Feline Recipient Screening

Chapter 10
Feline Recipient Screening

Anthony C.G. Abrams-Ogg

Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada

Erythrocyte antigens

Introduction

A red cell has a complex surface consisting of a cell membrane surrounded by a glycocalyx, which is a network of polysaccharides, glycoproteins, and glycolipids; for the latter, the lipid component is within the outer layer of the phospholipid bilayer and the carbohydrate component is part of the glycocalyx. Some red cell surface molecules differ between individuals of a species, which upon transfusion can be antigenic and elicit an alloantibody (also known as isoantibody) response. The result is a hemolytic transfusion reaction. These cell surface antigens define the blood groups of animals (Andrews and Penedo 2010). The encoding genes and polymorphisms, biochemical structure, and normal function of red cell antigens are variably understood for different species, and it is likely that many have only been discovered because of transfusion reactions (Lin et al. 2009; Andrews and Penedo 2010). Many blood group molecules are glycolipids or glycoproteins, and the antigenic sites are often carbohydrates. Lipids, in particular, are only antigenic if coupled to a protein or carbohydrate. A “common antigen” is one that is present in most members of the species.

Compared to normal physiology of the blood group antigens, their pathophysiology is comparatively well characterized. The potential severity of a hemolytic transfusion reaction covers the spectrum from an acute intravascular crisis to a subacute event (delayed hemolysis), where transfused cells are destroyed by extravascular hemolysis over several days or weeks (see Chapter 11). Analogous to autoimmune hemolytic anemia, three key factors in the recipient influencing the severity of an alloimmune hemolytic transfusion reaction are alloantibody titer, type, and binding affinity. First, the higher the alloantibody titer of the recipient, the more severe the transfusion reaction. Second, alloantibodies can be hemolysins and/or agglutinins. Hemolytic reactions mediated by immunoglobulin (Ig)M alloantibodies (more likely to be hemolysins) are worse than reactions mediated by IgG alloantibodies (more likely to be agglutinins). This is at least in part because of greater complement fixation by IgM. Third, the higher the affinity/reactivity (binding strength) of the alloantibody for the blood group antigen, the more severe the reaction.

Two key factors from the donor also affect severity of reaction. The first is antigen expression on the red cell surface. The more the blood group antigen is expressed on donor red cells, the more severe is the reaction. IgM is especially good at binding an antigen that is highly expressed. The second factor is transfusion volume. The higher the dose of donor antigen, the more severe the reaction can be.

Alloantibodies can be naturally occurring, that is, they are present in an animal prior to ever receiving a transfusion. Alloantibodies can also be newly produced after receiving a transfusion, that is, the recipient is sensitized. Naturally occurring antibodies are not present at birth, but are believed to be formed mostly as a result of sensitization to gastrointestinal microorganism or food antigens. Naturally occurring antibody titer can be enhanced by further sensitization and it is possible that ongoing exposure to antigens sustains naturally occurring titers. Naturally occurring and acquired alloantibody formation is polyclonal. There is probably an epigenetic effect modifying blood group expression and alloantibody formation, but this has not yet been reported.

Blood groups are genetically determined and most follow simple Mendelian inheritance. A simple blood group is one where there are only two alleles at a gene locus, with the animal being positive or negative. A blood group system is one where there are three or more alleles at a gene locus. Blood groups as a consequence of transfusion medicine would not have had a role in evolutionary selection pressure. However, neonatal isoerythrolysis (NI) or hemolysis in a newborn animal due to maternal alloantibody directed against the newborn’s red cells is a naturally occurring condition, and it is possible that blood groups exerted some selection pressure via this disorder.

Blood types of the domestic cat

History of the AB blood group system

Incompatibility studies and inheritance

Agglutination and hemolytic incompatibilities in cats were first reported in the early 20th century in New York City (Ingebrigsten 1912). Out of 40 cats (breed and source not specified), tube crossmatches identified two cats (5%) with strong alloagglutinins that were likely type B cats. This study also identified incompatibilities with incubation at cold temperatures (cold agglutinins). Further experiments were reported in another 40 cats in New York City (Ottenburgh and Thalhimer 1915), but that study also identified a number of cases of autoagglutination, suggesting that intense rouleaux, which is characteristic of cats, was confused with agglutination in some instances. That study also reported that the degree of agglutination varied within an animal over time. Hemolysis was reported in only one cat.

These findings were expanded on by Holmes (1950, 1953) in the UK, by Eyquem and Podliachouk (1954) and Eyquem et al. (1962) in France (who proposed the current nomenclature of type A and type B), and by Suzuki (1966) and Ikemoto et al. (1981) in Japan. Suzuki (1966) concluded that there were four blood groups. The largest group (10 cats, named type C₀) would have been type A. At least two of the other cats in this study were probably type B. The other two cats might have been A or B with A–A or B–B minor incompatibilities, or type AB. In the study by Ikemoto et al. (1981), cats with strong alloantibody were designated anti-Ca (for anti-cat), likely representing type B cats with anti-A antibody. Two blood groups were identified and named Ca and Cb, fortuitously corresponding to A and B. Auer and Bell (1980, 1981) first formally reported type AB in Australia. Numerous studies then established that the AB system was the main blood group system of cats, that a null phenotype devoid of A and B antigens does not occur, and that type A was more common than type B except in some breeds, especially British shorthairs and Rex breeds. (“AB system” is used in this chapter when discussing the whole group to avoid confusion with “type AB”, although it is acknowledged that type AB is probably not allelic to type A and type B.)

The A and B antigens were demonstrated in fetal liver and spleen tissue, and on fetal red cells as early as 46 days, supporting their genetic basis (Eyquem et al. 1962; Symons and Bell 1985). Pedigree and breeding studies established that type A and type B were allelic and followed simple Mendelian inheritance, and that the A allele was dominant to the b allele (Auer and Bell 1981; Giger et al. 1991a; Griok-Wenk et al. 1996). These studies also established that type AB was rare, and that the mode of inheritance was not clear. Numerous studies have not identified any association of the AB system with sex, coat color, eye color, or size (other than breed association), nor have any diseases other than NI been associated with blood type.

Transfusion reactions and alloantibodies

Early reports of experimental and unintentional incompatible transfusions provided a clinical picture that transfusions of type A blood to type B cats could be severe and acutely fatal, with less severe reactions causing anemia and jaundice, whereas transfusion of type B blood to type A cats would usually only result in a transfusion not lasting as long as expected and transient change in blood typing results (Auer et al. 1982; Auer and Bell 1983; Giger and Akol 1990; Giger and Bücheler 1991; Bücheler and Giger 1993; Niggemeier et al. 2000). Transfusion reactions were due to naturally occurring antibodies and the severity of observed reactions was due to type B cats having high anti-A titers, while the anti-B titers of type A cats were low or non-existent. Eyquem et al. (1962) reported that titers could be boosted to as high as 1:8,000 with sensitization by incompatible transfusion, but did not report if this was in type A or type B cats. Auer and Bell (1981, 1983) subsequently reported that anti-B titers, but not anti-A titers, could be boosted by sensitization. However, Giger and Bücheler (1991) reported sensitization of both type A and type B cats. Alloantibodies were not present in fetuses or at birth, but in type B cats developed by 4–6 weeks of age and reached adult levels by 12 weeks; in type A cats developed by 12 weeks of age, if at all (Auer and Bell 1981; Bücheler and Giger 1993). There was evidence that titers would increase somewhat with age (Ejimah et al. 1986) and fluctuate somewhat through the year (Auer and Bell 1981, 1983).

Analogous to the human ABO blood groups, it was proposed that alloantibodies developed in response to gastrointestinal A and B antigen-like epitopes, but these epitopes were not present on Toxocara cati or Salmonella isolated from the cats (Eyquem et al. 1962). Anti-A antibodies were proposed to develop more rapidly than anti-B antibodies because epitopes similar to the A antigen are either more common or are stronger stimulants than B-mimicking epitopes (Knottenbelt 2002). The transmission of alloantibodies to neonates via colostrum, the mechanism for NI, was also reported by Eyquem et al. (1962). The A antigen is expressed on lymphocytes, but the B antigen is not (Symons and Bell 1985). It is possible that chronic immunosuppression might lower alloantibody titers, but this has not been reported. Interestingly, using flow cytometry, anti-B antibody binding to type B red cells was greater than anti-A binding to type A red cells (Griot-Wenk et al. 1993), and a similar pattern was seen with immunostaining (Silvestre-Ferreira et al. 2011).

Biochemical characterization

Concurrent and subsequent studies using thin-layer chromatography (TLC), high-performance liquid chromatography (HPLC), and other methods in Japan and the United States and later in Spain, described the neuraminic (sialic) acids in the red cell membrane. As with other eukaryotic cell membranes, mammalian red cell membranes contain glycolipids. The carbohydrate moieties are found on the outer surface and contribute to the glycocalyx. The first studies of feline red cells revealed that they contain more glycolipids than those of other species examined (Yamakawa et al. 1960), and of these glycolipids, seven gangliosides were identified (Ando and Yamakawa 1982; Furukawa et al. 1988a,b). The most abundant ganglioside identified in non-pedigree cats was the disialoganglioside NeuGc-NeuGc-Galactose-Glucose-Ceramide [abbreviated (NeuGc)₂G_D3], where NeuGc refers to the carbohydrate N-glycolyl neuraminic acid (Handa and Handa 1965). Another disialoganglioside, NeuAc-NeuAc-Galactose-Glucose-Ceramide [ $c10-math-0001$ ], where NeuAc refers to N-acetyl neuraminic acid, was identified in a Persian cat (Hamanaka et al. 1979). This preliminary work was expanded upon by examining the gangliosides in type A and type B cats, and established that the neuraminic acids define the AB system (Butler et al. 1991b; Andrews et al. 1992; Griok-Went et al. 1993; Silvestre-Ferreira et al. 2011). Type A is due to NeuGc and type B is due to NeuAc (mnemonic: type B has Ac).

In addition to disialogangliosides, the different blood types have small quantities of mono- and trisialogangliosides as well. Neuraminic acids are ubiquitous in mammalian cell membranes. Their physiologic functions include cell synaptogenesis, neural transmission, and cell signaling (Schauer 1982; Wang and Brand-Miller 2003). Pathophysiologic roles include roles in oncogenesis and infectious diseases (e.g., NeuAc is the receptor for influenza virus). They can be absorbed intact from the gastrointestinal tract and incorporated into cell membranes (Bardor et al. 2005).

Genetic basis

Most recently, the genetic basis of the AB system has been extensively investigated. NeuAc is converted to NeuGc by the enzyme cytidine monophospho-N-acetylneuraminic acid hydroxylase (CMAH), therefore the CMAH gene was investigated as the genetic basis of the AB system (Bighignoli et al. 2007). The entire gene was sequenced and six single nucleotide polymorphisms (SNPs, substitution of one nucleotide for another) and an 18 nucleotide insertion/deletion (indel) were identified in type B cats. Five SNPs and indel 18 formed haplotypes (sets of polymorphisms on the same strand of DNA that tend to be inherited together) that corresponded to type A and type B phenotypes. The entire sequence of the gene can be found at NCBI (http://www.ncbi.nlm.nih.gov/gene/?term=cmah%20felis) (along with the rest of the feline genome), and multiple sequences of the polymorphic regions have also been deposited into GenBank (http://www.ncbi.nlm.nih.gov/nuccore/?term=cmah%20felis).

Two mutations (SNP G139A, indel 18) were used to genotype cats world-wide in three laboratories (Table 10.1). In a small number of cases there were discordant results between the two mutations, suggesting that not all type B cats had identical genotypes. The study did not identify mutations responsible for the type AB phenotype, and the genotypes of type AB cats were the same as the genotypes of homozygous and heterozygous type A cats (with the exception of two Sphinx cats homozygous for indel 18). The genetics of the AB system was proposed to be $c10-math-0002$ , where $c10-math-0003$ is at a different gene locus.

Table 10.1 Genotyping results of 1407 cats (Bighignoli et al. 2010)

Breed	AA	Ab	bb	N
Abyssinian	49	35	18	102
Balinese	3	0	0	3
Bengal	1	0	0	1
Birman	71	77	24	172
British Shorthair (4)^a	125	227	190	546
Cornish Rex	5	18	8	31
Chartreux	0	1	0	1
Domestic Med. Hair	0	1	0	1
Devon Rex (1)^a	17	32	21	71
Domestic Shorthair	2	2	0	4
Exotic Shorthair	9	5	2	16
Himalayan	4	1	0	5
LaPerm	1	0	0	1
Maine Coon (1)	2	1	1	5
Norwegian Forest (1)^a	6	0	0	6
Persian	35	9	4	48
Ragdoll (4)^a	193	35	3	235
Siamese	1	0	0	1
Scottish Fold	9	10	3	22
Siberian Forest	6	0	0	6
Somali	18	11	0	29
Selkirk Rex	5	20	7	32
Sphynx	9	17	5	31
Turkish Angora	8	1	0	11
Turkish Van	2	0	0	2
Unknown and crossbred	20	3	0	3
Total	602	506	286	1407

^a Number of cats tested that had discordant results between indel 18 and SNP G139A genotyping.

A recent study reported another less common CMAH mutation, SNP C136T, and genotyping based on G139A and C136T was used to examine concordance between genotype and phenotype in cats in the UK (Tasker et al. 2014). There was 100% concordance between type A phenotype and genotype (either homozygous AA or heterozygous Ab). As in the previous study, type AB phenotype had type A genotype (either AA or Ab) and mutations determining type AB were not found. All genotype AA cats had nucleotide G for SNP G139A and nucleotide C for SNP C136T. The study demonstrated that the b allele can be contributed to by either nucleotide A at SNP G139A or nucleotide T at SNP C136T, and concluded that genotyping based only on G139A might result in falsely identifying a genotype Ab as AA and a genotype bb as Ab in a small number of cases. The transfusion consequences of such misgenotyping would not be life-threatening, as it would at worst result in a type A cat receiving type B blood, but it could have severe consequences for breeding to avoid NI.

Type B

Although type B is far less common than type A (Table 10.2), the clearest picture of this blood type emerges from an integrated summary of current knowledge. The type B phenotype results from mutations that render the CMAH enzyme non-functional. The SNP G139A has been investigated the most, and appears to be present in all type B cats in at least one b allele. About two-thirds of type B cats have SNP G139A in both b alleles, while about one-third are compound heterozygotes with SNP G139A at one b allele and SNP C136T in the other b allele (Tasker et al. 2014). Genotype discordancy between SNP G139A and indel 18 has not been reported in detail, and whether other mutations must also be present to confer the type B phenotype has not been reported. Thus, there might be other combinations of mutations that result in type B. Regardless of the mutations or combinations thereof that render the CMAH enzyme non-functional, the resulting phenotype is the same for transfusion purposes, with only NeuAc being present on the red cell membrane, as it cannot be converted to NeuGc. The main resulting ganglioside on the type B red cell is $c10-math-0004$ ; there are also minor amounts of $c10-math-0005$ , as well as trisialogangliosides.

Table 10.2 Prevalence (percentage) of blood type A and B in pedigree cats in the United States and Canada (most cats from the United States) determined by tube hemagglutination, based on published and unpublished observations (Giger 2005)

Breed	Type A	Type B
Abyssinian	84	16
American Shorthair	100	0
Birman	82	18
British Shorthair	64	36
Burmese	100	0
Cornish Rex	67	33
Devon Rex	59	41
Exotic Shorthair	73	27
Himalayan	94	6
Japanese Bobtail	84	16
Ocicat	100	0
Maine Coon	97	3
Norwegian Forest	93	7
Oriental Shorthair	100	0
Persian	86	14
Scottish Fold	81	19
Siamese	100	0
Somali	82	18
Sphinx	83	17
Tonkinese	100	0
Turkish Angora	46	54

Type AB all <1% and not included.

When Triticum vulgaris lectin is used to agglutinate type B cells (see the section on blood typing), there is some slight variation in strength of agglutination, suggesting there might be variable expression of the B antigen on the red cell. It has been shown by TLC immunostaining that the naturally occurring anti-A antibodies are directed against $c10-math-0006$ (Andrews et al. 1992). The mechanism of natural alloimmunization of type B cats has not been proven, but neuraminic acids are present in all mammalian cells, as well as in some plants, fungi, and bacteria. Cats will be exposed to these in their diets (including in milk) and by other routes of exposure, and they can be absorbed intact from the intestinal tract. The type B cats have no NeuGc on their cells, so ingested NeuGc could be recognized as foreign and incite an immunologic response, resulting in development of anti-A antibodies that consist predominantly of strong IgM hemagglutinins and hemolysins.

The strength of the agglutinating anti-A titers varies from as low as 1:2 to as high as 1:2,048, with an approximately bell-shaped curve with median titers of 1:16–1:128 (Auer and Bell 1981; Wilkerson et al. 1991; Leidinger et al. 1993; Bücheler and Giger 1993; Knottenbelt et al. 1999b; Arikan and Akkan 2004; Gurkan et al. 2005; Almeida Lacerda et al. 2011). Anti-A antibodies can also be hemolysins, although the titers are lower, with a median of 1:8. One type B cat with no antibodies was reported (Haarer and Grunbaum 1993), as was a type B cat with no agglutinins (Auer and Bell 1981), and in two studies the lowest titers were reported as <1:4. It is therefore possible, although rare, for a type B cat to have no anti-A antibodies. It is likely that the strength of the anti-A titers depends on the degree of exposure to type A-like epitopes, as well as other host immunity factors, although this has not been investigated.

A type B cat with a high anti-A titer will develop severe shock after receiving as little as 0.5 mL of type A or type AB blood. A type B cat with a low anti-A titer will develop early loss of the transfusion with extravascular hemolysis and icterus. In one report, the mean half-life of transfused type B red cells to a type B recipient was 36.3 days, while the mean half-life of transfused type A red cells was 1.3 hours (Giger and Bücheler 1991). Type B cats are particularly prevalent in certain breeds (Table 10.2), but unfortunately the notoriety of these breeds has anecdotally resulted in belief by many veterinarians and veterinary technicians that the main risk of an AB system incompatible transfusion reaction is in pedigreed cats. In fact, because for most clinics the non-pedigree feline patient population likely far outnumbers the pedigree population (unless a practice has breeders of high type B prevalence breeds as clients), a clinic is more likely to encounter a non-pedigree type B cat.

Crossmatch incompatibility between two type B cats was reported (Suzuki 1966), as were anti-B antibodies at low titer (1:2) in type B and type AB cats (Knottenbelt et al. 1999b). These could represent non-AB system incompatibilities or subgroups of type B.

Type A

In type A cats, the CMAH gene is not mutated and the CMAH enzyme is functional, resulting in conversion of NeuAc to NeuGc. However, unlike the type B phenotype, the type A phenotype does have variation in the ganglioside patterns by TLC and HPLC, including between homozygous and heterozygous cats (Griot-Wenk et al. 1993; Silvestre-Ferreira et al. 2011). The predominant ganglioside is $c10-math-0007$ , but $c10-math-0008$ , $c10-math-0009$ , $c10-math-0010$ , $c10-math-0011$ , and $c10-math-0012$ are also variably present. In addition, various anti-A murine monoclonal antibodies (MoAbs) do not recognize all type A and type AB red cells, indicating phenotypic subgroups (Green et al. 2000). These differences might represent genotypes $c10-math-0013$ , $c10-math-0014$ , and $c10-math-0015$ (Silvestre-Ferreira et al. 2011). In the majority of Ab heterozygous cats, the b allele is due to SNP G149A, with a very small number due to SNIP C136T (Tasker et al. 2014). There might be other mutations in the b allele of heterozygous cats or elsewhere in the genome that affect the type A phenotype. The source of NeuAc could either be NeuAc that does not get converted to NeuGc by CMAH or NeuAc of dietary origin.

In initial reports, about one-third of type A cats had anti-B antibodies, consisting of weak IgM hemagglutinins and weak IgM and IgG hemolysins (Ejima et al. 1986; Auer and Bell 1981; Wilkerson et al. 1991; Bücheler and Giger 1993). Subsequently, anti-B antibody titers have been reported in 40–88% of type A cats (Leidinger et al. 1993; Knottenbelt et al. 1999b; Arikan and Akhan 2004; Gurkan et al. 2005; Almeida Lacerda et al. 2011). These higher rates may reflect regional differences and differences in laboratory techniques. Most titers are <1:4, with a highest reported titer of 1:128. Albeit at low titers, the presence of any such antibodies in some cats with NeuAc on their red cell membranes is intriguing. It is possible that the variable anti-B titers are related to varying amounts of NeuAc on the type A red cell membranes. However, unlike the binding of NeuGc by anti-A antibodies, the actual epitope recognized by anti-B antibodies has not been identified by immunostaining. It is possible that a type A cat’s anti-B antibodies recognize either different NeuAc gangliosides than on its own red cells, or NeuAc sialoproteins or other NeuAc-containing molecules, or that they are directed against non-AB system antigens (Silvestre-Ferreira et al. 2011). At this time, the genetic or other mechanisms responsible for the variable molecular structures of the type A phenotype and the variable anti-B titers have not been reported. The importance of the variable type A phenotype to AB system incompatibility is also not clear, but it is unlikely it has a major effect on the severity of a transfusion reaction in a type B cat.

Transfusion of type B or AB blood to a type A cat (of any phenotype) might result in a mild acute reaction or delayed hemolysis from the anti-B activity. In one report, the mean half-life of transfused type A red cells to a type A recipient was 33.4 days, while the mean half-life of transfused type B red cells was 2.1 days (Giger and Bücheler 1991). It should be noted that it has not been proven that type B red cell survival in a type A cat with undetectable anti-B antibodies is normal. Acute and delayed hemolysis can also result from the anti-A activity in the type B donor plasma. A type A cat transfused with type B blood might become sensitized and is at increased risk for an acute reaction upon the next mismatched transfusion. However, this scenario is not likely to happen given that type B blood is not common and feline blood banks are careful not to waste a precious resource.

Type AB

This phenotype is rare (see the section on prevalence of blood types). Pedigree and prevalence studies suggest that type AB can only occur in cats that can produce type B, but this would include non-pedigree cats and most breeds, with the possible exception of the Norwegian Forest Cat (Griok-Went et al. 1996). Type AB is the least understood of the AB system, but further studies are in progress to further characterize it. The CMAH genotype is the same as for type A ( $c10-math-0016$ or $c10-math-0017$ ); specifically, none of the type B mutations are present (except for indel 18 in two Sphinx cats). In TLC and HPLC studies, the type AB phenotype contains both NeuAc and NeuGc in approximately equal proportions, although, as with type A, there are different ganglioside patterns, but the mechanisms for producing the various phenotypes are not known (Andrews et al. 1992; Griot-Wenk et al. 1993; Silvestre-Ferreira et al. 2011).

Flow cytometry demonstrated that expression of the A and B antigens on type AB red cells were each about half of that on type A and type B red cells, respectively (Griot-Wenk et al. 1996). However, agglutination reactions of type AB cells with anti-B antibody were only slightly less strong than with type B cells, reactions were the same using T. vulgaris lectin, and anti-A antibody reactions were similar in strength between type AB and type A red cells. Given the genotype, the type AB phenotype cannot be produced by a mutated CMAH enzyme, although this does not preclude another mutation that modifies CMAH activity, or modifies incorporation of dietary NeuAc and NeuGc into the red cell membrane. Type AB cats do not have naturally occurring antibodies to either type A or type B red cells, with the previously noted exception of a low anti-B titer (Knottenbelt et al. 1999b).

Given the rarity of this blood type, it is unlikely that a type AB donor is available for a type AB recipient. A type AB cat can be safely transfused with type A blood if the donor has no anti-B antibodies. If the anti-B titer of the donor is not known, then it is best to transfuse only packed red blood cells (when most of the plasma has been extracted) and to consider washing the red cells prior to transfusion to remove type A plasma (Box 1).

Other blood groups

All other mammalian families investigated to date have more than one blood group system. During investigations of the AB system, occasional serologic incompatibilities between type A cats and between type B cats were noted and cold agglutinins were detected. There are also observations of delayed hemolysis developing in repeatedly transfused type A cats (K.J. Wardrop, personal communication 2015) and case series of crossmatches in clinical patients (see the section on crossmatching) revealing non-AB system incompatibilities. These findings suggest that other blood groups or common antigens might also exist for cats. In 2007, the Mik blood group was reported (Weinstein et al. 2007). There have been no molecular studies and the role of any such blood groups in NI is not known.

Mik blood group

The Mik antigen (named after Mike, a Mik-negative donor) was identified through crossmatching after transfusion of type A blood (ultimately deemed Mik-positive) to a type A community-owned renal transplant cat (ultimately deemed Mik-negative) resulted in acute hemolysis due to naturally occurring antibody (Weinstein et al. 2007). Upon further investigation of 65 type A blood donors (22 purpose-bred laboratory cats, 43 outbred community-owned cats), three unrelated cats ( $c10-math-0018$ ) were crossmatch incompatible with Mik-positive cats, indicating that they lacked the Mik antigen and had natural anti-Mik antibody. Three type B and one type AB cat also appeared to express Mik. The evidence from this study is that the Mik antigen is present in most cats, the phenotype is Mik-negative or Mik-positive with variable expression, and that Mik-negative cats had variable anti-Mik titers from 1:1 to 1:64, composed of both IgM and IgG. Additional Mik-negative cats were identified shortly after this report, but the limited supply anti-Mik antiserum precludes further investigation. In a recent study of 112 crossmatches of transfusion-naïve cats in the UK, no major incompatibilities were noted, suggesting that no Mik-negative cats were present (Tasker et al. 2014).

Acquired blood groups

Acquired (as opposed to inherited) blood groups are, by definition, not true blood groups, but might have genetic determinants (e.g., the Lewis system in humans). With neoplasia and gastrointestinal disorders in humans, blood group antigen expression can change and/or, analogous to the acquiring of autoantibodies, alloantibodies can be acquired (Matsushita et al. 1983; Mannessier et al. 1986; Murata et al. 1992; Matthes et al. 2002; Yazer et al. 2006). Non-AB system crossmatch incompatibilities were seen in 22.2% of 207 cats (a figure too high to represent all Mik incompatibilities), with an increased risk in cats with chronic kidney disease and other urinary tract disorders (Specht et al. 2007). A transfusion-naïve type A Mik positive cat with lymphoma at the author’s institution had an acute hemolytic transfusion reaction and was subsequently found to be incompatible to numerous prospective donors. A novel blood group antigen was not ruled out, but the possibility of acquired incompatibility was also considered. Mechanisms of disease-altering blood groups could include antigenic mimicry with red cell surface antigens or a change in CMAH activity.

Prevalence of blood types

Numerous studies have been performed using varying methods of blood typing for over 40 years (Tables 10.3–10.5). It is likely that there have been some typing errors, but these would not affect overall prevalence estimates. Among the most common cat breed, domestic shorthair (DSH), type A is the most common, whereas prevalence of type B is $c10-math-0019$ estimated or reported in eastern North America, South America, northern and southwest continental Europe, northern England and Scotland, and South Africa. Areas with type B prevalence of 10–20% in DSH include the west coast of North America, Ireland, and regions in southern England, Italy, Greece, Israel, and New Zealand. Areas with $c10-math-0020$ type B DSH cats include regions in southern England, Turkey, and Australia.

Table 10.3 Prevalence studies of blood type A, B, and AB, determined by hemagglutination, in non-pedigree cats, listed by country

Continent, country (region)	Type A (%)	Type B (%)	Type AB (%)	N	Typing method	Reference
North America
British Virgin Islands*^a	100	0	0	32	Tube-A	Bird et al. (1988)
Canada (Montreal)	94.4	5	0.6	178	Tube-L	Fosset and Blais (2014)
Canada (Southern Ontario)	90.1	9.9	0	121	IC-Alvedia	Blois (personal communication 2014)
USA and Canada	NR	NR	0.14	4148	Tube-A, Tube-L	Griot-Wenk et al. (1996)
USA and Canada (west coast)	80–90	10–20	Rare	NR	DMS-2, IC-Alvedia	Bland (personal communication 2015)
USA (New York)*	95	5	0	40	Tube crossmatch	Ingebrigsten (1912)
USA (New York)*	90	10	0	20	Tube crossmatch	Hayes et al. (1982)
USA (Boston)*	100	0	0	69	Tube-A	Bird et al. (1988)
USA (Philadelphia)	100	0	0	82	Tube-A	Kiltrain and Giger (1987)
USA (≈50% Philadelphia)	99.8	0.2	0	432	Tube-A	Giger et al. (1989)
USA (Kansas)	100	0	0	100	Tube-A	Giger et al. (1989)
USA (82% Philadelphia)	99.7	0.3	0	1072	Tube-A	Giger and Bücheler (1991), Giger et al. (1991a)
USA	98.1	1.7	0.1	3785	Tube-A, MTP-A	Giger et al. (1991b)
USA (northeast)	99.7	0.3	0	1450	Tube-A, MTP-A	Giger et al. (1991b)
USA (North Central and Rockies)	99.4	0.4	0.2	506	Tube-A, MTP-A	Giger et al. (1991b)
USA (southeast)	98.5	1.5	0	534	Tube-A, MTP-A	Giger et al. (1991b)
USA (southwest)	97.5	2.5	0	483	Tube-A, MTP-A	Giger et al. (1991b)
USA (Washington, lab colony)	90	10	0	22	Tube-A	Wilkerson et al. (1991)
USA (west coast)	94.8	4.7	0.5	812	Tube-A, MTP-A	Giger et al. (1991b)
South America
Argentina (Buenos Aires)	96.1	2.6	1.3	76	Tube-A	Jacomet et al. (1997)
Brazil (Paraíba)	98.1	1.2	0.7	178	Tube-L	Mendes et al. (2013)
Brazil (Porto Alegre)	97.0	3.0	0	100	DMS-2, Tube-A	Almeida Lacerda et al. (2011)
Brazil (Rio de Janeiro)	94.8	2.9	2.3	172	Tube-L (type B), MTP-A	Medeiros et al. (2008)
Europe
Austria	97.0	3.0	0	101	Tube-A	Leidinger et al. (1993)
DSH	97.8	2.2	0	89
DLH	91.7	8.3	0	12
Denmark (Copenhagen), DSH	98.1	1.9	0	105	Tube-A	Jensen et al. (1994)
Finland	100	0	0	61	Tube-A	Giger et al. (1992)
France*	85.1	14.9	0	350	Tube-A	Eyquem et al. (1962)
Greece (various regions)	78.3	20.3	1.4	207	DMS-1	Mylonakis et al. (2001)
DSH	NR	NR	NR	176
DLH	NR	NR	NR	31
Germany (Gieben area)	94.1	5.9	0	404	Tube-A	Haare and Grünbaum (1993)
Germany (Berlin, Brandenburg)	98.7	1.1	0.3	372	Slide-L	Weingart et al. (2006)
Hungary (Budapest area)	100	0	0	73	MTP-L	Bagdi et al. (2001)
Ireland (Dublin)	84.7	14.6	0.7	137	IC-Alvedia	Juvet et al. (2011)
Italy (Tuscany)	87.1	12.9	0	363	Tube-A	Continenza et al. (1992)
Italy (Lombardy)	89.5	8.8	1.7	57	Tube-L	Proverbio et al. (2008)
Italy (Milan)	90.7	7.1	2.1	140	Gel	Proverbio et al. (2013)
Italy (Milan, Perugia)	92.3	5.1	2.6	195	IC-Alvedia	Spada et al. (2014)
Italy (Piedmont)	86.9	7.4	5.7	122	Tube-L	Cavana et al. (2007)
Netherlands	95.8	3.1	1.1	95	Tube-A	Giger et al. (1992)
Portugual (northern)	89.1	4.1	6.8	147	Tube-L	Silvestre-Ferreira et al. (2004a)
DSH	90.2	3.8	6.0	132
DLH	80.0	6.7	2	15
Portugual (Lisbon), DSH	97.5	2.1	0.4	515	Slide-L, Tube-L, IC-Alvedia Marques et al. (2011)
Spain (Barcelona)	94.0	4.0	1.0	100	DMS-1+ slide crossmatch	De Gopegui et al. (2004)
Spain (Gran Canaria)	88.7	7.2	4.1	97	Tube-L	Silvestre-Ferreira et al. (2004b)
Sweden	98.1	0	1.9	54	NR	Sköld (2013)
Switzerland	99.6	0.4	0	1014	Tube-A	Hubler et al. (1993)
Turkey (Istanbul, Izmit, Kirikale, Giresun)	72.8	25.0	2.2	312	Tube-L, MTP-L	Gurkan et al. (2005)
	73.1	24.6	2.3	301	Tube-L, slide-L	Arikan et al. (2006)
Turkey (Mediterranean)	72.1	25.4	2.5	240	Slide-L	Arikan et al. (2010)
UK (Edinburgh, Glasgow, northern England)	87.1	7.9	5	139	DMS-1, MTP-A	Knottenbelt et al. (1999a)
DSH	88	8	4	125
DLH	78.6	7.1	14.3	14
UK (Scotland)	97.1	2.9	0	70	Tube-A	Giger et al. (1992)
UK (Bristol)	79.3	12.2	8.5	82	MTP-A, MTP-crossmatch	Tasker et al. (2014)
DSH	NR	NR	NR	74
DLH	NR	NR	NR	8
UK (London)	67.6	30.5	1.9	105	DMS-1	Forcada et al. (2007)
DSH	65.0	33.0	2.0	95
DLH	90.0	10.0	0	10
UK (Manchester)*	97.1	2.9	0	477	Slide-A	Holmes (1950)
	95.15	3.88	0.97	103	Tube-A and slide-A	Holmes (1953)
Asia
China (Beijing)	88.2	11.4	0.4	262	Tube-L	Zheng et al. (2011)
India (Mumbai)*	88.0	12.0	0	100	Tube-L	Dahanukar et al. (2001)
Israel (various)	69.5	16.0	14.5	213	Gel	Merbl et al. (2011)
Japan*	>80			14	Tube crossmatch	Suzuki (1966)
Japan*	99.3	9.7	0	207	Tube crossmatch	Ikemoto et al. (1981)
Japan (Tokyo)	90.0	0.8	9.2	261	Tube-A	Ejima et al. (1986)
South Korea (Seoul, Kangwon)	96.4	3.6	0	336	Tube-L	Ban et al. (2008)
Africa
Republic of South Africa	>90	<10	Rare	NR	DMS-2	Goddard (personal communication 2015)
Oceania
Australia
(Brisbane)*	73.3	26.3	0.4	1895	MTP-A	Auer and Bell (1981)
(Sydney)	62.0	36.0	1.6	187	MTP-A, DMS-1	Malik et al. (2005)
New Zealand	85.6	13.5	0.8	245	Tube-L	Cattin (2016)

^a The large majority of cats were DSH. Separate values for DSH and DLH cats are presented when specifically reported. In studies identified by “*”, pedigree and non-pedigree cats were not distinguished, but the majority were DSH.

DLH, domestic longhair; DSH, domestic shorthair; NR, not reported.

DMS-1: RapidVet-H Feline Typing Card (DMS Laboratories) with type B cat derived anti-A serum to agglutinate type A cells and Triticum vulgaris lectin to agglutinate type B cells.

DMS-2: RapidVet-H Feline Typing Card (DMS Laboratories) with monoclonal anti-A antibody to agglutinate type A cells and Triticum vulgaris lectin to agglutinate type B cells.

Gel: gel column card (DiaMed) using monoclonal anti-A antibody to agglutinate type A cells and Triticum vulgaris lectin or monoclonal anti-B antibody to agglutinate type B cells. No longer commercially available.

IC-Alvedia: QuickTest A+B (Alvedia), using monoclonal anti-A antibody to agglutinate type A cells and monoclonal anti-B antibody to agglutinate type B cells.

MTP: microtitre plate.

MTP-A: microtitre plate agglutination using type B cat derived anti-A serum to agglutinate type A cells, and high-titre anti-B serum, either naturally occurring or from sensitized type A cats, to agglutinate type B cells.

MTP-L: microtitre plate agglutination using type B cat derived anti-A serum to agglutinate type A cells, and Triticum vulgaris lectin to agglutinate type B cells.

Slide-A: slide agglutination using type B cat derived anti-A serum to agglutinate type A cells, and high-titre anti-B serum, either naturally occurring or from sensitized type A cats, to agglutinate type B cells.

Slide-L: slide agglutination using type B cat derived anti-A serum to agglutinate type A cells, and Triticum vulgaris lectin to agglutinate type B cells.

Tube-A: tube agglutination using type B cat derived anti-A serum to agglutinate type A cells, and high-titre anti-B serum, either naturally occurring or from sensitized type A cats, to agglutinate type B cells.

Tube-L: tube agglutination using type B cat derived anti-A serum to agglutinate type A cells, and Triticum vulgaris lectin to agglutinate type B cells.

Table 10.4 Prevalence studies (number of cats with each blood type, <10 of each breed) of blood type A, B, and AB, determined by hemagglutination, in pedigree cats, listed by breed and country (region)

Breed	Type A	Type B	Type AB	N	Method	Reference
Abyssinian
Austria	7	0	0	7	Tube-A	Leidinger et al. (1993)
Germany	9	0	0	9	Slide-L	Weingart et al. (2006)
Hungary	6	0	0	6	MTP	Bagdi et al. (2001)
Ireland (Dublin)	2	0	0	2	IC-Alvedia	Juvet et al. (2011)
Japan (Tokyo)	6	0	0	6	Tube-A	Ejima et al. (1986)
South Korea (Seoul, Kangwon)	2	1	0	3	Tube-L	Ban et al. (2008)
Italy (Milan, Perugia)	4	2	0	6	IC-Alvedia	Spada et al. (2014)
UK (Edinburgh, Glasgow, northern England)	2	0	2	4	DMS-1, MTP-A	Knottenbelt et al. (1999a)
USA and Canada	NR	NR	2	NR	Tube-A	Griot-Wenk et al. (1996)
Australian Mist (Spotted Mist)
Australia (Sydney)	1	0	0	1	MTP-A, DMS-1	Malik et al. (2005)
Bengal
Ireland (Dublin)	2	0	0	2	IC-Alvedia	Juvet et al. (2011)
UK (Edinburgh, Glasgow, northern England)	4	0	4	8	DMS-1, MTP-A	Knottenbelt et al. (1999a)
UK (southeast England)	6	1	0	7	DMS-1 card	Forcada et al. (2007)
Birman
Australia (Sydney)	2	2	0	4	MTP-A, DMS-1	Malik et al. (2005)
Canada (Montreal)	2	0	0	2	Tube-L	Fosset and Blais (2014)
Denmark (Copenhagen)	2	3	0	5	Tube-A	Jensen et al. (1994)
Germany (Berlin, Brandenburg)	9	0	0	9	Slide-L	Weingart et al. (2006)
Ireland (Dublin)	3	0	0	3	IC-Alvedia	Juvet et al. (2011)
South Korea (Seoul, Kangwon)	2	0	0	2	Tube-L	Ban et al. (2008)
Italy (Milan, Perugia)	7	0	0	7	IC-Alvedia	Spada et al. (2014)
UK (Bristol)	0	1	0	1	MTP-A, MTP-Xmatch	Tasker et al. (2014)
USA and Canada	NR	NR	3	NR	Tube-A	Griot-Wenk et al. (1996)
Bombay
UK (Edinburgh, Glasgow, northern England)	1	0	0	1	DMS-1, MTP-A	Knottenbelt et al. (1999a)
British shorthair
Australia (Sydney)	3	5	0	10*	MTP-A, DMS-1	Malik et al. (2005)
Canada (Montreal)	8	0	0	8	Tube-L	Fosset and Blais (2014)
Canada (southern Ontario)	0	1	0	1	IC-Alvedia	Blois (personal communication 2015)
Hungary	1	0	0	1	MTP-A	Bagdi et al. (2001)
South Korea (Seoul, Kangwon)	0	1	0	1	Tube-L	Ban et al. (2008)
Italy (Milan, Perugia)	6	0	0	6	IC-Alvedia	Spada et al. (2014)
UK (Bristol)	2	1	0	3	MTP-A, MTP-Xmatch	Tasker et al. (2014)
USA and Canada	NR	NR	13	NR	Tube-A	Griot-Wenk et al. (1996)
Burmese
Austria	2	0	0	2	Tube-A	Leidinger et al. (1993)
Canada (Southern Ontario)	1	0	0	1	IC-Alvedia	Blois (personal communication 2015)
Germany	1	0	5	6	Tube-A	Haare and Grünbaum (1993)
Denmark (Copenhagen)	9	0	0	9	Tube-A	Jensen et al. (1994)
Ireland (Dublin)	5	0	0	5	IC-Alvedia	Juvet et al. (2011)
UK (Bristol)	2	0	0	3	MTP-A, MTP-Xmatch	Tasker et al. (2014)
UK (London)	5	0	0	5	DMS-1	Forcada et al. (2007)
Chartreux
Italy (Milan, Perugia)	5	0	0	5	IC-Alvedia	Spada et al. (2014)
Chinchilla
UK (Edinburgh, Glasgow, northern England)	1	0	0	1	DMS-1, MTP-A	Knottenbelt et al. (1999)
Colourpoint longhair
Ireland (Dublin)	2	0	0	2	IC-Alvedia	Juvet et al. (2011)
Devon Rex
Germany	0	3	0	3	Tube-A	Haare and Grünbaum (1993)
Italy (Milan, Perugia)	3	3	0	6	IC-Alvedia	Spada et al. (2014)
UK (Bristol)	1	4	0	5	MTP-A, MTP-Xmatch	Tasker et al. (2014)
UK (Edinburgh, Glasgow, northern England)	2	0	0	2	DMS-1, MTP-A	Knottenbelt et al. (1999a)
Europée (European Shorthair)
Denmark (Copenhagen)	1	0	0	1	Tube-A	Jensen et al. (1994)
Exotic shorthair
Denmark (Copenhagen)	1	0	0	1	Tube-A	Jensen et al. (1994)
Ireland (Dublin)	3	0	0	3	IC-Alvedia	Juvet et al. (2011)
Italy (Milan, Perugia)	3	0	0	3	IC-Alvedia	Spada et al. (2014)
Havana
Ireland (Dublin)	1	0	0	1	IC-Alvedia	Juvet et al. (2011)
Himalayan
Canada (southern Ontario)	3	0	0	3	IC-Alvedia	Blois (personal communication 2015)
Ireland (Dublin)	1	0	0	1	IC-Alvedia	Juvet et al. (2011)
Japan (Tokyo)	5	0	2	7	Tube-A	Ejima et al. (1986)
USA (Philadelphia)	0	1	0	1	Tube-A	Kiltrain and Giger (1987)
LaPerm
UK (Bristol)	1	0	0	1	MTP-A, MTP-Xmatch	Tasker et al. (2014)
Maine Coon Cat
Austria	1	0	0	1	Tube-A	Leidinger et al. (1993)
Canada (southern Ontario)	1	0	0	1	IC-Alvedia	Blois (2014)
Denmark (Copenhagen)	3	0	0	3	Tube	Jensen et al. (1994)
UK (Bristol)	1	0	0	1	MTP-A, MTP-Xmatch	Tasker et al. (2014)
Manx
Australia (Sydney)	0	1	0	1	MTP-A, DMS-1	Malik et al. (2005)
Norwegian Forest Cat
Austria	1	0	0	1	Tube-A	Leidinger et al. (1993)
Canada (southern Ontario)	2	0	0	2	IC-Alvedia	Blois (personal communication 2015)
Denmark (Copenhagen)	2	0	0	2	Tube	Jensen et al. (1994)
Germany	2	0	0	2	Slide-L	Weingart et al. (2006)
Ireland (Dublin)	2	0	0	2	IC-Alvedia	Juvet et al. (2011)
Italy (Milan, Perugia)	7	0	0	7	IC-Alvedia	Spada et al. (2014)
USA and Canada	NR	NR	4	NR	Tube-A	Griot-Wenk et al. (1996)
Oriental Shorthair
Germany	4	0	0	4	Slide-L	Weingart et al. (2006)
Persian and/or Persian cross
Australia (Sydney)	6	2	1	9	MTP-A, DMS-1	Malik et al. (2005)
Canada (southern Ontario)	3	1	0	4	IC-Alvedia	Blois (personal communication 2015)
Canada (Montreal)	8	8			Tube-L	Fosset and Blais (2014)
Hungary	14	3	0	17	MTP-A	Bagdi et al. (2001)
Ireland (Dublin)	2	1	0	3	IC-Alvedia	Juvet et al. (2011)
Italy (Milan, Perugia)	4	1	3	8	IC-Alvedia	Spada et al. (2014)
Portugual (Northern)	6	0	1	7	Tube-L	Silvestre-Ferreiraet al. (2004a)
UK (Bristol)	2	1	0	3	MTP-A, MTP-Xmatch	Tasker et al. (2014)
UK (London)	4	1	0	5	DMS-1	Forcada et al. (2007)
USA and Canada	NR	NR	1	NR	Tube-A	Griot-Wenk et al. (1996)
Pixie bob
Ireland (Dublin)	1	0	0		IC-Alvedia	Juvet et al. (2011)
Ragdoll
Australia (Sydney)	4	1	0	5	MTP-A, DMS-1	Malik et al. (2005)
Canada (southern Ontario)	4	0	0	4	IC-Alvedia	Blois (personal communication 2015)
Germany	3	0	0	3	Slide-L	Weingart et al. (2006)
UK (Bristol)	4	0	0	4	MTP-A, MTP-Xmatch	Tasker et al. (2014)
UK (Edinburgh, Glasgow, northern England)	5	2	0	7	DMS-1, MTP-A	Knottenbelt et al. (1999a)
Russian Blue
Australia (Sydney)	4	1	0	5	MTP-A, DMS-1	Malik et al. (2005)
Austria	5	0	0	5	Tube-A	Leidinger et al. (1993)
Canada (southern Ontario)	1	0	0	1	IC-Alvedia	Blois (personal communication 2015)
Israel	5	0	0	5	Gel	Merbl et al. (2011)
Italy (Milan, Perugia)	1	0	0	1	IC-Alvedia	Spada et al. (2014)
Savannah	2	0	0	2	IC-Alvedia	Abrams-Ogg (unpublished data 2015)
Scottish Fold
Canada (Montreal)^b	7	0	0	7	Tube-L	Fosset and Blais (2014)
Germany	1	0	0	1	Slide-L	Weingart et al. (2006)
USA and Canada	NR	NR	6	NR	Tube-A	Griot-Wenk et al. (1996)
Siamese
Canada (Montreal)^c	4	0	0	4	Tube-L	Fosset and Blais (2014)
Canada (southern Ontario)	3	0	0	3	IC-Alvedia	Blois (personal communication 2015)
Germany	6	0	0	6	Slide-L	Weingart et al. (2006)
Hungary	3	0	0	3	MTP-A	Bagdi et al. (2001)
Denmark (Copenhagen)	3	0	0	3	Tube-A	Jensen et al. (1994)
Ireland (Dublin)	3	0	0	3	IC-Alvedia	Juvet et al. (2011)
Italy (Milan, Perugia)	3	0	0	3	IC-Alvedia	Spada et al. (2014)
UK (Bristol)	2	0	0	2	MTP-A, MTP-Xmatch	Tasker et al. (2014)
UK (Edinburgh, Glasgow, northern England)	4	0	0	4	DMS-1, MTP-A	Knottenbelt et al. (1999a)
Siberian Forest Cat
Italy (Milan, Perugia)	3	0	0	3	IC-Alvedia	Spada et al. (2014)
UK (Bristol)	3	2	0	5	MTP-A, MTP-Xmatch	Tasker et al. (2014)
Singapura
Australia (Sydney)	1	0	0	1	MTP-A, DMS-1	Malik et al. (2005)
Snowshoe
UK (Bristol)	1	0	0	1	MTP-A, MTP-Xmatch	Tasker et al. (2014)
Somali
Denmark (Copenhagen)	9	0	0	9	Tube-A	Jensen et al. (1994)
UK (Bristol)	1	0	0	1	MTP-A, MTP-Xmatch	Tasker et al. (2014)
UK (Edinburgh, Glasgow, northern England)	7	0	2	9	DMS-1, MTP-A	Knottenbelt et al. (1999a)
USA and Canada	NR	NR	6	NR	Tube-A	Griot-Wenk et al. (1996)
Sphynx
Canada (southern Ontario)	1	0	0	1	IC-Alvedia	Blois (personal communication 2015)
Italy (Milan, Perugia)	5	2	0	7	IC-Alvedia	Spada et al. (2014)
Tiffanie (Chantilly)
UK (Bristol)	1	0	0	1	MTP-A, MTP-Xmatch	Tasker et al. (2014)
Tonkinese
Canada (southern Ontario)	2	0	0	2	IC-Alvedia	Blois (personal communication 2015)
Turkish Angora
Germany	0	4	0	4	Slide-L	Weingart et al. (2006)
Turkish Van
UK (Edinburgh, Glasgow, northern England)	1	0	0	1	DMS-1, MTP-A	Knottenbelt et al. (1999a)

See Table 10.3 for abbreviations.

^a Results inconclusive for two cats.

^b Included Highland Fold and Foldex (Scottish Fold × Exotic derived breed).

^c Included Siamese and Siamese crossbreds.

Table 10.5 Prevalence studies (percentages, >10 of each breed) of blood type A, B, and AB determined by hemagglutination in pedigree cats, listed by breed and country (region)

Continent, country (region)	Type A	Type B	Type AB	N	Typing method	Reference
Purebred overall (only listed if some or all breeds not distinguished in survey)
Denmark (Copenhagen)	89.2	10.8	0	139	Tube-A	Jensen et al. (1994)
Ireland (Dublin)	97.4	2.6	0	39	IC-Alvedia	Juvet et al. (2011)
USA	78.5	21.5	0	1110	Tube-A	Giger et al. (1991a)
USA and Canada	80.3	19.6	0.14	5091	Tube-A	Griot-Wenk et al. (1996)
UK (London)	75.0	19.0	6.0	16	DMS-1	Forcada et al. (2007)
Purebred crosses overall
Germany (Berlin, Brandenburg)	91	9	0	11	Slide-L	Weingart et al. (2006)
Abyssinian
Australia (Sydney)	89.0	11.0	0	16	MTP-A, DMS-1	Malik et al. (2005)
Australia	100	0	0	36	DMS-2, Gel	Barrs et al. (2009)
Denmark (Copenhagen)	100	0	0	20	Tube-A	Jensen et al. (1994)
USA	79.9	20.1	0	194	Tube-A	Giger et al. (1991a)
USA	86.5	13.5	0	230	Tube-A	Giger et al. (1991b)
Abyssinian, Somali, Ocicat grouped together
Germany	97.2	2.8	36		Tube-A	Haare and Grünbaum (1993)
American Shorthair
USA	100	0	0	15	Tube-A	Giger et al. (1991a)
Bengal
UK	100	0	0	100	DMS-2, MTP-L	Gunn-Moore et al. (2009)
Birman
UK (Edinburgh, Glasgow, northern England)	62.5	29.2	8.3	24	DMS-1, MTP-A	Knottenbelt et al. (1999a)
USA	82.4	17.6	0	216	Tube-A	Giger et al. (1991a)
British Shorthair
Austria	70	30	0	30	Tube-A	Leidinger et al. (1993)
Denmark (Copenhagen)	66.7	33.3	0	30	Tube-A	Jensen et al. (1994)
Germany	54.5	45.5	0	33	Tube-A	Haare and Grünbaum (1993)
Germany (Berlin, Brandenburg)	71.4	28.6	0	35	Slide-L	Weingart et al. (2006)
USA	41.2	58.8	0	85	Tube-A	Giger et al. (1991a)
UK (Edinburgh, Glasgow, northern England)	39.7	58.7	1.6	121	DMS-1, MTP-A	Knottenbelt et al. (1999a)
Burmese
Australia (Sydney)	93.4	3.3	3.3	71	MTP-A, DMS-1	Malik et al. (2005)
UK (Edinburgh, Glasgow, northern England)	90.0	10.0	0	10	DMS-1, MTP-A	Knottenbelt et al. (1999a)
USA	100	0	0	25	Tube-A	Giger et al. (1991a)
Chartreux/Carthusian
Germany (Berlin, Brandenburg)	77.8	18.5	3.7	27	Slide-L	Weingart et al. (2006)
Devon rex
Australia (Sydney)	45.0	54.0	1.4	71	MTP-A, DMS-1	Malik et al. (2005)
USA	57.0	43.0	0	100	Tube-A	Giger et al. (1991a)
USA	50.3	49.7	0	288	Tube-A	Giger et al. (1991b)
Himalayan
USA	80.0	20.0	0	35	Tube-A	Giger et al. (1991a)
Maine Coon Cat
Germany	100	0	0	23	Tube-A	Haare and Grünbaum (1993)
Germany (Berlin, Brandenburg)	96.0	4.0	0	25	Slide-L	Weingart et al. (2006)
Italy (Milan, Perugia)	100	0	0	75	IC-Alvedia	Spada et al. (2014)
Ireland (Dublin)	100	0	0	11	IC-Alvedia	Juvet et al. (2011)
Norwegian Forest Cat
USA	100	0	0	20	Tube-A	Giger et al. (1991a)
Oriental Shorthair
USA	100	0	0	15	Tube-A	Giger et al. (1991a)
Persian
Austria	81.7	18.3	0	71	Tube-A	Leidinger et al. (1993)
Denmark (Copenhagen)	96.4	3.6	0	56	Tube-A	Jensen et al. (1994)
Germany	91.7	7.6	0.6		Tube-A	Haare and Grünbaum (1993)
Germany (Berlin, Brandenburg)	95.5	0	4.5	22	Slide-L	Weingart et al. (2006)
Israel	100	0	0	15	Gel	Merbl et al. (2011)
Italy	97.4	2.6	0	38	Tube-A	Continenza et al. (1992),
Japan (Tokyo)	72.7	9.1	18.2	11	Tube-A	Ejima et al. (1986)
South Korea (Seoul, Kangwon)	97.6	2.4	0	42	Tube-L	Ban et al. (2008)
UK (Edinburgh, Glasgow, northern England)	88.2	11.8	0	24	DMS-1, MTP-A	Knottenbelt et al. (1999a)
USA	75.9	24.1	0	170	Tube-A	Giger et al. (1991a)
USA	90.4	9.6	0	230	Tube-A	Giger et al. (1991b)
USA (WA, Persian cross colony)	82	18	0	23	Tube-A	Wilkerson et al. (1991)
Ragdoll
Italy (northern)	77.1	4.9	18.0	61	Gel	Proverbio et al. (2013)
Italy (Milan, Perugia)	68.0	8.0	24.0	25	IC-Alvedia	Spada et al. (2014)
UK (Edinburgh, Glasgow, northern England)	71.4	28.6	0	24	DMS-1, MTP-A	Knottenbelt et al. (1999a)
Russian Blue
South Korea (Seoul, Kangwon)	100	0	0	19	Tube-L	Ban et al. (2008)
Scottish Fold
USA	85.2	14.8	0	27	Tube-A	Giger et al. (1991a)
South Korea (Seoul, Kangwon)	100	0	0	11	Tube-A	Ban et al. (2008)
Siamese
Australia (Sydney)	100	0	0	12	MTP-A, DMS-1	Malik et al. (2005)
(including Oriental Shorthair)
Austria	100	0	0	11	Tube-A	Leidinger et al. (1993)
Germany	100	0	0	46	Tube-A	Haare and Grünbaum (1993)
Italy	96.2	3.8	0	26	Tube-A	Continenza et al. (1992)
Japan (Tokyo)	92.9	0	7.1	14	Tube-A	Ejima et al. (1986)
South Korea (Seoul, Kangwon)	100	0	0	30	Tube-L	Ban et al. (2008)
Portugual (Northern)	100	0	0	19	Tube-L	Silvestre-Ferreira et al (2004a)
USA	100	0	0	99	Tube-A	Giger et al. (1991a)
UK (London)	100	0	0	13	DMS-1	Forcada et al. (2007)
Siamese cross
Portugual (northern)	9.7	8.3	0	12	Tube-L	Silvestre-Ferreira et al (2004a)
Somali (also see Abyssinian)
Australia	100	0	0	24	DMS-2, Gel	Barrs et al. (2009)
Germany (Berlin, Brandenburg)	71.4	23.8	4.8	35	Slide-L	Weingart et al. (2006)
USA	77.8	22.2	0	27	Tube-A	Giger et al. (1991a)
Tonkinese
USA	100	0	0	31	Tube-A	Giger et al. (1991a)
Turkish Angora
South Korea (Seoul, Kangwon)	94.4	5.6	0	36	Tube-L	Ban et al. (2008)
Turkey	53.6	46.4	0	28	Tube-L and Slide-L	Arikan et al. (2003)
Turkish Van
Turkey	40.0	60.0	0	85	Tube-L and Slide-L	Arikan et al. (2003)

See Table 10.3 for abbreviations.

Geographical variations in the prevalence of blood types are not as pronounced in pedigree cats, probably in part because of the international travel of breeding cats, although this has been variably affected by import restrictions (Giger et al. 1991a; Bighignoli et al. 2010).

In all breeds except the British shorthair, Rex breeds, Turkish angora, and Turkish Van, type A is most common; whereas in these breeds type A and type B are roughly equally distributed (Tables 2, 4, and 5). Siamese cats are widely considered to have a type A prevalence of 100%, but studies by Continenza et al. (1992) and Ejima et al. (1986) identified one type B and one type AB Siamese cat, respectively. The possibility of misclassification based on older agglutination methods must be considered. However, anecdotally, one phenotypically Siamese cat from Austin, Texas, United States (Veterinary Information Network 2003), and one phenotypically Siamese cat from Vancouver, British Columbia, Canada (K. Bland, personal communication 2015) were type B based on strong DMS typing card results. The Canadian cat was transfused with type B blood without a reaction. It is possible that these cats were Siamese crossbred cats, but it emphasizes the point that even cats that are Siamese in appearance should be blood-typed.

Type AB is rare in all breeds. The notable exception is the ragdoll cat in Italy (Proverbio et al. 2013). In a study of 4148 non-pedigree cats in the United States and Canada, there were only six type AB cats, four of which were from California (Griot-Wenk et al. 1996). In Table 10.3, the percentage value in the type AB column for each breed only represents one or two cats.

Prevalence studies have involved various numbers and combinations of colony cats, healthy cats presented for wellness visits, breeding cats being tested to assess risk for NI, healthy cats being screened as blood donors, and sick hospitalized cats, which will all affect prevalence. Although there is no evidence that type B or AB cats are at increased risk for hematologic or other diseases, prevalence studies from referral hospitals with blood banks in low type B prevalence areas might be biased for type B prevalence because of referral for access to type B blood. For example, the prevalence of type B blood for hospitalized cats at the author’s institution is approximately 10%, while the estimated prevalence from screening healthy cats as donors is approximately 3%, a significant difference (χ², P < 0.05) (S. Blois, personal communication 2015). Similarly, a study population involving breeder-owned cats being screened for risk of NI might either increase or decrease prevalence depending upon the breed (Malik et al. 2005). Overall, there might be a trend for certain purebred cats to have a decreasing prevalence of type B as breeders select against those cats (Fossett and Blais 2014).

Many studies have calculated risks for transfusion reactions based on blood type prevalence and alloantibody titers. The risks might be low in some areas, but the consequences can be high. A compatibility test is easy and quick to perform, and no risk is worth taking. In the author’s opinion, it is malpractice to perform a blood transfusion in a cat without a compatibility test of some sort, and the admonition of “B careful” should be remembered whenever performing a feline transfusion.

Compatibility testing

A small volume “test dose” transfusion cannot be used as a compatibility test, both because this dose of type A or type AB cells given to a type B cat might be fatal, and because it might fail to detect incompatibility of type B blood given to a type A or type AB cat. Compatibility testing must be performed by serologic methods, which in increasing order of precision are crossmatching, antibody screening, and blood typing. Serology is the foundation of immunohematology and although molecular methods are advancing, serologic tests will remain necessary for some time, especially for point-of-care testing. Although severe transfusion reactions in feline veterinary patients were noted at least as early as the 1960s (Thornton 1964) and there was mounting evidence of serious AB system incompatibility reactions in the 1980s, compatibility testing did not start to become routine in many general and referral practices until the 1990s. Although simple point-of-care crossmatching techniques could always be performed, it was the promotion of blood typing services (Giger et al. 1989) and introduction of a point-of-care typing card (Rapid Vet®-H Feline, DMS Laboratories, Flemington, NJ) in 1995 that established blood typing as standard of care.

Crossmatching

The crossmatch is an in vitro simulation of what will happen in vivo if a transfusion proceeds. It is the most comprehensive test and the foundation serology test. In a major crossmatch, recipient serum is mixed with donor red cells; in a minor crossmatch, donor serum is mixed with recipient red cells. The mixtures are then observed for agglutination and/or hemolysis. Rapid-slide, tube, and microplate methodologies can be used. The rapid-slide and tube methods are shown in Boxes 10.2–10.5. The rapid slide method is roughly equivalent to the immediate spin crossmatch of the tube method. The tube method is more cumbersome, but allows for longer incubation time, which facilitates detection of weakly reacting antibodies. The microplate method facilitates using smaller volumes for conducting large surveys and measuring titers.

Tags: Manual of Veterinary Transfusion Medicine and Blood Banking

Sep 27, 2017 | Posted by admin in GENERAL | Comments Off

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