Abstract
While resistance to anticoagulant rodenticides is known to occur in many European populations of Norway rat and house mouse, to-date no data is available on the occurrence in Ireland of such resistance. No genetic evidence for the occurrence of resistance was found in 65 Norway rat samples analysed, indicative of an absence, or low prevalence, of resistance in rats in at least the Eastern region of the island of Ireland. The presence of two of the most commonly found amino acid substitutions Leu128Ser and Tyr139Cys associated with house mouse resistance to anticoagulant rodenticides was confirmed. The occurrence of two such mutations is indicative of the occurrence of resistance to anticoagulant rodenticides in house mice in the Eastern region of the island of Ireland.
Highlights
Following their introduction in the 1950s, warfarin and the structurally similar anticoagulant rodenticides, resulted in radical changes in rodent pest management practice
The rat sequences were aligned with the NCBI Rattus norvegicus VKORC1 reference sequence (NM_203335.2)
There were no polymorphisms in exons 1 and 3 of the rat samples when compared with the Rattus norvegicus VKORC1 reference strain (NM_203335.2)
Summary
Following their introduction in the 1950s, warfarin and the structurally similar anticoagulant rodenticides (e.g. chlorophacinone and coumatetralyl), resulted in radical changes in rodent pest management practice. Reflecting the higher tolerance of house mice (Mus musculus) to such compounds, the use of warfarin and other first generation anticoagulants for their control was frequently unsatisfactory[1]. As a consequence of increasing concerns generated by the identification of warfarin resistant rodent populations, industry developed the more potent anticoagulant rodenticides bromadiolone, brodifacoum, difenacoum, difethialone and flocoumafen, known as second generation anticoagulant rodenticides. As in the case of the first-generation compounds, these reflect the 4-hydroxycoumarin structure, but display increased lipophilicity that results in their having longer half-lives[8]. As a consequence of anticoagulant binding with VKOR, a deficiency of vitamin K and coagulation factors occur, resulting in spontaneous bleeding and eventual death
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