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May 1999

Norm Auspitz, Abyssinian Breed Council Secretary

 1110 Lodge Hill Rd.

Louisville, KY 40223

Home/Work: (502) 244-6133/ (502) 452-4868


E-Mail: auspitzn@yahoo.com

Abyssinian Breed Council URL: http://www.AbyssinianBC.org


To the Abyssinian Breed Council, this is my first newsletter, after a somewhat slow start this year. I am getting this out in anticipation of the CFA Annual Meeting in Sacramento, CA. There are only a couple of items I want to cover herein, (1) recap of the results of the Abyssinian Breed Ballot, (2) announcement and suggested agenda for our usual breed council meeting at the annual, (3) details of a new Winn Foundation study proposal for amyloid in Abyssinians.


These last few years have been very tumultuous for CFA with the WIAB controversy, the ever-present animal rights activist agenda against our hobby, the spate of natural disasters, which have engulfed the world. The next couple of years look to be just as tumultuous since the WIAB controversy is still with us, there is war in the Balkans, a continued expectation of even more natural disasters, and the possible man-made problems arising from the fabled millennium bug <a.k.a. the Y2K problem>.


However, through all this, the Abyssinian breed has remained a constant in that once the wording of the color standards was updated, there have been no major changes to the standard, only necessary refinements. We have seen the Abyssinian evolve to a somewhat more stylistic cat without losing its "out of the forest" charm. However, as this year’s top Abyssinians prove, we still have a range of acceptable styles all of which have done well in the show rings.


There does appear to be some who are in favor of merging the Abyssinian and Somali breeds into a shorthair and longhair division of Abyssinians. Personally, I believe most Abyssinian breeders and most Somali breeders would like to retain the status quo, but we must maintain an awareness that there are those, both in these two breeds and without, who would like to see this happen.

Respectfully Submitted,
Norman Auspitz Abyssinian Breed Ballot Results


Total Members: 159

Ballots Received 104

60% of voting: 63


Item 1: Add to penalize section the following clause: White undercoat on blue or fawn Abyssinians

Yes: 79

No: 24


The Board of Directors voted in favor of this in February and it was added to the Abyssinian standard as of May 1, 1999.


Item 2: Do you favor deleting the current 360 breed identification number from Ruddy and Red Abyssinians that have the dilute gene in their pedigrees.

Yes: 45

No: 57


As this was advisory to the Board and not a change to the Abyssinian standard, the Board of Directors could still take up this issue. The Board of Directors did not delete the 360 prefix.

Abyssinian Breed Council Breakfast Announcement


As per our normal custom, our annual Abyssinian Breed Council breakfast will be on Saturday morning June 26, 1999 at 7:00 AM. And is scheduled for 2 hours (until the delegate meeting starts up again). The price is $14.25 per person, payable to CFA. Please make your reservations before June 15, 1999.


The following is a tentative agenda for the meeting:


  • Introductions and announcements 
  • Awards 
  • Whole Foods Program for Aby’s – Mimi Cary 
  • Winn Foundation Amyloid Study Proposal – Hilary Helmrich/Leslie Lyons 
  • Open Discussion



Amyloidosis is actually a diverse group of diseases seen in many species of animals that was first identified about 150 years ago. In all these diseases, a type of protein is deposited in major body organs that eventually can impair organ function and lead to illness or death.


Background: Human and Feline Amyloidosis


In humans, the various amyloidosis syndromes have been classified into three groups: reactive, immunoglobulin-associated, and heredofamilial. In domestic animals, the only type of systemic amyloidosis found is reactive. These protein deposits are made of amyloid protein AA, which is a breakdown product of the serum protein called serum amyloid A (SAA) which is produced in the liver. SAA is commonly associated with chronic inflammatory disorders. However, in most affected cats, the predisposing cause of amyloidosis is not known.


In cats, systemic amyloidosis usually occurs infrequently. However, we have known since the early 1980’s that the Abyssinian breed has a high rate of amyloidosis. This has been called familial amyloidosis in Abyssinians. While the disease primarily affects the kidneys, amyloid deposits are also found in other organs, such as the adrenal and thyroid glands, the stomach and intestine, the liver, and the heart. In recent years, another form of systemic amyloidosis that primarily affects the liver has been identified in the Oriental breeds.


 History of Abyssinian Familial Amyloidosis Research


The history of familial amyloidosis research in Abyssinians goes back over 15 years, and Abyssinian breeders have been instrumental from the start. The first researcher to become involved was Dr. Steve DiBartola of The Ohio State University. In 1983, the Robert Winn Foundation and Abyssinian breeders funded his first project. The project was renewed in 1985 and in 1987, again with considerable financial and research support from the Abyssinian community. Dr. DiBartola’s work uncovered some very important facts about familial amyloidosis in Abyssinians, including the nature of the amyloid protein itself.


Isolation and analysis of the amyloid protein from the kidneys of Abyssinians has proven that this is a form of reactive systemic amyloidosis based on amyloid protein AA. This is distinct from the more common form of amyloid often found incidentally in the pancreas of domestic cats, which is called islet amyloid polypeptide.


Dr. Erik Gruys’ lab at Utrecht University has sequenced feline protein AA and compared the amino acid sequences of the Abyssinian/Somali amyloid to that from the Oriental breeds and also that found occasionally in domestic shorthair cats. He has found that these three protein AA sequences all differ slightly from one another. This work suggests that there are different genes responsible for the different feline SAAs, the precursor to amyloid protein AA.



Inheritance and Testing


Work at The Ohio State University has demonstrated that familial amyloidosis in Abyssinians is an inherited disease, but the mode of inheritance has been very difficult to determine. The disease has a variable presentation in affected cats, so that only those cats who have moderate to severe disease are usually detected. In order to determine the mode of inheritance, it is necessary to have an accurate test that can identify all cats with the disease, including those very mildly affected. Amyloid deposits have been found in the kidneys of older Abyssinians who died of other causes and never showed signs of kidney disease. Yet some of these cats did produce offspring confirmed with familial amyloidosis.


Unfortunately, there is also no foolproof way to detect mildly affected cats. The disease is usually diagnosed by kidney biopsy, but even this method can be inaccurate and it is certainly invasive. Dr. DiBartola worked on developing a blood test for SAA in an effort to try to predict which cats were at risk of developing familial amyloidosis. However, the blood test has not been suitable for screening cats because SAA will increase in response to any tissue injury and also in response to inflammation and cancers.


Over the years, research into familial amyloidosis in Abyssinians has also increased the knowledge of amyloidosis in humans as the cat has been used as a model for familial Mediterranean fever. This approach has enabled both humans and cats to benefit immeasurably from research. A great deal of information has been acquired about the pathogenesis of this disease and treatment methods. The link between environmental stresses, stress response dysfunction, the immune system and amyloidosis has been investigated. However, many questions still remain to be answered in these areas and further research is needed.



Identification of Genetic Causes


Work to identify a gene responsible for familial amyloidosis in Abyssinians started over 10 years ago, using DNA hybridization techniques. Several researchers, including Dr. DiBartola and Dr. Brenda Connor of the Beckman Research Institute of the City of Hope, have directed intensive efforts toward this goal. Identification of a gene or genes responsible for amyloidosis will enable researchers to examine the pathogenesis of the disease further. There may be a complex interplay of genetics, environment, stress, and other factors that results in amyloidosis.


Identification of a gene for familial amyloidosis in Abyssinians will also enable breeders to have a screening test for breeding cats. The most powerful tool in the fight against this disease will be one that allows kittens to be screened so that predisposed cats can be eliminated from breeding.


Recent revolutions in molecular genetic techniques have opened new doors in the hunt for a genetic basis for familial amyloidosis. Over the past 5 years, analysis methods to investigate familial diseases that do not have a clear mode of inheritance have been developed. In humans, several genes have been identified as related to the inherited forms of amyloidosis. One of these genes could also be related to amyloidosis in Abyssinians.


The other important recent development is the mapping of the feline genome which greatly increases the ability of researchers to investigate feline diseases.


Proposed Research Project


Dr. Leslie Lyons, who has been instrumental in the feline genome project, has developed a research proposal to hunt for a gene responsible for familial amyloidosis in Abyssinians. Her approach is based on a technique called sib pair analysis. To use this technique, breeders will have to identify living cats with amyloidosis, or deceased cats where blood and/or tissue samples still exist. A diagnosis of amyloidosis will be established using several criteria, including the results of veterinary examinations, patient history profiles, and laboratory testing. Attempts will be made to include cases without the need for kidney biopsies wherever possible. Certainly, if a diagnosis of amyloidosis has previously been made using a biopsy or at necropsy, this is the ideal situation. Once an affected cat is identified, available siblings will be examined to determine if one other affected cat is present in the family. Blood samples will then be collected and submitted to Dr. Lyons. Ideally, blood samples will also be collected from the parents of the affected cats to confirm parentage, as this is extremely important to the accuracy of the study.


Specific regions of the feline genome will be investigated. The regions will be selected because they are similar to regions on the human chromosome that are known to carry genes for human amyloidosis. Hopefully, the project will identify one or more candidate genes. One of the factors the success of the project will depend on is the diversity of the blood samples from the Abyssinian population. Therefore, it is important to have as many family lines as possible represented, as well as related breeds such as the Somali.



Project Requirements


This study requires that about 200 affected sibling pairs be identified. Samples from the parent cats will be required to verify parentage, but their amyloidosis status is less imperative to the study. Therefore, blood samples from about 400 affected cats plus parents, a possible total of 600 samples, will be required. Identification of this many cats will no doubt be a time consuming process, but the study has great potential to rule in or rule out specific genes as important to familial amyloidosis in Abyssinians.


Funding for the project is estimated at $15,000.00 over 2 years. The budget will cover the veterinary costs for biopsies, the histology reports on the biopsies, and blood sample collection and shipment. It is hoped that many of the samples can be collected from previously identified affected cats to minimize the number of new biopsies that must be performed. Dr. Lyons will attempt to arrange special rates from certain labs and vet facilities for sample collection and biopsies to help minimize costs.


The Winn Feline Foundation recognizes the importance of this study, not only to the Abyssinian breed, but to advancing the knowledge of amyloidosis in all cats. At the board meeting in February 1999, Dr. Lyons’ project was approved, but there is a lack of funds available for it to go ahead. Once again, help is required from Abyssinian breeders and fanciers to fund research. We are closer than ever to development of a screening test for this disease, a critical step in eliminating it from the breed.



What You Can Do?


Dr. Lyons and her collaborators from Ohio State and Utrecht need your help to continue the research work outlined in the article above.

  1. Funding:
  2. The Winn Foundation did not have sufficient funds this year to go forward with this research project. However, they will accept your donation (specified for the "Aby Project") and will apply those funds to Dr. Lyons' proposal. Send funds to

    The Winn Feline Foundation

    1805 Atlantic Avenue

    PO Box 1005

    Manasquan, NJ 08736-0805


  3. Sib pairs:

Dr. Lyons and the colleagues need at least 200 examples from affected cats and their littermates. If you have a cat that is affected, and know where the littermates are, contact Dr. Lyons directly and she will provide information about collecting blood samples and shipping them to her facility. (Remember to include a pedigree with every sample).


Dr. Leslie Lyons


Bldg 560, Rm 11-10

Fort Detrick, 7th Street

Frederick, MD 21702


phone: 301-846-1299

fax: 301-846-1909

email: lyons@NCIFCRF.gov

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