How Second Generation Anticoagulant rodenticides affect bird species
Intro
The use of Second Generation Anticoagulant rodenticides (SGARs) have been a controversial topic since the development of them in the late 1970s. (Valchev et al 2008) In this essay I will be focusing on how SGARs affect different bird species around the globe. I will be focusing on all different aspects of SGARs; what they are, How they work, What are the dangers to vertebrates which have ingested the anticoagulant toxins (primary and secondary) The application of SGARs. Throughout this essay I will be focusing predominately on Brodifacoum.
Brodifacoum is the most toxic out of all the SGARs and has the greatest impact on mammals and birds. Compared to First generation Anticoagulant rodenticides (FGARs) it has a high residual persistence in liver tissue (Eason. et al. 1996). This is the main site where inhibition takes place. The essay will also be focusing a lot around New-Zealand; this is because Brodifacoum around other parts of the world are for in-door use only. This is including the UK unless the buyer has a license to buy the product (Hoare & Hare 2006). The essay will also include different SGARs
What are SGARs?
A SGAR is a rodenticide which is designed to kill rodents; rats and mice for example. Before the development of SGARs; Chlorophaninone, disphacinone and warfarin were used. These are examples of First Generation Anticoagulant Rodenticides which were discovered in the 1940s. (Hadler and Buckle 1992) The reason for the development of SGARs is due to some species of rats becoming resistant to certain rodenticides using warfarin. SGARs are more persistent than FGARs; Brodifacoum a SGAR can persist in the liver of sheep for over 16 weeks (Parmar et al. 1987).
How do SGARs Work?
A SGAR works in a similar way to an FGAR. Anticoagulant toxins act by interfering with the synthesis of vitamin K- dependent clotting factors in the liver of vertebrates therefore ‘blocking’ the recycling of vitamin K. As the body will have less vitamin K there will be a deficiency. When this inhibition occurs over a prolonged period of time blood will not coagulate, typical clinical signs of anticoagulant toxicity are haemorrhage and anaemia, with death through massive haemorrhage occurring several days after a lethal exposure (Pelfrene 2001). Research has been taking out and suggested that they don’t affect invertebrates due to the different blood clotting systems of vertebrates (Shirer 1992). The
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To slow the rate at which blood clots in a patient, a doctor may or may not administer a course of anticoagulant therapy. Anticoagulant therapy is a course of drugs taken by the patient, who might have one or more cardiovascular diseases, to prevent clots from forming. The most common use for anticoagulants is atrial fibrillation, an irregular heart rhythm [7]. They’re also administered for patients who have mechanical heart valves or patients who have blood clots [7]. There are many types of anticoagulants used, most commonly administered was Warfarin (Coumadin) [5]. However, due to recent advances in medicine many new anticoagulants have surfaced such as Apixaban, Dabigatran, Edoxaban, Rivaroxaban and many others [4]. Practitioners have more
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