BLOOD TYPE INCOMPATIBILITY AND OTHER CAUSES OF NEWBORN KITTEN DEATHS

Dr. Giger first thanked the Winn Foundation for their support for the last three years. The Winn Feline Foundation is the major funder of feline research at this time; it is very difficult to get funding for the sort of research he is involved with from any other sources. Not only do CFA breeders raise the funds, we have also raised the issues and stimulated his interest in the area of blood group incompatibility in cats, the topic of this talk.

Kitten mortality is a distressing, as well as, an economic problem which occurs to some extent in any breeding program. A study by Scott et al, 1976, of over 3,000 kittens in over 800 litters indicated 34.5% mortality between birth and one year, which is a considerable number. Of these, 10% were stillborn, and 15.2% died during the first week. The role of infection was studied by Young in 1973 in a specific pathogen free colony. In litters from 56 queens totaling 633 kittens, there was 15% preweaning mortality, almost all during the first week. Of these kittens, 3% were stillborn, 24% had obvious malformations, 12% died of infections (such as pneumonia), and 62% were from unknown causes.

The causes of early kitten mortality are:

• inappropriate environmental conditions (probably not an issue with conscientious breeders).
• maternal neglect and cannibalism
• lack of colostrum or milk and/or improper supplementation
• infections such as septicemia or pneumonia
• metabolic abnormalities or immune deficiency
• neonatal erythrolysis

This last cause, neonatal erythrolysis has recently been recognized to be a major one in some breeds of cats. The term means hemolysis of the newborn, or the destruction of the red blood cells by the action of maternal antibodies which gain access to the neonatal circulation. In cats, this entrance is through the colostrum.

To understand the problem, we need to know about blood types in cats. The most numerous cells in the blood, the red blood cells, carry protein markers on their surfaces. The kinds and numbers of markers differ in different species. The blood type is determined by incubating blood from an individual with antisera to the different markers found in that species. Cells which have the marker will clump. For instance, blood from a type B cat will agglutinate when mixed with anti-B antiserum, but not when it is mixed with antiA antiserum.

Studies in Australia had indicated that cats had two blood types, A and B. In the United States over 3,000 domestic shorthair cats have been tested now and the frequency of type B blood is much lower than it is in Australia. There are definite geographic differences in the frequency of type B. In the northeast and midwest, over 99% of the domestic shorthair cats have type A blood. In Florida and the southeast, 1% to 2% have type B blood, while on the west coast 4% to 6% have type B. This knowledge is important for the management of anemic cats. Veterinarians on the west coast should be aware of the increased need to know blood type before giving a transfusion.

Studies of blood type in purebred cats were started after breeders realized that problems existed in some breeds. The frequency of type B blood varies greatly. Some breeds have no known type B individuals. Over 300 Siamese, Burmese, and Oriental Shorthairs have been tested, and all have type A blood. Breeds in which over 50 individuals have been typed which have higher frequencies are:

• 1% to 5% type B
  Maine Coon, Manx, Norwegian Forest Cat
• 10% to 20% type B
  Abyssinian, Scottish Fold, Persian,
  Japanese Bobtail, Birman, Somali
• 25% to 50% type B
  British Shorthair, Devon Rex, Cornish Rex

The genetics of the A and B blood types in cats is not the same as the ABO system in humans, the markers are not the same and the reagents for testing blood types are not the same. In all breeds of cats type B is recessive to type A. There is no type O blood, and type AB is extremely rare (and the genetics of this type is not understood yet). There are apparently no other blood groups in cats (unlike humans who have the Rh system in addition to the ABO system.)

Two problems may arise because of blood type incompatibility. The first is transfusion reactions especially when a type B cat is transfused with type A blood, a fatal reaction may result. The second is neonatal erythrolysis, which occurs when type A kittens are born to a type B queen.

Unlike Rh factor incompatibility in humans, neonatal erythrolysis may be seen in first litters as well as subsequent litters of a queen. It may affect some or all kittens in a litter (even if all of them have type A blood), and may not occur at all in some litters in which it should be expected. We still do not understand why some type A kittens born to type B queens are not affected. Typically, kittens will be vigorous and healthy at birth, and symptoms occur within hours to days of first nursing. Maternal antibodies cross the gut wall for a day or two after birth, which gives the kittens immediate passive immunity. Unfortunately, type B mothers have strong antiA antibodies, which also are transferred to the kittens, and can cause the lysis of their blood. After a few days, the intestinal wall becomes impermeable to proteins. Clinical signs vary between kitten and between queens. In general, the earlier the signs appear, the more serious they are. Nonspecific signs include the kitten ceasing to nurse, general failure to thrive, and sudden death. Specific signs are pigmenturia (urine which is colored red or brown), anemia, jaundice, and tail tip necrosis (which may occur at one to two weeks of age).

There are several ways that feline neonatal erthrolysis can be prevented. One is to type all cats and avoid mismatched matings with type B queens. If such a breeding occurs, type A kittens should not be allowed to nurse from their mother for two days, after which time the maternal antibodies will no longer be absorbed by the kitten. Newborn kittens can be typed using blood from the placenta (only a few drops are necessary), sent by overnight mail to Dr. Giger. Kittens may be foster nursed by a type A queen or tube fed until it is safe to return them to their mothers. Some breeders plan to have a litter about a week older than the litter due to a type B mother, and switch the litters for a few days, to keep the type B mother producing milk, since the older kittens will not absorb the anti-A antibodies. Any type B kittens in the litter may also be left with the mother. Since some kittens at risk will not be affected, kittens may be left with their mother and watched carefully, removing them if they show symptoms. This strategy is not as successful as the others, because, unfortunately, once kittens show symptoms it is often too late to save them.

The important thing to remember is that blood type is not a disease! Blood type reactions are significant problems, but ones which can be managed or avoided.

At the conclusion of this talk, Dr. Giger answered questions from the audience:

Where can blood typing be done?

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