Comparison of the results of abdominal ultrasonography and exploratory laparotomy in the dog and cat

Results of preoperative ultrasonography and exploratory laparotomy were reviewed retrospectively in a series of 100 small animals to assess the agreement between ultrasonographic and surgical findings and to identify abdominal lesions likely to be missed by ultrasonography. Good agreement occurred between ultrasound reports and surgical reports in 64% of the animals, which supported the use of ultrasonography in potential surgical candidates. A major discrepancy was observed between the ultrasound report and surgical findings in 25% of the animals. Of the various types of pathology encountered in the study, gastrointestinal ulceration or perforation was the most likely lesion to be missed by ultrasonography.     

Nucleotide sequence of the canine alphaIIb gene from platelet-derived cDNA

OBJECTIVE: To determine the nucleotide sequence of the alphaIIb gene from canine platelet-derived cDNA. ANIMALS: 3 adult dogs. PROCEDURE: First-strand cDNA was prepared from total RNA isolated from canine platelets. The cDNA was amplified, using specific primers in polymerase chain reaction (PCR), and the nucleotide sequence was obtained from purified PCR products. RESULTS: Except for the nucleotide at position 694, results of all sequencing reactions of alphaIIb were identical for canine platelet-derived cDNA. Canine alphaIIb had 3 fewer codons than alphaIIb of humans. The nucleotide and deduced amino acid sequences of full-length canine alphaIIb shared > or = 83% similarity with the sequences established for humans. Segments of canine alphaIIb nucleotide and deduced amino acid sequences were > or = 78% similar to alphaIIb associated with 7 functional domains (extracellular, transmembrane, cytoplasmic, and 4 calcium-binding domains) in humans, with the highest degree of similarity correlating with the sequences of the 4 calcium-binding domains. Amino acid residues associated with development of alloantibodies in humans (Met837, Val837, Ile843, Ser843) are not encoded by canine alphaIIb. CONCLUSIONS AND CLINICAL RELEVANCE: The nucleotide variation at position 694 of canine alphaIIb may represent a polymorphism. The species differences in the alphaIIb sequence may contribute to variations in receptor-li gand interactions. The high degree of alphaIIb sequence conservation of the 4 calcium-binding domains implies functional importance. Some disorders associated with alphaIIbbeta3 in dogs are clinically analogous to diseases in humans, and results indicate that dogs are an appropriate model for the evaluation of gene therapy and other treatments of platelet-associated disorders.     

Asymmetric densitometric and mechanical adaptation of the left fifth metacarpal bone in racing greyhounds

The densitometric and mechanical structural properties of the left and right fifth metacarpal bones of 10 racing greyhounds with a fracture of the central tarsal bone and 10 without a fracture were investigated by dual energy x-ray absorptiometry and a servo-hydraulic materials testing machine. In all the greyhounds the bone mineral density of the left fifth metacarpal bone was significantly greater than that of the right (P<0.001), but there was no significant difference between the degree of asymmetry in bone mineral density in the two groups. The ultimate torque and energy-to-failure of the left fifth metacarpal bone of the greyhounds with a fracture of the right central tarsal bone were significantly higher than in the right fifth metacarpal bone and higher than in both the left and right fifth metacarpal bones of the greyhounds with no fracture (P<0.05). The ultimate torque and energy-to-failure were significantly related to bone mineral density (P<0.005), and 22 per cent of the variation in these structural properties could be explained by variations in bone mineral density. Fifth metacarpal remodelling in response to asymmetric cyclic loading is bone-specific, and structural properties are enhanced in the left fifth metacarpal of greyhounds with a fracture of the right central tarsal bone.     

Clinical, biochemical, and molecular aspects of Glanzmann's thrombasthenia in humans and dogs

Glanzmann's thrombasthenia (GT) is an inherited, intrinsic platelet function defect that involves the platelet glycoprotein complex IIb-IIIa, also known as the fibrinogen receptor and the integrin alphaIIbbeta3. The defect was originally described by Dr. Glanzmann in humans in 1918 as a bleeding disorder that differed clinically from other known coagulopathies. Over the decades that followed, researchers determined the biochemical and molecular basis for the disease in humans. Otterhounds with thrombasthenic thrombopathia, described in the 1960s, were the only animal model that closely resembled the disease described in humans until 1996. At that time, a Great Pyrenees dog was identified with unequivocal clinical and biochemical features of Type I GT The cDNA encoding for glycoproteins IIb and IIIa were sequenced in normal dogs in 1999, allowing for identification of specific mutations causing Type I GT in both Otterhounds and Great Pyrenees dogs. Knowing the molecular basis for Type I GT in dogs as well as the cDNA sequences in normal dogs should enhance the understanding of structure/function relationships of the alphaIIbbeta3 integrin and provide an excellent animal model for studies aimed at correction of GT in humans. The following review focuses on the structure and function of this platelet receptor and reviews the molecular, biochemical, and clinical aspects of Glanzmann's thrombasthenia in humans and dogs.     

Disseminated histoplasmosis in an Atlantic bottlenose dolphin (Tursiops truncatus).

An approximately 37-yr-old female Atlantic bottlenose dolphin (Tursiops truncatus) died after a 4-mo illness characterized by intermittent anorexia, lethargy, mild neutrophilic leukocytosis, and mild nonregenerative anemia. At necropsy, the lungs were diffusely consolidated, and histopathology of the lungs revealed severe pneumonia with macrophages containing clusters of numerous yeast cells. Inflammatory lesions and yeast also were found in pulmonary, mediastinal, prescapular, and duodenal lymph nodes, spleen, liver, kidneys, urinary bladder, pancreas, right adrenal gland, and the pyloric stomach. Histomorphology, fungal culture, and polymerase chain reaction analysis indicated that the fungus was Histoplasma capsulatum var. capsulatum. This is the first report of histoplasmosis in a cetacean.     

Complications and long-term outcomes of the ligation of congenital portosystemic shunts in 49 cats

Only two of 49 cats undergoing surgical ligation of congenital extra- and intrahepatic portosystemic shunts died perioperatively, a mortality rate comparable with the mortality rates of dogs undergoing surgical attenuation of congenital portosystemic shunts and cats in which the shunts are attenuated with an ameroid ring constrictor. Thirty (83 per cent) of the 36 cats for which long-term information was available were still alive at a median follow-up period of 47 months (range six to 105 months); the outcome was excellent (no clinical signs) in 20 of them (median follow-up 37 months, range six to 105 months) and good (minimal clinical signs) in seven (median follow-up 39 months, range 10 to 73 months) and none of these 27 cats was on any long-term medication or special diet. The only major cause of morbidity was the development of neurological signs in 18 (37 per cent) of the cats. These included seizures and a wide variety of other neurological signs, and their development and persistence was not affected by the presence of preoperative seizures, the type of shunt, the degree of shunt attenuation or the age of the cat. The serum concentrations of ammonia and preprandial bile acids were normal or significantly below normal in the cats with neurological signs. Liver histopathology was similar in the cats with and without neurological signs. Ten (56 per cent) of the 18 cats that developed neurological signs recovered normal neurological function long term.     

Circadian rhythms in rats: effects of random lighting

Increase in body weight, spontaneous running activity, and adrenal cortical function have been studied in rats exposed to a random lighting schedule. In two separate experiments, grouped control animals were given 12 or 14 hours of light alternating with 12 or 10 hours of darkness, respectively, while coresponding grouped experimental animals were given the same total amounts of light and darkness per 24 hour period in a randomized pattern. Random light for periods of 17 to 40 days exerted no influence on growth rate, on weights of endocrine organs, or on adrenal response to adrenocorticotrophic hormone. However, the physiological fluctuation of group running activity and adrenal steroid secretion was abolished. Group desynchronization and the development of circadian rhythms having periods both shorter and longer than 24 hours appear to have replaced the synchronized group rhythmicity.