Coton de Tulear’s are a relatively healthy breed, there expected lifespan is around 12 - 16 years but can live longer.
There are few genetic health problems within the breed, and at present the UK Kennel club require no health testing. But there are tests available for Coton’s and most breeders in Europe carry out these as routine, as most Cotons in the UK derive from European lines, we feel it is important to use the health tests where available.We carry out the following tests on our dogs.
Primary Hyperoxaluria type 1 (PH1)
Primary hyperoxaluria (PH) is a rare autosomal recessive disorder of glyoxylate. It is characterized by the accumulation of oxalate and subsequent precipitation of calcium oxalate crystals, primarily in the kidneys, leading to progressive kidney failure. If the storage capacity of the kidneys is exhausted, the crystals are accumulated in other tissues including bones, joints, cartilages, retina and muscles.
The symptoms may include intense abdominal pain radiating to the groin, blood that can be seen in the urine, and the passage of kidney stones.
Canine Multifocal Retinopathy type 2 (CMR2)
Canine multifocal retinopathy (CMR) is a hereditary disease. It is a retinal disorder caused by mutation in VMD2 gene (Vitelliform Macular Dystrophy 2 Gene). VMD2 gene is coding a protein bestrophin which is responsible for right forming of pigment epithelium in retina. Mutations in VMAD2 gene cause pigment epithelium atrophy which is leading to serious damage of sight.
CMR disease usually arises before 4th month of age in an affected puppy. Clinically, rose-grey coloured lesions are remarkable in retina. These lesions are of different size and shape and are occurred in both eyes of affected individual. Total blindness usually comes in higher age.
The mutation causes raised lesions to form on the retina which alters the appearance of the eye but usually does not affect sight. The lesions may disappear, or may result in minor retinal folding. Symptoms of the mutation usually appear when a puppy is only a few months old, and generally do not worsen over time.
Von Willebrand Disease type 1(vWD1)
Von willebrand disease (vWD) is caused by plasmatic von willebrand factor (vWF) insufficiency. VWF is a blood glycoprotein (not enzyme) important for blood coagulability. Its primary function is to bind itself to other proteins, and also facilitates aggregation and adhesion of the thrombocytes to wound site. The deficiency or failure of vWF function causes bleeding which is most apparent in tissues having high blood flow shear in narrow vessels, VWD manifests oneself as a tendency to bleeding from skin and tissues. The disease can be inheritable or acquired.
VWD type 1, the type that occurs in the Coton De Tulear is the most frequent occurring and the least serious form of vWd. It is inherited autosomal recessively. The disease is characterized by low plasma vWF concentration and normal vWF protein structure. Most affected animals have few if any symptoms. Dogs with mild to moderate forms of the disease may not be diagnosed for years.
Banderas Syndrome (BNat)
Also referred to as Bandera’s Neonatal Cerebellar Ataxia, BNAt, or NCA, Bandera’s Syndrome is a hereditary disease found only in the Coton de Tulear dogs. The cerebellum is the part of the brain that coordinates movement. If it does not function normally, the dog will lack the ability to control their movement which is referred to as “ataxia”. There are other and varied forms of ataxias in dogs and other animals, including humans. While some ataxias are caused by an infection or injury to the brain, we know that BNAt is the result of a genetic mutation; the University of Missouri, Animal Genetics Laboratory has isolated the very gene responsible for this disease in the Coton de Tulear. In BNAt, the mutation is in a glutamate receptor gene. These receptors are responsible for the ability of the puppies’ brains “to learn” motor skills– walking, eating, standing, eliminating, etc. All genes come in pairs and as long as a dog has one normal gene, their cerebellum develops normally. In the mating of two dogs that carry one copy of the gene with mutation, the two mutant genes will be paired in some of the pups. Then the glutamate receptors do not develop in the cerebellum and the puppy has Bandera’s Neonatal Cerebellar Ataxia.
The Patella or kneecap is part of the stifle joint (knee). In patellar luxation the kneecap luxates or pops out of place either in a medial or lateral position. Medial patellar luxation should be considered an inherited disease and is often seen in puppies.
Luxated patella is categorised in four grades, depending on the severity of the condition:
Grade I: This is when the kneecap manually dislocates but goes back into place
once the pressure is released. Considered as a mild case, with treatment not
necessary, However, you need to keep a close eye on your dog in case the
condition gets worse.
Grade II: The kneecap dislocates more often, either manually or automatically,
when the joint is being flexed and continues to be dislocated until the joint
is extended and the leg is turned into the opposite direction of the
dislocation. Considered as the middle ground between mild and severe, dogs with
grades I and II should be closely monitored in case the condition gets worse.
Grade III: The kneecap dislocates on a regular basis, whenever the joint is flexed
and extended. Dislocation is manually decreased when the joint is extended.
This is considered to be severe enough to warrant surgery.
Grade IV: The kneecap is permanently dislocated and cannot manually be put back
into place. This is because the groove is too shallow or, in some cases,
completely missing. Surgery is needed to fix this problem.
Degenerative Myelopathy (DM)
Degenerative Myelopathy is a progressive disease of the spinal cord in older dogs. The disease has an insidious onset typically between 8 and 14 years of age. It begins with a loss of coordination (ataxia) in the hind limbs. The affected dog will wobble when walking, knuckle over or drag the feet. This can first occur in one hind limb and then affect the other. As the disease progresses, the limbs become weak and the dog begins to buckle and has difficulty standing. The weakness gets progressively worse until the dog is unable to walk. The clinical course can range from 6 months to 1 year before dogs become paraplegic. If signs progress for a longer period of time, loss of urinary and faecal continence may occur and eventually, weakness will develop in the front limbs. Another key feature of DM is that it is not a painful disease.
Intervertebral Disc Disease
Intervertebral disc disease (IVDD) occurs when the cushioning intervertebral discs between the vertebrae of the spinal column become displaced, deteriorate, bulge out, rupture, or burst (herniate) into the spinal cord space. When this happens, the discs press on the nerves that run through the spinal cord, which can cause pain, nerve damage, and in severe cases, paralysis.
IVDD is sometimes referred to as a slipped or herniated disc. IVDD is one of the most common neurological disorders in canines and reportedly affects 2% of the domestic dog population.
Progressive retinal Atrophy, progressive Rod-cone degeneration or PRA-prcd
Progressive retinal Atrophy, progressive Rod-cone degeneration, or PRA-prcd, is a disorder in which the cells in the retina of a dog degenerate and die. PRA is the dog equivalent of retinitis pigmentosa in humans. Most affected dogs will not show signs of vision loss until 3-5 years of age. Complete blindness can occur in older dogs. Progressive Rod-Cone Degeneration is a form of PRA known to affect over 40 different breeds.
The retina is a membrane located in the back of the eye that contains two types of cells known as photoreceptors. These cells take light coming into the eyes and relay it back to the brain as electrical impulses. These impulses are interpreted by the brain as vision. In dogs suffering from PRA-prcd, the photoreceptors begin to degenerate, causing an inability to interpret changes in light resulting in loss of vision. Rod cells, which are normally function in low-light, begin to degenerate first, leading to night-blindness. The cone cells, which normally function in bright-light or daytime conditions, will deteriorate next. This often leads to complete blindness over time.
Hereditary Hyperuricosuria (HUU)
Dogs with this genetic mutation metabolize waste product s as uric acid in their urine. The uric acid forms into hard stones in the bladder, causing pain and inflammation as the stone moves through the urinary tract.
A dog that has difficulty urinating or appears to have an inflamed bladder may have HUU. Other signs can include blood in the urine and frequent urination. If the dog is unable to pass the urate stones without medical intervention, surgery may be required to remove them. And if the urinary tract is blocked, the condition can be life-threatening. Even in the best-case scenario, HUU is uncomfortable and painful for the dog.
The mutation is autosomal recessive. Both parents will need to be carriers of the mutation to pass it on to their offspring. Carriers will not show any symptoms of HUU and even affected dogs may not show any signs, so it is important to test dogs for HUU prior to breeding.