Neonatal Isoerythrolysis

This is a potentially life-threatening disorder that affects kittens of blood type A that are born to queens of blood type B. If the kittens are allowed to suckle maternal colostrum in the first 18-24 hours of life they may absorb significant amounts of maternal anti-A antibodies, which cause haemolysis (destruction) of the kitten’s red cells. Depending on the amount of antibody absorbed this may be rapidly fatal, more slowly fatal, or the kittens may survive but suffer necrosis (death) and sloughing of the extremities, typically the ears and tail tips.
The condition can be prevented by planned breeding, if the blood types of queen and tom are known. Blood type B is recessive, blood group A is dominant (blood group AB is distinct from either and inherited separately), so avoiding using type B cats altogether, or only putting type B queens to type B toms avoids producing type A kittens. Alternatively type A kittens born to a type B queen can be prevented from suckling maternal colostrums for the first 18 hours of life – by fostering them to another lactating queen, or bottle feeding with artificial milk-replacer. All these preventive strategies require knowledge of the cats’ blood types. Blood typing cards are available and produce an immediate result, useful for breeders wishing to type kittens at birth (using drops of cord blood). Veterinary laboratories also offer blood typing of EDTA blood samples, and recently a genetic test has become available which utilises DNA extracted from buccal swabs. For more information regarding this gene test go to http://www.vgl.ucdavis.edu.

Estimated Frequency of Blood Type B in Various Pedigree Breeds
NB: For some breeds only small numbers of cats have been tested, so the figures may not be as accurate as they would be if results were available for larger numbers of cats. The proportion of group B cats within a breed may change with time, depending on breeding choices and patterns within that breed. A recent Australian study concluded that the distribution of A and B blood types for pedigree cats was in general agreement with data reported previously for cats in North America and Europe.

* Figures supplied by Dr. Giger, University of Pennsylvania
^ Figures from a study of UK cats conducted by C. Knottenbelt, University of Glasgow
“ Figures supplied by Dr Addie, University of Glasgow

A gene test is now available for the detection of A and B blood types. It is available from Dr. Leslie Lyons U.C. Davis Genetics Laboratory www.vgl.ucdavis.edu
For information on blood types within different breeds go to www.fabcats.org/owners/blood_groups
Knottenbelt, C.M (2002) The feline AB blood group system and its importance in transfusion medicine, Journal of Feline Medicine & Surgery 4:69-76
Giger, U., Bucheler, J., Callan, M.B., Casal, M., Griotwenk, M. Feline Neonatal Isoerythrolysis and Transfusion Reactions, Kleintierpraxis 38:715, 1993.
Giger, U., Kilrain, C.G., Filippich, L.J., Bell, K. Frequencies of Feline Blood Groups in the United-States, Journal of the American Veterinary Medical Association 195:1230-1232, 1989.
Griotwenk, M.E., Giger, U. Feline transfusion medicine - blood types and their clinical importance, Veterinary Clinics of North America - Small Animal Practice 25:1305 ff., 1995.
Weinstein, N. M., Blais, M. C., Greiner, K., Oakley, D. A., Hyson, A., Giger, U.A new blood group antigen in domestic shorthair cats: The feline mik red cell antigen, Journal of Veterinary Internal Medicine 3:400-401 (abstract), 2005.
Knottenbelt CM, Addie DD, Day MJ, Mackin AJ. Determination of the prevalence of feline blood types in the UK. J Small Anim Pract. 1999 Mar;40(3):115-8.
Arikan S, Gurkan M, Ozaytekin E, Dodurka T, Giger U., Frequencies of blood type A, B and AB in non-pedigree domestic cats in Turkey. J Small Anim Pract. 2006 Jan;47(1):10-3
Malik R, Griffin DL, White JD, Rozmanec M, Tisdall PL, Foster SF, Bell K, Nicholas FW. The prevalence of feline A/B blood types in the Sydney region. Aust Vet J. 2005 Jan-Feb;83(1-2):38-44.
Silvestre-Ferreira AC, Pastor J, Almeida O, Montoya A. Frequencies of feline blood types in northern Portugal.
Vet Clin Pathol. 2004;33(4):240-3.
Ruiz de Gopegui R, Velasquez M, Espada Y. Survey of feline blood types in the Barcelona area of Spain.
Vet Rec. 2004 Jun 19;154(25):794-5.
Bagdi N, Magdus M, Leidinger E, Leidinger J, Voros K. Frequencies of feline blood types in Hungary. Acta Vet Hung. 2001;49(4):369-75.
Forcada Y, Guitian J, Gibson G. Frequencies of feline blood types at a referral hospital in the south east of England. JSAP 2007: 48: 570-573
Gunn-Moore DA, Simpson KE, Day MJ. Blood types in Bengal cats in the UK. J Feline Med Surg. 2009;11(10):826-8

Hyperlipidaemia (i.e. too much fat in the blood)

Fat metabolism is very complex and a number of diseases are known to occur when it goes wrong, some of which have a heritable nature. The best understood of these conditions are ‘transient hyperlipidaemia and associated anaemia’ and ‘inherited hyperchylomicronaemia’.

Transient hyperlipidaemia and associated anaemia
Transient hyperlipidaemia and associated anaemia has been seen with reasonably frequency in non-pedigree cats and in a number of different breeds, including Siamese and Oriental cats. Affected kittens become ill at 3-5 weeks of age. They stop feeding, become very weak, and usually die within a few days. On clinical examination, affected kittens have very pale mucous membranes, are breathing fast and have very fast heart rates. Some kittens may show hind limb paralysis. The entire litter is usually affected, and most affected kittens die if they are left untreated. The mother cat is unaffected. Diagnosis can be made by collecting a blood sample. Grossly, the blood looks like strawberry milk shake! This results from the very high fasting triglyceride levels (5-126 mmol/l; reference range 0-1.0 mmol/l) and severe anaemia (PCV <11 %; reference range 24-45%). If a blood sample is not collected and/or a post mortem examination is not performed then this condition is very easy to miss. Lipid analysis reveals marked increases in chylomicrons, with moderately raised very low-density lipoproteins. While the cause of the disorder is not yet known, a number of factors are thought to be involved; including genetics, nutrition, age, and infectious agents. The underlying defect is believed to be a transient error in fat metabolism. Genetics appear to be involved as the lipoprotein lipase (LPL) activity of affected kittens is significantly reduced compared with unrelated healthy cats (Gunn-Moore et al 1997). Interestingly, the LPL activity in the affected kittens’ parents and non-affected siblings is also reduced, but to a lesser degree. LPL is an enzyme that is essential for normal fat metabolism, and reduced activity results in hypertriglyceridaemia. Further study has failed to find the LPL gene mutation reported previously in LPL-deficient cats from New Zealand (Ginzinger, 1996).
Interestingly, while the LPL activity is reduced throughout life, affected cats only show clinical disease as kittens. Other factors must therefore be involved, the most important of which is probably age. This is because all young kittens have low levels of LPL activity. The combination of the age-related lack of enzyme activity with a mild genetic insufficiency may result in disease. Diet may also play a role. Queens’ milk and proprietary kitten diets contain high levels of fat. Therefore, the kittens receive a high fat diet at a time when they can least cope with it. The effect of the queens’ milk can be further exaggerated by feeding the queen a high fat diet, since this is then passed onto the kittens in the milk. While these factors may explain the presence of the hyperlipidaemia, the cause of the anaemia is less well understood. It may relate directly to the fat disorder or, perhaps to other factors, such as the flea burdens and/or Haemobartonella felis infections that have be seen affecting some of the kittens. If diagnosed and treated promptly affected kittens can be saved. The kittens typically need a blood transfusion, and their diet must be changed to one with a low fat content. This also means first weaning them from their mother. Any fleas or other anaemia-inducing parasites must be removed.

Inherited hyperchylomicronaemia
Inherited hyperchylomicronaemia is seen only rarely and causes affected cats to develop xanthomata (fatty masses) when their fatty blood leaks out of damaged blood vessels. The xanthomata then compress peripheral nerves, leading to nerve damage. The fasting hyperlipidaemia is characterized by hypertriglyceridaemia with elevation of chylomicrons and often mild very low density lipoprotein elevation. Some affected cats also anaemic. Lipoprotein lipase (LPL) activity is absent or reduced. The defect is inherited as an autosomal recessive trait. It is suggested that a point mutation is present in the heparin binding domain of the protein.

Ginzinger, D.G., Lewis, M.E.S., Ma, Y.H., Jones, B.R., Liu, G.Q., Jones, S.D., Hayden, M.R. (1996) A mutation in the lipoprotein lipase gene is the molecular basis of chylomicronemia in a colony of domestic cats, Journal of Clinical Investigation 97:1257-1266
Gunn-Moore, D.A., Watson, T.D.G., Dodkin, S.J., Blaxter, A.C., Crispin, S.M., Gruffydd-Jones, T.J. (1997) Transient hyperlipidaemia and anaemia in kittens, Veterinary Record 140:355-359
Jones, B.R. (1993) Inherited Hyperchylomicronaemia in the Cat, Journal of Small Animal Practice 34: 493-499
Reginato, C.F., Backus, R.C., Rogers, Q.R. (2002) Improved growth of lipoprotein lipase deficient kittens by feeding a low-fat, highly digestible diet, Journal of Nutritional Biochemistry 13:149-156
Watson, TDG; Gaffney, D; Mooney, CT; Thompson, H; Packard, CJ; Shepherd, J (1992) Inherited hyperchylomicronaemia in the cat: lipoprotein lipase function and gene structure. Journal of Small Animal Practice 33(5): 213-217

Bleeding disorders (r)

Blood clotting involves a complex series of reactions and many different components (e.g. platelets, clotting factors). While heritable defects in the clotting system are not seen commonly, there are a number of well recognised defects that are known or presumed to be genetic in nature that have been seen in pedigree and DSH cats. In all cases affected individuals are predisposed to bleeding after trauma or surgery.
Devon Rex Vitamin K-dependent coagulopathy is an autosomal recessive defect that has been seen quite frequently in cats of this breed all over the world. Haemophilia A (Factor VIII deficiency; classical haemophilia) (r) has been seen very occasionally in Persian cats. Haemophilia B (Factor IX deficiency, Christmas disease) (r) has been seen very occasionally in Birman, BSH and Siamese cats. Since the genes for factors VIII and IX are both located on the X chromosome, these two disorders are usually recessive and sex-linked. A combined Factor I and Factor XI deficiency has recently been seen in a number of Maine Coon cats in the UK. Hageman factor deficiency results in a deficiency of clotting factor XII, and in prolonged APTT clotting times (which is a laboratory test), but does not appear to result in signs of bleeding. It is believed to be inherited as an incomplete dominant trait.

Factor I & Factor XI deficiency in Maine Coon cats in the UK – contact Danielle.Gunn-Moore@ed.ac.uk
Brooks M. (1999) Hereditary bleeding disorders in dogs and cats. Veterinary Medicine, June: 555-564
Brown R. Haemophilia in Maine Coon cats. Vet Rec. 2008;163(22):667
Gookin, J.L., Brooks, M.B., Catalfamo, J.L., Bunch, S.E., Munana, K.R. (1997) Factor X deficiency in a cat, Journal of the American Veterinary Medical Association 211:576
Goree, M., Catalfamo, JL., Aber, S., Boudreaux, MK. (2005) Characterization of the mutations causing hemophilia B in 2 domestic cats., J Vet Intern Med 19:200-204
Hoskins JD (1995) Congenital defects of cats. Compendium of Small Animal Practice 17(3): 385-405
Kier A B & Bresnahan J-F (1982) Animal models of human disease: Hageman trait. Animal model: factor XII deficiency in domestic cats. Comparative-Pathology-Bulletin14, 3
Kier, A.B., Mcdonnell, J.J., Stern, A., Ratnoff, O.D. (1990) The Arthus Reaction in Cats Deficient in Hageman Factor (Factor-XII), Journal of Comparative Pathology 102:33-47
Littlewood, J.D. (1989) Inherited bleeding disorders of dogs and cats, Journal of Small Animal Practice 30:140-143
Littlewood, J.D., Evans, R.J. (1990) A Combined Deficiency of Factor-VIII and Contact Activation Defect in a Family of Cats, British Veterinary Journal 146:30-35
Littlewood J D et al (1995) Vitamin K-dependent coagulopathy in a British Devon Rex cat, Journal of Small Animal Practice 36, 115-118
Maddison, J.E, Watson AD, Eade IG, Exner T (1990) Vitamin-K-Dependent Multifactor Coagulopathy in Devon Rex Cats, Journal of the American Veterinary Medical Association 197:1495-1497
Maggio-Price, L., Dodds, W.J. (1993) Factor IX Deficiency (Hemophilia B) in a Family of British Shorthair Cats, Journal of the American Veterinary Medical Association 203:1702-1704
Soute B A M et al (1992) Congenital Deficiency of All Vitamin-K-Dependent Blood Coagulation Factors Due to a Defective Vitamin-K-Dependent Carboxylase in Devon Rex Cats, Thrombosis and Haemostasis 68:521-525
Troxel, M.T., Brooks, M.B., Esterline, M.L. (2002) Congenital factor XI deficiency in a domestic shorthair cat, Journal of the American Animal Hospital Association 38:549-553

Updated May 2010

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KEY

Genetics confirmed and/or test available
Breed predisposition/strongly suspected as inherited
Potential breed predisposition is recognised but it is not currently known if the condition is inherited or not, only single case reports are available or evidence is anecdotal

* well recognised within the breed
r  rare or only seen in specific line/group