[Rodenticide resistance and consequences]

Resistance to anticoagulant rodenticides, such as warfarin was first described in 1958. Polymorphisms in the vitamin K epoxide reductase complex subunit 1 (VKORC1) gene and respective substitutions of amino acids in the VKOR enzyme are the major cause for rodenticide resistance. Resistant Norway rats in Germany are characterized by the Tyr139Cys genotype, which is spread throughout the northwest of the country. Resistant house mice with the VKOR variants Tyr139Cys, Leu128Ser and Arg12Trp/Ala26Ser/Ala48Thr/Arg61Leu (spretus type) are distributed over a number of locations in Germany. Resistance can reduce management attempts with consequences for stored product protection, hygiene and animal health. Anticoagulants of the first generation (warfarin, chlorophacinone, coumatetralyl) as well as bromadiolone and difenacoum are not an option for the control of resistant Norway rats. The same applies for house mice whereby the tolerance to compounds can be different between local incidences. Due to the higher toxicity and tendency to persist, the most potent anticoagulant rodenticides brodifacoum, flocoumafen and difethialone should be applied but only where resistance is known. In other cases less toxic anticoagulants should be preferred for rodent management in order to mitigate environmental risks. Resistance effects of further VKOR polymorphisms and their combinations, the spread of resistant rats and conditions supporting and reducing resistance should be investigated in order to improve resistance management strategies.