Thrombocytopenia in Cats: A Retrospective Study of 41 Cases

The prevalence of feline thrombocytopenia (<200,000 platelets/L) at North Carolina State University, College of Veterinary Medicine Teaching Hospital, from January 1985 to March 1990, was 1.2% (41/3300). Cats were divided into six categories based on clinical diagnoses: 29% (12/41) had infectious disease, 20% (8/41) had neoplasia, 7% (3/41) had cardiac disease, 2% (1/41) had primary immune-mediated disease, 22% (9/41) had multiple diseases, and 20% (8/41) had disorders of unknown etiology. The mean platelet count for all thrombocytopenic cats was 52,000/μL ± 46,000/μL (1 SD) with a range of 1000–190,000/μL. No significant differences were found between groups with respect to platelet count, packed cell volume, or white blood cell count, though anemia and leukopenia were common among the cats as a whole. Bleeding disorders (hemorrhage or thrombosis) were observed in 29% (12/41) of thrombocytopenic cats and were more likely to be associated with neoplasia, cardiac disease, and platelet counts less than or equal to 30,000/μL. Disseminated intravascular coagulopathy was diagnosed in 12% (5/41) of the cats. Infections and/or neoplasia affecting the bone marrow were the most common diseases associated with thrombocytopenia. Feline leukemia virus and myeloproliferative neoplasia accounted for approximately 44% (18/41) of the specific diagnoses in thrombocytopenic cats. (Journal of Veterinary Internal Medicine 1993; 7:261–265. Copyright © 1993 by the American College of Veterinary Internal Medicine.)     

The diagnostic significance of different blood parameters and liver biopsy in chronic copper poisoning of sheep

In a flock of sheep to which food with excess copper (= Cu) had been fed for some months 39 animals died of chronic copper toxicosis. In 5 sheep of this flock the plasma concentrations of the enzymes glutamate dehydrogenase (GLDH), sorbitol dehydrogenase (SDH), aspartate-amino-transferase (ASAT) and copper were measured several times over a period of 100 days. At day 23, 58 and 97 needle biopsies of the liver were taken. The biopsies were used for histological examination and Cu-analysis. After 100 days the sheep were slaughtered and chronic copper poisoning was diagnosed by raised Cu concentration and typical histological alterations in the liver. The activities of GLDH and SDH in the plasma of the 5 sheep were consistently above normal, ASAT activity and the plasma Cu level were raised only occasionally. The results of Cu determination in biopsy samples were of little predictive value compared with post mortem Cu analysis of the liver.     

In vivo kinetic study on uptake and distribution of intramuscular tritium-labeled polysulfated glycosaminoglycan in equine body fluid compartments and articular cartilage in an osteochondrial defect model

The uptake and distribution of intramuscularly (IM) administered tritium-labeled polysulfated glycosaminoglycan (³H-PSGAG) in serum, synovial fluid, and articular cartilage of eight horses was quantitated, and hyaluronic acid (HA) concentration of the middle carpal joint was evaluated in a pharmacokinetic study. A full-thickness articular cartilage defect, created on the distal articular surface of the left radial carpal bone of each horse served as an osteochondral defect model. ³H-PSGAG (500 mg) was injected IM, between 14 and 35 days after creation of the defects. Scintillation analysis of serum and synovial fluid, collected from both middle carpal joints at specific predetermined times up to 96 hours post-injection, revealed mean ³H-PSGAG concentrations peaked at 2 hours post-injection. ³H-PSGAG was detected in cartilage and subchondral bone 96 hours post-injection in samples from all eight horses. There were no statistically significant differences in ³H-PSGAG concentration of synovial fluid or cartilage between cartilage defect and control (right middle carpal) joints.

HA assay of synovial fluid revealed concentrations significantly increased at 24, 48, and 96 hours post-injection in both joints. The concentration nearly doubled 48 hours post-injection. However, no statistically significant differences were found between synovial concentrations of HA in cartilage defect and control joints.

³H-PSGAG administered IM to horses, was distributed in the blood, synovial fluid, and articular cartilage. HA concentrations in synovial fluid increased after IM administration of polysulfated glycosaminoglycan.     

Response of Mustard to Ethrel Spray and Basal and Foliar Application of Nitrogen

In a field trial conducted during 1992–93 and 1993–94, the effect of basal (B) nitrogen (N) (45 and 60 kg N ha⁻¹) and foliar application (F) of water (W) or 10 kg N ha⁻¹ and 400 or 600 ppm ethrel (E) (2-Chloro ethyl phosphonic acid) at 70 days after sowing was studied on leaf area index and dry mass at 90 days and pod number per plant, seeds per pod, 1000 seed weight, seed yield, oil content and oil vield at harvest of mustard ( Brassica juncea L. Czern & Coss.) cv. T-59. Recommended basal (B) application of 90 kg N ha (BN₉₀) was used as control. On the basis of 2 year data it was found that basal application of 60 kg N and foliar spray of 10 kg N ha ⁻¹ and 600 ppm ethrel gave higher values for growth and yield characteristics and enhanced seed yield and oil yield by 12.5 and 14.8%, respectively over control BN_90.     

Effect of Integration of Fertilizer and Green Manure Nitrogen on Yield Attributes, Nitrogen Uptake and Yield of Lowland Rice (Oryza sativa L.)

Field experiments were conducted at Tamil Nadu Rice Research Institute, Aduthurai, India, during the wet seasons of 1992 and 1993 to study the effect of full and partial substitution of fertiliser N with green manure N (Sesbania rostrata) on nitrogen uptake, yield attributes and yield of rice. The experiment consisted of eight treatments with two levels of N (100 and 200 kg ha⁻¹) and three sources of N application viz., fertilizer, integrated (1:1 fertilizer and green manure N) and green manure N compared to the recommended practice (150 kg fertilizer plus 6.25 t ha⁻¹ (72 kg N) green manure) and a no N control. Nitrogen application markedly increased the N uptake. Combined use of the two N sources at 200 and 222 kg N ha⁻¹ and of single fertilizer N at 200 kg N ha⁻¹ recorded the maximum N uptake, increased the yield attributes such as number of panicles per unit area, weight per panicle, number of total and filled grains per panicle and test weight. At 200 kg N ha⁻¹ full substitution of N by green manure reduced the grain yield but only partial substitution of N by green manure resulted in almost similar yield as single fertilizer N. Thus 200 kg N ha⁻¹ applied in equal proportions of fertilizer and green manure N can be recommended for medium duration rice cultivars.     

Coagulopathic Effects and Therapy of Brodifacoum Toxicosis in Dogs

The clinical signs and laboratory changes of brodifacoum (BDF) intoxicated dogs and their response to vitamin K1 treatment were examined. Brodifacoum, a second-generation anticoagulant rodenticide, was fed to four dogs for 3 consecutive days producing a cumulative dose of 1.1 mg BDF/kg body weight. Clinical observations of the animals were made daily throughout the study. Monitored laboratory parameters included: one-stage prothrombin time (OSPT), activated partial thromboplastin time (APTT), activated coagulation time (ACT), complete blood counts, thrombocyte counts, and serum chemistry values. Response to vitamin K1 therapy was evaluated clinically and by laboratory tests. Serum BDF concentrations were monitored. Inappetence and hemorrhagic tendencies were exhibited by day 5 postrodenticide exposure. One-stage prothrombin time, APTT, and ACT were 25% greater than time zero values at 24, 24, and 72 hours postdosing, respectively. All laboratory parameters returned to normal within 48 hours of initiating vitamin K1 therapy (0.83 mg/kg orally, TID for 5 days). Serum brodifacoum concentrations were highest (1065-1215 ng/mL) during the 3 days after BDF dosing and were detectable (3.0-7.5 ng/mL) until day 24 postexposure. A mean BDF elimination half-life of 6 +/- 4 days was observed.     

Citrullinaemia in Friesian calves

Six Friesian calves from a pedigree herd died or were killed within 1 week of birth because of progressive central nervous disease in which the only consistent lesion was cerebral oedema. The cause was citrullinaemia, resulting from an autosomally inherited dysfunction of the urea cycle enzyme arginosuccinate synthetase. Citrullinaemia was diagnosed by demonstrating markedly elevated concentrations of citrulline in the blood of one calf and in the cerebral spinal fluid of another. One of two sires used in the herd was a heterozygous carrier of the disease. Heterozygocity was demonstrated using a polymerase chain reaction/restriction endonuclease test designed to detect the genetic mutation that causes citrullinaemia in cattle.