Health


Miniature Bull Terrier Health Overview

[Eyes- Primary lens luxation]
[Ears- Congenital deafness]
[Heart- Heart disease]
[Kidneys- Renal disease]
[Skeletal- Patellar luxation]
[Skin- Allergies]
[Skin- Lethal acrodermatitis]
[Neurological- Behavioral disorders]

Overall the miniature bull terrier is a fairly wholesome breed when health screenings are performed properly on mature individuals. But even the best dogs from the best kennels can fall victim to common ailments associated with bullies. Diagnostic tests do not guarantee a dog will remain in perfect health, they simply reassure that a dog is not showing symptoms of disease at the present time. Certain conditions such as kidney disease may not arise until much later in life even though a dog consistently passed routine screening. Most buyers are under the false impression that screened parents only produce ailment-free puppies. This is far from the truth. Medical screenings cannot guarantee the health of offspring either. The purpose of health testing is to promote wellness in the breed, not guarantee lifelong health. While breeders utilize health screenings in an attempt to minimize issues, there is always moderate risk associated with purchasing a miniature bull terrier. Because miniature bull terriers are not as common as other breeds, many vets have little (if any) experience with the breed. Always try to choose a vet based on qualifications rather than convenience.

In recent years the miniature bull terrier has become prone to health issues. Many of them are throwbacks to ancestral defects. Deafness, for example, was notoriously common in solid white English terriers and documented by dog handlers in the nineteenth century. Unfortunately these issues are becoming more and more prevalent with each generation. Frequently miniature bull terriers require veterinary assistance to bear pups or even conceive at all. The probability of skin allergies has drastically increased. Head-types are emerging, so convex in shape, that the upper and lower mandibles do not meet correctly. This results in faulty tooth alignment, soft palate deformities, or respiratory issues. There is a brewing debate over the ramifications of over-corrected traits like those seen in terriers with extreme head shapes. However, there is little scientific data to support or refute claims from either side. Nevertheless, one thing is certain. All of these conditions are heritable in one form or another which means they can be passed along to future offspring.

In all truth, “improvements” made by breeders since the early twentieth century (1915-present) led to the elevation in genetic defects. This in no way suggests it was done purposefully. No responsible dog breeder would intentionally generate excessive health problems within a breed. In miniature bull terriers the defects are a result of limited gene pools, fragmented populations, rise and decline of breed popularity, and society’s view of “what looks good”. Vintage breeders would likely assert that contemporary terriers are deviant with their short, stubby body and roman head. But modern breeders adamantly defend their beloved minibulls and the distinctive head that makes them so unique. The breed standard is an ever-evolving set of guidelines and, as such, varies according to society and the time period. Two centuries from now the breed will likely have diverged from the current standard. A new set of guidelines will be adopted and only old photos of today’s bull terrier will endure.

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Primary Lens Luxation

Primary lens luxation, or PLL, is a hereditary condition caused by a recessive allele. The mutation responsible for the disease affects miniature bull terriers and multiple other breeds. In unaffected dogs specialized fibers (zonules) in the eye hold the eye-lens in the correct position. However, in dogs impacted by PLL the fibers detach from the ciliary muscle resulting in blindness. The condition can hit suddenly and is very painful. The first sign of luxation is usually redness and swelling of the eye and, by that time, the outcome is usually complete vision loss. In other cases, the lens doesn’t completely detach and the eye can be partially salvaged with surgery. Even then there is still significant vision loss. According to a study published in The Open Genomics Journal, the disease is late-onset and typically manifests around 5 years old (Gharahkhani et al., 2012). PLL has been documented as early as age 2 and as late as age 8.

It is important that breeds with high frequencies of PLL be tested. By 5 years old many dogs have produced offspring and, if untested, may have inadvertently passed the trait to puppies. The gene associated with PLL operates under simple Mendelian inheritance patterns. There is a dominant version, the normal type, which results in proper fiber attachment. The mutative version of the gene is recessive and causes a deficiency in fiber attachment during adulthood. As a result, there are 3 possible allelic combinations. A terrier can possess the “DD” combination (2 normal copies), the “Dd” combination (1 normal copy, 1 recessive copy), or the “dd” combination (2 recessive copies). The affected dog does not possess a dominant allele and will have a “dd” genotype, exhibiting lens luxation 100% of the time. Under most circumstances the locus that codes for normal functioning can operate properly as long as there is atleast 1 normal allele (a big “D”). This means that carriers and non-carriers (DD and Dd) typically don’t suffer from lens luxation. However it should be noted that carriers (Dd) do have a slightly elevated risk of developing a luxating lens. Interestingly, of 196 PLL-affected dogs involved in a 2010 study, 23 were carriers (Dd) and 12 actually possessed two normal copies of the gene (Farias et al., 2010). Roughly 10% of carriers and 3% of PLL-clear adults will exhibit lens luxation. Researchers have suggested environmental factors or modifier genes may influence the development of the disease in carriers and non-carriers. Old age may also play a role in the appearance of PLL in clear terriers but this is a rare occurrence.

Approximately 50% of all miniature bull terriers are carriers of this disease. This is concerning because researchers in the United Kingdom documented carrier frequencies at 39% in 2011 (Gould et al., 2011). This means the frequency of the mutation in miniature bull terriers has risen 11% in only 5 years. Breeders attempt to mitigate PLL through health screenings and selectively pairing adults to ensure puppies don’t fall victim to the disease. A responsible kennel will never cross a male PLL-carrier with a female PLL-carrier. In a litter of 4, carrier-crosses result in 1 clear pup, 2 carrier pups, and 1 affected pup. On the other hand, the AKC and OFA allows breeding of carriers to clear genotypes due to the limited gene pool and relatively low risk associated with PLL emergence. Annual eye exams, regardless of PLL status, are recommended for all miniature bull terriers.

To order a test kit or learn more about the condition, visit the OFA website:  [PLL Test- Orthopedic Foundation for Animals]

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Deafness

Deafness or hearing loss is a common occurrence in miniature bull terriers. A BAER hearing test is the most effective method of diagnosing congenital deafness in terriers. Dogs can exhibit unilateral deafness (one ear) or bilateral deafness (both ears). Usually this condition is present in puppies but often goes unnoticed. This congenital defect is a result of bull terrier ancestry. Deafness in solid white English terriers was documented as early as the mid 1800’s. It’s possible James Hinks may have unwittingly introduced the defect around 1868 during his pursuit for the perfect bull terrier. Unlike PLL, there are no simple diagnostic tests available to determine which dogs will produce affected offspring or which offspring will inherit the defect. The only preventative measure is to have a BAER hearing test performed. Dogs with confirmed hearing loss should be withheld from breeding programs to avoid conveying the trait to offspring.

As with most tests or screenings, the BAER hearing test can provide false results in some instances. There have been cases of normal dogs diagnosed with deafness because of outside factors, such as improper procedures or ear infections. Unless BAER screening is performed on a young puppy, determining the exact cause of hearing loss can sometimes be difficult. Hearing loss can be permanent or temporary and caused by chronic or persistent ear infections, trauma, or old age. Congenital deafness is a permanent form of hearing loss resulting from a birth defect and puppies are typically born with it. Deafness arising in adult dogs is not congenitally-linked. This is not to say that late-onset deafness is not caused by hereditary factors, it just means adult hearing loss is not a birth defect. The root of deafness can be better established if the puppy has routine vet exams and a BAER hearing test during the first year of life. BAER tests are relatively inexpensive but do require veterinary specialists trained to interpret results.

A state-by-state list of BAER testing sites is available here: [BAER Testing Locations]

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Heart Disease

Two types of heart disease are prominent in miniature bull terriers: subaortic stenosis and mitral dysplasia. Both maladies can cause fatality in the first few months of life or go unnoticed for years. Subaortic stenosis results when lesions form below the aortic valve and obstruct bloodflow in the left ventricle. It is common for dogs suffering from subaortic stenosis to die before 3 years of age. Mitral valve dysplasia is a leading cause of congestive heart failure in miniature bull terriers. In this case, the mitral valve fails to close properly, allowing blood to backflow into the atrium. Audible heart murmurs exist with both conditions. Heart dopplers, a type of imaging echocardiogram, are used to check for murmurs. Auscultation is another useful detection method inwhich a qualified individual listens for low grade murmurs with a specialized stethoscope. These diagnostic tools examine heart valves to ensure there is no misappropriation of blood flow in the heart. Based on severity (or lack thereof) some murmurs may not be an issue.

Tests require the expertise of a board certified animal cardiologist. Echocardiograms are expensive but are sometimes offered at discounted rates through veterinary colleges or other organizations. The Orthopedic Foundation for Animals maintains a cardiac database that tracks auscultation and doppler results, though listing is completely optional for pet owners. Treatment depends on severity. In extreme cases surgery has been met with moderate success but is quite costly. A single exam does not guarantee cardiac conditions won’t arise at a later time.

To locate a cardiologist in your area, click here:  [Board Certified Veterinary Cardiologists]

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Kidney Disease

Renal failure is prevalent in the breed. Hereditary nephritis and polycystic kidney disease are the two main culprits. In miniature bull terriers hereditary nephritis is caused by a dominant gene with inheritance patterns similar to those of primary lens luxation. Dogs with the condition should not be utilized in breeding programs. Nephritis can easily be diagnosed with a urine protein creatinine test. UPC tests should be performed annually. Recently there have been rumors about the potential development of a DNA-based test for renal nephropathy in the United Kingdom. However these is no confirmation as of yet. If true, the test would be similar to the one used for PLL and eliminate the need for annual UPC screenings. A project of this magnitude would require years of formulation and testing, so it will likely be a while before it hits the market.

Diagnosis of polycystic kidney disease is slightly more complex and requires an ultrasound to scan for cysts. A renal ultrasound is only needed once in a dog’s lifetime. Like nephritis, a dominant gene is also responsible for polycystic kidney disease (Gharahkhani et al., 2011). It only requires one copy of the gene to induce the disease. After an extensive investigation into the deaths of 47 bull terriers with PKD, researchers found that each dog was heterozygous (carriers) for the lethal allele, further supporting predictions that pups carrying two copies died before birth (Gharahkhani et al., 2011). In some cases the disease may not be detected especially if there is delayed cyst enlargement. The TaqMan SNP Genotyping Assay is a diagnostic test useful in detecting the allele responsible. Furthermore, Gharahkhani et al. suggests the TaqMan test would allow breeders to screen for PKD, promote early treatment, and reduce prevalence of the condition in bull terriers (Gharahkhani et al., 2011). However the test has not been developed for private use or made available to the general public.

Read the article on polycystic kidney disease published by researchers in Queensland, Australia:  [PKD in Bull Terriers- Gharahkhani et al. 2011]

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Patellar Luxation

Slipping or dislocation of the knee cap in the hind leg is known as patellar luxation. Miniature bull terriers naturally have a predisposition for the condition. It is similar to hip dysplasia except that it deals with the knee joint. Affecting one or both knees, patellar luxation can be triggered by blunt trauma or result from a congenital defect. The American College of Veterinary Surgeons recommends that afflicted dogs not produce offspring. Symptoms include a bow-legged or knock-knee appearance, limping, and lameness. Diagnosis is made through a series of evaluations and usually involves referral to an orthopedic surgeon. At that time the orthopedic surgeon can provide a detailed description of treatment. Both surgical and non-surgical methods are possible and depend on the grade of patellar luxation as determined by the specialist.

This condition is less common than others observed in minibulls. More often than not, the luxation is triggered by blunt-force trauma. Owners should discourage puppies from jumping off furniture or overexertion. Puppies are sometimes misdiagnosed with patellar luxation at an early age. During the first year a puppy is still developing. It is not unusual for a puppy’s knees to be slightly loose until the muscles and tendons have a chance to strengthen. Unless the puppy is showing symptoms of luxation there is usually no need to have them evaluated. The Orthopedic Foundation for Animals recommends a dog be atleast 12 months of age before a patellar luxation examination is completed.

Learn more about patellar luxation here:  [American College of Veterinary Surgeons]

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Allergies

Allergies can occur in any breed. Miniature bull terriers are no exception. Skin-related issues are more common in white dogs but can also be exhibited by colored dogs. Minibulls can react to nearly anything including dogfood, fleas, grass, or shampoo, as well as numerous other allergens. Signs of allergies are extreme hair loss/shedding, persistent scratching (especially at ears), constant licking or chewing of the legs and feet, vomiting for no apparent reason, hotspots, chronic ear infections, wheezing and hacking, and redness of the skin. Frequently the allergy can be resolved with a simple diet change. The most common food allergens are chicken, dairy, wheat, corn, eggs, beef, and fish. When food is the problem a diet change is advised. A dog currently eating a chicken-based food should be switched to a lamb, fish, venison, or buffalo-based food made by a different manufacturer. The general idea behind the switch is to introduce an unfamiliar protein; one the dog has not previously encountered. Sometimes it is not the protein causing the reaction. Before searching for a new food, check the ingredients of the current food. Look for other known allergens in that particular food and steer clear of all of them.

Unlike the allergic reaction, which generally has sudden onset, a diet change takes time to work. It requires around 8 weeks to see results or know if the allergy is food-related. Old toxins aren’t eliminated from the digestive system for 2-3 weeks. The remaining 4-6 weeks allow the dog to heal from previous reactions. During this trial period the dog cannot have any other type of edible products; trash, bones, treats, tablescraps, nothing. If symptoms disappear the culprit has been discovered. Continue feeding the same food from then on out, as you don’t want to trigger any more allergic reactions.

Most vets will recommend trying a expensive dogfood with hydrolyzed proteins, but this is something that should be attempted as a last resort (meaning after a couple other foods have been tried first). In the case of true protein allergies hydrolyzed foods are necessary because the dog reacts to proteins in general, not a specific ingredient. Hydrolyzed proteins are broken into smaller components so the immune system doesn’t react adversely to them. Common brands of hydrolyzed dogfood are Purina Veterinary Diets, Royal Canin Veterinary Diet, and Hill’s Prescription Diet. Each one comes in a 25 pound bag and costs between $85-100 dollars. However a majority of dogs do well with a much cheaper alternative (usually one not sold at the vet’s office).

When food is not the problem it becomes incredibly difficult to diagnose skin disorders. There are numerous diseases of the skin including pyoderma, alopecia, atopic dermatitis, and dozens more. Conditions resulting from a simple hotspot, mange, or staph infection can easily be treated. Others, however, may require thousands of dollars and trial-and-error before a definitive cause is determined. Skin disorders can be a sign of autoimmune deficiencies. Medication, steroids, skin scrapings, or intradermal testing might be utilized to diagnose the condition. Ideally a vet can pinpoint the root cause rather than treat symptoms. Medications and steroids are not for long-term use. They only mask the problem, not treat it, and dogs build immunity to them after repetitive use. Natural methods are sometimes recommended to help alleviate symptoms. Epsom salt baths, probiotics, raw diets, vitamin supplements, and chamomile soaks or tablets are effective holistic remedies. Do not be afraid to get a second opinion if results are not forthcoming after a reasonable amount of time. Sadly, most vets do not have experience with bull terriers or their associated health problems.

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Lethal Acrodermatitis

Lethal acrodermatitis is a relatively new congenital disorder currently being studied by researchers. The disease has been documented for decades but the number of LAD-affected bull terriers is on the rise. This genetic disorder is exclusive to bull terriers, usually resulting in death before two years of age. Puppies exhibiting symptoms of LAD suffer from stunted growth, painful skin lesions, chronic skin infections, and aggression or abnormal behavior. As affected pups mature their coat fades due to lack of pigmentation. Hydrocephaly causes behavioral changes. In general, quality of life is low for dogs inflicted with the disease. Immune deficiencies lead most to succumb to respiratory-related illness or bacterial infections.

Fortunately, a veterinary research and diagnostic organization based in the United Kingdom developed a swab test for LAD in 2018. The simple, cost-effective test is now widely available to the public and should become a mandatory component of vigorous health screening in the future, much like PLL. The autosomal mutation follows a recessive pattern of inheritance, meaning there is still a high probability of the mutation cropping up within the population. Two parents carrying the LAD mutation will produce 1 affected pup in a litter of 4. However, carriers can still be utilized in breeding programs as long as breeders adhere to strict guidelines similar to those employed with carriers of primary lens luxation. It is extremely important for both breeders and buyers to be aware of this condition to help reduce cases of LAD going forward.

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Behavioral Disorders

Obsessive compulsive disorder, compulsive tail chasing, and sudden-onset aggression have been documented in bull terriers. They are all examples of neurological disorders. Behaviors such as hucklebutting (rapid spinning) appear harmless but should not be encouraged. Excessive licking, barking, pacing, and tail-chasing are alternate forms of obsessive behavior. Obsessive compulsion can be learned or hereditary and triggers include anxiety, excitement, and confinement. Many times these behaviors can be controlled or stopped altogether with proper training. Sudden-onset aggression (aka rage syndrome) is a neurological disorder of unknown origin where dogs suddenly suffer from uncontrollable fits of rage. In all cases the dog is unaware of what is happening and the condition cannot be mitigated with training or behavioral modification. This form of aggression is extremely rare but a majority of cases result in euthanasia due to the unpredictable nature of the dog.

Example of obsessive spinning:  [Hucklebutting Behavior in Mini Bull Terrier]
Example of sudden onset aggression:  [Rage Syndrome in Bull Terrier- Video 1]
Another example of SOA:  [Rage Syndrome in Bull Terrier- Video 2]

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Additional Resources

Farias, F., Johnson, G., Taylor, J., Giuliano, E., Katz, M., & Sanders, D. et al. (2010). An ADAMTS17 Splice Donor Site Mutation in Dogs with Primary Lens Luxation. Investigative Opthalmology & Visual Science, 51(9), 4716. http://dx.doi.org/10.1167/iovs.09-5142 [Farias PLL Research Study]

Gharahkhani, P., O’Leary, C., Kyaw-Tanner, M., Sturm, R., & Duffy, D. (2011). A Non-Synonymous Mutation in the Canine Pkd1 Gene Is Associated with Autosomal Dominant Polycystic Kidney Disease in Bull Terriers. Plos ONE, 6(7), e22455. http://dx.doi.org/10.1371/journal.pone.0022455 [Gharahkhani Polycystic Research Article]

Gharahkhani, P., O’Leary, C., Duffy, D., Bernays, M., & Kyaw-Tanner, M. (2012). Primary Lens Luxation in Australian Tenterfield and Miniature Bull Terriers is Due to An Old ADAMTS17 Mutation and is an Additive Trait. TOGENJ, 5(1), 7-13. http://dx.doi.org/10.2174/1875693×01205010007 [Gharahkhani PLL Research Study]

Gould, D., Pettitt, L., McLaughlin, B., Holmes, N., Forman, O., & Thomas, A. et al. (2011). ADAMTS17 mutation associated with primary lens luxation is widespread among breeds. Veterinary Ophthalmology, 14(6), 378-384. http://dx.doi.org/10.1111/j.1463-5224.2011.00892.x [Gould PLL Research Study]

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