The prevalence of feline A/B blood types in the Sydney region

OBJECTIVE: To determine the distribution of A/B blood types in pedigree and crossbred cats in the Sydney region, and to estimate the associated risk of administering incompatible blood in an unmatched random transfusion. DESIGN: A prospective/retrospective study of blood specimens collected from both sick and healthy cats. MATERIALS AND METHODS: Blood was collected from 355 cats from the Sydney region over a 12-year period from 1992 to 2003. Specimens were obtained from 187 domestic crossbred cats (short and long-haired) and 168 pedigree cats. The blood type of each cat was determined by one of three different laboratories using standard methods that varied over the duration of the survey. RESULTS: The distributions of blood types obtained by the three laboratories were not significantly different. The prevalence of type-A, type-B and type-AB blood types in crossbred cats was 62%, 36% and 1.6%, respectively. This is the highest percentage of type-B cats so far reported for an outbred population of domestic cats, and is significantly higher than the 26% reported previously for cats in the Brisbane region. The calculated frequency for the type-B allele assuming Hardy-Weinberg equilibrium for this feline population is 0.60; the corresponding frequency of the type-A allele is thus approximately 0.40. The calculated proportion of random transfusions from this population giving rise to an incompatible blood transfusion is 46%, with half of these being life-threatening events. The calculated proportion of random matings from this population at risk for developing neonatal isoerythrolysis is 23%. 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, suggesting that the distribution of blood types in these purebred populations is relatively consistent throughout the world. CONCLUSIONS: The prevalence of type B cats in the owned domestic and pedigree cat population is so high that blood typing or cross matching prior to transfusion should be mandatory, except in Siamese/Oriental cats.     

Quantitative assessment of hepatic function by means of 99mTc-mebrofenin in healthy horses

99mTc-mebrofenin is used in humans and small animals to assess hepatic function. This study was undertaken to measure hepatic clearance of 99mTc-mebrofenin in healthy horses and to determine whether feed deprivation and increased serum total bilirubin (TBIL) concentration alter 99mTc-mebrofenin clearance. Plasma clearance of 99mTc-mebrofenin was determirned in 7 healthy horses at 0, 48, and 96 hours of feed withholding. Serum TBIL and nonesterified fatty acid (NEFA) concentrations were measured every 24 hours. 99mTc-mebrofenin (4.16 +/- 0.62 mCi, mean +/- SD) was injected into a jugular vein, and blood samples were retrieved from the contralateral jugular vein. A plasma time-activity curve of 99mTc-mebrofenin was generated, from which the area under the curve (AUC) and the T1/2 of the fast-phase (T1/2) and slow-phase (T1/2f) were calculated. Mean +/- SD AUC was 17,700 +/- 4,257, 18,616 +/- 8,078, and 16,168 +/- 6,031 counts per minute (cpm) at 0, 48, and 96 hours, respectively; mean +/- SD T1/2f was 2.80 +/- 0.38 minutes, 3.52 +/- 1.46 minutes, and 3.82 +/- 1.29 minutes at 0, 48, and 96 hours, respectively; median T1/2s was 63.9, 49.2, and 45.8 minutes at 0, 48, and 96 hours, respectively. No difference was detected between the values of AUC, T1/2f, and T1/2s at 0, 48, and 96 hours. There was a significant increase in TBIL with fasting, with a mean +/- SD of 6.3 +/- 1.3 mg/dL at 26 hours. NEFAs increased, reaching a plateau at 48 hours (650 +/- 152 micromol/L). Plasma TBIL concentrations did not correlate with AUC or T1/2s but correlated weakly with T1/2f (r = 0.50). Plasma NEFA concentrations did not correlate with AUC, T1/2s, or T1/2f values. This study suggests that 99mTc-mebrofenin plasma clearance is not affected by feed withholding and that hyperbilirubinemia associated with feed withholding does not affect the hepatic extraction efficiency of this radiopharmaceutical.     

High throughput,high resolution selection of polymorphic microsatellite loci for multiplex analysis

Background  

Large-scale genetic profiling, mapping and genetic association studies require access to a series of well-characterised and polymorphic microsatellite markers with distinct and broad allele ranges. Selection of complementary microsatellite markers with non-overlapping allele ranges has historically proved to be a bottleneck in the development of multiplex microsatellite assays. The characterisation process for each microsatellite locus can be laborious and costly given the need for numerous, locus-specific fluorescent primers.     

Polymerase chain reaction (PCR) amplification of parvoviral DNA from the brains of dogs and cats with cerebellar hypoplasia

Cerebellar hypoplasia in cats is caused most commonly by an in utero or perinatal infection with feline panleukopenia virus (parvovirus). Cerebellar hypoplasia has been reported infrequently in dogs, but no viral etiology has been identified to date. DNA was extracted from archival, paraffin-embedded, cerebellar tissue from 8 cats and from 2 canine littermates with cerebellar hypoplasia, 2 canine littermates with cerebellar cortical abiotrophy, 6 dogs with congenital cerebellar vermal defects, 1 dog with congenital hydranencephaly, and 15 dogs and cats with various encephalitdes. The DNA extracted from each cerebellum was subject to polymerase chain reaction (PCR) amplification by 3 primer pairs specific for parvovirus DNA. Sequence analysis of PCR products from each of the 8 cats and 2 dogs with cerebellar hypoplasia confirmed their identity with parvoviral DNA. The 6 dogs with cerebellar vermal defects, 2 dogs with cortical abiotrophy, 1 dog with congenital hydranencephaly, and all control samples were PCR negative for parvovirus. Parvoviral structural proteins were not identified by immunohistochemistry in either dog with cerebellar hypoplasia. This study shows that parvoviral DNA can be amplified from feline and canine archival brain tissue and that cerebellar hypoplasia in dogs might be associated with in utero parvovirus infection.     

Early postnatal development of central corneal thickness in dogs

Objective To investigate the changes in corneal thickness that occur during maturation of the canine eye over the first months of life. Animals studied Dogs of two different breeds with ages ranging from 14 days to 42 weeks of age. Procedures The central corneal thickness was measured by ultrasonic pachymetry every week for the first month after eyelid opening (around 14 days) and then every month until 42 weeks of age. Segmented regression was applied to capture the two phases observed in the central corneal thickness plotted against age. Breed, eye and gender were also included in the model. Results Mean central corneal thickness (CCT) values initially decreased following eyelid opening, with the lowest point being reached at around 6 weeks of age. Then CCT gradually increased as the dogs matured. Differences between left and right eye were not significant. Breed and gender effects were significant factors in the statistical model. Conclusions Following eyelid opening there is an initial decrease in corneal thickness until approximately 6 weeks of age, which presumably mirrors maturation of corneal endothelial cell function. After 6 weeks of age the CCT increases with age until approximately 30 weeks of age after which there was only a gradual increase over the remainder of the study period. A similar pattern of changes in corneal thickness in humans has been previously recorded.