Health Testing

DEGENERATIVE MYELOPATHY (DM)

Degenerative Myelopathy (DM) is a progressive disease of the spinal cord commonly seen in older Corgi dogs. This condition has an insidious onset, typically manifesting between 8 and 14 years of age. It begins with a loss of coordination (ataxia) in the hind limbs, causing the affected dog to wobble while walking, knuckle over, or drag their feet. Initially, one hind limb may be affected before the other follows suit. As the disease progresses, limb weakness worsens, and the dog may struggle to stand, ultimately leading to an inability to walk. The clinical course can vary, lasting anywhere from 6 months to 1 year before dogs may become paraplegic. Prolonged progression of symptoms can result in loss of urinary and fecal continence, and eventually, weakness may develop in the front limbs. Notably, DM is not considered a painful condition. While any dog can be tested for DM, certain genetic backgrounds prevalent in some breeds may prevent symptom development, even in dogs testing at risk. Current evidence linking the genetic mutation to actual spinal cord evaluations has primarily been established in the breeds listed. For more information on Corgi breeding health standards and DM diagnosis, please visit http://www.ofa.org/dnatesting/dmexplanation.html and http://www.caninegeneticdiseases.net/DM/ancmntDM.htm.

EXERCISE INDUCED COLLAPSE (EIC)

Exercise Induced Collapse (EIC) is a genetic disorder affecting canine muscle control that occurs following periods of extreme exercise. Episodes generally happen after 5 to 25 minutes of excessive activity, such as prolonged running. The severity of these episodes varies between dogs, often starting with a rocking motion, leading to weakening of the hind limbs and eventual collapse. Typically, these attacks are brief, lasting less than 20 minutes, and dogs usually recover quickly. In some limited cases, episodes may prove fatal. Symptoms typically manifest from a few months of age to 3 years old, particularly at an age when more intensive training begins. Owners of dogs affected by EIC should be well-informed about activities that may trigger an episode to aid in effective Corgi disease prevention.

VON WILLEBRAND'S DISEASE TYPE I (VWD1)

Von Willebrand disease (vWD) is a genetic disorder that impairs normal blood clotting, potentially leading to prolonged bleeding after an injury. This condition is due to a deficiency or lack of sufficient von Willebrand factor (vWf), which serves as a binding protein during blood clotting. To date, three types of vWD (Types 1, 2, and 3) have been identified in dogs, alongside five different genetic mutations that cause canine vWD. Von Willebrand’s disease type 1 (VWD1) is marked by a reduction in normal vWf levels to approximately 5-10% of what is considered normal. Since some vWf is produced in dogs homozygous for the VWD1 mutation, this form is seen as less severe than types 2 and 3. The mutation involves a G>A substitution and has variable penetrance, being recessive and requiring two copies for affected dogs. Symptoms commonly include excessive bleeding after injuries or blood in bodily secretions (urine, feces, etc.).

HEREDITARY CATARACTS (HC)

Cataracts characterize a clouding of the lens in the eye, caused by tissue breakdown, resulting in impaired vision, and potentially total blindness. In canines, hereditary mutations can lead to cataracts, with conditions referred to as Hereditary Cataracts (HC), Juvenile Cataracts (JC), or Early Onset Cataracts (EOC). One specific mutation in the HSF4 gene leads to cataracts in several dog breeds. This type of cataract is typically bilateral, affecting both eyes. HSF4-associated cataracts often begin small and grow progressively, but the growth rate varies significantly among dogs. Some may experience slow growth, maintaining relatively clear vision, while others might go blind quickly. Corrective surgery is viable but can be costly and is not always successful. One HSF4 mutation causes the recessive form of HC in breeds such as Boston Terriers, Staffordshire Bull Terriers, and French Bulldogs. Since it is recessive, a dog must have two copies of this mutation to develop this form of cataracts. This mutation primarily leads to early-onset HC, typically occurring between 12 months and 3 years of age in Staffordshires and between 2-3 years in Boston Terriers. Boston Terriers may also suffer from late-onset HC, although the HSF4 gene mutation is not responsible for this variant. A separate mutation affecting Australian Shepherds relates to HC, presenting dominantly but with incomplete penetrance, meaning only one mutation copy is needed to predispose the dog to the disease. Research indicates that this mutation increases the likelihood of developing posterior bilateral cataracts significantly, although secondary genetic interaction may explain cases where dogs with the HC mutation do not develop cataracts. It's crucial to understand that not all cataracts are hereditary; some may result from age or injury. Cataracts located in different parts of the lens may also exhibit familial traits, though not necessarily attributed to the HSF4 mutation.

PROGRESSIVE RETINAL ATROPHY ROD-CONE DYSPLASIA 3 (PRA-RCD3)

Progressive retinal atrophy (PRA) encompasses various progressive conditions leading to retinal atrophy and potential blindness. Breeds including Cardigan Welsh Corgis, Pembroke Welsh Corgis, Chinese Cresteds, and Pomeranians can be affected by a specific type of PRA known as PRA-RCD3. Symptoms may arise as early as 1 year old and are usually detected during eye examinations. The rod cells responsible for low-light (night vision) gradually deteriorate, causing dogs to exhibit symptoms of “night blindness,” which is characterized by an increased difficulty in navigating outside at night. Around 2-3 years of age, the degeneration of cone cells begins, leading to a loss of color vision and inability to see in bright conditions, eventually culminating in complete blindness.