Mastiff Health
Cystinuria Update 6/17/2011
Dr. Paula Henthorn and her colleagues have found a set of DNA Markers for at least one type of Cystinuria in Mastiffs that are found in two copies (one from mom & one from dad) in intact male boys that have formed stones between 1 1/2 years and 4 years of age and.......
when there is only one copy of the "bad" version of the markers, some of the intact boys have elevated cystine in the urine and some of those form stones (usually at an older age, but they have seen a range from 3 years to 9 years of age when the dog first forms stones), and yet other dogs with only one copy of the "bad" markers don't have elevated cystine.
Dr. Henthorn said she is hoping to turn this finding into a DNA Marker test for Mastiffs in the next few months.
She also let us know that a number of Cystinuria positive boys that are neutered stop dumping excess cystine into their urine, so neutering appears to be a treatment for the disease, and should prevent stone formation. While Drs. Henthorn and Giger have seen this in a number of dogs (at least ten), please contact the researchers if you know of a Cystinuria positive dog that still tested positive more than a month after he was neutered. It is important to determine if neutering will lower the urine cystine levels for all dogs with elevated urine cystine.
We will need to continue testing the urine of the intact boys (at least two tests at or after 24 months of age) that have no copies, or only one copy to help figure out the other form of Cystinuria (remember that there are some boys that do NOT have the bad marker but have elevated cystine in the urine). While there have been NO reports of stones from the C+ boys that do not have the bad marker, the researchers do not have DNA from very many dogs that don't carry the bad marker, so they need to keep looking.
Good News: we'll have a genetic DNA marker test for both females and male Mastiffs that will predict which male puppies are at risk for early stone formation and which breeding pairs are at risk for producing these boys, AND neutering should help prevent the males from expressing the disease (in both the dogs that form stones early and those that form stones later). In other words, the new DNA Marker test will help us identify the male Mastiffs that are at a high risk of forming stones and it will identify both the males and
females that have the bad markers which will help us make our breeding decisions and eventually breed this problem out of our gene pool. Knowing that neutering has a good chance of curing the disease gives us many more options for managing this disease, both for individual dogs, and for our beloved breed.
Other News: We will need to continue the research to fully understand it all...
We'll send out more announcements to let everyone know when the Cystinuria
DNA Marker Test is available for Mastiffs.
Please share the news with everyone you know that has Mastiffs.
Anna
Cystinuria
AKC Canine Health Foundation Grant 1388-A: Validation of a SNP Haplotype Associated with Mastiff Cystine Stone Formation for Use in Genetic Testing Primary Investigator: Dr. Paula S. Henthorn, PhD Institution: University of Pennsylvania - School of Veterinary Medicine Sponsor(s): Danny's Fund, Joe & Carla Sanchez of Southport Mastiffs, Mastiff Club of America, Mastiff Club of America Charitable Trust
“Cystinuria is an inherited disorder that causes kidney and urinary tract stones in dog, man and other animals and has been
documented in over 60 breeds of dogs. In humans, mutations in the protein-coding regions of two genes are found in affected individuals. In some dog breeds, cystinuria is an autosomal recessive trait caused by mutations in one of the genes. However, in
many dog breeds, the genetic basis of cystinuria is much more complex. We recently obtained data suggesting:
1) that in at least one breed of dogs (Mastiffs), DNA changes near one of the "cystinuria genes" are associated with early cystine
stone formation, and
2) that gender and reproductive status may affect the level of cystine in the urine. Our most recent study has more precisely defined the region associated with early cystine stone formation in Mastiffs and analyzed DNA polymorphisms from the region in additional dogs. The data generated further supports the finding that polymorphisms near one of the cystinuria genes are associated with high risk of early stone formation.
In summary, the studies indicate that it will be possible to develop a DNA-based test for breeders to use to reduce the incidence of particular (but not all) cystinuria predisposing alleles in the Mastiff.” We will share more updates as they become available! Although it appears that we are getting much closer to a DNA Marker test for at least one type of Cystinuria in Mastiffs, there is more research that needs to be done as this is a very complex disease in Mastiffs with genetic polymorphisms and it appears that there are environmental and metabolic influences that are associated with the gene expression of this genetic disease in our breed.
Reminder: If you have a dog that has tested positive on a nitroprusside urine test or that has formed cystine stones,
PLEASE send blood and urine to UPenn to have your dog added to the research study and let them know what you've been
feeding and giving your dogs. And please share this information with anyone with a cystinuric dog to encourage them to participate
in the research, too! http://www.mastiff.org/ CYSTINURIARESEARCH.htm
If you are planning on neutering your Cystinuria positive dogs, please contact Dr. Henthorn and make arrangements to donate
blood and urine before the neuter and then monthly urine samples after the surgery. Treat the blood & urine like you're shipping semen for a special breeding. Notify Dr. Henthorn that you are shipping the samples and let her know when they will arrive. Make sure she’ll be there or that she will arrange to have someone there to receive the package. They are closed on weekends and during the holidays!
Keep the samples cool in an insulated container with frozen freezer packs and ship it overnight delivery through FedEx (NOT the United States Post Office). Track the package & call Dr. Henthorn when it arrives at UPenn to make sure she received it in good condition.
Central Kentucky Veterinary Center www.vetmail.com Georgetown, KY 502-863-0868
Beechwold Vet and Reproductive Hospital, Columbus, Ohio 614-268-8666
Dr Urlich Mostosky, OFA without sedation
269-275-4265
20250 17 Mile Rd
Marshall, MI 49068
This is Bella's story.
Our journey began on October 7, 2006. We lost our GSD of almost 13 years back in May and I thought it would be a very long time before I could find enough love in my heart for another dog. But, by the grace of God, I woke up that Saturday morning, came downstairs, and told my husband, "I have to have a puppy today!" He looked at me quizzically and gave a long "okayyyyy". So our search began in the local newspaper. I really wanted another Shepherd, but there were none listed. Tim kept searching and he said, "Hey, what about a Mastiff?" Now the only dealing I had ever had with a Mastiff was seeing a couple of them hauled around in the back of a pickup by a guy in the little town we lived in. And, we had no idea there was a difference between a Mastiff and a Bullmastiff! So, after a phone call or two later, we were on our way to go look at this person's puppies. She had 3 puppies remaining to choose from, 2 fawns and an apricot. We wanted a fawn female, but the only fawn female kept running away and hiding under the table. This cute little apricot girl just kept coming up to us and really just stole our hearts. So, we paid the lady and came home with our girl! At the time we were told she was 8 weeks old. We were calling her "Bella" (pronounced Bay-ah) which is Spanish for beautiful. Upon filling out the registration papers, we noticed that her date of birth was 8/22/06, which put her at only 6 weeks old. The "breeder" was from Eastern WA but had these pups over in Western WA for the past 2 weeks trying to get them sold. This means they had been away from their mother since 4 weeks of age. (This should have been our first red flag)
After having her home for 6 days she began having diarrhea and vomiting. We ran her in to the Emergency Vet who immediately ran a test for Parvo. Thankfully she was negative! They suspected some kind of bacterial infection. After giving her a bolus of fluids and $180 later, we brought her home with instructions for a special diet. She recovered fully after a few days. Approximately a week later she began urinating blood. Her diagnosis was cystitis, for which she was given antibiotics. Two days after finishing her round of antibiotics, we were back at the vet with cystitis again. By the end of October we had spent approximately $1,719 on her. Her urinary tract issues continued into November with another 3 vet visits totaling approximately $191. Bella continues to have chronic urinary tract infections for which we make several trips to the vet for per year.
In January of 2007, we noticed that Bella had some strange, cloudy spots on her corneas and that she was having trouble navigating the stairs in our house. It was recommended that she see a Canine Ophthalmologist. We had heard about Mastiffs being one of the breeds prone to have PRA – Progressive Retinal Atrophy – and we were praying that this wasn't the case with our sweet girl. We took her in to see the Ophthalmologist and her diagnoses were: endothelial dystrophy (white plaques on the corneas), juvenile cataracts, CMR (Canine Multifocal Retinopathy), Micro-ophthalmia, retinal dysplasia, and entropion. We sent blood off to Opti-Gen to be tested for PRA and CMR. She tested "normal" for PRA, but "affected" for CMR. Needless to say we were heartbroken to find out that our sweet girl will eventually be totally blind, not because of the CMR, but because of the combination of the cataracts, the CMR, and the retinal dysplasia. She is not a candidate for cataract surgery because of this. She is at high risk for developing glaucoma. She is now almost 2 ½ years old and almost completely blind. To date we have spent over $800 on her ophthalmology visits and medications. Attempts to phone or email the person who sold Bella to us have gone unanswered.
Around this same time, my husband had read an article about a blind horse and how that horse was able to find its way around the pasture by following another horse which had a bell hung on its halter. The blind horse would follow the ringing of the bell. We figured "if this works for horses, why couldn't it work for our dog?!" So our search began for a "seeing-eye companion" for Bella. My husband began researching reputable Mastiff breeders to find a healthy, life-long companion for Bella. His searches brought him to a Breeder in our state and they began a series of correspondence. She was very gracious to answer all of our questions and she helped a great deal in educating us in the importance of health testing on Mastiffs. She never tried to "sell" us on one of her dogs. She places her dogs according to their temperament and where they will fit it best with family dynamics. She absolutely does not place according to gender or color of the dog. It was very clear to us that this person has a great deal of love for her dogs and wants to find homes for them with people who are willing to keep in contact for the entire duration of the pet's life. This was appealing to us because we felt like in Bella's case, we had so many questions left unanswered. She, in turn, had questions regarding Bella's diagnoses in order that she could get a more clear picture of what our needs were and what Bella's needs were going to be, so that she could make an informed decision on whether or not she would even have a puppy for our home.
She had a litter in February, 2007, and informed us that she would watch them closely as they began to mature, for the temperament that might match our home. She ultimately chose a little boy puppy for us. She described him as being "very serious and very quiet." We picked him up when he was 8.5 weeks old and brought him home. He was absolutely adorable and just as she had described him. Even as a young puppy he just seemed to "know" that there was something "different" about Bella. As he grew and their relationship grew, it became very apparent that he knew his job was to take care of her. We've never had to formally train him to be her eyes or to protect her. It's as if he's always known that she needs him. If they are out in the yard and he feels she is too far away from the house, he will "bump" her with his shoulder to redirect her toward the house, almost as if he is "herding" her. If she's defiant and continues on, he grabs her by the scruff of the neck and pulls her back. Most of the time though, he just follows closely behind her. When we call them to come inside, Boaz will either wait for her near the door, or in the case that she doesn't come quite fast enough for his liking, we say to him, "Go get Bella," and he will run off to herd her back inside. He never comes inside without waiting for her. It is really something quite phenomenal to watch. One would think this would only frustrate Bella, but in reality she looks to him for security. We've come to realize that Bella does not do well if we try to take her out anywhere without Boaz. She becomes frightened and once back home, sinks into a depression where she doesn't want to eat or even come out of her bed (kennel). An example of this is when she went in for her yearly vet check and vaccination booster. In the past she has always loved the attention she gets from everyone in the vets' office. This last time she was scared, shaking, and unsure of her steps. When we got home, it took her two days to recover enough to want to even ambulate around the house! So as an experiment of sorts, the next time we took her out, we took Boaz as well. She was confident, happy, and not insecure at all. Once we were home, she didn't exhibit any signs of being depressed. The way the two of them wrestle and play is another example of Boaz sensing her needs. He knows that her vision is limited so he's very good at not running away, asking her to pursue, but instead stays in close proximity so she can feel his whereabouts. They wrestle like a couple of kids! If she whines or barks for any reason, he is right there beside her for protection and comfort.
We wish we would've been more responsible in our education of health testing and what questions to ask and what red flags to look for. But we cannot imagine what our home would be like without Bella.
Mastiff Standard
--------------------------------------------------------------------------------
Mastiff Breed Standard
Working Group
General Appearance
The Mastiff is a large, massive, symmetrical dog with a well-knit frame. The impression is one of grandeur and dignity. Dogs are more massive throughout. Bitches should not be faulted for being somewhat smaller in all dimensions while maintaining a proportionally powerful structure. A good evaluation considers positive qualities of type and soundness with equal weight.
Size, Proposition, Substance
Size--Dogs, minimum, 30 inches at the shoulder. Bitches, minimum, 27½ inches at the shoulder. Fault--Dogs or bitches below the minimum standard. The farther below standard, the greater the fault.
Proportion--Rectangular, the length of the dog from forechest to rump is somewhat longer than the height at the withers. The height of the dog should come from depth of body rather than from length of leg.
Substance--Massive, heavy boned, with a powerful muscle structure. Great depth and breadth desirable. Fault--Lack of substance or slab sided.
Head
In general outline giving a massive appearance when viewed from any angle. Breadth greatly desired.
Eyes set wide apart, medium in size, never too prominent. Expression alert but kindly. Color of eyes brown, the darker the better, and showing no haw. Light eyes or a predatory expression is undesirable. Ears small in proportion to the skull, V-shaped, rounded at the tips. Leather moderately thin, set widely apart at the highest points on the sides of the skull continuing the outline across the summit. They should lie close to the cheeks when in repose. Ears dark in color, the blacker the better, conforming to the color of the muzzle.
Skull broad and somewhat flattened between the ears, forehead slightly curved, showing marked wrinkles which are particularly distinctive when at attention. Brows (superciliary ridges) moderately raised. Muscles of the temples well developed, those of the cheeks extremely powerful. Arch across the skull a flattened curve with a furrow up the center of the forehead. This extends from between the eyes to halfway up the skull. The stop between the eyes well marked but not too abrupt.
Muzzle should be half the length of the skull, thus dividing the head into three parts-one for the foreface and two for the skull. In other words, the distance from the tip of the nose to stop is equal to one-half the distance between the stop and the occiput. Circumference of the muzzle (measured midway between the eyes and nose) to that of the head (measured before the ears) is as 3 is to 5. Muzzle short, broad under the eyes and running nearly equal in width to the end of the nose. Truncated, i.e. blunt and cut off square, thus forming a right angle with the upper line of the face. Of great depth from the point of the nose to the underjaw. Underjaw broad to the end and slightly rounded. Muzzle dark in color, the blacker the better. Fault snipiness of the muzzle.
Nose broad and always dark in color, the blacker the better, with spread flat nostrils (not pointed or turned up) in profile. Lips diverging at obtuse angles with the septum and sufficiently pendulous so as to show a modified square profile. Canine Teeth healthy and wide apart. Jaws powerful. Scissors bite preferred, but a moderately undershot jaw should not be faulted providing the teeth are not visible when the mouth is closed.
Neck, Topline, Body
Neck powerful, very muscular, slightly arched, and of medium length. The neck gradually increases in circumference as it approaches the shoulder. Neck moderately "dry" (not showing an excess of loose skin). Topline--In profile the topline should be straight, level, and firm, not swaybacked, roached, or dropping off sharply behind the high point of the rump. Chest wide, deep, rounded, and well let down between the forelegs, extending at least to the elbow. Forechest should be deep and well defined with the breastbone extending in front of the foremost point of the shoulders. Ribs well rounded. False ribs deep and well set back. Underline--There should be a reasonable, but not exaggerated, tuck-up. Back muscular, powerful, and straight. When viewed from the rear, there should be a slight rounding over the rump. Loins wide and muscular.
Tail set on moderately high and reaching to the hocks or a little below. Wide at the root, tapering to the end, hanging straight in repose, forming a slight curve, but never over the back when the dog is in motion.
Forequarters
Shoulders moderately sloping, powerful and muscular, with no tendency to looseness. Degree of front angulation to match correct rear angulation. Legs straight, strong and set wide apart, heavy boned. Elbows parallel to body. Pasterns strong and bent only slightly. Feet large, round, and compact with well arched toes. Black nails preferred.
Hindquarters
Hindquarters broad, wide and muscular. Second thighs well developed, leading to a strong hock joint. Stifle joint is moderately angulated matching the front. Rear legs are wide apart and parallel when viewed from the rear. When the portion of the leg below the hock is correctly "set back" and stands perpendicular to the ground, a plumb line dropped from the rearmost point of the hindquarters will pass in front of the foot. This rules out straight hocks, and since stifle angulation varies with hock angulation, it also rules out insufficiently angulated stifles. Fault--Straight stifles.
Coat
Outer coat straight, coarse, and of moderately short length. Undercoat dense, short, and close lying. Coat should not be so long as to produce "fringe" on the belly, tail, or hind legs. Fault Long or wavy coat.
Color
Fawn, apricot, or brindle. Brindle should have fawn or apricot as a background color which should be completely covered with very dark stripes. Muzzle, ears, and nose must be dark in color, the blacker the better, with similar color tone around the eye orbits and extending upward between them. A small patch of white on the chest is permitted.
Faults--Excessive white on the chest or white on any other part of the body. Mask, ears, or nose lacking dark pigment.
Gait
The gait denotes power and strength. The rear legs should have drive, while the forelegs should track smoothly with good reach. In motion, the legs move straight forward; as the dog's speed increases from a walk to a trot, the feet move in toward the center line of the body to maintain balance.
Temperament
A combination of grandeur and good nature, courage and docility. Dignity, rather than gaiety, is the Mastiff's correct demeanor. Judges should not condone shyness or viciousness. Conversely, judges should also beware of putting a premium on showiness.
Approved November 12, 1991
Effective December 31, 1991
Click on links:
WHAT IS IT: "Hip dysplasia" simply stated means an "abnormal formation" of the hip joint. Think of the condition first as a looseness in a joint that should be snug - then most of the problems attendant to hip dysplasia are a result of this "looseness".
The normal anatomy of the hip joint is a classic Ball and Socket joint. The head of the femur (the "Ball") is supposed to match the acetabulum (the "Socket"). A good hip joint has a neat, snug fit between the ball and socket - that is, the head of the femur should not be slipping and slopping around somewhere in the neighborhood of the acetabulum! There are infinite variations of dysplasia - ranging from only very slight changes from normal to complete dislocation. Consequently, no two dogs will be affected by CHD exactly alike.
HOW IS CHD ACQUIRED? This is one disorder that has been proven, positively, to have a genetic basis. How much of a genetic origin in each case can vary from 25% to 85%. A condition that is completely determined by genetics, for example gender, has a Heritibility Factor of 1. A condition totally unaffected by genetics, for example a broken leg, has a Heritibility Factor of zero.
Studies have shown that CHD's Heritibility factor ranges from .25 to .85; this is a significant genetic contribution. So the Heritibility Factor for a given dog is the result of a combination of the Heritibility Factors from each parent. Simply put . . . if the parents are carrying genetic material for hip dysplasia - so will the offspring. And the greater the genetic contribution for loose hips or malformed bone or abnormal muscle mass (Heritibility Factor) from the parents, the greater the chances for hip dysplasia in the offspring.
The expression of hip dysplasia in any dog has other determinants, though; genetics play only a varying role in the total picture. The effect of the developing dog's environment does play a role in the clinical (observable) signs of dysplasia, although just like the genetic component the effects of environment are variable and not completely understood. To illustrate the complexity of the environmental issue, listen to this: It is possible for a dog with known genetic components for hip dysplasia (called genotype) to not show any clinical signs of trouble if the environmental factors are favorable. So the dog can be dysplastic and not show observable signs of it until middle or old age. This is seen commonly in practice and it is always an important issue with breeders who assume that their dog is normal just because it hasn't shown any signs of hip trouble. Why take pelvic x-rays for dysplasia when the dog has always acted perfectly fit, they reason. There is no excuse for NOT taking pre-breeding x-rays. If two dogs that have the same genotype (genetic makeup) are exposed to different environmental conditions, their expression of hip trouble can be quite dissimilar. Little wonder that the topic has such a wide range of information and misinformation regarding it.
Some of the environmental aspects that can affect the observable expression of hip dysplasia are the following:
1. Nutrition - There are reports that in puppies a restricted calorie intake could restrict the growth rate, and in turn will lessen the potential for the dog to develop hip dysplasia. (Do NOT do this to any pup... it makes as much sense as stealing money from your own checking account!) The problem is that some restricted diets restrict the fat and protein content and increase the carbohydrate content of the food. Bad! The real goal should be to keep growing pups from becoming OVERWEIGHT. Restricting fat and protein in a growing pup can be a disaster. A high quality, meat-based diet is absolutely necessary for growing pups, just don't feed so much of it that the pup becomes overweight.
2. Physical Activity - In a young, growing dog with a genotype (genetic makeup) for CHD who will eventually develop some trouble because of it, will develop more arthritis and have more eventual difficulty if it is highly active physically. Climbing stairs, jumping into and out of pick-up trucks, running with other normal dogs can all subject the growing hip structures to unwarranted stress and trauma and increase future discomfort for the dog. The effects of this excessive activity is worsened in an overweight pup. (In a normal, growing dog, all these activities will not cause hip dysplasia!) There are many activities that a fast-growing mastiff pup should not do, but this has nothing to do with CHD.
3. Bedding - There is no scientific proof, but lots of observational conclusions, that pups reared (especially during the nursing period) on slippery surfaces such as newspapers will be prone to hip difficulties. That is not to say that smooth concrete, wood or newspaper surfaces cause dysplasia, just that they can make a bad situation worse. Better surfaces for newborn pups would be blankets or towels... something they can get a better grip on.
MUSCLE AND CHD: Research has shown that dogs with CHD have significantly decreased sizes of total pelvic musculature surrounding and acting on the hip joint. Whether this is a contributing factor or a result of hip dysplasia remains to be proven.
One muscle that can contribute to worsening of hip dysplasia is the Pectineus Muscle. In dogs with a strong genetic background for CHD, the microscopic makeup and contractibility of the Pectineus Muscle are strikingly different from the same muscle of normal dogs. The theory is that a tight or inelastic Pectineus Muscle causes tension in such a direction that the force tends to pull the head of the femur away from the acetabulum. So the tight muscle creates more looseness in the joint. There have been good results in about 50% of the cases where they have surgically excised a portion of the Pectineus Muscle. The patients were more comfortable and mobile almost immediately. This Pectineal Myotomy surgery has no effect on the arthritic changes in the hip joints; it simply can make the dog more comfortable.
LIGAMENT OF THE HEAD OF THE FEMUR: Attaching to the head of the femur from the center of the hip socket is a tough fibrous ligament called the Ligament of the Head of the Femur. If this ligament is stretched or torn, the hip joint will be less stable . . . and this is exactly what happens to dogs with dysplasia. In fact, some of the first changes to take place in young dogs developing hip dysplasia occur in this ligament especially if the muscle mass of the pelvis is underdeveloped. The ligament swells, develops tiny tears and stretches. In advanced CHD this ligament can totally break down and cause more harm than good.
JOINT CAPSULE: This tissue, which if you could hold it, would feel like the wall of a thick balloon It surrounds the joint and produces synovial fluid to nourish and lubricate the joint cartilage. In addition, the joint capsule provides some support to the joint. In dysplastic joints the capsule becomes irritated, stretched, and scarred. In advanced cases the capsule will lose its elasticity and inhibit a full range of motion in the joint. A large percentage of the pain associated with hip dysplasia originates from inflamed nerve endings in the joint capsule so any pathology here will have a noticeable affect on the dog.
CARTILAGE: The surfaces of the head of the femur and the acetabulum are covered with what is termed hyaline cartilage. In a dysplastic joint the points of pressure and the amount of pressure applied to areas of cartilage surfaces are abnormal. The cartilage is being asked to do things it physically cannot accomplish, so it changes or disintegrates as a response. The changes range from thickening in abnormal areas to thinning in others. Sometimes the pounding it gets erodes the cartilage down to the underlying bone! The outcome is more pain and discomfort, more inflammation, more calcium deposits from inadequate healing attempts and eventual breakdown of the joint as a unit. Nutriceuticals such as Chondroitin Sulfate and Glucosamine may be effective in aiding the repair and maintenance of this articular cartilage.
BONE CHANGES: Since bone is alive it responds to stress and grows in a manner that tends to distribute weight loads evenly. As a result of posture changes brought on by discomfort, the dog's weight bearing forces stress the bone in unnatural ways. The bone does what it is supposed to do as a response and changes its shape. The bone doesn't know that the shape it changes to is abnormal.
Ultimately, this abnormal shape to the thigh bone and acetabulum create more difficulty with stability and a vicious cycle ensues that spells trouble for the dog. The final outcome of bony remodeling in unstable hip joints is Degenerative Joint Disease.
SIGNS OF CHD IN YOUNG DOGS: What you will see first is a pup that runs with both back legs nearly together, almost like a rabbit would run. After exercise the pup will be reluctant to rise, will sit back as if unsteady and will have difficulty climbing stairs or inclines. The pup might look slightly underdeveloped in the rear quarters. When it stands the rear legs may not be parallel, but rather too near each other at the hocks (ankles) called "cow hocked". You might notice a boniness to the pelvic area from lack of good muscle development. Another hint of trouble is an inability to extend the leg backward very far (decreased range of motion). Note: Many pups rest or sleep in a frog-like position with knees extended out to either side - this is a good sign and shouldn't alarm you.
In severe cases of dysplasia, the young dog will rock forward to support more weight on the front legs (which can create trouble in the shoulders and elbows). When dogs do this it seems as if they are tip-toeing or walking very lightly on their rear legs. A dysplastic pup will be reluctant to jump or "stand up" on its hind legs. Signs usually begin between five and eights months of age. But remember, as we learned above, some dogs do not show any signs at all of hip joint degeneration until mature adults.
SIGNS OF CHD IN OLDER DOGS: Some dogs with dysplasia escape pain or simply accept it as a fact of life and don't complain until degenerative joint disease sets in. Affected dogs will sit rather than stand, have trouble arising, run with the rear legs together and not be able to keep up any more on Sunday walks. Every veterinarian has been mystified on occasions where an x-ray of an older dog, who only recently seemed to be having hip trouble, reveals extensive degenerative changes in the hips due to long term dysplasia.
It is very important to keep this fact in mind: A dog can appear normal and yet have hip dysplasia. Just because a four-year-old dog isn't showing signs of trouble is not sufficient evidence to state "it couldn't possibly have hip dysplasia".
DETERMINING THE PRESENCE OF CHD: Dogs with obvious signs of CHD (hip soreness, difficulty arising or climbing inclines, muscle atrophy over the rump, limping) are not a challenge to confirm as such. So this discussion will apply more to the dog that seems to be normal but you are either not sure or need to know for breeding or training/working reasons. The minimum data required is a pelvic x-ray taken under anesthesia . . . PERIOD! You MUST have the x-ray to know if the dog is normal!
PennHIP: (University of Pennsylvania Hip Improvement Program)
Commercially available since 1993, this procedure has been and was developed as an objective method of evaluating dogs’ hip structure. It evolved as a direct result of the subjectivity factors and age constraint (maturity) limitations inherent to evaluation and certification of dogs by the OFA and other screening programs. PennHIP research published in peer reviewed journals has shown that different breeds have different susceptibility to osteoarthritis. Therefore, in PennHIP evaluations each breed is compared to its own. Only PennHIP certified veterinarians can do the PennHIP evaluation but many veterinarians are becoming certified in this procedure.
Why is anesthesia required in order to have the dog radiographed? To have an x-ray that yields the information you're trying to discover the dog must be perfectly relaxed. Because the position required to take a diagnostic x-ray is a somewhat unnatural one, even very gentle, cooperative dogs cannot relax enough to be x-rayed properly. Nothing is more frustrating for the veterinarian than to have an owner say "I need to know if this dog has any signs of hip dysplasia. Take an x-ray, but I don't want you to use anesthesia; this dog will do anything you tell it to do, so an anesthetic isn't necessary." Unless at the time of exposure of the x-ray, the dog is positioned precisely, with no movement, the x-ray will not be credible. You won't get the information you need!
Another great advantage of anesthesia is that the veterinarian can only then palpate and manipulate the hips to actually feel the degree of looseness. Also, the tension of the Pectineus Muscle is best assessed under anesthesia. Any grating or grinding from calcium deposits along the hip joints can be evaluated better than attempting to do so on an awake patient. If you need the information, the dog needs the anesthetic.
If the pelvis is tipped only slightly to one side or the other, one hip can appear normal that isn't and one can appear dysplastic that isn't! To complicate things, 10% of dysplastic dogs will be affected in only one hip! Better do the x-ray right!
The importance of radiography cannot be overstated. It can be done early, say five or six months of age, if dysplasia is suspected. If the results are questionable, reserve breeding until a time when the x-rays are conclusive. Generally, by the time the dog is full grown the x-rays will properly reveal the status of the hips. The OFA (OFA.org) will not classify hips in dogs until they are two years of age.
The advantage of radiography in a younger animal is that if you plan on breeding it you can eliminate fruitless time and financial and emotional expense related to breeding if the x-rays show unquestionable hip dysplasia. There have been many disappointed, depressed dog owners whose expectations for breeding were high and were shocked back to reality when their two-year-old dog showed x-ray evidence of dysplasia... two years of planning, training and dreams of great litters down the tube. If only the parents had been x-rayed. If only preliminary x-rays were taken eighteen months ago. Again, the advantage of the PennHIP procedure is obvious since dog over 4 months of age cane be evaluated.
It is very sad indeed for any pet owner to see their special pal affected by the discomfort and mobility problems associated with Canine Hip Dysplasia. Fortunately, armed with knowledge and forethought, highly selective breeding is your best defense against CHD.
Hip Dysplasia
Verification for All OFA testing link:
The OFA’s policy regarding permanent identification is an extension of the AKC’s policy in that the AKC will only accept OFA numbers into their registry for inclusion on registration papers and pedigrees IF the dog is permanently identified. While DNA profiles are able to uniquely identify individual dogs, it is also the AKC’s policy to limit permanent identification for health screening
purposes to tattoo or microchip. The rationale is that DNA profiles are not immediately verifiable, they require a sample to be taken and subsequent laboratory analysis. The AKC’s premise is that tattoos are visually immediately verifiable, microchips are immediately verifiable using a scanner, and that the verification should be done at the time of testing. Until January 1, 2008, the OFA will accept applications regardless of whether the dog has been tattooed or microchipped. Dogs with acceptable permanent id are assigned a PI suffix to their OFA number, dogs without permanent identification are assigned a NOPI suffix. The OFA Policy on Verification of Permanent Identification In order to add a higher level of integrity to the OFA databases, the OFA Hip and Elbow application form has been modified to include an area for the attending veterinarian to indicate whether or not they verified the
supplied permanent identification. The revised application form is available above After January 1, 2008, the verification step must be performed in order for the data to be forwarded to the AKC for inclusion in their records. Dogs with the verification step done will have a suffix of VPI assigned to their OFA numbers.
tick borne diseases
There are four major tick borne diseases that affect the dog in the United States:
Ehrlichiosis, Babesiosis, Rocky Mountain Spotted Fever and Lyme Disease.
All, with the usual exception of Lyme disease, may be fatal unless diagnosed in time and treated aggressively.
If you cannot get a firm diagnosis and nothing you do seems to help; if you cannot and will not settle for anything as vague as "compromised immune system"; if the symptoms you see make no sense and/or the treatment your dog is given does no good, you should consider the possibility that your dog has tick disease. Sites listed farther down the page are highly recommended to help you learn about and combat it.
Important! Here is the treatment your dog should be given for Ehrlichiosis or Lyme disease.
Doxycycline, a semi-synthetic tetracycline, is the drug of choice, the most effective against Ehrlichiosis and Lyme. It is given at 10 milligrams per kilogram (1 kg = 2.2 lbs.) of the dog's body weight every twelve hours for six to eight weeks. Another way to figure this, on the basis of pounds, is 5 mg. per pound of body weight. The result for the dog is exactly the same as doxy comes in 100 mg. tabs and the result of figuring in milligrams is usually adjusted up accordingly. If nausea is a problem, you can divide the dose further, as long as the dog gets what he needs in any twelve hour period.
This is twice the amount recommended in the Merck Veterinary Manual and is given for a longer period of time than the VMM recommends; however, vets who deal with tick disease all the time say that the higher doses and longer administration are successful far more often in treating this disease and preventing its recurrence.
Doxy is not used to treat Babesiosis and has little to no effect on it.
Dogs with Lyme disease that cannot tolerate doxycycline may be treated with amoxicillin as an alternative; it has no effect on Ehrlichiosis. I have read reports of IV Rocephin being used to save dogs in extremely bad cases of neurological Lyme..
Ehrlichiosis, a Silent and Deadly Killer
Betsy Easton has generously rescued this very important article from the web archives, linked in the title above, and posted it again on her site. Two links, one article; we are determined not to lose it.
The Hawk's Nest
============================
For those of us who are not vets, which is most of us, this is the best, most comprehensive, easily understood article on the web about Ehrlichiosis. For those who are vets, there is a foreword by Dr. Ibulaimu Kakoma, DVM, PhD, an acknowledged authority on rickettsial diseases in dogs, as well as a section on being awake to the possibility of TBD when a dog presents vague symptoms that don't seem to add up to much, or treatment for a suspected disease has little or no effect. Since this was written in 1996, tick disease has burgeoned as a problem that is still largely overlooked and it is all the more vital that vets inform themselves about it.
Ehrlichiosis is more than E. canis. Way too few vets seem to know much about tick-borne disease, fewer seem to realize that a dog that tests free of E. canis on the popular Snap test for heartworm, E. canis and Lyme, may still have another strain of it or another form of TBD altogether. (Some are resistant to even considering testing for tick disease and if you run up on one of these, don't let the door hit you on the way out! Go find a vet who will.)
If it's not E. canis, it could be equi, platys (a form that attacks the red blood cells), ewingii or risticii, though there are others, some unnamed. And, worse luck, cross infections with more than one type of TBD are common.
My dog died of E. risticii, the only form of this awful disease that is 'not' carried by ticks. The vector has only recently been found to be the larvae of the flukes that live on water snails. Think of it, imagine how tiny they are. It is believed that they may be ingested by dogs as they drink from river water, water in fields flooded or irrigated by rivers, or that these extremely small organisms may conceivably pass through the dog's skin with their deadly cargo. There is a possibility that E. risticii, now known as Neorickettsia risticii, is also harbored in horse manure, and it has been proven that horses which ingest caddis flies infected with this rickettsial organism can come down with the disease. The likelihood is that dogs may be infected in this way as well.
Ehrlichiosis, a Silent and Deadly Killer is the article that told me I shouldn't lose any time having my dog tested for TBD. It is invaluable. If you read nothing else, read this.
More links to information on Ehrlichiosis and other TBDs.
Tick Borne Ehrlichiae and Rickettsiae of Dogs
Tick FAQ: Pam Barbe's compendium of links and facts
Hemotropic Diseases of the Dog, Cat and Horse: Dr. Cynthia Holland, director of Protatek Reference Labs.
ProtaTek Reference Laboratory has made a specialty of these diseases and is the lab most used by vets on Tick List. Turn-around time on blood samples sent overnight for tick panels is between 24-48 hours, usually the former, and Dr. Cynthia Holland, PhD, the director, has been very helpful about discussing the results with the vets. The usual panel consists of IFA tests for E. canis, Babesia canis, Rickettsia rickettsii (Rocky Mountain Spotted Fever) and Borrelia burgdorferi (Lyme disease). Arrangements can be made to test for the less common forms of TBD as well as Valley Fever.
Tick Diseases: an Overview
Ehrlichiosis - Antech Diagnostics
Update on Ehrlichiosis - Antech Diagnostics. This is a .pdf file.
Imizol: Imizol (Imidocarb diproprionate) is the drug of choice for Babesiosis and is used off-label for knocking out stubborn cases of Ehrlichiosis, as well. This is a link to the product label on Schering-Plough's website. Read it carefully. If you use it, be sure to give your dog some form of liver support.
Bartonellosis - Antech Diagnostics
Bartonellosis - Dr. Ed Breitschwerdt 2001 - World Small Animal Veterinary Congress
AIHA, IMHA and ITP: Auto-Immune Hemolytic Anemia, Immune Mediated Hemolytic Anemia and Immune-mediated Thrombocytopenia are often concurrent with tick disease, making the treatment that much harder and more dangerous.
Lyme Disease: Allen Schoen, DVM
Lyme Borrelliosis in Dogs: R.K. Straubinger, DVM An excellent, detailed report on Lyme disease.
Signs of Tick Disease in Dogs: Cornell University's "Consultant Service". Select "Search by Diagnosis" and type in the name of the disease for a fairly complete list of the signs you might possibly see if a dog is infected with tick disease. For ehrlichiosis risticii, type in "neorickettsia risticii", the name by which it is now known.
The western blot: the definitive test, at present, for distinguishing Lyme disease from "vaccine induced Lyme".
Advanced Topics in Lyme Disease: Diagnostic Hints and Treatment Guidelines for Lyme and Other Tick Borne Illnesses by Dr. Joseph Burrascano. This page is unusual in that it is concerned with Lyme disease in humans, yet what Dr. Burrascano has to say is also largely applicable to dogs.
Rocky Mountain Spotted Fever in Dogs
Tick Disease and Epilepsy My thanks to Deborah Histen, who has an epileptic Golden named Henry, for bringing up a very real concern about the possibility of phenobarbital getting in the way of a diagnosis when a seizuring dog is suspected of having tick disease. Links to in-depth information on phenobarbital and to the Epil-k9 subscription page are here.
Online Medical Dictionary: where to look up all those technical medical terms you may be floored by.
PubMed The National Library of Medicine: Search for abstracts and sometimes complete articles on various diseases, human and canine.
The Australian Paralysis Tick: For the Aussies, vital information. For anyone, the flash animation of the feeding tick is repulsive, fascinating and clearly shows the way tick disease is transmitted.
Google: Google is always your best friend when looking for information. Use only the most necessary words, such as "ehrlichiosis +dog". (Quotes are not necessary and caps are ignored. Generally, the singular "dog" will get better results than the plural.) To emphasize a word, put a + directly in front of it; to make sure you don't get references you don't want, put a minus sign there, i.e.: ehrlichiosis +dog -human.
Tick List If you are dealing with tick disease in your dog or simply suspect that you might be, I strongly suggest that you join Tick List. The members of Tick-L have all been through what you are going through and are always ready to help with advice gained from experience that's sometimes been pretty painful. There are also vets on the list; most notable is Dr. Tom Beckett in Texas, who is endlessly patient with help when we need it. I don't know what we'd do without him.
To join
Tick borne disease is becoming epidemic in the United States, it's serious and it's deadly. My German Shepherd Dog Thunder died of TBD because he was diagnosed too late. Nancy Garcia's Australian Shepherd Adamdied of it. Pam Barbe's beautiful Samoyeds have lived with constant pain thanks to tick borne disease and countless other dogs may have lost their lives to it with no one the wiser due to misdiagnosis.
Read about it. Save this page and those it links to against the day that I hope never comes, the day you need what you read here.
Spaying or Neutering your Mastiff
Most veterinarians recommend spaying or neutering a puppy at or before six months of age. With animal shelters full of accidentally bred dogs and their puppies, their belief in early altering is understandable. Vets also recommend to spay early to prevent mamary (breast) cancer in females and neuter to avoid temperament or marking issues or testicular cancer in an intact male. Most veterinarians, however, have little first-hand knowledge about Mastiffs and the special needs associated with these big guys. Early spaying/neutering is NOT recommended for giant breed dogs. Mastiffs need the hormones present when they reach sexual maturity to reach their full potential physically. Spaying and neutering early (before at least a year old) often has adverse effects on both the look and health of a Mastiff. A Mastiff's growth plates need the hormones to close, as well as to develop bone density.
Females: Mamary cancer is a rarity, and chances of contracting it or other reproductive system cancers goes up only slightly when spaying at over a year of age versus spaying at under a year old, but it's been proven that spaying early does increase the chance of her contracting bone or lung cancer later in life or developing permanent problems with incontinence and bladder leakage that are often tough to deal with. Mastiffs need the hormones of at least the first heat cycle to help their organs mature and develop. Anyone who owns a female Mastiff can tell you how much their girl "bloomed" after her first heat cycle. Also, puppies that are prone to frequent urinary tract infections (UTIs) often outgrow them after their first heat cycle. Mastiffs usually come into their first heat at about 9-12 months of age. An average heats last 3 weeks, which is a minor inconvience that makes a world of difference in your girl's overall health. Just be sure to take precaustions so she is not accidentally bred, either by your own male or a neighborhood dog. Some people opt to board their girls while they're in heat to make sure this doesn't happen.
Males: The chance of a male Mastiff developing cancer later in life from being neutered closer to 2 years of age instead of earlier is very slight. However, when male Mastiffs are neutered too young, before their hormones are at full tilt, they often do not gain the muscle or mass that an adult male should have and tend to look like a gangly puppy their whole life. Neutering males early usually effects overall bone size, and you end up with a tall, lanky dog with no bone and a small head--they end up looking like badly bred Great Dane, not a Mastiff. Mastiffs need their sexual hormones for proper growth. If you buy a well-bred Mastiff, you want one that looks like a Mastiff, not a Dane.
If you spay or neuter after a year and before two years of age, you still get many of the same health benefits for your dog that comes with an early spay or neuter, without the negatives. We recommend spaying and neutering around 18 months of age. Remember, Mastiffs are not just big Labs. They are a special breed with needs all their own. Small breeds often do well when spayed or neutered at an early age, but with giant breeds it is better to wait. **NOTE If your dog will be sedated for any surgery or procedure, be sure to tell your veterinarian "NO ACE." Acepromazine is a commonly used tranquilizer for dogs and cats, and has been known to slow the heart down so much in our guys that they never wake up, dying on the table or shortly after. Always remind your vet's office.
Leptospirosis-An Update
By Beth Davidow, DVM DACVECC
Leptospirosis is a bacterial disease that can cause acute kidney shut down and
sometimes liver failure in dogs. The bacteria can be carried asymptomatically by
wildlife such as opossums, rats, and raccoons, and shed in the urine where it
can contaminate stagnant water. The bacteria is inactivated by freezing, very
hot temperatures and direct sunlight so it is most common in mild wet seasons.
This fall, we have seen an increase in acute kidney failure in dogs and have
diagnosed 6 cases of leptospirosis since October. The Department of Health had a
total of 29 cases in 2010 reported through the beginning of November. While the
prevailing thought has been that large breed dogs that roam are most at risk,
our 6 cases have been 2 Papillons, a Shih Tzu, a Miniature Schnauzer, a Terrier
mix, and a Boston Terrier. The Papillons had been to Camano Island but the other
dogs were only in their backyards or within the city limits. One case became
acutely ill while at a boarding facility over the holidays so many questions
have been asked about accurate diagnosis, treatment, prevention, and how to
address those dogs that were potentially exposed.
Here are my thoughts on some commonly asked questions.
1) What have been the common presenting signs in cases you have diagnosed?
All of the cases presented with not eating, vomiting, and lethargy. They did not
have fevers and were only mildly dehydrated initially. Because it is very hard
to determine who is at risk from history alone and to tell who has emerging
kidney failure from physical exam alone, I strongly recommend at least some
bloodwork (BUN, glucose, PCV/TS and electrolytes) on animals that have vomiting
and lethargy. In the past, we have identified some early leptospirosis cases
with mild changes in bloodwork. The animals caught early and started immediately
on antibiotics have the best prognosis.
2) What is the treatment?
Penicillin type drugs are the antibiotic of choice for treating clinical
leptospirosis. However, these medications do not get rid of the carrier state.
Tetracyclines both treat the bacteria and eliminate shedding but because they
cause nausea, they are not recommended in the acute phase. For acute cases, the
recommendation is 3 weeks of amoxicillin and 3 weeks of doxycycline. IV fluids
and medications to help with nausea are very important. Back pain is seen in
some dogs and pain medication should be considered. In addition, some dogs with
leptospirosis can develop breathing problems so radiographs and oxygen may be
needed. Complete renal shutdown is a very real risk. Hemodialysis can be very
effective in treating dogs that have worsening renal values despite IV fluids
and antibiotics.
3) How is leptospirosis diagnosed?
Usually a blood test is done to look for an elevated titer. This means the body
has made antibodies to fight the disease and the antibody level can be measured.
The problem with this test is that vaccines will also make somewhat of an
elevated titer (causing a false positive) and some animals get sick before their
body has time to make antibodies (causing a false negative). Knowing your pet's
vaccine history is important in interpretation. In addition, many animals need a
repeat titer in 7-14 days. Some animals who have a negative result or low titer
will have a high titer when rechecked, confirming the infection.
4) Can people in the household get leptospirosis?
Leptospirosis is shed in the urine. Exposure to urine from infected animals into
cuts, mucus membranes or orally can potentially lead to infection, especially in
people or animals with immunosuppression. Most common disinfectants kill
leptospires including bleach, povidone-iodine, and chlorhexadine. Any stagnant
water sources on the property should be drained if possible and rodent control
should be instituted. Thorough hand washing, avoiding contact with urine,
wearing gloves when cleaning potentially infected material and avoiding spraying
water when cleaning to avoid aerosolizing the bacteria will limit the infection
risk.. It is very important to consult with your physician if your pet is
diagnosed with leptospirosis. Because of this potential risk to people, we
highly recommend that any dog with suspected leptospirosis be tested, even if
treatment is not going to be pursued.
During 2005, there were 55 cases of leptospirosis diagnosed in dogs in Western
Washington. There were also 3 human cases the same year. None of the human cases
were directly related to dogs but these people were probably exposed to similar
contaminated water sources. Thus, dogs may be a sentinel for the disease and
reports may help Public Health to identify potential risk sites for people.
Leptospirosis is a reportable disease and your veterinarian will contact your
county and state public health department with information if your pet is
diagnosed with this disease. Public health will then contact the owners to get
more information to try to identify the source.
5) What is the risk to other animals in the household?
I have rarely seen more than one animal in a household with leptospirosis.
However, this year we treated a pair of Papillons who both had it. However, they
most likely contracted it from the same contaminated water source rather than
from each other. Dogs in the household are at risk if they drink water
contaminated by urine, if there is a fight or if there is mucus membranes or a
laceration exposed to contaminated urine. The incubation period between exposure
and signs is 4-12 days.
6) Should dogs exposed to a dog with leptospirosis be treated and if so, with
what antibiotic?
The safest course of action would be to consider checking renal values, urine,
and leptospirosis titers and/or urine PCR on exposed dogs in a household,
especially if there are any clinical signs of anorexia, lethargy or vomiting. If
values and clinical signs are normal, the recommendation is to use doxycycline
alone for 3 weeks to prevent both infection and development of a carrier state.
If there are any symptoms, then the combination of amoxicillin and doxycycline
is recommended.
7) Should I be vaccinating my pet for leptospirosis and if so, how often? How
much protection does it provide?
I do believe that we should be considering vaccination for dogs in this area
using a 4 serovar vaccine that contains L. canicola, L.icterohemorrhagica,
L.grippotyphosa, and L.pomona. Many of the cases we are seeing have the highest
titers to L. autumnalis but there is evidence that vaccination with L. pomona
might provide some protection against this serovar. Dogs do need 2 initial
vaccines 3 weeks apart and then at least yearly for coverage.
Recommendation is not to use the lepto vaccine until puppies are 12 weeks of
age. The greatest incidence of cases appears to be in the fall so vaccinating
dogs at risk in the late summer or early fall may provide the best coverage. The
downside to these vaccines is that the immunity probably doesn't last a full
year and they are more associated with vaccine reactions than some of the other
vaccines. Toy breeds appear to be more at risk of a reaction so this should be
considered.
More information:
http://www.cdc.gov/ncidod/dbmd/diseaseinfo/leptospirosis_g_pet.htm
Selected References:
-Barr SC, McDonough PL, Scipioni-Ball RL, Starr JK. Serologic responses of dogs
given a comercial vaccine against Leptospira interrogans serovar Pomona and
Leptospira kirschneri serovar grippotyphosa. Am J Vet Res 2005; 66: 1780-4.
-Davis MA, Evermann JF, Petersen CR, VanderSchalie J, et al. Serological Survey
for Antibodies to Leptospira in Dogs and Raccoons in Washington State. Zoonoses
and Public Health. 2008; 55: 436-442.
-Greene CE, Sykes JE, Brown CA, Hartmann K 2006: Leptospirosis. In Greene CE ed.
Infectious Diseases of the Dog and Cat. 3rd edition. 2006, pp.402-417.
Saunders/Elsevier, Philadelphia, PA.
-Harkin KR, Roshto YM, Sullivan JT. Clinical application of a polymerase chain
reaction assay for diagnosis of leptospirosis in dogs. JAVMA 2003; 222:
1224-1233.
Please note this article was published in the February issue of ShowSight Magazine and was beautifully written by Diane Klumb.
--------------------------------------------------------------------------------
The Mystery of the "Bad Bite"
Elementary, My Dear Watson
by Diane Klumb
Anyone who knows me at all probably also knows how totally excited I am by the ability of molecular genetics to solve the mysteries inherent in the breeding of purebred dogs. In addition to allowing us to actually "breed for improvement" instead of just blithely throwing the term around, I firmly believe that if used wisely, this new store of knowledge represents out best hope for both preserving the sport of dog breeing for future generations, and for fending off our own personal Professor Moriarty in the guise of Ingred Newkird & Co. But actually using this new knowledge to our benefit, and to the benefit of dogs, often requires us to discard long-held and long-cherished beliefs.
Realizing that something we were taught years ago (and in many cases have passed on to the next generation of breeders) was based on an incorrect assumption, and may actually be flat-out WRONG, can be a difficult mental pill to swallow, and some people just can't seem to do it.
For others, it provides an "Ah-HA!" moment, when the seemingly inexplicable suddenly becomes clear.
One such moment for me occurred a few years ago, when I learned that prenatal disruption (via genetics or environment) of a regulatory gene with the delightfully improbable name sonic hedgehog (SHH) often results in asymmetry, where the two sides of a dog don't exactly match. (It's a lot commoner than you'd expect, actually, and occurs in people to varying degrees as well. And symmetry in people has been linked to both beauty and longevity. Probably true in dogs as well.)
More to the point, an asymmetric dog will invariably crab, as he has longer reach and more drive on one side than the other, causing his forward progress to eerily resemble that of a '63 Ford Fairlane with a bent frame. Yet stacked in profile the dog displays flawless balance, which has confounded judges and breeders since time immemorial.
When I shared that discovery in a column a few years back, an amazing number of judges who read it made a point of telling me that it was an "Ah-HA! moment for them, too. (One told me that now whenever she sees a dog crabbing, she checks the elbows on both sides, and one is invariably set higher on the ribcage than the other.) An old dog show mystery solved by molecular genetics. Cool.
I had another of those "Ah-HA! moments recently, when I stumbled upon a fascinating research paper while looking for something else entirely. (Happens to me all the time.)
It seems that scientists have discovered that the size and shape of the mammalian mandible (or lower jaw) is controlled by a surprisingly large number of genes - over 15 have been identified to date.
A little more digging revealed that an equally large number are involved in the development of the maxillary complex, or what we refer to as the upper jaw.
The kicker is......they are different genes, and inherited pretty much independently. Which means, in terms expressed as simply as humanly possible: A DOG CAN INHERIT HIS UPPER JAW FROM ONE PARENT, AND HIS LOWER JAW FROM THE OTHER. Ah-HaH! Another dog-breeding mystery solved, and a long-cherished belief laid to rest.
Putting this into an everyday breeding scenario, here's what too often happens. A young health-screened dog of quality with a magnificent head is widely used by breeders on bitches whos heads could use some improvement--depending on the breed standard, their muzzles could be a little shorter, or a little longer, or maybe a little more or less refined.
But rather than the overall improvement in the first generation breeders are hoping for, they get maybe one nice bite (if they're lucky and depending upon what the bitch's parents looked like) and a basketful of "bad" bites. (What constitutes a bad bite varies from breed to breed, of course.) Soon the word goes round that this lovely-headed dog "throws bad bites" and his stock drops faster than Lehman Brothers. Happens all the time.
And now we learn that it wasn't his fault at all, poor guy. Breeders have been laboring for years under the misconception that an off-bite is the result of an AR gene, and that some dogs are carrying a recessive gene that causes them to "throw bad bites." I've heard it said a thousand times over the years, and so have you.
But it is simply NOT TRUE. Turns out there is no single AR gene for an undershot bite, or an overshot bite, either. There are literally dozens of genes involved, all inherited more or less independently.
So, from this day forward (unless you are one of those people now recognized as incapable of changing a long-held opinion in the face of new evidence due to insufficient activity in the anterior singulate cortex and I'm wasting my time here) we can all stop blaming the poor stud dog.
What is actually happening genetically is this: Given Mendel's Law of Independent Assortment, which is still scientifically valid after all these years, a percentage of the pups from an "unlike-to-unlike" breeding in the head department will inherit a larger percentage of the genes for a longer mandibular (under) jaw from one parent, and a larger percentage of the genes for a shorter upper maxillary (upper) jaw from the other, resulting in bites that are undesirable per a particular breed's standard. NEITHER parent is to blame - malocclusions of the jaw, we now know, are polygenic.
Now, hopefully most of us already understand that there is a huge genetic difference between a MALOCCLUSION OF THE JAW and MISALIGNMENT OF INCISORS, which cause a reverse scissors bite in a dog whose jaws align according to the standard, and whose "puppy bite" is often perfect. Misalignment of incisors is usually caused by no more than the particular timing of the eruption of the individual permanent teeth - if it is off, the upper incisors will force the lower ones out, resulting in a reverse scissors. (That's why it's correctable with mere pressure.) There's no sense blaming this one on either parent, either:
Research has shown there are more than FIFTY different genes that influence the development, and timing of eruption, of teeth.
Some of these genes, it turns out, are involved in other processes and also code for traits that we've actually selected FOR over the years---the MITF gene, for example, which is involved in pigment development (parti-colored dogs are parti-colored because they carry a mutation on this gene) is also involved in toogh development and timing of eruption, which is likely why the parti-colored pups in a litter often get their teeth later than their solid-colored brethren. The RSPO2 gene is also involved in tooth development, and a mutation on this one is responsible for canine head furnishings. (And that's just two off the top of my head- no doubt there are dozens more, as we now know that genes "multi-task.)
The route to overall improvement in bites within a breed
IS THE SAME ROUTE THAT HAS REDUCED HIP DYSPLASIA
in several breeds over the last few decades ----
SELECTION.
This probably explains why wolves -uniformly long-muzzled, solid-colored, and generally free of head furnishings - rarely display the anomalies in dentition that plague purebred dogs.
Now, I'm NOT suggesting for a moment that we should be trying to put a ''wolf head" on all our dogs, or to make them all solid-colored or clean faced-- to do so would seriously affect breed type in probably two-thirds of them, and not necessarily for the better.
What I AM suggesting is that simply understanding that malocclusion of the jaw and misalignment of incisors both appear to be polygenic, rather than the result of a single recessive gene, allows us to make more informed breeding decisions. Breeding a male with a gorgeous head to a bitch who is lacking and expecting the resulting puppies to all end up with his head (and bite) is about as silly as breeding a dog who is OFA Excellent to a dysplastic bitch and expecting the resulting pups to all end up OFA Excellent. No one with half a brain would blame the sire in that situation, because (hopefully!) we now all understand that canine hip dysplasia is polygenic, and represents a threshold characteristic.
The route to overall improvement in bites within a breed is the same route that has reduced hip dysplasia in several breeds over the last few decades--SELECTION. And as the German Shepherd breed has proven conclusively with its OFA ratings, you can do it without sacrificing breed type. Rather than discarding a quality health-screened male with a correct head per his standard who produces off-bites when bred to bitches with poor heads, it would make more sense to selectively linebreed off him, using only those offspring who inherited his head and petting out the rest. After three or four generations of this, the line should be homozygous for his head, the pedigree will have both depth and breadth in that regard, and malocclusions will be few and far between. What we'd be doing is simply combining time-honored animal husbandry practices with knowledge gained from cutting edge molecular genetics. It's the future of responsible dog breeding.
However, refusal to change one's long-held beliefs regarding mode of inheritance (i.e. continuing to believe that there is a single recessive gene for "bad bites" and that a dog who produces one is "a carrier") as new information becomes available to us will untimately result in failure to improve. Why? Because the breeding techniques used to reduce or eliminate the incidence of a trait caused by an AR gene will always be different than those used to reduce or eliminate the incidence of a threshold trait caused by polygenics, where gene testing is not a viable possibility.
And consistently producing sounder, healthier dogs is more important now than ever because, make no mistake about it, the wolf is at our door.
See you at the shows, and remember to have fun out there!
-DK
