Background:Naturally occurring alloantibodies produced against A and B red cell antigens in cats can cause acute hemolytic transfusion reactions. Blood incompatibilities, unrelated to the AB blood group system, have also been suspected after blood transfusions through routine crossmatch testing or as a result of hemolytic transfusion reactions. Hypothesis:Incompatible crossmatch results among AB compatible cats signify the presence of a naturally occurring alloantibody against a newly identified blood antigen in a group of previously never transfused blood donor cats. The associated alloantibody is clinically important based upon a hemolytic transfusion reaction after inadvertent transfusion of red cells expressing this red cell antigen in a feline renal transplant recipient that lacks this red cell antigen. Methods: Blood donor and nonblood donor cats were evaluated for the presence of auto‐and alloantibodies using direct antiglobulin and crossmatch tests, respectively, and were blood typed for AB blood group status. Both standard tube and novel gel column techniques were used. Results: Plasma from 3 of 65 cats and 1 feline renal transplant recipient caused incompatible crossmatch test results with AB compatible erythrocytes indicating these cats formed an alloantibody against a red cell antigen they lack, termed Mik. The 3 donors and the renal transplant recipient were crossmatch‐compatible with one another. Tube and gel column crossmatch test results were similar. Conclusions and Clinical Importance: The absence of this novel Mik red cell antigen can be associated with naturally occurring anti‐Mik alloantibodies and can elicit an acute hemolytic transfusion reaction after an AB‐matched blood transfusion.

Objective—To compare the ease of use and accuracy of 5 feline AB blood-typing methods: card agglutination (CARD), immunochromatographic cartridge (CHROM), gel-based (GEL), and conventional slide (SLIDE) and tube (TUBE) agglutination assays. Sample Population—490 anticoagulated blood samples from sick and healthy cats submitted to the Transfusion or Clinical Laboratory at the Veterinary Hospital of the University of Pennsylvania. Procedures—Sample selection was purposely biased toward those from anemic, type B, or type AB cats or those with autoagglutination. All blood samples were tested by use of GEL, SLIDE, and TUBE methods. Fifty-eight samples were also tested by use of CARD and CHROM methods. The presence of alloantibodies in all cats expressing the B antigen as detected by use of any method was also assessed. Results—Compared with the historical gold-standard TUBE method, good to excellent agreement was achieved with the other typing tests: CARD, 53 of 58 (91% agreement); CHROM, 55 of 58 (95%); GEL, 487 of 490 (99%); and SLIDE, 482 of 487 (99%; 3 samples were excluded because of autoagglutination). Four of the samples with discordant test results originated from cats with FeLV-related anemia. Conclusions and Clinical Relevance—Current laboratory and in-clinic methods provide simple and accurate typing for the feline AB blood group system with few discrepancies. Retyping after in-clinic typing with the GEL or TUBE laboratory methods is recommended to confirm any type B or AB cats.

Background Cystinuria, one of the first recognized inborn errors of metabolism, has been reported in many dog breeds. Hypothesis/Objectives To determine urinary cystine concentrations, inheritance, and mutations in the SLC3A1 and SLC7A9 genes associated with cystinuria in 3 breeds. Animals Mixed and purebred Labrador Retrievers (n = 6), Australian Cattle Dogs (6), Miniature Pinschers (4), and 1 mixed breed dog with cystine urolithiasis, relatives and control dogs. Methods Urinary cystinuria and aminoaciduria was assessed and exons of the SLC3A1 and SLC7A9 genes were sequenced from genomic DNA. Results In each breed, male and female dogs, independent of neuter status, were found to form calculi. A frameshift mutation in SLC3A1 (c.350delG) resulting in a premature stop codon was identified in autosomal‐recessive (AR) cystinuria in Labrador Retrievers and mixed breed dogs. A 6 bp deletion (c.1095_1100del) removing 2 threonines in SLC3A1 was found in autosomal‐dominant (AD) cystinuria with a more severe phenotype in homozygous than in heterozygous Australian Cattle Dogs. A missense mutation in SLC7A9 (c.964G>A) was discovered in AD cystinuria in Miniature Pinschers with only heterozygous affected dogs observed to date. Breed‐specific DNA tests were developed, but the prevalence of each mutation remains unknown. Conclusions and clinical importance These studies describe the first AD inheritance and the first putative SLC7A9 mutation to cause cystinuria in dogs and expand our understanding of this phenotypically and genetically heterogeneous disease, leading to a new classification system for canine cystinuria and better therapeutic management and genetic control in these breeds.

Objective —To compare accuracy and ease of use of a card agglutination assay, an immunochromatographic cartridge method, and a gel-based method for canine blood typing. Sample —Blood samples from 52 healthy blood donor dogs, 10 dogs with immune-mediated hemolytic anemia (IMHA), and 29 dogs with other diseases. Procedures —Blood samples were tested in accordance with manufacturer guidelines. Samples with low PCVs were created by the addition of autologous plasma to separately assess the effects of anemia on test results. Results —Compared with a composite reference standard of agreement between 2 methods, the gel-based method was found to be 100% accurate. The card agglutination assay was 89% to 91% accurate, depending on test interpretation, and the immunochromatographic cartridge method was 93% accurate but 100% specific. Errors were observed more frequently in samples from diseased dogs, particularly those with IMHA. In the presence of persistent autoagglutination, dog erythrocyte antigen (DEA) 1.1 typing was not possible, except with the immunochromatographic cartridge method. Conclusions and Clinical Relevance —The card agglutination assay and immunochromatographic cartridge method, performed by trained personnel, were suitable for in-clinic emergency DEA 1.1 blood typing. There may be errors, particularly for samples from dogs with IMHA, and the immunochromatographic cartridge method may have an advantage of allowing typing of samples with persistent autoagglutination. The laboratory gel-based method would be preferred for routine DEA 1.1 typing of donors and patients if it is available and time permits. Current DEA 1.1 typing techniques appear to be appropriately standardized and easy to use.