European
Maine Coons
Mantorville
Minnesota
Health of the Maine Coon
(common health concerns and disease you should know about)
High Risk
HCM - Hypertrophic Cardiomyopathy
Notable Risk
SMA - Spinal Muscular Atrophy
PKD - Polycystic Kidney Disease
Of Concern
Gingivitis / Dental Disease
HD - Hip Dysplasia
PL - Patellar Luxation
FELV - Feline Leukemia Virus
FIV - Feline Immunodeficiency Virus
FCoV / FIP - Feline Corona Virus / Feline Infectious Peritonitis
Breeder's Concern
Pk Def - Pyruvate Kinase Deficiency
Blood Type
Other Concerns
Heartworm
Cancer
Vaccine-Preventable Infections
Deafness
About the Concerns
HCM - Hypertrophic Cardiomyopathy
(Information taken from UC Davis and Wisdom Panel)
Hypertrophic cardiomyopathy (HCM) is the most common cardiac disease in cats worldwide. It is relatively certain that about two thirds of Maine Coons around the world are free of the mutation, and one third of them have one or two copies of the mutation. The disorder is characterized by an increase in wall thickness of the left ventricle and the intraventricular septum. This causes turbulence in blood flow and increased venous pressure in the left atrium and lungs, which may or may not coincide with a cardiac murmur upon auscultation. The clinical signs most commonly noted with the disease are respiratory signs associated with congestive heart failure such as tachypnea, exercise intolerance and panting, difficulty breathing, and (rarely) coughing. Thromboembolism may also occur and affected cats have an increased risk of sudden cardiac death. Clinical and echocardiographic signs typically appear after the cat has reached breeding age. In the Maine Coon, a point mutation (A31P) in the MYBPC3 gene has been found causative for the disease. The most common age of diagnosis for HCM is 5 to 7 years. Cats with two copies (homozygous) of the mutation have earlier onset and increased severity of the disease than those with only one copy (heterozygous) of the mutation. The relative risk for developing HCM is around 1.8 in Maine Coons heterozygous for the mutation and 18 in Main Coons homozygous for the mutation compared to Maine Coons negative for the mutation. The mode of inheritance is autosomal dominant with incomplete penetrance. HCM has also been found in about 5.4% of Maine Coons negative for A31P, thus this mutation is not sole cause of HCM in Maine Coons. Please note: It is possible that disease signs similar to the ones caused by the HCM mutation could develop due to a different genetic or clinical cause.
The other causes are not known at this time. However, additional information from publications suggests that male cats may be twice as likely to be affected as females, and that heavier cats are more prone to develop HCM than lighter cats. However, this latter relationship may itself be attributable to a larger size for males than females.
What can breeders do?
With HCM being observed in around 1/3rd of the breed's population and the majority coming from a the same mutation. Breeder's should genetically test for HCM in their cattery. This drops the the percentage down from around 30% risk to around 5%. Genetic tests is an easy and inexpensive way to help reduce heart disease in the breed, but it's not perfect. Another test for breeders to do, is during examination, have the vet or specialist perform a Heart Auscultation (listing to the heart) this is also cost effective test for the breeder. One of the only ways to diagnose HCM is by echocardiogram (heart ultrasound) done by a cardiologist. This can not tell you that your cat will develop or not develop HCM, it can only tell you at the time of ultrasound if your cat has it or not at the time of the test. Most veterinarians recommend doing a yearly echocardiogram during the ages 1-7. This is an expensive option costing around $400-$800 each time depending on your area and vet. This can cost thousands of dollars over the life of your pet. Also HCM can develop outside the age of breeding, so make sure your breeder guarentees the health of your pet from any genetic disease.
SMA - Spinal Muscular Atrophy
(Information taken from UC Davis and Wisdom Panel)
Spinal muscular atrophies are hereditary diseases caused by the degeneration of lower motor neurons of the spinal cord. In cats, the disease has an early onset. Progressive weakness and atrophy of skeletal muscles is visible in kittens around 12 weeks of age. The changes are first seen in the proximal musculature of the hindlimbs. Clinical signs progress to gait instabilities, postural abnormalities, and visible muscle loss. Muscle loss and inability to jump is typically observed at 5 months of age. In time, distal musculature may also become atrophied. After an initial progression of disease for several months, the ongoing loss of muscle function will likely slow with affected cats reaching a plateau of variable muscle atrophy, weakness, and mobility. Despite the severe clinical signs, the disease is not painful and affected cats may survive with varying degrees of disability into adulthood. The mode of inheritance is autosomal recessive.
The disease is not painful or fatal, but it is disabling. As there is no cure, treatment is limited to supportive care dictated by the severity of the clinical signs. Owners should be advised that affected cats cannot be safely allowed outdoors unattended due to their compromised mobility.
What can breeders do?
Breeder's can preform a cost effective genetic test to help eliminate the chances of SMA.
PKD- Polycystic Kidney Disease
(Information taken from UC Davis and Wisdom Panel)
Polycystic kidney disesae (PKD), also named autosomal dominant PKD, is characterized by variously sized, fluid-filled cysts in the renal cortex and medulla with hepatic and pancreatic cysts also possible. The cysts develop from birth and enlarge with age. The cysts destroy the renal parenchyma and disturb renal function, eventually causing renal failure. Affected cats present with signs of renal insufficiency such as weight loss, decreased appetite, increased drinking and urination, poor body condition, and vomiting. Biochemical labwork and ultrasonography examination are helpful tools in identifying the severity of an affected individual. A point mutation in the PKD1 gene has been identified as the most common genetic mutation for the disease. The inheritance pattern is autosomal dominant. No homozygous cats have been identified, suggesting the mutation is a homozygous lethal mutation in utero. While there is no known sex linkage to the inheritance of the mutation, research has shown male cats have a higher prevalence of the mutation.
There is no treatment specific for feline polycystic kidney disease. As the symptoms are similar as for patients with feline chronic kidney disease, therapy is guided towards the same supportive care methods such as special diets, fluid therapy, medications to reduce nausea and to block absorption of phosphorus, along with other support options for feline kidney failure.
What can breeders do?
Breeder's can preform a cost effective genetic test to help eliminate the chances of PKD.