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Anticoagulant rodenticides were first discovered during ingvestigations into mouldy sweet clover poisoning in cattle<sup>1</sup>. In this condition, naturally occuring coumarin in clover is converted by fungi to a toxic agent, dicumarol, which causes a haemorrhagic syndrome when ingested. Initially, warfarin was synthesised and used in this way for rodent control, but as rodents have developed a resistance to the substance new, second generation anticoagulant rodenticides have been developed. These include coumarin (bromadiolone and brodifacoum) and indandione (pindone and diaphacinone) rodenticides, which along with warfarin may cause toxicity following accidental ingestion in animals.  
 
Anticoagulant rodenticides were first discovered during ingvestigations into mouldy sweet clover poisoning in cattle<sup>1</sup>. In this condition, naturally occuring coumarin in clover is converted by fungi to a toxic agent, dicumarol, which causes a haemorrhagic syndrome when ingested. Initially, warfarin was synthesised and used in this way for rodent control, but as rodents have developed a resistance to the substance new, second generation anticoagulant rodenticides have been developed. These include coumarin (bromadiolone and brodifacoum) and indandione (pindone and diaphacinone) rodenticides, which along with warfarin may cause toxicity following accidental ingestion in animals.  
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Anticoagulant rodenticide toxiticy is one of the most common causes of acquired coagulopathy in small animals. Warfarin itself has a short half-life and a fairly low toxicity in non-rodent species, so unless large or repeated doses are consumed clinical bleeding is rare. However, the second generation anticoagulant rodenticides are far more potent, with  tendency to accumulate in the liver and a long half life (4-6 days) owing to high levels of plasma protein binding<sup>2</sup>. This means it is possible for a domestic animal to acquire secondary poisoning by ingesting a killed rodent.
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Anticoagulant rodenticide toxiticy is one of the most common causes of acquired coagulopathy in small animals. Warfarin itself has a short half-life and a fairly low toxicity in non-rodent species, so unless large or repeated doses are consumed clinical bleeding is rare. However, the second generation anticoagulant rodenticides are far more potent, with  tendency to accumulate in the liver and a long half life (4-6 days) owing to high levels of plasma protein binding<sup>2</sup>. These newer drugs are therefore more commonly implicated in cases of poisoning<sup>3</sup>, and it is possible for a domestic animal to acquire secondary poisoning by ingesting a killed rodent<sup>2</sup>.
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anyway!
 
anyway!
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Another group of agents frequently involved in poisoning
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events are the anticoagulant rodenticides. They are
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Their effects are frequently
frequently scavenged by dogs and, although few animals
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display clinical signs, there are nevertheless the
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occasional cases where prolonged vitamin K, therapy
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and sometimes even blood transfusions are required.
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Poisonings have also occurred as a result of ingestion of
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rodents killed with these baits. The 'second generation'
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rodenticides such as difenacoum, bromadiolone, coumatetralyl
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and chlorophacinone appear to be more commonly
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implicated, although they now have a larger share
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of the market than the older warfarin-based and
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alphachloralose-type rodenticides. Their effects are frequently
   
delayed, and this often results in the late presentation
 
delayed, and this often results in the late presentation
 
of affected animals to veterinary practices once
 
of affected animals to veterinary practices once
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