbow dysplasia, but it doesn' t limp. Can I breed it?

The OFA acknowledges that breeding decisions are personal and that health testing is a tool to be used by the breeder. So, they will not tell a breeder NOT to breed a dog. . OFA and MCOA (Mastiff Club of America) do not regulate breeding practices or impose testing requirements.

The OFA’s main function still remains to provide breeders with the tools and information to make more informed breeding decisions and their purpose remains to assist breeders in reducing the incidence of genetic disease including elbow dysplasia.

The OFA strongly recommends that dogs from the "at risk breeds "being considered for a breeding program, as well as their siblings, be radiographed to determine their elbow status. This information should be an important and carefully considered part of breeding decisions.

Can a dog only have Elbow Dysplasia in one elbow?

Since an injury can lead to the changes associated with ED , sometimes you will note that an injury may cause a dog to get a "fail"in one elbow. As a breeder--this then becomes a judgement call. IMO-if it was "genetic" both elbows would have and demonstrate changes. IF a dog has no other "joint" issues (i.e the other elbow and both hips are normal) and there are no related dogs (1/2 and full siblings, parents, and grandparents) with ED---I do not consider ED in one elbow as genetic.

Breeding a dog that has ED in one elbow is a judgement call. I have used a stud dog that has ED in one elbow--but he had been bred before and had never produced ED and he also has a Vet documented injury to that elbow. My Vidalia injuried her right elbow at age 22 months--twisting and damaging the joint in a fall down some icy steps.

When I did her pernament OFAs, her right elbow did not pass. I had pre-limned her at 10-12 months and knew her elbows were normal; I had witnessed her injury--so I bred her. None of her puppies have ever developed ED--nor have any on her grandpuppies. I also knew that none of her 1/2 and full siblings had ED--and her grand parents were clear. By knowing all the doigs behind in her pedigree, I was confident that her failed elbow was due to the previous injury and was not genetic.


It is only through a proper exam (x-ray) and evaluation can elbows be "cleared" of elbow dysplasia and be determined to be "normal". If siblings (full or 1/2 brother and sisters) have bilateral ED, one could predict that a littermate or sibling would have an increased risk of having or passing on ED.

It is essential to any breeder to fully know the health issues within the lines of the dogs they breed. Health testing is not a 100% guarrentee, but it can certainly stack the odds in your favor to produce a sound healthy puppy.

Please feel free to foward any questions or comments to me at Thank you. Catie Arney