News & Events

Winn Feline Foundation Announces 2006 Grant Recipients

Winn Foundation President Susan Little, DVM announces the award of eleven grants for feline health studies totaling $131,364. Dr. Little commented, "The Foundation was pleased to receive proposals from veterinary researchers around the world who are interested in improving feline health. Out of over 40 proposals for 2006, our team of outstanding veterinary consultants helped the Foundation select the best studies for funding. We look forward to seeing the results of these studies and being able to share them with the veterinary community as well as cat owners and breeders of pedigreed cats."

Inherited blindness in Persian cats: Heritable progressive retinal atrophy in Persians. Leslie Lyons, PhD. University of California, Davis, CA.

Like humans, cats experience types of naturally occurring inherited vision problems, called progressive retinal atrophy (PRA). Because research has been extensive for human blindness, we can use this information to improve the health of felines. Our goal is to investigate the progression of an inherited blindness in Persians and decipher which gene results in the disease. Persian cats are the most popular cat breed throughout the world. Many other breeds use Persians to change the body and facial structures of other breeds as allowable outcrosses. Thus, health problems in Persians can be spread quickly and widely in the cat world if unchecked. The Persian vision problems start very early, at about 4 - 8 weeks of age and progress very rapidly. Cats become completely blind by 15 weeks of age, but do not have other health issues. This disease is caused by a mutation in one gene and two copies of that mutation are required to cause blindness. Carrier cats, cats with one copy of the mutation, are perfectly healthy, but when bred, they can pass the mutation on to their offspring. Thus, a genetic test is required to detect these cats so that they do not spread the mutation. The disease has to be clinically very well defined in order to match this disease to one that is found in humans. If a good match can be made, then markers for that gene can be developed for the cat rather efficiently and used to detect carriers. Also, if we know which gene is mutated, we may understand how the genes function and be able to give better medications to slow or stop the blindness. A chromosomal segment has been recently identified that is statistically associated with the Persian form of PRA. It is most likely that a gene within the segment is responsible for the Persian blindness and a mutation test will be feasible in the near future.

Heart Disease:

Hypertrophic cardiomyopathy in Ragdoll cats: Molecular evaluation of the feline myosin binding protein C gene in Ragdoll cats with familial hypertrophic cardiomyopathy. Kathryn M. Meurs, DVM, PhD, DACVIM; Mark D. Kittleson, DVM, PhD, DACVIM. College of Veterinary Medicine, Washington State University, Pullman, WA (Meurs) and School of Veterinary Medicine, University of California, Davis, CA (Kittleson). Feline hypertrophic cardiomyopathy (HCM) is the most common cause of heart disease in the adult cat. Affected cats are at risk of sudden death, breathing difficulties, or development of a blood clot. Increasingly, feline HCM is noted to be inherited, with examples reported in the Maine Coon, Ragdoll, British Shorthair, and Scottish Fold breeds, among others. We demonstrated that HCM is associated with a mutation in the myosin binding protein C gene in the Maine Coon cat. In human beings, the disease is commonly associated with a mutation in one of several genes that encode for sarcomeric proteins, most commonly the myosin binding protein C and the beta myosin heavy chain gene. Causative mutations have been identified in over 140 regions of the cardiac myosin binding protein C gene alone. The Ragdoll cat also has a heritable form of the disease. We prospectively collected pedigrees and medical information and DNA samples from 3 families of Ragdoll cats with familial HCM. We performed an initial study of affected Ragdoll cats and determined that the Maine Coon defect is not present. However, we only evaluated one small region of the gene. Given the importance of this gene in both humans and Maine Coon cats with HCM we hypothesize that a mutation in a different region of the gene is associated with the development HCM in the Ragdoll. The objective of this study is to evaluate the DNA of this gene in both affected and unaffected cats for a causative mutation.


Contact: Janet Wolf, Executive Director, 856-447-9787 winnfeline@aol.com
Susan Little DVM, President,613-741-2460 SusanLittleDVM@compuserve.com