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.     

The effects of ultraviolet-B (UV-B: 290–320 nm) radiation on blister blight disease of tea (Camellia sinensis)

Sunlight is known to reduce the incidence of blister blight disease of tea, caused by Exobasidium vexans . The effects of the ultraviolet-B (UV-B: 290–320 nm) component of solar radiation on the disease and the development of E. vexans were studied in the field in Sri Lanka using UV-screening filter materials held over a commercial crop. Exclusion of UV-B radiation by Polyester, which reduces fluxes in the UV-B region by approximately 75–85%, increased both the number of translucent spots (immature sites of infection) and number of sporulating blisters (mature sites of infection), but it had little or no effect on the sporulation of the pathogen. When basidiospores were artificially inoculated on leaves, and were exposed to full or filtered solar radiation, their survival and germination increased when UV-B wavelengths were removed; significant differences were found 62 h after inoculation. However, UV-B did not affect the extension of germ tubes. This study indicates that the UV-B component of solar radiation plays an important role in the natural regulation of blister blight disease in the field.     

Development of a powder formulation of Pseudomonas fluorescens for control of rice blast

Pseudomonas fluorescens strain Pf1, inhibitory to the growth of the rice blast pathogen Pyricularia oryzae in vitro , was developed as a talc-based powder formulation. When rice seeds were treated with this formulation, the bacteria spread to roots, stems and leaves of the plants and protected against leaf infection by P. oryzae . When applied as a foliar spray, the bacteria survived on the leaves. The powder formulation controlled leaf blast under greenhouse conditions. In tests as a seed treatment and foliar spray in four field trials it effectively controlled the disease and increased grain yield.