Abstract/Summary

Anticoagulant resistance has been present in Norway rats (Rattus norvegicus) in Hampshire and Berkshire for forty years. All first-generation anticoagulants and two of the second generation, bromadiolone and difenacoum, are resisted by rats carrying the L120Q single nucleotide polymorphism (SNP). A regulatory restriction on the use of resistance-breakers brodifacoum, difethialone and flocoumafen in the UK effectively prevented their use against Norway rats for more than 30 years. During this time, L120Q spread from original localised foci eventually to cover most of central-southern England; with other more dispersed foci elsewhere in the UK. We summarise research on L120Q Norway rats and the field performance of anticoagulant baits against them. Bromadiolone (50 ppm), difenacoum (50 ppm) and brodifacoum (23 ppm) baits were each applied on two farmsteads where it had been established that Norway rats carried the L120Q SNP. Preliminary DNA resistance tests conducted at the farms found only one of 107 rats to be susceptible and 86.9% to be homozygous resistant. The bromadiolone and difenacoum applications were either partially or wholly ineffective; brodifacoum treatments were fully effective. Quantities of active substances used varied between farms and substances; but more bromadiolone and difenacoum baits were applied than brodifacoum baits during the treatments. Results confirm the high incidence of resistance and support advice that bromadiolone and difenacoum should not be used against the L120Q SNP. Prolonged use of resisted anticoagulants has resulted in a high prevalence of homozygosity and resistance spread. Failed treatments result in prolonged feeding on anticoagulant bait and leave Norway rats alive carrying, presumably, high residues. It remains to be seen whether the use of now-permitted effective substances, and the introduction of a rodenticide stewardship regime, will curtail the spread of resistance and reduce anticoagulant residues in wildlife.