BackgroundBased upon serology, >10 canine blood group systems have been reported.ObjectiveWe surveyed dogs for dog erythrocyte antigen (DEA) 1 and 2 new blood types (Kai 1 and Kai 2), and some samples also were screened for Dal and DEA 3, 4, and 7.MethodsBlood samples provided by owners, breeders, animal blood banks, and clinical laboratories were typed for DEA 1 by an immunochromatographic strip technique with a monoclonal antibody and analysis of band intensity. Both new antigens, the Dal and other DEAs (except DEA 7 by tube method), were assessed by a gel column method with either monoclonal or polyclonal antibodies. The same gel column method was applied for alloantibody detection.ResultsOf 503 dogs typed, 59.6% were DEA 1+ with 4% weakly, 10% moderately, and 45.6% strongly DEA 1+. Regarding Kai 1 and Kai 2, 94% were Kai 1+/Kai 2‐, 5% were Kai 1‐/Kai 2‐ and 1% were Kai 1‐/Kai 2+, but none were Kai 1+/Kai 2+. There was no relationship between Kai 1/Kai 2 and other blood types tested. Plasma from DEA 1‐, Kai 1‐, Kai 2‐ dogs, or some combination of these contained no detectable alloantibodies against DEA 1 and Kai 1 or Kai, respectively.Conclusions and Clinical ImportanceThe new blood types, called Kai 1 and Kai 2, are unrelated to DEA 1, 3, 4, and 7 and Dal. Kai 1+/Kai 2‐ dogs were most commonly found in North America. The clinical relevance of Kai 1 and Kai 2 in canine transfusion medicine still needs to be elucidated.

BackgroundThe Dog erythrocyte antigen (DEA) 1 blood group system was thought to contain types DEA 1.1 and 1.2 (and possibly 1.3 [A3]). However, DEA 1.2+ dogs are very rare and newer typing methods reveal varying degrees of DEA 1 positivity.ObjectivesTo assess if variation in DEA 1 positivity is because of quantitative differences in surface antigen expression. To determine expression patterns in dogs over time and effects of blood storage (4°C). To evaluate DEA 1.2+ samples by DEA 1 typing methods.AnimalsAnticoagulated blood samples from 66 dogs in a research colony and from a hospital, and 9 previously typed DEA 1.2+ dogs from an animal blood bank.MethodsResearch study: Samples were analyzed by flow cytometry and immunochromatographic strip using a monoclonal anti‐DEA 1 antibody.ResultsTwenty dogs were DEA 1−, whereas 46 dogs were weakly to strongly DEA 1+. Antigen quantification revealed excellent correlation between strip and flow cytometry (r = 0.929). Both methods reclassified DEA 1.2+ samples as weakly to moderately DEA 1+, but they were not retyped with the polyclonal anti‐DEA 1.1/1.X antibodies. Dogs and blood samples retained their relative DEA 1 antigen densities over time.Conclusions and Clinical ImportanceThe blood group system DEA 1 is a continuum from negative to strongly positive antigen expression. Previously typed DEA 1.2+ appears to be DEA 1+. These findings further the understanding of the DEA 1 system and suggest that all alleles within the DEA 1 system have a similarly based epitope recognized by the monoclonal antibody.

BackgroundDifficulties with the direct antiglobulin test (DAT) and its apparent lack of sensitivity and specificity for immune‐mediated hemolytic anemia (IMHA) in dogs have raised skepticism regarding its diagnostic value.ObjectiveTo compare different DATs and other hematologic parameters in dogs.AnimalsAnticoagulated blood samples from 59 nonanemic and 46 anemic dogs (± IMHA) from a research colony and veterinary clinics.MethodsProspective observational study: Immunochromatographic strip, gel microcolumn, and capillary techniques were compared with standard microtiter DAT using 2 polyvalent antiglobulins. Spherocytosis, autoagglutination, osmotic fragility, and clinical data were assessed.ResultsBlood samples from all 59 nonanemic dogs were DAT‐. Among 46 anemic dogs, 33 were suspected of IMHA, but only 20 were DAT+. Old and new DAT methods yielded comparable and consistent results even after storage of chilled blood samples for 1 week. Spherocytosis and autoagglutination (that did not persist after washing) were noted in 15 and 16 DAT+ dogs, respectively. The other 26 anemic dogs, including 21 previously transfused dogs and 4 with autoagglutination, tested DAT‐ by the other methods. Osmotic fragility was increased in 70% (19/27) of anemic and all 15 DAT+ dogs tested. Limited follow‐up testing revealed DAT+ results for 3–70 days.Conclusions and Clinical ImportanceThe novel strip and capillary DAT methods are promising adjunct in‐clinic tools. Despite prior immunosuppressive treatment and presence of autoagglutination, the DAT was positive in anemic dogs with IMHA. Transfusion did not cause false DAT+ results. Our results support DAT as a cornerstone in the diagnosis of canine IMHA.

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.

Background Finding compatible feline blood donors can be challenging. Canine blood has been occasionally used when compatible feline blood was not available in emergency situations. Objectives The study goals were to describe the effects of xenotransfusion in two anemic cats receiving canine blood because of discordant blood types and acute transfusion reaction, respectively, and to report in vitro heterotyping and – crossmatching results between canine and feline blood samples. Material and Methods Blood samples from patients and other cats and dogs were typed, crossmatched, and assessed for alloantibodies using gel, card, and immunochromatographic strip techniques. Results Cat 1 was found to have type AB blood. Cat 2, which experienced an acute transfusion reaction, had type A blood. Neither had detectable alloantibodies against feline RBC. Both cats transiently improved after transfusion with canine blood, however, acute intravascular hemolysis occurred and the PCV rapidly declined. Blood typing post xenotransfusion with DEA 1 strips revealed a positive control band that was absent in feline blood, thus allowing for the identification of transfused canine RBC. Longitudinal assessment revealed that canine RBC could no longer be detected 4 days after xenotransfusion. Major crossmatching (feline plasma with canine RBC) resulted in both positive and negative reactions, depending on the cat. Minor crossmatching results showed mostly incompatibility. Conclusion While both cats survived xenotransfusion, the positive control band on the DEA 1 strip revealed that transfused canine RBC were short-lived, and intravascular hemolysis occurred. Crossmatch results between cats and dogs showed varied incompatibilities, and may not predict transfusion reactions.