Gall Bladder Mucocele (GBM) results when the inside lining of the gallbladder produces a solidified mucus. The mucus remains attached to the lining of the gallbladder and over time fills the entire lumen of the gallbladder leading to obstruction to the flow of bile or rupture of the gallbladder. GBM has received a lot of attention recently. In the past it may not have been diagnosed correctly, however the availability of abdominal ultrasound has made it easy to diagnose. In the UK (where there are at least 5 times the registration of Border Terriers than we see in the US) there has been a concern about the incidence of GBM. Surgery to remove the gall bladder is often the outcome. Late diagnosis does not help as the dogs are often a poor surgical risk at that time.
CECS aka, Spike’s Disease, appears to be Paroxysmal Gluten-Sensitive Dyskinesia (PGSD) in many dogs. Symptoms include a seizure like disorder where the dog remains fully conscious during episodes. But signs can vary. Age of onset is widely variable but often occurs in young adulthood. The definitive diagnosis is to test for gluten and gliadin antibodies prior to being put on a Gluten Free diet. At this time these tests are not available in the US. Dogs that respond to a strict Gluten free diet are presumed to have PGSD. No genetic markers have been associated with this disorder at this time (2022).
Idiopathic epilepsy is a term used for a group of seizure disorders that occur due to abnormal electrical activity in the brain where no structural brain abnormalities exist. Epilepsy is a rule-out disease. Trauma, toxins, viral diseases and brain tumors can also cause seizure-like activity. New anti-epileptic drugs allow many dogs with epilepsy to live normal lives. Idiopathic epilepsy has many presentations and is not always a grand mal seizure where the dog loses consciousness and thrashes around.
There are some dogs that have Paroxysmal Dyskinesia episodes that do not fit the diagnosis of PGSD or idiopathic epilepsy. Paroxysmal Dyskinesia (PD) is an umbrella term given to a range of movement disorders, existing both in humans and domestic animals, characterized by intermittent episodes of involuntary motor movements that are debilitating, sometimes even on daily basis. These disorders were originally suspected to be seizure events, however, some differences in clinical presentation were noted. As opposed to seizures, many times during the episodes consciousness is intact, autonomic signs are absent and abnormal post-ictal behavior is not observed. The episodes can last minutes to hours which is uncommon for epileptic seizures.
Cranial Cruciate Ligament (CCL) disease concerns tears and ruptures of the knee ligament. At first we thought these might be associated with luxating patellas (which may contribute) or with poor rear angulation conformation. However, one cause may be associated with the increased number of Border Terriers participating in Agility and similar high impact activities. Weekend Warrior syndrome can occur in dogs as well as in humans. It is important that dogs participating in high impact and acute turning sports be properly conditioned. Luxating patellas are familial in some breeds but we do not have evidence at this time to support that in Border Terriers. The same applies to dogs with CCL disease.
Hip dysplasia is the abnormal development and growth of a dog’s hip joint. It has been reported in Border Terriers. Some dogs have presented with severe lameness. Canine hip dysplasia (CHD) is a complex disease with a high environmental component associated with the expression of lameness. Inheritance is complex with multiple genes contributing to the expression of CHD. Responsible breeders evaluate the hip status of dogs, as well as their siblings and parents, when making selections on breeding pairs. In Sweden hip scores are required for registration. Where breeders have selected for better scores there has been an improvement in total scores. Unfortunately, in the US not all hip results are entered into the OFA Open database.
Congenital Cardiac Disease. Ventricular septal defects (VSDs) have been reported as well as congenital mitral valve dysplasia. The BTCA recommends that every puppy have a careful cardiac exam by a veterinarian prior going to its new home and that the pediatric cardiac form is submitted to OFA. If a murmur is heard and if it persists beyond 14 weeks, we recommend that a cardiologist do an echocardiogram with the results submitted to OFA for the OPEN Database. VSDs in Border Terriers have been known to close by the time a pup is 6 months old. Great for the life of the dog, but not one you want to breed from. Congenital cardiac disease appears to be complex inheritance. The genetic basis is still unknown.
Juvenile (developmental) cataracts have been reported. These may appear between 2 and 4 years of age. Cataracts that appear at a young age and that are bi-lateral are presumed to have an inherited basis. No genes have been identified in Border Terriers to date. Breeding dogs should have yearly eye exams until at least age 8. Exams beyond that provide useful information. Young dogs with cataracts should have eye exams every year for at least 3-4 years and the results entered in the OFA database. Depending on the rate of progression exams may be spread out after that. Longitudinal data can provide useful information.
Progressive retinal atrophy, a degenerative disease that affects the photoreceptor cells in the eyes, has been reported very rarely. Dogs were removed from the breeding population and there have been no cases reported in recent years.
SLEM (Shaking Puppy) is a neonatal neurologic disorder identified in Border Terriers. In 2017 the gene mutation that causes SLEM was identified. The test is currently available through OFA. It is inherited as a simple autosomal recessive. It is important that ALL SLEM (including carriers) results be entered on the open database. Knowing the SLEM status of an individual allows us to make sure we do not breed two carriers together. Carriers can be used in breeding programs with the hope that we can gradually reduce the frequency of the SLEM gene in the population without putting the breed through a genetic bottleneck. (See the articles by Jerold Bell, DVM.)