Abstract/Summary

Anticoagulant resistance was discovered in Norway rats in the United Kingdom nearly 70 years ago, and since then the number of resistance mutations and resistance foci has increased. In no other country are mutations that are thought to confer serious practical resistance so widespread. Numerous studies have shown multiple resistance genotypes and phenotypes across south-east England. Despite this, the extent of these resistance foci and the resistance factors possessed by these rats are not known. The experiments described herein were designed to reveal the extent and impact of resistance mutations in south-east England. 304 tissue and faecal samples were taken from rats across the study area, in order to identify and delimit foci of VKORC1 resistance conferred by mutations in the VKORC1 gene. The L120Q resistance mutation was found to be prevalent across the study area, with the majority of rats possessing the homozygous form of the mutation, suggesting that for years, resistance has been selected for through use of ineffective second generation anticoagulant rodenticides (SGARs). Two strains of L120Q-resistant laboratory rats were dosed with SGARs and their prothrombin times (PT) measured, and resistance factors generated by comparison with data from susceptible strains. L120Q in its strongest form was found to confer practical resistance to bromadiolone and difenacoum, but not to resistance breakers such as brodifacoum. Finally, field trials were carried out in the L120Q resistance focus of central-southern England, which showed conclusively that brodifacoum is efficacious against L120Q-resistant rats in both Berkshire and Hampshire. The UK rodenticide stewardship scheme, proposed by the Campaign for Responsible Rodenticide Use (CRRU) will see “resistance breaking” SGARs available for use against Norway rats only by competent users as of April 2017. Results indicate this development is both timely and necessary for proactive Norway rat control in the UK.