Please Note: MCBFA provides the feline health information on this site as a service to the public. Diagnosis and treatment of specific conditions should always be in consultation with one's own veterinarian. Your own veterinarian is, of course, your best source for information. MCBFA disclaims all warranties and liability related to the veterinary advice and information provided on this site.

MCBFA Health Information & References

Health articles including information about:
  Hypertrophic Cardiomyopathy (HCM), Spinal Muscular Atrophy (SMA), Polycystic Kidney Disease (PKD), Hip Dysplesia (HD), Chronic Gingivitis, and other Health Information.

Hypertrophic Cardiomyopathy

Discovery of Gene Defect Linked to Heart Disease in Cats

You can’t help but wonder if Dr. Kathryn Meurs hollered “Bingo!” when she found a gene mutation in Maine Coon cats that is clearly associated with feline hypertrophic cardiomyopathy, the most common form of heart disease in cats. After years of scratching for research dollars and laboriously sequencing genes, she finally discovered the genes that were linked to sarcomeric proteins in the heart and was recently able to publish the findings.

Dr. Mark Kittleson, a cardiac veterinary specialist at the School of Veterinary Medicine at the University of California, Davis has partnered with Meurs. “First we’ll confirm this finding is really true of Maine Coon cats in the general population (outside a lab setting), and then we look for other mutations in other breeds. Meanwhile, we’re able to identify individual Maine Coon cats with the mutation. So, yes, this discovery is potentially important for saving lives.”

Feline hypertrophic cardiomyopathy (HCM) is by far the most common heart disease in cats. According to several studies, it is also the number one cause of spontaneous death in all indoor adult cats.

Just as the rare football star who drops suddenly and dies on the field  – the same thing occurs in cats. Except, in cats, sudden death due to HCM is surprisingly common, and often the first – and only - symptom. In people HCM is generally diagnosed. In cats, when diagnosed, one symptom may be a clot, causing debilitating stroke-like symptoms, which can be treated. The problem is that these stroke-like events continue and typically worsen.

“This is very difficult to deal with emotionally and also financially,” says Dr. Susan Little, executive director of the Winn Feline Foundation, a not for profit organization that helped to fund the ground-breaking research. “Sudden death though is especially traumatic to witness – you’re just not prepared for it.”

Kittleson explains that HCM is a thickening of the left chamber of the heart, causing the heart to over-work. Sometimes vets can diagnose HCM hearing a murmur or an exceedingly rapid heartbeat (though neither is always necessarily indicative of HCM). Cardiac vets can identify HCM using an ultra-sound. 

While any cat, including mixed breeds, can have HCM, it was Kittleson who learned years ago, there is a genetic and also a breed tendency, among the American Shorthair, Devon Rex, Ragdoll, Persian and the Maine Coon.

Since HCM often isn’t found until cats are young adults or older, breeding out genetic carriers is challenging if not downright impossible. A male cat, for example, can sire several litters before he reaches, say 5 years, and then is unexpectedly diagnosed with HCM – even if there is no immediate family history. Kittleson says naturally that cat is neutered, but gene mutations – which ‘till now have remained a mystery - have already been potentially passed on. 

Kittleson says the hopes now that the mystery is unraveled – at least for Maine Coons – the hope is HCM carriers can be identified as kittens.

Meurs, who was at Ohio State University College of Veterinary Medicine – Columbus, has been sniffing for the HCM gene abnormality since 1995. Several years of research focused on sarcomeric proteins associated with the thickening of the heart that occurs in HCM in people. The “Bingo” winner and breakthrough came when Meurs discovered cardiac myosin binding protein C doesn’t get properly incorporated into the muscle of the Maine Coon cats with HCM. Meurs then traced the gene responsible for this abnormality.

Little, who is in Ottawa, Ontario, Canada says, “By identifying the gene and the protein the gene produces, it’s more likely a drug may be created to intervene.”

While there are drugs currently used to hopefully control HCM (in the cats who are lucky enough to be diagnosed), the reviews on their effectiveness are mixed at best.

Kittleson is now researching the potential efficacy of two medications that would successfully treat HCM. To determine the impact of these meds, Kittleson is looking at the hearts of the cats using MRI imaging, a first for revealing changes in cats’ hearts.  

Generating Funds for Feline Research

The research conducted by Meurs and Kittleson was financed through the Ricky Fund of the Winn Feline Foundation, private donations to Ohio State and the University of California, Davis.

The Morris Animal Foundation is another funder of animal health studies, and executive director Dr. Patricia Olson says there’s actually a shortage of proposals on feline health.

“With so much to learn, and so much to do it’s shocking and it’s inexcusable there’s money (for funding research) that isn’t being used,” says veterinary cardiologist Dr. Paul Pion, co-founder and president of the Davis, CA-based Veterinary Information Network.

“I’m grateful for the dollars I’ve received, but it’s a struggle,” says Kittleson. “I assume my colleagues see a lot more money being thrown at the problem of HCM in humans without a significant breakthrough – so they figure, how can we ever solve the problem in cats?”

Pion, isn’t as diplomatic, “With the progress Kate (Meurs) has made, it’s flabbergasting there aren’t more investigators interested.”

Meurs, who is in the process of setting up a new lab at Washington State University College of Veterinary Medicine – Pullman, as the Dr. Richard L. Ott Endowed Chair in Small Animal Medicine & Research points out there are many mutations in human HCM, so it’s likely the mutations will vary as she investigates other breeds. “The prospects are exciting, but we have a long ways to go,” she says.

Kittleson – who with Pion – helped to solve the mystery of a related heart disease in cats several years ago says, “I just think about all the cats who suffer with this disease or die early. My hope is that one day we can do something about it.”

Steve Dale writes "My Pet World," a newspaper column syndicated by Tribune Media Service. He can be heard at 7:30 p.m. on Pet Central on WGN Radio (or www.wgnradio.com) Saturdays, and on his syndicated radio programs, Steve Dale's Pet World and the Pet Minute. He also a contributing editor to USA Weekend. Steve's website is www.petworldradio.net.

MCBFA is raising funds for additional research on hypertrophic cardiomyopathy if you would like to donate please follow this link to our fund raising page.

*Please note at this time there are varied opinions in dealing with the issue of HCM and the newly developed DNA test for one genetic cause of the disease.  MCBFA has listed information from a number of different sources expressing opinions on the subject. The content is solely the opinion of the author(s). 

Recommendation by Drs. Mark Kittleson, Rebecca Gompf, and Susan Little

PawPeds Recommendation For Testing And Breeding 

Recommendation by Dr. Jerold S Bell

Recommendation by Dr. Jens Haggstrom

Veterinary Cardiac Genetics Lab - A genetic test has been developed for the cMyBP-C mutation causing HCM in Maine Coons. Information about HCM and instructions to order the test kit.

Update from Kathyrn M. Meurs, DVM, PhD, Professor

Frequently Asked Questions about the test for the HCM Mutation

Q & A from Dr. Mark Kittleson

Feline Hypertrophic Cardiomyopathy - by Jody Chinitz, Marcia Munro, and Dr. Mark Kittleson

Feline Cardiomyopathies - by Dr. Paul Pion

CVCA's FAQ on cardiac diseases - the feline section is halfway down the page 

Hypertrophic Cardiomyopathy in Cats by PetPlace - by Dr. Bonagura
Summary page 
or In-depth article 

Listing of Board Certified Veterinary Cardiologists with contact information, websites, and email

ACVIM Specialty of Cardiology - Alphabetic and Geographic lists of veterinary cardiology diplomates

 

The genetic cause of spinal muscular atrophy (SMA) in Maine coon cats (MC) was determined in May 2005, culminating a cooperative, 8-year effort of breeders, veterinarians, and researchers at Michigan State University, University of California at San Diego, the National Center for Biotechnology Information, and the National Cancer Institute. A convenient and reliable DNA based carrier test is now available.

SMA is a disorder caused by death of spinal cord neurons that activate skeletal muscles of the trunk and limbs. Loss of neurons in the first few months of life leads to muscle weakness and atrophy that first becomes apparent at 3-4 months of age. Affected kittens develop an odd gait with a sway of the hindquarters and stand with the hocks nearly touching. They may also stand with toes out in the front. By 5-6 months of age they are too weak in the hindquarters to readily jump up on furniture and often have a clumsy landing when jumping down. The long hair MC may hide it, but careful feeling of the limbs will reveal reduced muscle mass. Affected kittens are not in pain, they eat and play avidly, they are not incontinent, and most live very comfortably as indoor cats for many years. As of this writing, the oldest affected cats of which we know are 8-9 years of age. Known affected kittens have occurred in breeding programs across the United States, and, in retrospect, likely carriers have been exported widely.

Studies have demonstrated that the disorder is inherited as a simple autosomal recessive trait. For a kitten to have the SMA disorder, it must receive the mutated copy (allele) of the disease gene from both parents, and male and female kittens are equally affected. The parents of affected kittens show no outward signs of disease, but they are obligate carriers, by definition. In a breeding program, both male and female carriers will pass on their mutant alleles to 50% of all their offspring, on average. When two carriers are inadvertently mated, on average 25% of the kittens will have SMA. That means that in litters from such matings, there may be some combination of SMA and normal kittens, all SMA kittens, or all normal kittens. Unidentified carriers in breeding programs continue to spread the mutant gene throughout the MC breed.

SMA in MC is caused by large deletion on cat chromosome A1 that removed 2 genes.  Identification of the SMA mutation has allowed design of a laboratory test to detect the deletion in DNA from cat cheek cells, blood, or frozen semen. DNA isolated from samples is subjected to a polymerase chain reaction (PCR) to amplify the portion of the genome harboring the deletion.  Normal and deleted alleles are differentiated by the size of the amplification products separated by agarose gel electrophoresis. Carrier cats can be positively identified in the laboratory on the basis of both the mutant and normal allele PCR products amplifying from their DNA. If one thinks a kitten may be affected, the test can also be used for definitive diagnostic confirmation.

The SMA test is offered to MC breeders, owners, and veterinarians through the Laboratory of Comparative Medical Genetics at Michigan State University in hopes that it will be used to stop the spread of SMA. Testing results are kept strictly confidential and are returned only to the person submitting the cat’s sample. Test results for each cat will be returned as a printed certificate by US post and also by email if desired.

The cost of the test is $65/cat. To obtain cheek brushes and instructions for sample collection, please contact the laboratory by email (fyfe@cvm.msu.edu) indicating how many cats you wish to test and providing a mailing address. For additional information, please contact Dr. John C. Fyfe by email or by mail at Laboratory of Comparative Medical Genetics, 2209 Biomedical Physical Sciences, Michigan State University, East Lansing, MI 48824



Polycystic Kidney Disease
by: Dr. Arnold Plotnick

Polycystic kidney disease (PKD) is a slowly progressive, irreversible, inherited kidney disease once thought to be only in Persian and Persian-related cats. Clinical signs of the disorder typically occur around the age of seven. Ultimately, PKD can result in renal failure, with clinical signs similar to those of cats with naturally occurring kidney failure.

          What to Watch For

  • Depression

  • Anorexia or reduced appetite

  • Increased thirst and urination

  • Weight loss

  • Occasional vomiting

    Diagnosis

  • Radiography with or without contrast 

  • Ultrasound


Treatment

There is no specific treatment for PKD. Treatment is the same as that for chronic kidney failure of any cause, for example:

  • Restricted protein and phosphorus diets

  • Possible subcutaneous fluids

  • Phosphorus binders

  • Calcitriol (Vitamin D) 

  • Erythropoietin

         Home Care and Prevention

There is no specific home care for cats with PKD that have no symptoms. Cats with PKD that have developed chronic kidney failure undergo home care typical for that condition including:

  • Prescription diet

  • Possible subcutaneous fluid therapy 

  • Medication


There is no way to slow the progression or prevent the onset of chronic renal failure once PKD has been diagnosed. Prevention requires responsible breeding to eliminate PKD from Persians and Persian-related breeds.
In-depth information about PKD or
The Feline PKD

Hip Dysplesia

Resources: Karl and Gale Bowman, DVM

Hip Dysplasia is defined as an abnormality of development of the hip joint, affecting one or both hip joints. Hip dysplasia is an inherited trait involving multiple gene pairs. In order for an animal to have hip dysplasia both parents are either affected by or carriers of the disease. HD is not congenital (meaning an animal is not born with it); the condition develops over time from instability in the hip joint. This instability results from an improper fit of the femoral head (ball-like structure on the end of the femur) into the acetabulum (hip socket). This instability, or "joint laxity", results in abnormal weight bearing within the hip joint. From this, secondary changes and remodeling occur in an effort to stabilize the joint or avoid bone-on-bone contact. When cartilage disintegrates from abnormal wear, the femoral head and acetabulum rub together with every step, often causing osteoarthritis.

Other Hip Related Sites:

The Feline Hip Dysplasia Awareness Site
Orthopedic Foundation for Animals (OFA) 
Penn Hip

Chronic Gingivitis

Chronic Gingivitis in the Cat
A Winn Foundation Health Article On Chronic Gingivitis in the Cat. 
Chronic Gingivitis in the Cat by Judy Zinn, DVM


Links to other General Health Information

Merck Veterinary Manual - for general reference
Dr. Susan Little - helpful info and resources for breeders, rescuers, and pet owners
The Winn Feline Foundation - dedicated to the health of the cat
Cats International - general cat care and behavior site not specific to any breed
Drs Foster and Smith - general cat care 
Declawing.com - by Dr. Christianne Schelling - considering declawing your cat, please read this
Maine Coon Breed Rescue
- list of Maine Coon rescue groups
Antibody Titers vs. Annual Vaccination
Feline Vaccination-Associated Sarcoma - the case against adjuvant

Please Note: MCBFA provides the feline health information on this site as a service to the public. Diagnosis and treatment of specific conditions should always be in consultation with one's own veterinarian. Your own veterinarian is, of course, your best source for information. MCBFA disclaims all warranties and liability related to the veterinary advice and information provided on this site. 

 

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