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
20250 17 Mile Rd
Marshall, MI 49068
Dr. Joe Bando
Berwick Animal Clinic, Ltd.
3372 Refugee Road
Columbus, Ohio 43232
Mastiff Breed Standard
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.
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.
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 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.
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.
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.
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.
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
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.
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. (see homeopathic treatment)
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.
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.
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 Adam
died 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.
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
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
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
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
-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:
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 ----
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!
In keeping with the spirit of the MCONO Code of Ethics, Mastiff breeders are encouraged to inform puppy buyers of developmental conditions (that may or may not be hereditary or genetic) that are known to exist in Mastiffs, as well as methods to test and/or monitor some of these conditions.
Please keep in mind that all purebred and mixed breed dogs can have health concerns and health testing is simply a tool....not a guarantee.
EYE PROBLEMS IN THE BREED
• Canine Multi-focal Retinopathy (CMR), also known as Retinal Dysplasia/Retinopathy - Abnormal development of the retina present at birth and recognized to have three forms: folds, geographic, and detachment. A Mastiff with folds will currently pass CERF and the folds may disappear over time while the geographic and detached forms may cause loss of vision or blindness. There is a DNA test available though OptiGen www.optigen.com for CMR in Mastiffs.
• Cataract - Lens opacity that may affect one or both eyes and some forms may cause blindness.
• Distichiasis - Eyelashes abnormally located in the eyelid margin which may cause ocular irritation.
• Ectropion - Conformational eyelid defect, which may cause ocular irritation due to exposure.
• Entropion - Conformational defect where eyelid margins invert or roll inward, toward the eye causing eyelashes and hair to rub against the cornea which may result in ocular irritation.
• Macroblepharon - Abnormally large eyelid opening; may lead to secondary conditions associated with corneal exposure.
• Persistent Pupillary Membranes (PPM) - Persistent blood vessel remnants in the anterior chamber of the eye which fail to regress normally in the neonatal period.
• Progressive Retinal Atrophy (PRA) - Degenerative disease of the retinal visual cells which leads to blindness. In Mastiffs the age at which PRA can be detected varies from as young as 6 months to as late as 42 months. Typically Mastiffs with PRA go blind gradually, first loosing their night vision and then their day vision. Many do not go completely blind until they are 8 years old or older. There is a DNA test available through OptiGen www.optigen.com for PRA in Mastiffs.
ORTHOPEDIC, NEUROLOGICAL, STRUCTURAL, AND JOINT PROBLEMS IN THE BREED
• Anterior Cruciate Ligament (ACL) Rupture - The knee along with the external support (i.e., collateral leg) has two ligaments inside the joint that help prevent forward movement (i.e., cruciate). Insult/injury can cause this ligament to rupture and result in acute lameness (not want to bear weight) on the limb.
• Degenerative Myelopathy (DM) – This is a progressive, degenerative, late onset disease of the spinal cord seen in older dogs. The symptoms usually begin with hind end weakness, lack of coordination and shuffling or dragging of the rear feet. There is a DNA test for DM through OFA www.offa.org
• Elbow Dysplasia - Elbow dysplasia encompasses several different conditions, all of which are indicative of abnormally formed or fused elbow joints and all can cause lameness and pain:
o Fragmented Coronoid Process (FCP) - This form of elbow dysplasia is generally the most difficult to treat if the fragments are actually loose in the joint.
o Osteochrondritis Dissecans (OCD) - A defect in the joint cartilage overlaying or attaching to the bone. OCD most commonly occurs in the elbows, shoulders, hocks and stifles.
o Ununited Anconeal Process (UAP) - In giant breeds such as Mastiffs the Anconeal Process can close later than in smaller breeds, often as late as one year of age or older.
• Hip Dysplasia - Hip dysplasia is a painful condition caused by abnormally formed hips. The animal may become lame in the hind quarters due to the pain associated with the degeneration of the hips.
• Hypertrophic Osteodystrophy (HOD) - A developmental disorder that manifests with toes turning in or out, roached toplines, pinched rears, and in advanced stages fever, lethargy, pain in joints, inability to stand or function. This is a problem of intake in calories versus output of energy - too many calories consumed and/or unbalanced diet disrupted by supplementing.
• Panosteitis (Pano or Wandering Lameness) – A developmental problem that affects the long bones during rapid growth periods typically between 6-16 months of age. The exact cause is unknown although genetics, diet, stress, infection, and metabolic or autoimmune problems have been suspected. Lameness can occur in one limb or over time in all limbs. It often is intermittent affecting one leg then another and back again… It is self-limiting and spontaneously disappears.
• Spondylosis – is a degenerative disease that causes excessive bone production of osteophytes along the spinal vertebrae which can cause lameness. In advanced cases the vertebrae can fuse together. In many cases there are no clinical symptoms, but the acute expression of the disease such as lameness, severe pain and disabilities are often seen in adults and older Mastiffs.
• Wobblers Syndrome – Cervical Vertebral Instability (CVI) is caused by pressure and pinching of the cervical spinal cord and the nerves in the neck due to ligament problems and/or vertebrae malformation. The compression on the spinal cord in the neck may cause the Mastiff to stand and move abnormally. This is believed to be an inherited genetic disorder with environmental influence. Rapid growth and nutrition may influence the expression of the disease.
MISCELLANEOUS OTHER PROBLEMS IN THE BREED
• Allergies – Some Mastiffs have allergies to certain foods, pollens, etc. Allergies are due to autoimmune problems and since they often run in certain lines they are believed to be inherited.
• Cancer - Most forms of cancer have been diagnosed in some members of the breed. Cancer can be hereditary while others occur spontaneously or even due to environmental toxins. Although there are several forms of cancer found in Mastiffs, the most common types are: Osteosarcoma (Bone Cancer), Lymphoma, Hemangiosarcoma, Mast Cell Tumors, Squamous Cell Tumors, & Breast Cancer. Today there are advanced medical treatment options such as radiation, chemotherapy and medications to reduce the size of the tumors and offer pain management to help maintain a good quality of life.
• Cystinuria - An inherited metabolic disease caused by a defective kidney transporter for cystine and some other amino acids. Because cystine readily precipitates in acid urine, crystals and later calculi (stones) can form in the kidney and bladder. Cystinuria in Mastiffs primarily affects males and can result in serious illness and may be life threatening.
• Epilepsy – A seizure disorder which can have multiple causes. The age of onset of the inherited form is normally around 6 months to 5 years of age. Epilepsy is often difficult to treat successfully in Mastiffs and other large breeds.
• Gastric Dilation, Torsion, Volvulus (Bloat) - Bloat is a hideous killer of giant breed animals, and Mastiffs are no exception. Without warning, the stomach fills with air (dilation), can twist 180 degrees (torsion) on its long axis, or more than 180 degrees (volvulus) thereby cutting off blood and oxygen to vital organs. Bloat can be primary or secondary, caused by emotional or physical stress, improper nutrition or feeding habits, guzzling water, inappropriate exercise, as well as other causes that we do not understand. Every Mastiff owner needs to familiarize themselves with bloat symptoms and have a plan of action to get the animal to an emergency medical facility at the onset of the first symptom. A dog that is bloating often has approximately 3 hours to live without medical intervention.
• Heart Disease - The most common heart problems in Mastiffs are aortic stenosis, mitral valve dysplasia and cardiomyopathy. Early detection and treatment are essential for a good prognosis. Some mastiffs have heart murmurs that are mild and not a cause for concern. If a heart murmur is detected it is essential to have it checked to see if it is an "innocent" murmur or a serious problem.
• Hypothyroidism - Hypothyroidism is the result of an abnormally functioning thyroid gland resulting in a lower than normal level of thyroid hormone. This lack of thyroid hormone can have serious health consequences including coat and skin problems, intolerance to cold, weight gain or loss, infertility, sudden aggression, and immune system malfunctions. The inherited form is autoimmune thyroiditis where the body's own immune system attacks and destroys the thyroid gland or reduces its function. Autoimmune thyroiditis is diagnosed by measuring the FT4D, cTSH & TgAA. Acquired hypothyroidism can be caused by various problems such as stress for long periods of time, poor nutrition, prolonged infections, and chemical agents.
• Reproductive Issues – There are several reproductive problems that can affect Mastiffs and it is encouraged that you research this area if you plan to breed. Some of the most common are pyometria (uterine infection), cryptorchidism (undescended testicles), failure to conceive, and vaginal hyperplasia.
• von Willebrand's Disease (vWD) - A rare abnormal bleeding disorder due to a lack of normal clotting. An animal's life can be threatened by bleeding due to an injury, or during spaying/neutering or any other condition resulting in bleeding.
TESTING AND RESEARCH INFORMATION: ORGAINIZATIONS, CONTACTS, AND REGISTRIES
Canine Health Information Center (CHIC) DNA Repository - Please donate DNA (blood or semen)
Phone: (800) 442-0418 E-mail: firstname.lastname@example.org Website: http://www.caninehealthinfo.org/
Behavior Disorders, Cancer, Epilepsy & Wobblers –
Dr. Mark Neff - Van Andel Research Institute, Contact Alison Ruhe, Phone: 602-343-8693
email@example.com – http://www.vai.org/Research/Labs/NeurogeneticsCanineBehavior/kitrequest.aspx
Broad Institute of Harvard and MIT, Dog Genome Project
Fax: (617) 324-2722, e-mail: firstname.lastname@example.org website: http://www.dogDNA.org
Printable Brochure: http://www.broadinstitutte.org/mammals/dog/vet_samples.html
Orthopedic Foundation for Animals (OFA), 2300 E. Nifong Blvd, Columbia, MO. 65201-3806
Phone: (573) 442-0418 Fax: (573) 875-5073 e-mail: email@example.com
Cardiac: http://www.offa.org/cardiacinfo.html application: http://www.offa.org/cardappbw.pdf
Cystinuria Testing and DNA Research, University of Pennsylvania School of Veterinary Medicine
Dr. Giger – Cystinuria Nitroprusside Urine Testing, Metabolic Lab 215-898-3375
Dr. Paula Henthorn – Cystinuria DNA Research, Section of Medical Genetics 245-898-8894
Degenerative Myelopathy Testing and Research
University of Missouri-Columbia, College of Veterinary Medicine
Contact: Liz Hansen, Phone: (573) 884-3712 Fax: (573) 884-5414 e-mail: firstname.lastname@example.org
DM DNA Test Information: http://www.caninegeneticdiseases.net/DM/ancmntDM.htm
DM Research Information: http://www.caninegeneticdiseases.net/DM/ancmntDM.htm
Epilepsy DNA Research
Canine Genetic Analysis Project (CGAP), Anita Oberbaurer, PhD., Professor and Vice Chair
University of California, Davis Department of Animal Science
Phone: (530) 752-4997 Fax: (530) 752-0175 e-mail: email@example.com
Canine Epilepsy Network, Liz Hansen, Coordinator of Veterinary Information
Dr. Gary Johnson's Lab - Department of Veterinary Pathology
College of Veterinary Medicine, University of Missouri
209 A Connaway Hall, University of Missouri, Columbia, MO 65211
Phone: (573) 884-3712 Fax: (573) 884-5414 e-mail: firstname.lastname@example.org
Canine Eye Registration Foundation (CERF)
Phone: (217) 693-4800 e-mail: CERF@vmdb.org
OptiGen – DNA Tests
Progressive Retinal Atrophy (PRA) & Canine Multi-focal Retinopathy (CMR)
Cornell Business & Technology Park 767 Warren Road, Suite 300 Ithaca, New York 14850
Phone: (607) 257-0301 Fax: (607) 257-0353 e-mail: email@example.com
www.optigen.com online application: http://www.optigen.com/opt11_form.taf
Hip and Elbow Dysplasia
Orthopedic Foundation for Animals (OFA), 2300 E. Nifong Blvd, Columbia, MO. 65201-3806
Phone: (573) 442-0418 Fax: (573) 875-5073 e-mail: firstname.lastname@example.org
Hips: http://www.offa.org/hd_info.html Elbows: http://www.offa.org/ed_types.html
PennHIP - University of Pennsylvania's Hip Improvement Program
Phone: (215) 573-3176 e-mail: email@example.com
Hip Dysplasia and Osteoarthritis Research – Dr. Rory Todhunter, Cornell University
Identifying and verifying genetic markers of canine hip dysplasia. Phone: (607) 253-3041,
E-Mail: firstname.lastname@example.org Website: http://www.vet.cornell.edu/Faculty/Todhunter/research.htm
Research Information: https://www.vet.cornell.edu/research/awards/08September/Todhunter.htm
Orthopedic Foundation for Animals (OFA), 2300 E. Nifong Blvd, Columbia, MO. 65201-3806
Phone: (573) 442-0418 Fax: (573) 875-5073 e-mail: email@example.com
http://www.offa.org/pl_overview.html OFA Patella Application: http://www.offa.org/pdf/plappbw.pdf
It should be noted that the use of soloxine and other medications used to treat hypothyroidism makes the results of thyroid testing invalid. For a thyroid test to be valid the mastiff being tested must NOT have had soloxine or other thyroid medications for at least 3 months prior to testing. Please ship the SERUM sample CHILLED with frozen cold packs in an insulated container via overnight delivery to the OFA approved Lab with the OFA Thyroid Registry Application Form! Do NOT send the sample to OFA!
Recommended Lab for Thyroid Testing – MSU Diagnostic Center for Population and Animal Health,
Michigan State University – Please request the OFA Thyroid Registry Test Phone (517) 353-0621
OFA Thyroid Registry Information: http://www.offa.org/thy_info.html
OFA Thyroid Registry Application: http://www.offa.org/pdf/thyappbw.pdf
von Willebrand's Disease – von Willebrand Factor Assays (vWF)
AHDC, Cornell University College of Veterinary Medicine, Upper Tower Road, Ithica, NY 14853
Phone: 1-607-275-0622 Fax: 1-607-275-0720 http://diaglab.vet.cornell.edu/coag/
For Von Willebrand factor assay tests: please ship the PLASMA sample CHILLED with frozen cold packs in an insulated container via overnight delivery! Also verify receipt of package in good condition!
Wobblers & Multiple Other Disorders – Dr. Mark Neff - Van Andel Research Institute
Contact: Alison Ruhe, Phone: 602-343-8693 or email firstname.lastname@example.org
Mastiff Club of America Health Information Contacts:
Health Committee Anna May (951) 704-6022 email@example.com
Jan McNamee firstname.lastname@example.org
Cancer - Tricia Dalman Phone 816-453-0700 E-Mail Chamois06082000@yahoo.com http://mastiff.org/CANCER.htm
Cystinuria - Anna May Phone (951) 704-6022 E-Mail email@example.com - http://mastiff.org/CYSTINURIA.htm
Mary DeLisa Phone (720) 529-1954 E-Mail DevineMastiffs@gmail.com - http://mastiff.org/DNA.htm
Hip & Elbow Dysplasia Anna May Phone (951) 704-6022 E-Mail firstname.lastname@example.org - http://mastiff.org/HIPSANDELBOWS.htm
Progressive Retinal Atrophy (PRA) Carla Sanchez Phone (951) 696-4169 E-Mail Carlachez@aol.com http://mastiff.org/PROGRESSIVERETINALATROPHY.htm
Seizure Disorders - Epilepsy Doreen Dysert (503) 348-9347 email@example.com
Brucellosis canis is a venereal disease with no cure. There are 6 types of Brucellosis from varies species and canines can be infected with any of the various strains. This disease will cause spontaneous abortion in breeding females, usually late in pregnancy (45-59th day of pregnancy). Chronic infection from the disease can cause other serious disease states. Due to the fact that it is highly contagious, non-curable and causes fetal demise, any dog infected with the disease should immediately be removed from a breeding program and isolated from other animals. Unfortunately, since it is also contagious to humans, it is often recommended to euthanize the animal. Spaying and neutering can be an alternative, but since it is contagious to human, this option must be taken with extreme caution in order that other species (including humans) not be infected with the disease.
The test for Brucellosis is a simple blood test that can be drawn from you general veterinarian. Your veterinarian may choose to send the blood sample to a private lab or may have an in-house test available. This test is EXTREMELY important in all breeding animals and is required by most sperm banks that store frozen semen. To reiterate, this disease has no cure and is highly contagious. All breeders should verify testing prior to breeding. It is contagious through both sexual contact and casual contact through excreted urine; therefore all dogs that are frequently exposed to other dogs should be tested every six months. Since this disease can also infect humans, it is a reportable disease.
Question and Answers Updated January 2013
Good things to know/remember/remedies to keep on hand.
"If you live in a Lyme disease endemic area such as the Northeast upper Midwest and your dog is the outdoorsy type who picks up ticks on his adventures, you can use homeopathy to good effect in protecting him against Lyme disease.
Joette Calabrese, HMC, CCH, RSHom(NA) is a distinguished American homeopath, public speaker and author. Find her at joettecalabrese.com. Joette’s family lives in the country, with plenty of deer and other critters nearby. The surrounding woods are considered a Lyme tick Mecca. She’s successfully used the protocol described below for many years on Buster (described as “the bad office dog”) as well as her human family members.
This protocol is not for long-term, chronic Lyme disease; for that you’ll need to seek the expertise of a seasoned veterinary homeopath.
First, the tick
When you find a tick on your dog, the first thing to do is remove the tick as soon as possible. There are several techniques you can use; read about them here.
Save the tick by placing it in a covered jar with either 180 proof vodka, grain alcohol or brandy and label it with the date, on whom it was found and where on the body. In the unlikely event that all else fails, the tick can be made into a homeopathic remedy. This is known as isopathy, which works under principles similar to homeopathy.
But for now, just keep the tick in a jar.
Then follow whichever steps below are appropriate for your dog’s situation, depending on how long ago the bite occurred and whether he is displaying any symptoms of Lyme disease.
Step 1 – for prevention after a recent bite
This has been found to be highly effective for bites that are rather recent – say within a few weeks.
Remedy: Ledum palustre 200C
Ledum is the foremost remedy for any kind of animal bite.
•Give the first dose of this remedy at the time you remove the tick.
•Continue dosing with Ledum every 3 hours for the first day
•Then, dose twice daily for a week
•After the first week, dose twice weekly for a month
•Then once per week for another month
This is probably overkill, but worth the extra effort to be certain.
If the tick was discovered in the last few days, Step 1 is likely all you’ll need.
But if your dog has been diagnosed with Lyme disease that is older and more entrenched, follow Step 1 as above, then add Step 2 at any time after using Ledum.
Step 2 – in the event of a Lyme diagnosis
Remedy: Aurum arsenicum 200C
Aurum arsenicum is a capital choice for when a poisonous infection arises, and this is one of those times.
•Dose twice daily for one week
•After the first week, dose twice weekly for a month
•Then once per week for another month
For older cases in which it is critical to take all precautions because illness has set in, follow Step 3 along with the previous remedies.
Step 3 – when there are clinical symptoms of Lyme
Remedy: Borrelia burgdorferi 30C (also called Lyme Nosode 30C)
Borrelia is the remedy made from the Lyme tick.
•Dose with Borrelia once per day for three days and then stop, for a total of three doses
•This may need to be repeated every few months if the symptoms remain.
In older cases of Lyme, the most common symptoms in dogs are arthritis or painful joints and lameness; other symptoms may include fever, lack of appetite, depression or lethargy. Dogs do not exhibit the classic “bulls eye” rash that occurs in humans. Symptoms can occur two to five months after exposure. If your dog shows these symptoms, it’s best to consult an experienced homeopathic vet who can prescribe the correct remedy for his symptoms, along with the above procedures.
How effective is this protocol?
When Step 1 is used at the right time, it’s rare that Lyme disease will develop.
In older cases, where there is a Lyme diagnosis or symptoms, success can frequently be achieved, but may be affected by how entrenched the disease is, whether (and how often) antibiotics and other allopathic drugs have been employed, as well as the general vital force of the dog.
Joette Calabrese has generously shared this protocol and asks that if you know someone who should have this information, please pass it along. Spread the good news of how homeopathy can help"
Lyme disease - homeopathic treatment
changing to OFA Eyes in 2015