Field trials of bromadiolone against infestations of warfarin-resistant Rattus norvegicus.
(65/71)Baiting with 0.005% bromadiolone in medium oatmeal or soaked wheat completely controlled infestations of warfarin-resistant rats on farms when surplus amounts of the poisoned baits were maintained until rats ceased to feed on them. The speed with which control was achieved was the same as with other anticoagulants that have been tested in this way.Poison baiting with 0.005% bromadiolone for only 1, 4 or 7 days achieved respectively about 49, 77 and 81% control of similar farm rat infestations. (+info)
Trials of the anticoagulant rodenticides bromadiolone and difenacoum against the house mouse (Mus musculus L.).
(66/71)Laboratory and field trials were conducted to determine the efficacy of the anticoagulant rodenticide bromadiolone against the house mouse (Mus musculus). In laboratory feeding tests, family groups of warfarin-resistant mice maintained in pens and conditioned to feeding on plain foods were offered pinhead oatmeal bait containing bromadiolone at 0.005%. Overall mortality in replicated 21-day poison treatments was 55/58 or 94.8%. Six field trials were carried out, using the same poison bait, against mice infesting farm buildings. Treatment success, estimated from the results of census baitings conducted before and after treatment, ranged between 60.4% and 100%, mean 92.4%. In equivalent field trials using difenacoum, another newly developed anticoagulant rodenticide, the control achieved ranged between 70.2% and 100%, mean 96.0%. Five field trials, three involving bromadiolone and two difenacoum, were not completely successful and the surviving mice were removed for laboratory examination. In 21-day toxicity tests, each animal was fed the poison bait offered to it earlier in the field. Bromadiolone and difenacoum gave kills of 12/21 (57.1%) and 9/11 (81.8%) respectively. The possible emergence of mouse populations resistant to these anticoagulants is considered. (+info)
Evaluation of brodifacoum against T. indica, M. hurrianae and R. rattus.
(67/71)Brodifacoum was evaluated in the laboratory against the two gerbils, Tatera indica and Meriones hurrianae and the house rat, Rattus rattus. The acute oral LD50 for these rodents was found to be 0.10 mg/kg, 0.083 mg/kg and 0.77 mg/kg respectively. Feeding tests with 0.002% and 0.005% brodifacoum produced a 100% mortality after a 3-day feeding period in the gerbils and after a 4-day period in R. rattus. The anticoagulant is toxic at both the concentrations to all three species but is less palatable in comparison to plain baits. Results of this laboratory evaluation indicates that 0.002% brodifacoum-treated bait can be effectively used against T. indica, M. hurrianae and R. rattus. (+info)
The development and use of a test to identify resistance to the anticoagulant difenacoum in the Norway rat (Rattus norvegicus).
(68/71)Feeding tests were carried out in the laboratory to obtain basic data on the susceptibility of wild Norway rats to difenacoum. The results were used to derive a standard test procedure for the identification of difenacoum resistance in warfarin-susceptible and resistant rats. Details are given of tests on rats from suspected difenacoum-resistant infestations on farms. (+info)
Laboratory evaluation of bromadiolone as a rodenticide for use against warfarin-resistant and non-resistant rats and mice.
(69/71)Laboratory feeding tests were carried out to determine the efficacy of the anticoagulant rodenticide bromadiolone against Rattus norvegicus, R. rattus and Mus musculus. Using 0.005% bromadiolone, complete kills of R. norvegicus and R. rattus not resistant to warfarin were obtained after exposure to the poison for 1 and 5 days respectively. Warfarin-resistant R. norvegicus were all killed in 4 days, and resistant M. musculus in 12 days. In general, the results resembled those obtained with difenacoum. Acceptance of bromadiolone was very good. (+info)
Nutritional vitamin K-intake and urinary gamma-carboxyglutamate excretion in the rat.
(70/71)Using the rat as an experimental animal model we have found that prothrombin synthesis reaches its maximal level at a relatively low dietary vitamin K intake. At still higher vitamin K intakes, however, the urinary Gla-excretion was substantially increased, showing a different vitamin K requirement for liver and extrahepatic tissues. The increased urinary Gla-excretion was found for both phylloquinone and menaquinone-4, but not for menaquinone-8, which questions the bioavailability of higher menaquinones for extrahepatic tissues. A discrepancy was found between effects of nutritional vitamin K-deficiency and treatment with a vitamin K-antagonist (brodifacoum). With both regimens plasma prothrombin rapidly decreased to well below 10% of the starting values, but in case of K-deficiency urinary Gla had hardly decreased in 7 days, whereas after 3 days of brodifacoum treatment Gla-excretion had decreased to 17% of the starting values. An explanation for this observation is that prothrombin procoagulant activity does not decrease proportional to the prothrombin Gla-content, but that a wide range of undercarboxylated prothrombins have lost nearly all activity. During vitamin K-deficiency the remaining low levels of vitamin K would mainly give rise to undercarboxylated prothrombin, whereas during brodifacoum treatment only non-carboxylated prothrombin is formed. It seems plausible that in the latter case the urinary Gla originates from proteins with long half-life times, such as the bone Gla-proteins. (+info)
Induction of prothrombin synthesis by K-vitamins compared in vitamin K-deficient and in brodifacoum-treated rats.
(71/71)Vitamin K is a group name for a number of prenylated 2-methyl-1,4-naphtoquinones, which may differ in their ability to function as a cofactor for prothrombin biosynthesis. To quantify the bioactivity of different forms of vitamin K, two experimental animal systems are frequently used: vitamin K-deficient rats and anticoagulated rats. In this paper both models are compared, and it is shown that the results obtained depend on the model used. The main reason for this discrepancy is the difference in recycling of vitamin K-epoxide, which results in a 500 times higher vitamin K requirement in anticoagulated rats. Absorption and hepatic accumulation of long chain menaquinones seem to be restricted to a maximum, whereas also the lipophilic nature of long chain menaquinones may hamper the quinone-quinol reduction in anticoagulated animals. If these data may be extrapolated to patients, food items rich in K1 and MK-4 would be expected to influence the stability of oral anticoagulation to a much larger extent than food items primarily containing higher menaquinones. (+info)