Delayed-effect rodenticides operate via anticoagulation or metabolic disruption
the verdict
INSUFFICIENT LEANING
refutedsupported
the weight of evidence
8 sources for · 0 against
The retrieved literature partially supports the claim by establishing that certain rodenticides operate via anticoagulation (such as warfarin and superwarfarins), but the provided sources do not fully cover metabolic disruption as an operative mechanism for delayed-effect rodenticides.
Long-acting anticoagulant rodenticides (LAARs) inhibit vitamin K epoxide reductase (VKOR). Related bleeding may present a diagnostic challenge and require administration of blood component therapy, hemostatic agents, and vitamin K. This article intends to provide the reader a comprehensive understanding of LAAR poisoning. An exhaustive literature search of PubMed, Science Direct, US National Library of Medicine Toxicology Data Network, and Google Scholar yielded 174 reported cases of LAAR poisoning from which clinical data were extracted and reviewed. In addition, 25 years of epidemiologic data from the American Association of Poison Control Centers was reviewed. In the United States, on average, there were 10413 exposures reported with 2750 patients treated annually. For 25 years, there were 315951 exposures reported with nearly 90% among children and more than 100000 patients treated in a health care facility. Fortunately, only 2% of all exposures result in morbidity or mortality. Inhalational, transcutaneous, and oral routes of exposure have been documented. Most exposures are unintentional. The most frequently reported bleeding sites are mucocutaneous, with hematuria being the most common feature. Deaths were most commonly associated with intracranial hemorrhage. Long-acting anticoagulant rodenticide-induced paradoxical thrombosis and thrombotic complications accompanying hemostatic therapy have also been observed. Most patients present with coagulation assay values beyond measurable limits. Long-acting anticoagulant rodenticides have an extremely high affinity for VKOR compared with warfarin, characterized by rebound coagulopathy and bleeding after initial treatment and the need for high-dose, long-term therapy with vitamin K1. Treatment of acute hemorrhagic symptoms often required intravenous vitamin K1 in excess of 50 to 100 mg; chronic maintenance with 100 mg PO vitamin K1 daily was the most frequently used dose required to suppress coagulopathy. Treatment courses averaged 168 days. Adjunctive hemostatic therapy with recombinant factor VIIa and prothrombin complex concentrate has been reported, and phenobarbital has been used to expedite LAAR metabolism.
Superwarfarins are long-acting anticoagulant rodenticides developed from warfarin. The mechanism of action is by inhibition of vitamin K epoxide reductase, resulting in the inability of the body to recycle vitamin K. Deficiency of vitamin K thereafter leads to inability for the body to synthesise vitamin K-dependent coagulation factors, factor II, VII, IX, and X, leading to prolonged prothrombin time. Due to the bulky aromatic sidechains, superwarfarins have a much longer half-life when compared to warfarin, and exposure to superwarfarins results in a prolonged period of anticoagulation which can result in clinical bleeding. Diagnosis is straightforward in patients with known history of superwarfarin exposure but has proved difficult for patients who did not report superwarfarin intake. Superwarfarin poisoning should therefore be suspected in all patients with unexplained prolongation of prothrombin time, and can be confirmed by their detection in serum. Treatment for superwarfarin poisoning includes rapid correction of factor deficiencies with either 4-factor prothrombin complex concentrate or fresh frozen plasma in patients with active bleeding, and high dose vitamin K therapy given multiple times per day for a prolonged period of weeks to months.
Aspects of anticoagulant action: a review of the pharmacology, metabolism and toxicology of warfarin and congeners. Warfarin is the most widely used anticoagulant in the treatment of thromboembolism in man. It has also been used extensively as a rodenticidal agent. Insofar as its clinical use is concerned, it is now clear that many of the drug interactions observed in patients are mediated via metabolic or pharmacokinetic factors. An understanding of the disposition of warfarin is therefore essential if one is to predict the likely response in patients undergoing anticoagulant therapy with this compound. Warfarin-resistance has been reported in both man and rodents. Understanding resistance in both man and rodents is important for effective anticoagulant therapy, and in control of resistant strains of rodents. Warfarin resistance in rat strains does not appear to have a metabolic or pharmacokinetic basis; in this species, resistance is thought to be due to differences in permeability to, or affinity for a receptor.
Toxicology of selected pesticides, drugs, and chemicals. Anticoagulant, cholecalciferol, and bromethalin-based rodenticides.
The control of rodent pests is a continuing goal of mankind. To this end, a multitude of rodenticides have been produced, each designed to kill rodents by exerting their toxic effects on various body systems. As examples, veterinarians have had to manage companion animal poisonings due to anticoagulant, sodium fluoroacetate (compound 1080), thallium, barium carbonate, and zinc phosphide-based rodenticides. Many of these rodenticides were introduced because of their anticipated safety in relation to nontarget species; unfortunately, this has not been the case. Veterinarians must attempt to identify the specific rodenticide involved in poisoning cases. Therapeutic success in these poisonings is often more dependent upon symptomatic and supportive care rather than the use of antidotal therapy.
Published in The Veterinary clinics of North America. Small animal practice (1990)
A comparative assessment of efficacy of three anticoagulant rodenticides.
Results are presented of feeding tests carried out with three common anticoagulant rodenticides viz., coumatetralyl, fumarin and warfarin on three common species of commensal rodents i.e., Rattus rattus, Rattus norvegicus and Bandicota bengalensis. All three species of rodents were susceptible to anticoagulant rodenticides. However, the action of these compounds in B. bengalensis was comparatively slow. Coumatetralyl was found to be the most effective rodenticide followed by fumarin and warfarin. Liquid baits of these compounds are more effective in comparison to food baits.
Published in Journal of hygiene, epidemiology, microbiology, and immunology (1982)
Rodent resistance to the anticoagulant rodenticides, with particular reference to Denmark.
Inherited resistance to anticoagulant rodenticides was discovered in populations of Rattus norvegicus about 14 years ago. Similar resistance has now been reported from several countries in north-western Europe and from the USA. In order to detect resistance and to control it effectively, basic data on the susceptibility of rat populations are required for each country, and trapping surveys should be made in any area where resistance is suspected. Acute poisons are needed to control resistant rats although the shift from anticoagulants to acute poisons is a retrograde step as far as efficiency is concerned, and increases the hazard of control operations to man and other animals. Resistance to anticoagulants in Mus musculus has been reported from England, and resistant mice are probably to be found in other countries also in view of the great individual variation in susceptibility of this species to these rodenticides.
Published in Bulletin of the World Health Organization (1972)
[Effect of an anticoagulant rodenticide on the female albino rat with offspring].
Lactating female albino rats have been treated with coumatetralyl rodenticide, having anticoagulant activity. The letal effect on mothers was of 40% (using a maximum concentration of toxic substance) while it was of 54% in offsprings. Among the probable causes of death in offsprings, the authors suggest the hypothesis that an interference in the relationship mother-offsprings is due to the influence of coumatetralyl on parental behavior.
Published in Parassitologia (1978)
The response of the Egyptian spiny mouse (Acomys cahirinus) and two other species of commensal rodents to anticoagulant rodenticides.
The response of Acomys cahirinus to three anticoagulant rodenticides was investigated in the laboratory. In contrast to the other commensal rodents Rattus rattus and R. norvegicus, this species appears to be naturally very resistant to warfarin, difenacoum and brodifacoum. It is considered unlikely that anticoagulant poisons would be effective in the field for the control of A. cahirinus.
Published in The Journal of hygiene (1981)
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