Are Bull Terriers on their way to extinction?
According to The Kennel Club Bull Terriers have an effective breed population of only 41.9, which means that it is at high risk of suffering detrimental effects of inbreeding. What on earth does this statement mean?
Inbreeding is the mating of related animals. All matings within a breed involve matings of dogs which are related to some degree since they are all related ultimately to the limited number of dogs which were used to found the breed. Indeed, in the origins of any breed the desired characteristics were bred for and fixed by inbreeding, without inbreeding no distinctive breeds could have been produced. So why has inbreeding suddenly become undesirable? To try to answer this question I will first look beyond the world of dogs to other species for examples of problems caused by inbreeding before returning to dogs.
Recent research has shown that Tutankhamun, the “boy king” of Egypt was the product of a brother-sister marriage – the Pharaohs considered that no one outside the royal family was good enough to marry a royal, and brother-sister matings were the norm over many generations. As we all know Tutankhamun died young, scientists have now documented some of the serious physical deformities and other illnesses which afflicted him. Perhaps the most famous example of the dangers of inbreeding is King Charles II, the last of the Hapsburg rulers of Spain. The product of 200 years of inbreeding, Charles’ tongue was too large for him to speak properly, his infamous Hapsburg jaw was so pronounced that he was unable to chew, and his intellect was somewhat lacking. The behaviour of his ancestors in choosing close intermarriages to protect the crown ended up terminating their line instead. There are lots of similar examples in other royal families from most parts of the world. In our current human society matings between relatives closer than first cousins are illegal – evidently we have learnt from experience! Problems of close inbreeding are of considerable concern when breeding from the limited stocks of zoological gardens. To take just one feature as an example, a study of mammals of twelve species in zoos showed that juvenile mortality in inbred strains was double that of outbred strains (1). In dogs, Willis quotes two highly inbred colonies in the USA: a Beagle colony where… “very high inbreeding caused the death by ten days of age of some 75 per cent of all pups born” and a Foxhound colony where… “inbreeding led to reduced sperm counts in males which in turn led to reduced litter size at birth.” (2) Returning to Bull Terriers, inbreeding problems were noted several decades ago. In the 1930s and 1940s many of the best ‘pure white’ Bull Terriers, maintained as pure white lines since at least the 1860s, were observed to be lacking in vitality. Raymond Oppenheimer reached the conclusion that “… ceaseless white matings tended to a loss of substance and of pigmentation, as well as of head fill and power.” (3) Tom Horner wrote that “In the early thirties many southern breeders of whites were line breeding pretty heavily, and along with the good heads and quality they were getting signs of deterioration in some of their products, poor bone, lack of substance, poor pigmentation, slipping stifles and general effeteness were quite common.” (4) It seems probable that what Oppenheimer and Horner were observing in the inbred strains of white Bull Terriers was “inbreeding depression”.
As a group of animals becomes increasingly inbred it loses versions of genes (alleles) which have not been selected for, so these alleles gradually disappear from the gene pool. Many of these alleles relate to polygenic factors (factors under the control of many genes) such as conformation, health and general vitality. The gradual loss of alleles from populations is known as “genetic drift”, this is a random process which occurs naturally in all populations; it may not matter much in the large gene pool of a large population, but becomes increasingly serious over time in the small gene pools of smaller populations. Whilst some of the lost alleles may be deleterious versions of genes, the process may at the same time increase the proportion of other, mildly deleterious alleles, in the small gene pool, and thus increase the incidence of some diseases. However we may describe it, the ultimate result of inbreeding depression is a general lack of vitality. Scientists express the degree of inbreeding as a Coefficient of Inbreeding, which involves complex calculations, so it is often expressed in more readily understood measurements such as fertility and mortality. Clearly small gene pools are hazardous to the future of a breed (5). How small is the Bull Terrier gene pool? There may be many dogs but genetic analysis estimates their effective population as a mere 41.9. This is far below the level which is regarded as sustainable, our breed is in real danger of dying out.
What is the answer to the problem of excessive inbreeding?
Since the days of James Hinks, the principal founder of the breed, white Bull Terriers have not merely been predominant, for many years they were virtually the only ones shown. Colour was re-introduced to the breed, mainly from the older style of dog now termed Staffordshire Bull Terrier between 1910 and 1925 (6). The whites had become so different from the old style coloured dogs that the coloureds produced by these crosses were of very inferior type, and were disregarded by most white breeders. Indeed the Bull Terrier Club tried to prevent them being shown, they were however, according to the Kennel Club, Bull Terriers, and could be entered in shows, competing with whites. In the 1940s Oppenheimer had watched the emergence from relative obscurity of coloured Bull Terriers, which were then becoming increasingly successful in the show ring. The Bull Terrier Club’s members were long against the use of coloured or colour-bred white sires on ‘Pure White’ bitches and undertook “not to breed from Brindle-bred Whites as a foundation for a ‘White’ strain, and upon selling Brindle-bred Whites to point out the disadvantages of having ‘Coloured blood’ in a White strain” (7). The Club maintained a ‘Pure White Stud Book’ to protect the purity of the whites (Tom Horner was the last keeper of the ‘Pure White Stud Book’). So we had a situation where the breeders of coloureds could use the best whites but the breeders of whites were unable to use coloureds no matter how good they were. Oppenheimer declared that “…. I could see plainly that coloured blood carried with it factors for sturdiness….. I was now satisfied that the fate of the whites hung in the balance and that I must fight for what I knew to be vital to their ultimate survival” (8). Accordingly he led the move to free the Bull Terrier Club’s members from the pledges cited above, and this was done at the annual general meeting in 1950.
Led by Oppenheimer, breeders of whites began to use coloureds in crosses, and the whites were soon restored to full health. He decided that the “brindle factor” was responsible for this and pushed his theory with vigour “… if breeders here or elsewhere in the world, ever forget the overwhelming importance of the brindle factor they and the breed will suffer severely.” (9) Of course he was right that the coloureds had “saved” the whites but technically wrong in that it had nothing to do with the “brindle factor” it was all due to the outcrosses of the whites with the genetically different coloureds. As this brief excursion through Bull Terrier history illustrates, the answer to inbreeding depression is greater genetic diversity.
As an aside, we may note that the interbreeding between Miniature Bull Terriers and Bull Terriers to save the former breed whilst a DNA test was developed for Primary Lens Luxation, has resulted in such increased genetic diversity in Miniatures that their effective population size is now high enough to be officially described as sustainable. Their show quality has also improved dramatically, the best now look like genuine miniatures of their larger cousin Bull Terriers, which they very rarely did prior to interbreeding.
Effective population sizes and sustainability
The Kennel Club quotes the findings of the Food & Agriculture Organisation of the United Nations, “Breeding strategies for sustainable management of animal genetic resources” ( 2010) in expressing the relationship between effective population size and the sustainability of breeds thus:
Effective population sizes which are over 100 are sustainable.
Effective population sizes between 50 and 100 lead to the warning “The rate of loss of genetic diversity within a breed or population increases dramatically when the effective population size is less than 100.
Effective population sizes, which are less than 50, are “considered to be at high risk of detrimental effects of inbreeding.” I will go on to quote the KC’s expansion of this statement: “The breed is at risk of detrimental effects of inbreeding which could increase the chances of the breed being at risk for both known and unknown inherited disorders. The population is also at risk of inbreeding depression, which is an overall decrease in general fitness, or general health, and may reduce litter sizes and fertility across the breed.”
Clearly, with an effective population size of only 41.9, the future of our breed looks bleak!
The future of Bull Terriers depends on breeders’ decisions. The more closely related are the sires and dams of the litters you produce the more likely you are to contribute to the gradual shift towards inbreeding depression in the breed. But you can’t judge the closeness of relationships of possible mates from the ringside, and a layman’s examination of three or even five generation pedigrees will not be much help either. So how can you take into account the extent of inbreeding in mating decisions? Easy, if you make use of the Kennel Club’s Mate Select service you can check the extent of inbreeding involved in any crosses you are contemplating, examine it online on the KC’s web site (10), it is free, easy to use and will help you to produce healthier litters whilst at the same time aiding the genetic diversity of the breed. Remember the old adage “always cross the best with the best” but please, at the same time have in mind the health of the stock which genetic diversity maintains or improves. Beware of the prevalent practice of chasing the current winners to sire your litters, the overuse of popular sires is probably the major factor leading to excessive inbreeding. Selecting sires which have the features you are breeding for but which are not too closely related to your bitch is the way to go.
Wouldn’t it be ironic if inbreeding became so bad in our beloved breed that we had to seek interbreeding with Miniatures to save Bull Terriers!
Dr Brian E Hill (Bull Terrier Breed Health Coordinator)
THE BULL TERRIER CLUB HEALTH PROTOCOL
The Bull Terrier Club strongly recommends that its members health test their Bull Terriers at regular intervals.
BAER TESTING (HEARING)
BAER testing is a one off test which will determine whether your Bull Terrier can hear in both ears, one ear or none.
The best age to test a litter is around 5.5 to 6.5 weeks of age (ear canals don’t open until puppies are about 2 weeks old). The test can be carried out at any age after this, including on adult dogs; however, many breeders wish to know the hearing status of their pups before they go to their new homes. Also, at this age, puppies have an active period followed by a period of sleep, which is the perfect time to carry out the test.
The Kennel Club run a formal BAER testing scheme where results can be recorded on the dogs record and are available on the Kennel Club Health Test Results Finder. More details can be found at the following URL
Requirements for publishing results:
All participating dogs will need to be KC registered and microchipped (prior to screening).
The microchip of individual dogs will be scanned prior to screening to verify that the correct dog is being screened.
Owners are encouraged to submit copies of the certificates themselves directly to the Kennel Club, if the testing centre does not automatically do so.
THE BULL TERRIER CLUB HEART SCHEME
For heart testing 18 months of age is deemed the most reliable time to start testing your Bull Terrier. Kidney testing can be carried out from 1 year onwards.
1) Basic heart auscultation (listening with a stethoscope) – This should only be carried out by a Veterinary Cardiologist.
2) Ultrasound scan – To be carried out by a veterinary cardiologist, preferably on the panel of the Veterinary Cardiovascular Society.
3) Ultrasound scan with flow velocities – To be carried out by veterinary cardiologist, preferably on the panel of the Veterinary Cardiovascular Society. NB: Cardiologist’s view -Usually 1.8 m/s is the cut-off value for normal aortic flow. Further scanning is needed to get more information on what is normal in this breed. It is recommended that animals with measurements above 1.8 OR which have had their certificate marked equivocal only be considered for mating to animals with readings of 1.8 and below to attempt to reduce the incidence of heart disease in the BT**. NB; see point 1 above.
Auscultation/Ultrasound should be carried out prior to using any animal for breeding purposes.
As part of the Bull Terrier Club Heart Scheme data collection, we would appreciate it if copies of results (blue part of auscultation form) could be sent to the Secretary, Elaine Ball. They can be anonymised and will be held for data collection purposes only and not published. This should over time, allow us to form a useful picture of heart disease in the breed.
THE BULL TERRIER CLUB KIDNEY SCHEME
FAMILIAL NEPHROPATHY – POLYCYSTIC KIDNEY DISEASE – KIDNEY DISEASE
This can be a hereditary condition in Bull Terriers. You can get a UPC test done (urine protein:creatinine ratio) test carried out (it costs about £13) to test your dog’s kidney function. For breeding purposes this should be less than 0.3.
TO TRY AND ERADICATE THIS SERIOUS PROBLEM, THE BULL TERRIER CLUB STRONGLY RECOMMENDS THAT ALL IT’S MEMBERS CARRY OUT A UPC TEST AND/OR ULTRASOUND SCAN OF THE KIDNEYS PRIOR TO BREEDING AND DO NOT BREED FROM ANY BITCH WITH A UPC OF 0.3 OR MORE OR THAT SHOWS SIGNS OF POLYCYSTIC KIDNEY DISEASE AS THIS COULD HAVE AN IMPACT ON HER HEALTH OR WELFARE.
THE CLUB FURTHER STRONGLY RECOMMENDS THAT A DOG WITH A UPC OF 0.3 SHOULD ONLY BE CONSIDERED FOR BREEDING TO A LOW RISK BITCH.
**It is important to remember that the UPC test only tests the kidney function at that point in time and is not an indicator of future disease.
If your Bull Terrier, or one you have bred has suffered from kidney disease or is diagnosed as having kidney disease it would be incredibly valuable and kind, if you would ask your vet to take a DNA sample for the AHT. It is a simple cheek swab and you should be able to do this at home instead if you wish, as instructions are provided. If you would like a kit you can either contact the Bryan McLaughlan at the Animal Health Trust.
As part of the Bull Terrier Club Kidney Scheme data collection, we would appreciate it if copies of results could be sent to the Secretary, Elaine Ball. They can be anonymised and will be held for data collection purposes only and not published. This should over time, allow us to form a useful picture of kidney disease in the breed.
The demand for Canine blood is growing and more donors are needed to help save other dogs lives. One donation can help to save up to four other dogs!!
In order to donate, dogs must be over 25kgs, between 1-8 years old, not have travelled abroad, be fit and well and not on any medication.
Dogs have two main blood types – DEA 1.1 Positive or Negative, with more demand for Negative.
There are regular blood collections around the country and at the Veterinary Hospitals.
All the Donors receive a full health check before giving blood and it takes around 5-10 minutes to collect 450mls of blood. After each donation the special dogs are given a goody bag (if its the Pet Blood Bank).
Pet Blood Bank 01509 232 222
Royal Dick Edinburgh 01316517300
Glasgow Vet School 01413305848
Towards a DNA test for familial nephropathy.
For anyone new to the breed I must first explain what this disease is. Familial means it is an inherited disease, nephropaphy relates it to the kidneys. In short, it is an inherited disease which destroys the kidneys. It destroys the kidneys completely, it is fatal and there is no cure. Like us, dogs are “over-engineered” with respect to kidney capacity, both we and dogs have kidneys which can cope with several times the amount of work they are required to do. When this disease strikes, the kidneys are destroyed little by little, there is no noticeable effect on the dog until there is too little kidney tissue left to cope with the work load, then, quite suddenly the dog becomes obviously ill. In a matter of weeks or even days an affected dog goes from apparently normal to having a tremendous thirst, and what goes in must come out again so it becomes incontinent. Its weight declines rapidly regardless of food offered and eaten. By this stage the distressed owner will have visited a vet, who will have done a blood test and diagnosed a kidney problem. The vet may not know about the underlying disease because it is unique to Bull Terriers and may propose various treatments. These are likely to empty your bank account but not help the dog. As the kidney destruction progresses the dog will experience great pain and the and the only kind and sensible answer is euthanasia as soon as real discomfort is evident. This is a “late onset” disease meaning that the affected dog may appear to be perfectly healthy for several years before it succumbs, sadly, this may result in it having puppies before any problem is suspected. The disease may become apparent at any age from a few months up to seven years. Dogs older than that can be assumed not to have inherited the defective gene.
How is the disease inherited? The defective gene may be in either parent and if it is present it will cause the disease eventually. Because genes always exist in pairs one defective gene will be paired with one normal gene, but the normal gene will be “overcome” or dominated by the defective one. The disease affects dogs and bitches equally. If you are familiar with the terminology of genetics the disease is described as being inherited as an autosomal dominant. This mode of inheritance means that one affected dog crossed with one normal dog will produce puppies of which half, on average, will have the disease. Although the disease is fatal, its late onset nature results in it being perpetuated down the generations. It should be noted that the Bull Terrier which sired the breed record number of champions had the disease, died of it, and half of those champions produced died of it too.
Clearly the answer to this problem is to find a test which will identify which dogs have the defective genes before they are bred from. If all dogs could have such a test before mating, and not be mated if they had the gene, then the disease could be completely eliminated. At the moment there is a test available but it is a “rule of thumb” test, not the final answer. It has been developed by Dr Caroline O’Leary at the University of Queensland. It involves collecting a urine sample from the dog first thing in the morning before it has been fed anything, this sample then being tested for its protein/creatinine ratio. This UPC test is inexpensive and most vets will either do it or get it done for you. The desired ratio is below 0.3 but be aware that the “normal” interpretation of the test is that a reading less than 1.0 is satisfactory, which indeed it is for other breeds, but a reading above 0.3 for a Bull Terrier indicates that it most probably has the defective gene. A DNA test for the defective gene would provide a much better answer, a dog once tested would be guaranteed free for this inherited disease. The Animal Health Trust has agreed to develop a DNA test for us, but it does not involve them waving a magic wand, there is much work for them and we have to play our part too to make it possible.
What do we have to do to help develop a DNA test?
DNA tests are expensive to develop. The Kennel Club funds a Genetics Centre at the Animal Health Trust so most of the expense is taken care of, but resources such as consumables and laboratory materials are funded solely by donations from funding organisations, breed clubs and individuals.
We have been asked to make an initial contribution of £11,000 to enable research to begin. At the time of writing most of this sum has been raised. Many donations, both modest and generous have come from individuals in many European countries, large donations have come from Notts and Derby District Bull Terrier Club (£2000) The Dutch Bull Terrier Club (£1,514.51), The Coloured Bull Terrier Club (£1000), The Danish Terrier Club (£800) the Bull Terrier Clinical Studies Fund (£606) the Southern Miniature Bull Terrier Club (£589) and the Danish Bull Terrier Club (£570). Whilst expressing thanks to all of the individuals and clubs concerned we must include special thanks to Terry Heath who set the ball rolling by getting the AHT on side and setting up the donations mechanism through the Just Giving website.
We now need samples from affected dogs, possibly as many as fifty. Collecting these may be difficult because affected dogs don’t survive long and their distressed owners may not be aware of the importance of providing samples. So please be vigilant and if you know of any Bull Terriers which are suspected of the disease try to make sure that samples are collected. Here I am copying the advice of Dr Bryan Mclaughlin of the AHT:
“Due to the nature of this disease I realize that sampling is not always easy. May I suggest that if a dog is suspected of the condition, then a sample is taken prior to full diagnosis, and if renal nephropathy is determined post mortem we are informed. Tissue samples may also be taken if at all possible, but these must either be placed in a preservative solution (not formaldehyde) or frozen directly until we can supply the solution.”
The supply of whole kidneys or kidney tissue samples from affected dogs is the ideal because the diagnosis is then definitive instead of just being the opinion of a vet who may not have met the condition before. The AHT will send DNA cheek swab sampling kits free of charge together with the necessary documentation. Request kits by email to [email protected] putting Bull Terrier DNA study as the subject.
Working together we can and will remove this dreadful kidney disease from our breed. If anyone wishes to contact me about this subject I can reached on [email protected] Finally, donations for this study should be made through http://www.justgiving.com/Terry-Heath What happens to the money if donations exceed the study’s expenditure? Since the donations will have been made specifically for a Bull Terrier problem the AHT will consider them ring-fenced for the breed.
Dr Brian E Hill (Bull Terrier Breed Health Coordinator)
On Monday the 15th of January, the Animal Health Trust DNA testing service will be launching a new DNA test for Lethal Acrodermatitis in Bull Terrier and Miniature Bull Terriers.
Puppies Affected by Lethal Acrodermatits (LAD) have characteristic skin lesions and fail to thrive. These lesion consist of Erythema and adherent scales, primary on the feet, elbows, hocks and muzzle. Hyperkeratosis of the foot pads also occurs. Dogs with LAD are also immunodeficient, so frequently suffer from skin infections.
With the availability of this DNA test Breeders can use this tool as part of their breeding program to ensure that affected puppies are not produced.
This test will be available in January for the introductory price of £35, this is a saving of £13 on the standard prices of £48.
Test can be ordered at our website
www.ahtdnatesting.co.uk , select canine DNA tests and then “B” for Bull Terrier. Here you will see listed both Bull Terrier and Miniature Bull Terrier
To access the introductory discount please enter the following code at checkout.
We are also adding a new Bundle offer for Miniature Bull Terriers.
This will allow owners to test both Lethal Acrodermatitis and primary Lens Luxation for £65, which is a £25 saving on the cost of the two test individual.
Dr Brian E Hill (Bull Terrier Breed Health Coordinator)
The appearance of a liver tri-colour male Bull Terrier advertised at stud on the Internet has caused the BT fancier to question the value or risks associated with using this colour pattern in a breeding scheme.
In the 40 years I have been breeding, liver colour in Bull Terriers has popped up occasionally in reports, discussions and in personal observations. I have personally seen one liver brindle bitch, one all white bitch and now this most recent liver tri-colour dog.
All Bull Terriers carry the B locus gene which is a black overlay gene from production of black pigment (melanin). Review of dog coat colour inheritance publications, especially the most recent, state that all Bull Terriers are double dominant BB because all Bull Terriers have black black nose and pads pigmentation.
We know of course, that some Bull Terriers must be carriers of a recessive b gene since we have knowledge of liver coloured Bull Terriers. Therefore, when the B locus gene is resent in either BB or Bb the dog will have a black coat overlay with black nose and pads (melanin), but when present in red-brown (liver) in all the areas of normal melanin distribution. So in this instance (bb), the dog becomes liver coated with light yellowish eyes, a liver nose and liver pads in areas where it should have been black melanin coloured.
The medical studies of black pigment mutation centres around the change of melanin pigmentation to phaecomelanin pigmentation. Melanin pigment is present in many locations throughout the body in humans and dogs. These include the hearing apparatus, eyes, brain, skin and more. Melanin serves a an important anti-oxidant in these locations to protect against harmful oxygen free radicals which cause a myriad of destructive changes to cellular functions. Phaecomelanin is a poor anti-oxidant and does not function similarly to melanin in any of these organs systems.
There is documented proof that loss of melanin in the hearing apparatus of the ear (Cochlea) increases the rate of hearing loss from both loud noise exposure and aging loss in humans. Canine hearing research has linked the loss of melanin containing cells in the hearing apparatus directly to congenital deafness in the dog. Other research has shown a protective function for melanin in the light receptor layer of the eye (retina) as well.
The recessive b gene must occur with some frequency in the breed since it persistently but infrequently pops up. Whether this gene expression occurs with higher frequency depends on reporting from breeders, have they seen this? How often? What did they do? (Cull, place in pet home, etc.) I think that with the current breeding population so heavily slanted toward black tri-colour, there is a significant risk for many more liver coloured animals to be produced. Thus e may be leading the breed towards potentially more phaecomelanin complications spread widely through our breeding population. Certainly, if the currently offered stud dog is used, it will introduce the recessive b gene rapidly into our dogs as every offspring will carry at least oen copy of the recessive b gene an serve as carriers. Our early breed mentors who wrote the breed standard may not have been familiar with the science, but they certainly understood the importance of black (melanin) pigmentation.
A prominent breeder once said at a BTCA meeting about deafness “We all know deafness is bad, but if you want it, breed to it”. The same applies to liver colour in Bull Terriers, in my opinion, it’s bad, but “if you want it……”
CARL PEW DVM MRCVS
What is Lethal Acrodermatitis?
It is a progressively wasting disease that is usually seen at a young age and is lethal within a few months. There is no effective cure for lethal acrodermatitis, but there are some therapies and medication that can be used to help slow down the process and give your dog a better quality of life.
Lethal acrodermatitis is a serious inherited skin condition of Bull Terriers that usually causes death before the dog reaches two years of age. This disease causes severe retardation of growth, thick skin and painful blisters on the muzzle, eyes, nose, ears, feet, and mucous membranes which eventually leads to pneumonia and death. The most commonly affected areas are the muzzle, ears, feet, legs, and groin. Most breeders can recognize the disease in the puppy by the time it is six to eight weeks old because it is less than half the size of the other puppies in the litter and has flat, splayed feet with dermatitis.
Symptoms of Lethal Acrodermatitis in Dogs
If your dog has lethal acrodermatitis, the signs will most likely be evident by the time he is about three to six months old. Some of the most often seen complaints are:
• Thickened skin on legs and feet
• Painful eruptions on toes
• Pustules and lesions on face
• Blisters on mucous membranes (lips, nostrils, mouth, genitals, throat)
• Slow growth
• Standing with legs splayed apart
• Deformed and broken nails
• Difficulty eating
• Numerous bacterial infections
• Frequent nasal discharge
• Pneumonia (high body temperature, coughing, breathing difficulty)
Causes of Lethal Acrodermatitis in Dogs
In lethal acrodermatitis the skin thickening gets so severe that the dog is unable to walk or eat normally and secondary bacterial or yeast infections are a common side effect. Eventually, infection and wasting progresses to such an extreme that the dog will die, or the owner decides to euthanize.
Diagnosis of Lethal Acrodermatitis in Dogs
A full physical will need to be done along with diagnostic testing and radiographic imaging. The veterinarian will first need to know your dog’s medical history and whether he has had any recent illnesses or injuries as well as any medications your pet may have been given lately. You should also tell the veterinarian if you have tried a new food recently and if your dog’s appetite has been abnormal. A physical examination will be done, and your dog’s vital signs will be checked. The veterinarian will do a skin assessment and will look at the overall appearance of your dog’s physique.
Diagnostic tests will most likely reveal abnormal liver enzymes, including decreased activity of alanine transaminase (AST) and serum alkaline phosphatase (ALP) as well as a decreased lymphocyte blastogenic response. Histology will show inflammation in the outermost layer of skin. Blood tests, including a complete blood count, blood cultures, and a chemical profile usually indicate increased cholesterol, decreased zinc and copper, lymphocytes (white blood cells), and gamma globulins. Radiographs (x-rays) will need to be done of the chest and abdomen to check for bronchitis, pneumonia, and lesions on the mucous membranes in the intestinal tract. Often, the veterinarian will want to perform an MRI, ultrasound, and CT scans as well.
Treatment of Lethal Acrodermatitis in Dogs
There is no cure for lethal acrodermatitis, but there are treatments that can improve your dog’s quality of life and possibly slow the progress of the disease.
Natural foods high in zinc and omega-3 and omega-6 fatty acids are good choices for your dog. Some of the choices your veterinarian may suggest are fish, flaxseed oil, soybean oils, sunflower oils, liver, chicken, salmon, beef, and veal.
Supplements of omega-3 and omega-6 fatty acids and zinc can both be added to your dog’s diet as well. Some veterinarians offer injections of these supplements, but they should only be administered by the veterinarian.
Recovery of Lethal Acrodermatitis in Dogs
As the name implies, this disease is almost always fatal. In rare cases, a dog can live for several years with lethal acrodermatitis, but the quality of life must be considered. If your dog is in constant pain and suffering, the most humane thing to do is euthanize.