Feline Genetic Conference 2000

by Susan Manley

Published September 2000

On July 29-30, 2000, the 2nd International Conference on Feline Inherited Diseases was held at the University of California/Davis covering a wide variety of topics. Although the actual scientific study may have been conducted using a breed other than Persian or Exotic, some of the insights and data collected would be of interest to Persian and Exotic breeders, and so is included in this over view.

About the Author
From 1976 to 1984 Susan Manley was involved in feline rescue of feral cats for the City of San Jose Parks and Recreation at Happy Hollow Park. Returning to cat rescue several years ago, Sue successfully raised and subsequently adopted a 2 day old kitten, Solomon. Fascinated by the fact that Solomon carries his tail curled in a ring over his back, Sue has pursued a greater understanding of the genetics of his tail anomaly, purebred cat registries and good breeding practices in general. You can see photos and read about Solomon and his "special" tail at

Below is an alphabetical list of some of topics included in this synopsis. The individual topics are linked to the correseponding synopsis.

      1. Amyloidosis (Abyssinians)
        Amyloidosis (Siamese)
      2. Blood Type Incompatibility
      3. Cardiomyopathy (American Short Hairs)
        Cardiomyopathy (Maine Coons)
      4. Coat Color in Cats
      5. Feline Genomics
      6. Feline Urinary Syndrome
      7. Gangliosidosis
      8. Genetic Counseling and Genetic Diversity
      9. Genetics and Infectious Diseases
      10. Genetic Registry for Cats
      11. Hip Dysplasia
      12. Inherited Diseases
      13. Nutritional Pecularities in the Cat
      14. Polycystic Kidney Disease
      15. Ovarian Function
      16. Retinal Atrophy
      17. Spasticity
      18. Spinal Muscular Dystrophy
      19. Veterinary Information Network

1. Amyloidosis in Abyssinian Cats/Stephen DiBartola/Ohio State University/AA protein deposits found primarily in the kidneys of Abys (and other cats), but the Oriental-type cats primarily get them in the liver, causing sudden rupture/hemoabdomen. In all cats, only the lungs, bladder and nervous system have been found free of deposits. Chronic inflammation in some part of the body is associated with this disease. Mode of inheritance still not determined.

Pedigree analysis of death due to Amyloidosis in the Siamese cat breed/Bernard VanOost/Utrecht University (NL)/Started study three years ago (too small sample). Mean age of death was 4.1 years. Possible causes: overreaction of the immune system, metabolic storage defect, coagulopathy and familial. Malik mentioned study in AU of 22 Siamese cats. What is it? Deposition of insoluble amyloid fibrils leading to organ failure, in Siamese spontanious hepatic bleeding Usually goes unnoticed w/ sudden death. Necropsy finds ruptured liver & possibly other organs.

2. Blood Type Incompatibility Problems: Are you my type?/Urs Giger/Univ of Penn/Have not found B type blood in Siamese, Burmese, Tonkinese and Russian Blues. He needs 100+ of any breed to publish data on blood types (ASH is one large breed he needs samples from). Test cards that breeders can buy were shown. - Type B blood has more anti A antibodies: Type A blood has a lower B antibody count. - The biggest item of note for me is that sometimes blood type incompatibility does not kill the kitten and can cause the tail tip of the kitten to slough off. Some of the breeds have as high as 40% type B blood. DSH on the West Coast have the highest incidence of type B at 7%.

3. Familial Hypertrophic Cardiomyopathy in the ASH Cat/Kate Meurs/Ohio State University/Believed to be caused by an autosomal dominant gene (as yet unidentified).

Familial Hypertrophic Cardiomyopathy in the Maine Coon Cat/Mark Kittelson/UCDavis/Believed to be caused by an autosomal dominant gene (as yet unidentified). NOTE: common name for this disease in general is left ventricular hypertrophic cardiomyopathy (LVHC), and it is different from the dilated form of cardiomyopathy caused by lack of taurine in the diet (Paul Pion's research).

4. Coat Color in Cats: Solid Colors and Tabby Patterns/Heather Lorimer/Youngstown State University/More on color genetics and theories of tabby pattern inheritance.

5. Feline Genomics at UCDavis/Leslie Lyons (conference host)/Current projects include Burmese head defect (autosomal recessive), lymphosarcoma in Oriental-type cats, Bengal heart disease, Devon Rex spasticity, PKD and PRA in Persians, etc., Russian Blue heart disease, Munchkin dwarfism (FGFR3 gene?). Most interesting were the chromatographs of a sample of DSH compared to a sample of Havana Browns - very little gene variation evident> in the latter. Sues notes: lymphosarcoma in Oriental-type cats responds well to chemotherapy. Dr Lyons has been collecting genetic samples of many breeds and individuals> with genetic problems in those breeds. She stressed, that though many samples were in they were not all run and analyzed yet. It takes more time and probably more samples to identify problems. As she continues to build her library of samples the answers will hopefully come to light in the future.

6. FUS - Are Lower Urinary Tract Diseases Inherited/Tony Buffington/Ohio State University/I'd say the answer is "probably not". Since 1981 (and thanks to the reformulation of commercial pet foods - don't quote me ), the struvite (MAP) stones have been replaced with oxalate (CaOx) stones. Persians, Himmys and Burmese develop the latter. However, about 2/3rds of bladder problems are from what he calls "interstitial cystitis", which can be very difficult to cure. He advises watering down all dry food before feedings, particularly if you have cats with recurring FUS.Clinical signs of FUS: - Increased urination frequency - increased urination urgency - Pain in urination - Blood in urine - Inappropriate Elimination Causes: - Idiopathic - Urolithiasis ( stones either Struvite (MAP) or Calcium Oaxlate (CaOX) ) - Anatomy - UTI ( Urinary tract infection ) - Cancers in tests on 109 cats results were 63% Interstitial Cystitus 11% Anatomical Defect 9% Behavior disorder 7% MAP Struvite Crystals 5% Calcium Oaxalate Crystals Oxalate stones are found more often now then 20 years ago. Oxalate Crystals were most common in persian and cats of Persian decendance. Struvite crystals are found among all types of cats including DSHs. What causes Struvite stones? To much magnesium. In particular Salts of Magnesium that are used to raise urine PH levels. Cats with stone disease should never been fed food that is dry ( soak dry food before feeding) Interstitial Cystitus: Genetics : Occurrence ~ 6/1000 cats Breed Predilection to Persians and Norwegian Forest cats. Reoccurrence common despite treatment. Stress seems to bring it on. ( Change of weather, moving, change of relationships. Change of diet ( consistency, composition, texture) Treatment - Stress reduction - Feliway Phermone spray - Gags - Amitriptyline

7.An International Program to Eliminate the Gangliosidosis from Korats by Molecular Testing/Henry Baker*/Scott-Richey Research Center (Auburn Univ)/Testing and certification program (now required by FIFe) for autosomal recessive genes gm1 and gm2 in Korats and other breeds (gm1 gangliosidosis was originally found in Siamese). 351 Korats tested to date and 20% are carriers. NOTE: Dr. Baker will be speaking at the CFA Intl Show this year. Fables of genetics: Fable 1 Inherited diseases are rare The truth is inherited disease in people is rare, its quite common in purebred cats and dogs. Human Tay-sachs 1~300 .03% Concentrated in Easter European who have emigrated to NYC 3% in that population 1 in 5 Korats are carriers of Korat Gangliosidoses (20%) Fable 2 Phenotype Is what we have to pay attention to > In recessive disease phenotype is irrelevant. The first time you see a disease you must assume that 15% to 20% are carriers and that statistic goes up with more cases. Fable 3 Phenotype is more important then genotype 4 - to eliminate carriers you must properly identify them - So the genepool is not decreased mate carriers to normals - use the 50% normal, non carriers to breed furture generations Two types of Gangliosidosis GM1 See in Siamese korat mix Beagle Mix & Portuguese Water Dog Bovine (Friesian) GM2 4 different mutation all seen in Korats Progressive fatal disease Early clinical signs at 2-4 months Terminal by 8-18 months > Affects Korats/ Siamese & Domestics For each breed you must know the mutation in order to do the molecular genetics studies. Enzyme testing at UC Oregon was a failure There are 10K registered Korats Symptoms Progressive Neurological Similar to distemper at birth. Progressive loss of coordination in facial features GM2 have dwarf like features at the end of the line

8. Genetic Counseling and Genetic Diversity Considerations for Pedigreed (was Purebred ) Cats/Jerold Bell*/Tufts University/Covered breeding goals, inheritance of defects (autosomal dominant, autosomal recessive, sex-linked and maternal), methods of gene mapping, and how to eliminate recessive defects from a gene pool (overuse of certain studs is a big problem). Controlling dominant genes: - Replace Affected breeding cats with normal siblings, parent of prior born offspring. - Ideally don't want to breed and produce more affected/ Controlling Recessive Genes: - Breed carriers to genetically normal offspring . When testing for normal is possible - Replace carriers parents with genetically normal offspring - select against carriers for breeding animals. Identifying defective genes: - Candidate gene approach ( human, dog and equine genomes can help) - Search for abnormalities in gene sequence - Genes known to be involved in the defective system Linkage analysis: - Search for common series of genes in known affected animals - The problem with linkage is markers can be removed during Meiosis ( the making of sperm or egg ) and then you can have affected animals with no marker and unaffected animals with marker. Controlling Polygenic Disorders: ( multiple gene disorders) - Phenotypic health of pedigree provides information on the possibilities. - 2 Phenotyipcally normal parents produce affected = both parents must carry the genes to create the disorder - best remedies are Genetic diversity, don't line breed to the same line

9. Genetics and Infectious Diseases/Niels Pedersen/UCDavis/summary of where we are with FIP. Feline leukemia has three forms Types A, B & C only type A is passed from cat to cat B is manufactured when A combines with Felv genetic material that is in a cats genetic material. FIP Happens in 5% of catteries and shelters 100% of all catterys and shelters tested that had 11 or more cats had corona virus UC Davis itself has a very difficult time keeping this virus out of its pathogen free colony. It can ride in on the litter dust on your shoes, clothes etc. DR Pedersen thinks it impossible to segregate cats enough in a home to keep this virus from spreading. FIP has a fecal to oral transfer - anything that a cat gets on its fur will get into its mouth. Monitoring several catteries with FIP incidenced showed a decrease of incidence to zero or almost zero after 2 years with no changes made in the cattery management. 50-75% of cats that come into contact with FIP cannot fight it off. like this Could be new or environmental changes & keeping practices have brought it to the fore. FIP is not transmitted from a carrier cat to another. It mutates in the cats themselves. FIP cause is Feline Enteric Corona Virus Virus infects mature ephilium on the intestinal wall. No clinical signs for first infection 6-10 week old kittens replicate the virus at 100 to 1000 times greater then after they are 16 weeks FIP can cause disease as much as 15 years later 40-60% of cats in a cattery will be shedding FECV at any one time FIP hits, then hits hard, then disappears. These factors do not contribute to the risk of FIP - Husbandry practices - Degree of inbreeding - concurrent disease - number of cats (once its over 11) - mean age of all cats in cattery - gender These factors are seen as risk factors for FIP - Prevalence of long term FECV shedder 75% of risk - Proportion of cats shedding FECV at any given time - Genetic disposition *** The same family is more susceptible - Age 4 - 29 months - High Corona Virus antibody titer (High and keeps climbing is bad No test out currently can tell by PCR or Serology if a cat as FIP To know the status of your cattery for corona virus a viral RNA check can be performed on feces. It costs approx $200. per test and the tests need to be >run every day for every cat for a week. UC Davis will not run these tests.

10. Genetic Registry for Cats/Paul Poulos/Institute for GDC in Animals, UCDavis (Genetic Disease Control)/Says they are collecting data and will provide KinReports - genetic pedigrees - to owners/breeders planning matings, but at the same time he stated that the information gathered is confidential and no names are released (so I'm not sure what good the information is if you don't know what animals to avoid). Cats have about 150 known genetic defects. Note: Dogs have 400 known genetic diseases.

11. Hip Dysplasia in Maine Coon Cats/Gail Smith*/University of Pennsylvania/Believed to be inherited polygenetically. Notes: This talk was given using hard data from Dog breeding programs. The overall consensus is that 3 breeds of dogs are free of hip displasia and all other breeds are mildly to severely affected. (The 3 breeds including the Borzoi, and I am sorry I forgot to write down the other breeds). Radiographs were shown showing how the rating of the Hips and Patella were created. The ratings were then plotted per breed on a horizontal chart. The overall consensus of the data was have your breeding animals examined and breed the best hips and patella to the best to get the best.

12. Inherited Diseases in Burmese in the UK/Tim Gruffydd-Jones/University of Bristol/"FCKs" (flat-chested kittens) are found in Burmese, Bengals and Oriental-type cats. Small group of Burmese have hypokalemia (low blood potassium). One familial group has keloidosis (abnormal scarring). Burmese may be more susceptible to FIP (very small sample however). No craniofacial malformations (head defects) in UK Burmese have been found. Sues Notes: Flat chest was divided into two groups - Flat chested ( Chest was V shaped with a noticeable corner on the ribcage where the bones connect with cartilage) -Pectus Excavatum ( chest had a dimple in the middle of it with a noticeable line down the center.) Clinical signs of flat chested were: - weight loss - failure to grow - difficulty breathing 75% of kittens with flat chest survive. At 4 months old they usually catch up to their littermates and have no visible deformity. Of all of the flat chested kittens evaluated 9% have Pectus Excavatum and 6% had splay legs ( Back legs not able to support weight usually resolves at 2-3 months). - Flat chest appears to be familial, autosomal recessive, variable expression/penetrance. Variable expression and the fact that it can resolve makes it difficult to remove animals with the trait from the breeding population. Hypokalemia in Burmese: - Not seen in DSH - Experience based on 18 cases - Clinical signs usually at 4 months of age - Low potassium seems linked - Low potassium is not from inadequate intake or from excessive loss - Possibly related to Hypokalemic Periodice Paralysis in Humans. ( Sues thoughts: Possibly also related to HYPP in American Quarter Horses, although note this is Hyperkalamic, HYPP is mapped on the equine genome) - 5 affected litters - 12/32 kittens affected - In humans is associated with/ ion channel in muscle ( defect in calcium channel) Sometimes a defect in the sodium channel.

13. Nutritional Pecularities in the Cat/Quentin Rogers/UCDavis/12 deficiencies in diet are caused by man (let them eat mice ). Ratio of the small intestine to body length Cat 4:1 Dog 6:1 Rabbit 10:1 Pig 14:1 ( Domestic cats intestinal length is longer then their wild cousins due to human intervention pushing them to be more omnivorous (eating plants as well as animals) then they would in the wild state. Flavor preferences of the cat: Protein Hydrozates ++++ (Sues thoughts: same junk in human snack foods) Animal Fats +++ Cats normal eating pattern is 12-15-18 meals per day. Zinc deficiency linked to cleft pallet. Excess of liver in the diet also linked to cleft palate Excess liver can also cause poor growth and congenital defects. Treatment of hepatic lipidosis be off food 10-14 days of force feeding. Dr Rogers is not a fan of BARF diets. He thinks commercial diets are better.

14. Noninvasive Monitoring of Ovarian Function in the Domestic Cat/Brenda Griffin/Scott-Richey Research Center (Auburn Univ)/Fecal samples are checked daily for estradiol levels to determine when queens are in season. Visual signs coding system also used daily. Progesterone levels measured with twice weekly blood draws (NOTE: 85% of queens ovulate spontaneously!!). Young and low (pecking) order queens have silent heats. Notes: Dr Griffen had the most amazing food dyes that were fed through the cats to identify which feces in a multicat environment they were collecting to test. - Cats used in the test were DSH & DLH. - Collected feces was tested for Estradiol. ( Same process that large animal parks and zoos use) - One queen in her study had far less frequent heats ( once every year) then the other queens. When tested to see if a problem existed it was found that there was no problem and that was her normal cycle. Its possible by modern spaying and neutering practices we have accidentally been selecting for more frequent and earlier cyclers to have kittens and passing their predilections on.

15. Polycystic Kidney Disease (PKD) in Persians/David Biller/Kansas State University/Bilateral cysts caused by an autosomal dominant gene linked to PKD1 on human chromosome 16. 40-50% of Persians and their close relatives estimated to have the gene. Polycystic Kidney Disease in Humans has been found to be both recessive and dominant. Usual onset is 3-10 years with a mean of 6 years. Cysts in the Kidneys are " Proximal" with a sodium content like Plasma "Distal" with a sodium content like Urine. German research shows 5% of the PKD positive cats also have cysts in the liver. Ultrasound equipment necessary to definitively diagnose. 7 MHZ or higher. With correct Ultrasound and an experienced person running the machine (this was stressed) a diagnoses can be make in animals as young as 4 weeks. PKD homozygous mice died in Utero. 5K Persians have been tested. Of those 5K 33% have PKD w/ multiple cysts in both kidneys. The advice is to screen future breeding animals before breeding.

16. Abyssinian Retinal Atrophy/Matthew Binns*/Animal Health Trust (UK)/Two types - autosomal dominant and autosomal recessive. AHT does DNA testing and is currently researching PRA in Abys, PKD in Persian, amyloidosis in Oriental-type cats, chronic renal failure (all cats), cardiomyopathy, and hepatic shunts.

17. Spasticity in the Devon Rex/Richard Malik/University of Sydney/Believed to be a form of muscular dystrophy. The photos and movies were heart-wrenching to say the least. Death occurs from choking on food. Clinical Signs: Head sinks to chest in the litter box. Litter box takes a great deal of time. High stepping gait. Head bobbing, Difficulty chewing and swallowing, Abnormal head position with chin resting on chest, Painful for cat to bite, Scapula of shoulders prominent above back with a dip behind the shoulders, Megaosophagus in all cases ( enlarged esophagus that traps food) Believed to be some kind of muscular dystrophy. Dorsal cervical and proximal forelimbs most affected.

18. Spinal Muscular Dystrophy in Maine Coon Cats/John Fyfe*/Michigan State University/Study of a familial group (~15 cats) in Michigan. This disease is similar to Norwegian Glycogen Storage Disease. With Norwegian Glycogen Storage Disease a large percentage of Kittens are stillborn. - It appears that the nerves supplying the muscles are dying equaling a loss in motor neurons.

19. VIN/Paul Pion/Veterinary Information Network/www.vin.com, also has Pet Care Forum for lay people

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