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House mice (Mus musculus domesticus) vary considerably in their susceptibility to anticoagulants, and several non-synonymous sequence variants in the coding region of the vitamin K epoxide reductase subcomponent 1 gene (vkorc1) were found in Germany (Rost et al., 2009). It was the aim of our study to characterize the degree of resistance in relation to vkorc1genotypes in local mouse groups, and to test whether certain genotypes were selected by sequential treatments with the two anticoagulant rodenticides warfarin and difenacoum. Two successive treatments were conducted, the first with bait containing warfarin followed by a second using difenacoum. Their effects were determined on local sub-groups of mouse infestations in different sub-units on two livestock farms in Westphalia, Germany. The frequency of different vkorc1 genotypes, as determined by Sanger sequencing, was considered relative to the rodenticide treatment results for each sub-group and sampling period.Three tolerance types were identified on farm one: A=warfarin-susceptible, B=resistant to warfarin, but susceptible to difenacoum, C=approx. one half of animals resistant to both anticoagulants. On farm 2, only type A and B were identified. A high degree of resistance was observed in vkorc1 wild-type mice. In all cases, only the R58G vkorc1 variant was found, which appears not to be a resistance marker in house mice. Hence, in these mouse infestations, practical resistance to anticoagulants was not accompanied by any identifiable vkorc1 resistance marker.The study was funded by the Rodenticide Resistance Action Committee (RRAC) of CropLife International

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Field trials to assess resistance to warfarin and difenacoum of house mice in relation to the occurrence of variants in the vkorc1-gene before and after the treatments