Topic > How do second generation anticoagulant rodenticides affect...

How do second generation anticoagulant rodenticides affect bird speciesIntroThe use of second generation anticoagulant rodenticides (SGARs) has been a controversial topic since their development in the late 1970s. (Valchev et al 2008) In this essay I will focus on how SGARs affect different bird species around the world. I will focus on all the different aspects of SGARs; what they are, how they work, what are the dangers for vertebrates that have ingested anticoagulant toxins (primary and secondary) The application of SGARs. In this essay I will focus mainly on Brodifacoum. Brodifacoum is the most toxic of all SGARs and has the greatest impact on mammals and birds. Compared to first generation anticoagulant rodenticides (FGAR), it has a high residual persistence in the liver tissue (Eason. et al. 1996). This is the primary site where inhibition occurs. The essay will also focus heavily on New Zealand; this is because Brodifacoum in other parts of the world is for internal use only. This includes the UK, unless the purchaser has a license to purchase the product (Hoare & Hare 2006). The essay will also include several SGARs. What are SGARs? A SGAR is a rodenticide designed to kill rodents; rats and mice for example. Before the development of SGARs; Chlorophaninone, dysphacinone and warfarin were used. These are examples of first generation anticoagulant rodenticides discovered in the 1940s. (Hadler and Buckle 1992) The reason for the development of SGARs is that some rat species have become 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 similarly to an FGAR. Anticoagulant toxins work by interfering with the synthesis of vitamin K-dependent clotting factors in the vertebrate liver, thereby "blocking" the recycling of vitamin K. Since the body will have less vitamin K, a deficiency will occur. When this inhibition occurs for a prolonged period of time, the blood does not clot, typical clinical signs of anticoagulant toxicity are hemorrhage and anemia, with death from massive hemorrhage occurring several days after a lethal exposure (Pelfrene 2001). Research has suggested that they do not affect invertebrates due to the different blood clotting systems of vertebrates (Shirer 1992). THE