Saturday, December 12, 2009
We lost Mitch's dad in March 2009. Pop developed kidney failure and required dialysis 3 times a week. It took everyone's cooperation to care for him, but we were able to keep him at home. Pop was a proud man, strong willed and a bit stubborn--but we loved him and honored his wishes. The last few months were hard, but he knew we loved him. We will miss him.
In April, Mitch went out on the road driving long distance. For 6 months, he gave it his best shot--but he just was not happy being away from home. So back home he came. He got lucky, and took a job here close to home--so now I get to cook every night! LOL!
We had another big event in April--my daughter Amiee and her husband, JR became the proud parents of a baby boy--John Richard Snow. FINALLY! We have a boy in this family! Needless to say, we all think he is very special. John is named for his grandfathers--Amiee and JR's dads. I think he is going to be a redhead--so he does have just a little bit of Cook (my maiden name) in him after all! LOL!
Both my old ladies--Vidalia and Zena made it through the winter. Zena had been completely deaf for the last 3 years, and her eye sight was failing her. At one point during the winter, she stopped eating--and I felt sure the end was near. But she improved and began eating again, and was her old self again. Zena would spend most of the day lying on the south side of the house, waiting and watching for me to come home each day. She would always greet me as I opened the car door to give me a kiss. Vi developed problems with her right front leg--Initially I thought is was arthritis in an old elbow break--but an x-ray showed a tumor and we suspected the worst.
Both these grand old ladies left me in April. It was a sad day and extremely hard to say good bye to both of them on the same day. Zena was 1 month short of 13 and Vi was 2 months short of 12 years. These old girls were the last of my Maddie daughters and the heart of my breeding program. I see so much of each of them in their kids and grand kids. They will always be special in my heart.
In May, we went to Fontana Dam, NC and the MCOA National Speciality. So many beautiful Mastiffs from all over the country--what an experience. Diesel got 3rd in Open Fawn--Jimbo made the cut in the 12-18 month class, Gracie was shown in the BBE class, and Cooter was showed in the BOB competition. It was a great experience and one I hope to be able to repeat again.
We also showed at a few shows in June. Gracie's litter sister--Hope (Ch. Kiokee Lionhearted Hope and a Prayer) won BOB over 7 male specials at the Asheville, NC Show. Hope was proudly shown by her owner. Lillian Tolley Welenc. It was a wonderful win for Hope and Lillian.
In July, we finished Gracie (Ch. Kiokee Lionhearted Amazin" Grace) at the Greenville, SC shows. Gracie finished from the BEE class and is qualified to be entered at Eukanuba for 2009 & 2010. Gracie also turned 2 in July. When we get her health testing completed, we have a lovely breeding planned for her in 2010.
We spent most of August and September raising a litter of puppies--Rose & Leo's-- that we co-owned. It was a lot of work, but it was a good change. This was the first litter we have had here in almost 2 years. Rose was a wonderful mother and she produced some lovely puppies.
In October, we welcomed a new face here at Kiokee. A beautiful bullmastiff girl--Starrdogs SYLO at Kiokee--bred by Kathy Roberts of Acworth, Georgia. From day one, she came into this house and stole our hearts--esp. Mitch's. Sylo is a bundle of energy and very different from the Mastiffs! She is best friends with Gidget. She reminds he of her sire--Ch. Starrdogs He's A Player--who was one of the top ranked Bullmastiffs in 2009. We look forward to showing her in 2010.
In November, Our Mona delivered us 2 beautiful Brindle boys that look so much like their sire--Boss. Sadly we lost her a few hours after the c-section. Although, I know this is a chance we take anytime we breed one of our girls--Mona was the first Mother I have lost in 25+ years of breeding. The first few days were rough, but both of these little men (T-Beau and Piggy) were robust and healthy. I think they will do their Momma proud.
We hope to get back out and start showing again in 2010. We have some nice breedings planned and we have a few changes planned for 2010. We hope that all of our friends and family have a warm and happy holidays.
We wish you a happy and healthy 2010. Catie
Wednesday, November 11, 2009
First of all--never buy any puppy as a "surprise" gift for someone. How can you be sure that the recipient is ready and willing to care for a pet? How do you know they want a pet--and how do you what kind of pet is right for them?
As a breeder--I would NEVER sell a puppy that is to be given as gift. What happens to the puppy if the new owner doesn't want it--or can't provide for it? Giving a puppy as a "gift" is not a reason to buy a puppy. No ethical breeder would ever sell a puppy to be given to a second party-esp. someone they have never met or interviewed.
Secondly--the holidays can be stressful and confusing for us humans--how do you think a new puppy would feel? The confusing and ever changing environment can be overwhelming for a 8-10 week old puppy. Most children would quickly forget and ignore a puppy for the other more entertaining presents. Who is responsible for it's care? In most cases the puppy get shuffled off to a crate somewhere out of the way. Visitors coming into your home can present a management problem, too--esp. children who do not know proper pet etiquette. Too many changes and too many stressors.
Anytime you bring a new puppy into your home, the first few weeks should be kept as stress-free as possible with no changes in your home routine. Your puppy will adapt and fit in much quicker and easier if your home routine is stable. The holidays are not the time for "routine".
Some new owners think nothing about placing their "brand" new puppy in a boarding Kennel for a few days up to a couple of weeks while they leave and go out of town. This places the puppy is a very dangerous position to be exposed to illness and to suffer emotional trauma due to the separation and isolation from it's family. Talk about Stressors!
Those of us who work with rescue also see an influx of 6-7 month old (and older) puppies a few months after Christmas. The "cute" is gone; the puppy is not housebroke; the puppy is untrained; the puppy has behavior problems; They are just too "busy" for the dog, the puppy was a "gift" and now they don't want it.
At about this same time, We also begin to see the unsold Older Christmas puppies show up in animal shelters--once the cute is gone, they can't be sold--so they are dumped to make room for the next litter of "cute" puppies. Christmas gift puppies just are not a good idea.
So for all of you potential puppy buyers who are looking for a "Christmas puppy"--don't call me. I do not and never will sell or place puppies during the holidays.
It is my humble opinion that the holidays is not the best possible time for a puppy to enter your home. Boarding any puppy before it has completed it's puppy shot series is just asking to have your puppy get sick--or die. I always offer a "come to Grand-Ma's house" for my puppy owners--if they need to leave and go on Vacation--their dog can come back to saty with me. I don't like to see my puppies boarded until they are at least 2 years old.
The stress and turmoil of the holidays could also set up behavior issues that could take you months to correct and possible alter your dog's temperament for the rest of it's life. Often what we as humans view as insignificant can be life-altering to a puppy and lead to the development of a behavioral problem. I.E.: Visiting relative's children who are too rough with a puppy could alter it's attitude toward children leading to a lifetime distrust of children.
So as a parent, grand-parent, breeder, and dog owner; my advice is don't get your kids a puppy for Christmas. Wait until after the first of the year--put up your holiday decorations, settle back into your home routine, and then bring your new baby home.
A puppy is not a "fad" gift or a holiday whim. A dog is forever. Before getting your new canine family member, Please wait until you and your family are prepared and ready. Make it a homecoming you will always remember.
Catie C. Arney, Kiokee Mastiffs, Hickory, NC
Monday, July 6, 2009
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.
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.
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.
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.
slow heart rate (bradycardia) / cardiac arrhythmias / cardiomyopathys/ Gastrointestinal Disorders constipation / diarrhea / vomiting.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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 email@example.com. Thank you. Catie Arney Kiokee Mastiffs
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.
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.
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.
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.
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.
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 firstname.lastname@example.org. Thank you. Catie C. Arney
(1) Pathology involving the medial coronoid of the ulna (FCP)
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 email@example.com. Thank you. Catie Arney
Monday, March 9, 2009
What is Canine Hip Dysplasia (CHD)?
Canine Hip Dysplasia can affect millions of dogs each year and can also result in debilitating orthopedic disease of the hip. Many dogs will suffer from osteoarthritis, pain, and lameness costing owners and breeders millions of dollars in veterinary care, a shorten lifespan and reduced quality of life for affected dogs. The occurrence of HD is well documented in Mastiffs as well as many other large and giant breeds and is also prevalent in many toy and small dog breeds as well as cats.
The term hip dysplasia(HD) can be interpreted as the abnormal or faulty development of the hip. Abnormal development of the hip causes excessive wear of ther joint cartilage during weight bearing, eventually leading to the development of arthritis, often called degenerative joint disease (DJD) or osteoarthritis. The terms DJD, arthritis, and osteoarthritis are often used interchangeably.
Hip dysplasia was first described in 1937 by Dr. Gerry B. Schnelle in a paper entitled Bilateral Congenital Subluxation of the Coxofemoral Joints of a Dog. He wrote: "the condition described herein, rare thought it may be, should be recognized as being congenital and potentially hereditary, and the dog or bitch in which it occurs should be destroyed or sterilized in the eugenic interests of the breed."
In 1966, Henricson,Norberg, and Olsson refined the definition of CHD describing it as: "A varying degree of laxity of the hip joint permitting sublaxation during early life, giving rise to varying degrees of shallow acetabulum and flattening of the femoral head, finally inevitably leading to osteoarthritis."
Today, the general veterinary consensus is that hip dysplasia is hip laxity resulting in osteoarthritis.
Just by defination alone, we can see that CHD is a disease of complex factors based primarily on inheritance, and why ethical dog breeders and Veterinarians have attempted to eliminate CHD through selective breeding and care.
What is a Dysplastic Joint?
Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) which it can eventually produce that leads to pain, overall loss of range of motion in the hip joints, and debilitation.
The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged.
With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement.
Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells.
The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases.
No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.
FYI-One can not just "look" at the movement of a dog and determine that it does not have CHD. Only through x-rays can we determine if a dog is clear of hip dyspasia. As a breeder, one must evaluate any dog to be bred and determine if it is free of hip dysplasia before breeding!
How do you Test for CHD?
One "tests" for CHD by x-raying hips. This simply assures the breeder that the dog being bred does not have CHD. When a breeder health tests for CHD, it is the hope that with each succeeding generation that is bred from clear dogs, the puppies produced should have improved/better hips. OK. So what does these "scores" mean?
To a beginner, just looking at the hip "scores" can be confusing. What do they mean and how are they interprettted? Which ones are best? Here is the United States, the most common methods of evaluating hips is the OFA (Orthopedic Foundation for Animals) and the Penn Hip system (University of Pennsylvania Hip Improvement Program). Since many Mastiffs have imported lines from England, we will also look at the system used in the United Kingdom (England) and Austrialia : the British Veterinary Association (BVA).
When it comes to testing, various breeders have different opinions to which system is better and many a heated debate can result from discussing the pros and cons of each system. For the purpose of this entery, I will only discuss the basics priniciples of each system so as to provide an explaination. The most important aspect is to test and vertify your dogs are clear of hip dysplasia before breeding irregardless of the system you use. PERIOD.
The Good (Figure 2) classification is slightly less than superior (excellent) but a well-formed congruent hip joint is visualized. The ball fits well into the socket and good coverage is present.
The Fair (Figure 3) classification is assigned where minor irregularies in the hip joint exist. The hip joint is wider than a Good hip phenotype which is usually due to minor joint incongruency ( i.e. the ball slightly slips out of the socket). There may also be slight inward deviation of the weight-bearing surfaces of the socket(dorsal acetabular rim) causing the socket to appear shallow (Figure 4). This can be a normal finding in some breeds (i.e. Chinese Shar Pei, Chow Chow, and Poodle).
Thus, the higher the BVA score the greater the degree of dysplasia. I have provided a comparison to the OFA ratings in the table at the end of this entry.
International Hip Score Comparison Table
Copyright 1998 Tamaryn Hodge
This table is provided as an un-official means of comparing international hip scores, as there is currently no official FCI comparison data available for all countries listed here. Total accuracy cannot therefore be guaranteed. Please e-mail the originator at BritishLeos@aol.com with any corrections. Thanks from the originator goes to the following people for their assistance in creating this table: Arthur Muller, Gerie Groenendijk, Waltraut Zieher, Yves De Clerq, Susan Grosslight, Glen Ferguson, Jenny Bergdahl.
No signs of hip dysplasia
El - dysplasiaa "hyval"
Negatief geheel gaaf (1)
Kein Hinweis fuer HD
Total score of 0 - 4
No signs of hip dysplasia
El - dysplasiaa
Negatief niet geheel gaaf (2)
Kein Hinweis fuer HD
Total score of 5 - 10
Transitional Case (Tc)
Obergangs - form verdaechtig fuer HD
Total score of 11 - 18
Transitional Case (Tc)
Obergangs - form verdaechtig fuer HD
Total score of 18+
Licht positief (3)
Total score of 18+
Licht positief (3)
Total score of 18+
Total score of 18+
Total score of 18+
Total score of 18+
Positief optima forma (5)
Total score of 18+
Pleaase forward any comments or questions to firstname.lastname@example.org. Thank you. Catie Arney Kiokee Mastiffs