Health and The Boston Terrier
The Boston Terrier is generally a very healthy breed, but like any other breed of dog, there are some issues that can affect them. Here we will post any articles/papers which we consider to be of useful information for current owners and prospective new owners alike.
JUVENILE HEREDITARY CATARACT
Early-onset hereditary cataract in Boston Terriers is a condition that was first described in 1978 (Barnett 1978). In this disorder, cataracts are bilateral and can be diagnosed as early as 8-12 weeks of age, but are not congenital. Obvious cataracts occur between 9 and 15 months of age with further progression and maturity of the cataract between 2-4 years. The condition has an autosomal recessive mode of inheritance.
The mutation, or change to the structure of the gene, probably occurred spontaneously in a single dog but once in the population has been inherited from generation to generation like any other gene. The disorder shows an autosomal recessive mode of inheritance: two copies of the defective gene (one inherited from each parent) have to be present for a dog to be affected by the disease. Individuals with one copy of the defective gene and one copy of the normal gene - called carriers - show no symptoms but can pass the defective gene onto their offspring. When two apparently healthy carriers are crossed, 25% (on average) of the offspring will be affected by the disease, 25% will be clear and the remaining 50% will themselves be carriers.
The mutation responsible for the disease has recently been identified at the Animal Health Trust (Mellersh et al 2006, Mellersh et al 2007). Using the information from this research, we have developed a DNA test for the disease. This test not only diagnoses dogs affected with the disease but can also detect those dogs which are carriers, displaying no symptoms of the disease but able to produce affected pups. Under most circumstances, there will be a much greater number of carriers than affected animals in a population. It is important to eliminate such carriers from a breeding population since they represent a hidden reservoir of the disease that can produce affected dogs at any time.
The test is available now and information on submitting samples is given below.
Breeders will be sent results identifying their dog as belonging to one of three categories:
CLEAR: the dog has 2 copies of the normal gene and will neither develop Early-Onset Hereditary Cataract, nor pass a copy of the Early-Onset Hereditary Cataract gene to any of its offspring.
CARRIER: the dog has one copy of the normal gene and one copy of the mutant gene that causes Early-Onset Hereditary Cataract. It will not develop Early-Onset Hereditary Cataract but will pass on the Early-Onset Hereditary Cataract gene to 50% (on average) of its offspring.
AFFECTED: the dog has two copies of the Early-Onset Hereditary Cataract mutation and is affected with Early-Onset Hereditary Cataract. Carriers can still be bred to clear dogs. On average, 50% of such a litter will be clear and 50% carriers; there can be no affecteds produced from such a mating. Pups which will be used for breeding can themselves be DNA tested to determine whether they are clear or carrier.
The Animal Health Trust proudly announces the launch of a DNA test for Early Onset Hereditary Cataract in Boston Terriers. This test was developed in the Genetics Department of the Animal Health Trust by a team led by Dr Cathryn Mellersh.
Here is a link to the Animal Health Trust's website where you can find further information on this subject and request Testing Kits:
http://www.aht.org.uk/
LUXATING PATELLA
The most common orthopedic problem found in the Boston Terrier is patellar luxation, which can lead to rupture of the anterior cruciate ligament. Occasionally Bostons can suffer hip dysphasia, but this condition occurs more often in large breeds, while patellar luxation is more common in small breeds.
The canine patella is the equivalent of the human knee. Dogs have a ligament called the patellar ligament which slides in the patella groove on the lower end of the thigh bone at the front of the knee joint (stifle). When it luxates you can feel a popping at the knee cap as it moves medially (toward the middle of the body). Then the dog's patella ligament may assume its normal position again. This is called "medial patella luxation".
The patella is the kneecap, part of the structure of the stifle (knee) joint. A patella that is not stable but does not slip out of joint is said to be subluxating, while one that comes out of joint on its own is said to luxate. The cause of the problem can be from trauma but is more often genetic in nature. When the luxation is from trauma, something has occurred that has caused the knee to be forced out of normal alignment. A veterinary examination can determine if the knee structure is stable but an overzealous examination can stretch the ligaments. This type of examination is best left to the veterinarian and not done by the pet owner! Usually the traumatic injury occurs when the dog’s leg gets caught somehow and he struggles to pull free. Or during an overly enthusiastic playtime when the playmate grabs the foot and holds tight while the excited puppy tries to get away. Any other similar accident can permanently injure this small joint.
When the luxation is of a genetic nature, it is due to an abnormal development of the leg. There is a small groove that is a part of the structure that allows the patella to move freely but still remain in proper alignment. When this groove is too shallow or when the leg is slightly bowed, the ligaments holding the patella can be damaged. The ligaments themselves can be weak. Any or all of the above will lead to problems.
Signs of patellar luxation are limping, pain, and the dog may frequently stop to stretch his rear leg behind him. This straightening of the leg is done to allow the patella to pop back into its normal groove. There are several degrees of luxation, with the lower grade being the ability of the kneecap to pop back into place on its own and the highest grade (of four) being such severe luxation that only surgical repair can correct the dislocation. There are numerous reports of rupture of the anterior cruciate ligament. This term is familiar to any sports fan! Many a losing season can be blamed on injury to a key player’s ACL!
If your Boston Terrier has subluxating patellas, by all means keep his weight down. The obese dog will surely only become worse. When the patella(s) become loose enough to pop in and out, surgery is usually indicated. Obviously in Grades 3 and 4, surgery will be a necessity. The surgery will include deepening the groove in the thigh bone that the kneecap rides in. Recovery may take at least 6 weeks and may include physical therapy.
It is recommended that the Patella test be done every two years because of changes that may occur in the patella. However, it is most important that the patellas of a Boston Terrier be checked at these times. Most important is to do it before you breed your dog. and every time it is bred thereafter. This could be part of a prebreeding exam for a bitch. The dog should be checked every two years if he is regularly being used as a stud.
The form for the Putnam test to determine whther a dog is affected by Luxating Patella is available for download at the bottom of this page.
BOSTON TERRIER DEAFNESS
Deafness has been known in the Boston Terrier since the origins of the breed. Several of the old books make reference to dogs that were deaf. Today, both Dr. George Strain, world authority on canine deafness, and Dr. Bruce Cattanach, canine geneticist at Oxford University in England, agree that most deafness in Boston Terriers is undoubtedly caused by the gene that cause white/blue eyed deafness in almost 60 other canine breeds. (In some cases there may be other causes of deafness such as infection.) When the embryo is in the process of formation, pigment cells from the neural crest (embryonic spine) migrate outward and form the pattern of the Boston Terrier's markings that we are all familiar with. This pattern is called the Irish Spotting Pattern and is named by geneticists S(i). There is another gene that is found in some Boston Terriers called the piebald gene, and it is thought by some to be responsible for the white "overmarkings" found on some Boston Terriers. This gene is identified as S(p). It is thought that this gene is responsible for half white heads and white heads, or excessively wide collars, etc. There is actually much that isn't known about these color genes and exactly how they are expressed. There may also be little understood modifier genes at work. In any event, the amount of white, especially on the head, appears to have a close relationship to deafness in Boston Terriers.
Deafness in our breed has never been studied, so we have to make certain assumptions about what is known in other breeds. When the pigment cells migrate outwards from the neural crest in the embryo, pigment will eventually cover the body of the dog almost to its stomach and part way down its legs. Other pigment spots on the head will migrate to places on the ears and eyes. This will leave the white blaze, muzzle, chest, and feet unpigmented. (It is also of interest that when a Boston is crossed with a long tailed breed, the resulting puppies will usually have a spot of white at the end of the tail that the pigment doesn't reach.) If the pigment cells fail to reach the inner ear where there are hairs for hearing in the cochlea, the lack of pigment cells causes the death of these hairs about three weeks after a puppy is born. The lack of pigment which causes the death of the hairs results in deafness because the hairs are necessary to transmit sound. If the neural crest pigment cells do not reach the eye, the pigment of the eye remains bright blue. Normally vision in the eyes is not affected by the blue color. Because inheritance of deafness in Boston Terriers has never been studied, we do not know for sure why some Bostons with regular markings may turn up with a deafness problem. Some of the explanations might be that it is a different kind of deafness that is inherited differently, or the modifiers are of the nature that the excessive white color is not expressed.
In any event, what seems apparent is that most deaf Bostons (perhaps about 80 per cent) come from that group of Boston Terriers (perhaps as many as 20 per cent of the breed) that carry excessive white or have blue eye(s). Helpful for the elimination of pigment related deafness is the fact that most show/hobby breeders have been breeding for better markings for almost a hundred years. Dr. Cattanach feels that it should be relatively easy to reduce the amount of deafness in Boston Terriers by breeding for more conservative markings. He says "Therefore my key message is that if one wants to reduce the incidence of S locus associated deafness in a breed, then one should apply selection with as many indicators of pigment cell number and good migration as possible. Eye color appears to be the strongest indicator (in Dalmatians) so select against blue eyes. Size of pigment patches is another. In Bostons this should not be a problem. - at least compared to Dalmatians - and it might take a reappraisal of the Boston Terrier Standard to specify that less white rather than more whiteisdesirable."
"And then there is the direct hearing testing by BAER. Selection for hearing, especially in both ears, would be expected to be effective." "While I would not discount BAER, I would expect much faster progress with eye/patching selection. Why do I think the non-technical route better? Because every breeder can assess every dog he has, every litter, every pup born (alive or dead) by this method. He has a powerful range of measures to provide just about all the information he needs to select for hearing. And it costs not a penny. Were every breeder's individual data made generally available to all to aid in selective breeding, the breed could be transformed very quickly."
BAER TESTING: Only in recent years has BAER testing come into common practice in checking dogs for deafness. Dogs can be deaf in one or both ears. Dogs deaf in one ear are just as likely to pass deafness on to their progeny as those deaf in both ears. The only way that a unilaterally deaf dog can be identified is by BAER testing. This testing is done by attaching tiny electrodes to a dog's skin on his head and measuring the electric impulse produced. It only needs to be done one time in the life of most dogs. BAER testing can be done as early as six weeks, before a puppy leaves for his new home. (It shouldn't be necessary to anesthesize most Boston Terriers to do the BAER testing.) We also need to learn more about the dogs that are not obviously deaf because of a pigment cell deficit. Whether this is the same inherited deafness, or whether deafness in these dogs is caused by a separate genetic inheritance we do not know. The BTCA Health Committee would like to encourage all breeders to BAER test their dogs before breeding and to test all litters, but it recognizes that from a practical standpoint this is an impossibility for some people who live hundreds of miles from the nearest BAER testing center. You can find a list of BAER testers on the Internet at: http://www.lsu.edu/deafness/baersite.htm
Until we have a way to collect good data on deafness in Boston Terriers, it is recommended that you voluntarily refrain from breeding your overmarked and half white headed dogs, or dogs with excessive white on the body, or dogs with blue eyes. This could make a significant difference in the amount and extent of deafness in our breed both now and in future years.
AUTHOR: Dr Bruce Cattanach
Further information on this subject is available for download in PDF format at the bottom of this page. 'white factor packet'
JUVENILE HEREDITARY CATARACT
Early-onset hereditary cataract in Boston Terriers is a condition that was first described in 1978 (Barnett 1978). In this disorder, cataracts are bilateral and can be diagnosed as early as 8-12 weeks of age, but are not congenital. Obvious cataracts occur between 9 and 15 months of age with further progression and maturity of the cataract between 2-4 years. The condition has an autosomal recessive mode of inheritance.
The mutation, or change to the structure of the gene, probably occurred spontaneously in a single dog but once in the population has been inherited from generation to generation like any other gene. The disorder shows an autosomal recessive mode of inheritance: two copies of the defective gene (one inherited from each parent) have to be present for a dog to be affected by the disease. Individuals with one copy of the defective gene and one copy of the normal gene - called carriers - show no symptoms but can pass the defective gene onto their offspring. When two apparently healthy carriers are crossed, 25% (on average) of the offspring will be affected by the disease, 25% will be clear and the remaining 50% will themselves be carriers.
The mutation responsible for the disease has recently been identified at the Animal Health Trust (Mellersh et al 2006, Mellersh et al 2007). Using the information from this research, we have developed a DNA test for the disease. This test not only diagnoses dogs affected with the disease but can also detect those dogs which are carriers, displaying no symptoms of the disease but able to produce affected pups. Under most circumstances, there will be a much greater number of carriers than affected animals in a population. It is important to eliminate such carriers from a breeding population since they represent a hidden reservoir of the disease that can produce affected dogs at any time.
The test is available now and information on submitting samples is given below.
Breeders will be sent results identifying their dog as belonging to one of three categories:
CLEAR: the dog has 2 copies of the normal gene and will neither develop Early-Onset Hereditary Cataract, nor pass a copy of the Early-Onset Hereditary Cataract gene to any of its offspring.
CARRIER: the dog has one copy of the normal gene and one copy of the mutant gene that causes Early-Onset Hereditary Cataract. It will not develop Early-Onset Hereditary Cataract but will pass on the Early-Onset Hereditary Cataract gene to 50% (on average) of its offspring.
AFFECTED: the dog has two copies of the Early-Onset Hereditary Cataract mutation and is affected with Early-Onset Hereditary Cataract. Carriers can still be bred to clear dogs. On average, 50% of such a litter will be clear and 50% carriers; there can be no affecteds produced from such a mating. Pups which will be used for breeding can themselves be DNA tested to determine whether they are clear or carrier.
The Animal Health Trust proudly announces the launch of a DNA test for Early Onset Hereditary Cataract in Boston Terriers. This test was developed in the Genetics Department of the Animal Health Trust by a team led by Dr Cathryn Mellersh.
Here is a link to the Animal Health Trust's website where you can find further information on this subject and request Testing Kits:
http://www.aht.org.uk/
LUXATING PATELLA
The most common orthopedic problem found in the Boston Terrier is patellar luxation, which can lead to rupture of the anterior cruciate ligament. Occasionally Bostons can suffer hip dysphasia, but this condition occurs more often in large breeds, while patellar luxation is more common in small breeds.
The canine patella is the equivalent of the human knee. Dogs have a ligament called the patellar ligament which slides in the patella groove on the lower end of the thigh bone at the front of the knee joint (stifle). When it luxates you can feel a popping at the knee cap as it moves medially (toward the middle of the body). Then the dog's patella ligament may assume its normal position again. This is called "medial patella luxation".
The patella is the kneecap, part of the structure of the stifle (knee) joint. A patella that is not stable but does not slip out of joint is said to be subluxating, while one that comes out of joint on its own is said to luxate. The cause of the problem can be from trauma but is more often genetic in nature. When the luxation is from trauma, something has occurred that has caused the knee to be forced out of normal alignment. A veterinary examination can determine if the knee structure is stable but an overzealous examination can stretch the ligaments. This type of examination is best left to the veterinarian and not done by the pet owner! Usually the traumatic injury occurs when the dog’s leg gets caught somehow and he struggles to pull free. Or during an overly enthusiastic playtime when the playmate grabs the foot and holds tight while the excited puppy tries to get away. Any other similar accident can permanently injure this small joint.
When the luxation is of a genetic nature, it is due to an abnormal development of the leg. There is a small groove that is a part of the structure that allows the patella to move freely but still remain in proper alignment. When this groove is too shallow or when the leg is slightly bowed, the ligaments holding the patella can be damaged. The ligaments themselves can be weak. Any or all of the above will lead to problems.
Signs of patellar luxation are limping, pain, and the dog may frequently stop to stretch his rear leg behind him. This straightening of the leg is done to allow the patella to pop back into its normal groove. There are several degrees of luxation, with the lower grade being the ability of the kneecap to pop back into place on its own and the highest grade (of four) being such severe luxation that only surgical repair can correct the dislocation. There are numerous reports of rupture of the anterior cruciate ligament. This term is familiar to any sports fan! Many a losing season can be blamed on injury to a key player’s ACL!
If your Boston Terrier has subluxating patellas, by all means keep his weight down. The obese dog will surely only become worse. When the patella(s) become loose enough to pop in and out, surgery is usually indicated. Obviously in Grades 3 and 4, surgery will be a necessity. The surgery will include deepening the groove in the thigh bone that the kneecap rides in. Recovery may take at least 6 weeks and may include physical therapy.
It is recommended that the Patella test be done every two years because of changes that may occur in the patella. However, it is most important that the patellas of a Boston Terrier be checked at these times. Most important is to do it before you breed your dog. and every time it is bred thereafter. This could be part of a prebreeding exam for a bitch. The dog should be checked every two years if he is regularly being used as a stud.
The form for the Putnam test to determine whther a dog is affected by Luxating Patella is available for download at the bottom of this page.
BOSTON TERRIER DEAFNESS
Deafness has been known in the Boston Terrier since the origins of the breed. Several of the old books make reference to dogs that were deaf. Today, both Dr. George Strain, world authority on canine deafness, and Dr. Bruce Cattanach, canine geneticist at Oxford University in England, agree that most deafness in Boston Terriers is undoubtedly caused by the gene that cause white/blue eyed deafness in almost 60 other canine breeds. (In some cases there may be other causes of deafness such as infection.) When the embryo is in the process of formation, pigment cells from the neural crest (embryonic spine) migrate outward and form the pattern of the Boston Terrier's markings that we are all familiar with. This pattern is called the Irish Spotting Pattern and is named by geneticists S(i). There is another gene that is found in some Boston Terriers called the piebald gene, and it is thought by some to be responsible for the white "overmarkings" found on some Boston Terriers. This gene is identified as S(p). It is thought that this gene is responsible for half white heads and white heads, or excessively wide collars, etc. There is actually much that isn't known about these color genes and exactly how they are expressed. There may also be little understood modifier genes at work. In any event, the amount of white, especially on the head, appears to have a close relationship to deafness in Boston Terriers.
Deafness in our breed has never been studied, so we have to make certain assumptions about what is known in other breeds. When the pigment cells migrate outwards from the neural crest in the embryo, pigment will eventually cover the body of the dog almost to its stomach and part way down its legs. Other pigment spots on the head will migrate to places on the ears and eyes. This will leave the white blaze, muzzle, chest, and feet unpigmented. (It is also of interest that when a Boston is crossed with a long tailed breed, the resulting puppies will usually have a spot of white at the end of the tail that the pigment doesn't reach.) If the pigment cells fail to reach the inner ear where there are hairs for hearing in the cochlea, the lack of pigment cells causes the death of these hairs about three weeks after a puppy is born. The lack of pigment which causes the death of the hairs results in deafness because the hairs are necessary to transmit sound. If the neural crest pigment cells do not reach the eye, the pigment of the eye remains bright blue. Normally vision in the eyes is not affected by the blue color. Because inheritance of deafness in Boston Terriers has never been studied, we do not know for sure why some Bostons with regular markings may turn up with a deafness problem. Some of the explanations might be that it is a different kind of deafness that is inherited differently, or the modifiers are of the nature that the excessive white color is not expressed.
In any event, what seems apparent is that most deaf Bostons (perhaps about 80 per cent) come from that group of Boston Terriers (perhaps as many as 20 per cent of the breed) that carry excessive white or have blue eye(s). Helpful for the elimination of pigment related deafness is the fact that most show/hobby breeders have been breeding for better markings for almost a hundred years. Dr. Cattanach feels that it should be relatively easy to reduce the amount of deafness in Boston Terriers by breeding for more conservative markings. He says "Therefore my key message is that if one wants to reduce the incidence of S locus associated deafness in a breed, then one should apply selection with as many indicators of pigment cell number and good migration as possible. Eye color appears to be the strongest indicator (in Dalmatians) so select against blue eyes. Size of pigment patches is another. In Bostons this should not be a problem. - at least compared to Dalmatians - and it might take a reappraisal of the Boston Terrier Standard to specify that less white rather than more whiteisdesirable."
"And then there is the direct hearing testing by BAER. Selection for hearing, especially in both ears, would be expected to be effective." "While I would not discount BAER, I would expect much faster progress with eye/patching selection. Why do I think the non-technical route better? Because every breeder can assess every dog he has, every litter, every pup born (alive or dead) by this method. He has a powerful range of measures to provide just about all the information he needs to select for hearing. And it costs not a penny. Were every breeder's individual data made generally available to all to aid in selective breeding, the breed could be transformed very quickly."
BAER TESTING: Only in recent years has BAER testing come into common practice in checking dogs for deafness. Dogs can be deaf in one or both ears. Dogs deaf in one ear are just as likely to pass deafness on to their progeny as those deaf in both ears. The only way that a unilaterally deaf dog can be identified is by BAER testing. This testing is done by attaching tiny electrodes to a dog's skin on his head and measuring the electric impulse produced. It only needs to be done one time in the life of most dogs. BAER testing can be done as early as six weeks, before a puppy leaves for his new home. (It shouldn't be necessary to anesthesize most Boston Terriers to do the BAER testing.) We also need to learn more about the dogs that are not obviously deaf because of a pigment cell deficit. Whether this is the same inherited deafness, or whether deafness in these dogs is caused by a separate genetic inheritance we do not know. The BTCA Health Committee would like to encourage all breeders to BAER test their dogs before breeding and to test all litters, but it recognizes that from a practical standpoint this is an impossibility for some people who live hundreds of miles from the nearest BAER testing center. You can find a list of BAER testers on the Internet at: http://www.lsu.edu/deafness/baersite.htm
Until we have a way to collect good data on deafness in Boston Terriers, it is recommended that you voluntarily refrain from breeding your overmarked and half white headed dogs, or dogs with excessive white on the body, or dogs with blue eyes. This could make a significant difference in the amount and extent of deafness in our breed both now and in future years.
AUTHOR: Dr Bruce Cattanach
Further information on this subject is available for download in PDF format at the bottom of this page. 'white factor packet'
the_boston_terrier_club_of_scotland_putnam_test_sheet.pdf | |
File Size: | 233 kb |
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white_factor_packet_1.pdf | |
File Size: | 1260 kb |
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