INHERITANCE OF LOW-GRADE BRODIFACOUM RESISTANCE IN THE NORWAY RAT

We conducted a study to ascertain if an observed reduction of susceptibility to brodifacoum in Norway rats (Rattus norvegicus) present on at least 3 farms in Berkshire, United Kingdom, was heritable. This trait was demonstrated in individual rats by their survival after consumption of 0.0005% (m/m) brodifacoum in the diet for 7 days (Gill and MacNicoll 1991) and is termed "low grade" resistance. It is inherited through at least 5 generations and is not associated with vitamin K deficiency. Our data also suggest a different explanation for the inheritance of difenacoum resistance compared with that reported by Greaves and Cullen-Ayres (1988). We suggest that difenacoum resistance in these animals arises from an autosomal dominant anticoagulant resistance gene with a recessive sex-linked modifier. Brodifacoum resistance also is due to the same major gene with recessive sex linked modifiers, but with additional modifiers present that may or may not be sex-linked. The Berkshire anticoagulant resistance gene appears to be different from the Hampshire gene previously reported by Greaves and Cullen-Ayres (1988), because no vitamin K deficiency occurs after feeding for 4 days on vitamin K-free diet. Although these rats survived higher doses of brodifacoum than susceptible individuals in the laboratory, the practical results of this resistance on the outcome of field control treatments are unknown.