Rodenticide resistance: implications for seabird conservation and island restoration

Anticoagulant rodenticide resistance occurs when biocides lose their efficacy—even when used correctly—owing to inherited rodent traits that make these organisms less sensitive to the active ingredients. This phenomenon has been a concern on the mainland for decades, particularly in urban areas where it has become increasingly common among commensal rodents. More recently, resistance has been documented on islands, complicating conservation and restoration efforts. The best-described mechanism of resistance involves mutations in the Vkorc1 gene, which encodes the enzyme responsible for activating vitamin K and promoting blood coagulation. Normally, anticoagulants block this enzyme, thereby preventing blood clotting. However, mutations in the three exons of Vkorc1 can render rodenticides less effective, allowing resistant rodents to survive and reproduce. Resistance has also been linked to the overexpression of P-450 cytochrome enzymes, while mutations in the Vkorc1l1 pseudogene may also play a role (though this possibility has been less studied). Testing for resistance involves genetic screening (PCRs) for Vkorc1 mutations, lethal feeding period tests, blood clotting response tests, and in vitro assays of VKOR activity. In seabird conservation and island restoration, rodenticide resistance poses a serious threat. Invasive rodents are often the primary terrestrial predators of seabird eggs, chicks, and adults. However, the spread of resistance could undermine efforts to protect these vulnerable species and their ecosystems. As eradication programs target islands with a history of rodenticide use, testing for resistance should be a prerequisite for any control or eradication activities involving standard anticoagulant baits.