Tollers are generally healthy. However, like almost all dog breeds, they have specific potential genetic disorders. Luckily Toller breeders have several DNA tests available that allow us to avoid producing them. When you are searching for your next Toller please ensure the breeder is testing the Sire/Dam for the following:
- Hip Dysplasia – an abnormal formation of the hip socket that can lead to severe arthritis and lameness.
- Cardiac – A check for any malformation of the heart or great vessels.
- Eyes (CAER) – A check for any inherited eye disease.
- Collie Eye Anomaly (CEA) – an inherited disease causing defects in the formation of the eye.
- Progressive Retinal Atrophy (PRA) – a group of diseases that cause the retina of the eye to degenerate slowly over time.
- Juvenile Addison’s Disease (JADD) – a rare, early onset, chronic endocrine disorder in which the adrenal glands do not produce sufficient steroid hormones.
- Cleft Palate (CP1) – a birth defect whereby a hole in the roof of the mouth develops while the puppy is in utero.
- Degenerative Myelopathy (DM) – A debilitating disease that causes gradual paralysis
- Degenerative Encephalopathy (DE) – a new neurodegenerative disease
THE DYSPLASTIC HIP JOINT
Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.
The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint’s lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal’s body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint’s range of motion decreases.
No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.