Field trials of second-generation anticoagulants against difenacoum-resistant Norway rat populations

Abstract

SUMMARYTrials of rodenticidal baits containing 50 p.p.m. difenacoum, 50 p.p.m. bromadiolone or 20 p.p.m. brodifacoum were carried out on farmsteads against populations of Rattus norvegicus containing difenacoum-resistant individuals. Six difenacoum treatments failed in 14-42 days of baiting. Two treatments with bromadiolone succeeded in 23 and 33 days, but four further treatments lasting 35-56 days failed to eradicate the populations. Brodifacoum gave virtually complete control of six populations in 21-73 days and of the ten residual populations left behind by the other two compounds, after baiting for a further 11-85 days. The performance of both bromadiolone and brodifacoum was well below that reported by previous investigators, indicating the possibility of low-grade resistance to these compounds in the difenacoum-resistant strain.

Recent trends in the metabolism and cell biology of vitamin K with special reference to vitamin K cycling and MK-4 biosynthesis

“…At around the same time, reports of the spread of resistance to fi rst generation rodenticides were also being reported ( 88,89 ) and after the introduction of second-generation rodenticides (so called superwarfarins) to these compounds as well ( 90,91 ). The discovery of VKOR in 2004 as the target protein for VKAs ( 13,14 ) has resulted in the identifi cation of ‫ف‬ 30 mutations in humans ( 92 ) and ‫ف‬ 10 in rodents ( 93 ) associated with VKA resistance.…”

The Genetic Basis of Resistance to Anticoagulants in Rodents

“…However, resistance to most Animals: R. norvegicus: Rats of both sexes were analyzed. Animals of the laboratory outbred strains HW and HH were of these compounds was reported soon after their introobtained from two independent laboratory stocks [Central duction (Rowe et al 1981;Greaves et al 1982 Blood clotting response test: BCR resistance testing with was found mutated to serine (Tyr139Ser). Mutations warfarin was done as described (Martin et al 1979) with were absent from the anticoagulant-susceptible backmodifications .…”

“…A multiple sequence alignment of 37 related genes from archaebacteria, eubacteria, and metazoa activity has been measured in liver microsomes from a has identified three to four potential hydrophobic trans-2. Resistance to second generation anticoagulants has been reported for a proportion of resistant indimembrane domains, four cysteines and one serine/ threonine to be fully conserved between species, and a viduals (Rowe et al 1981;Greaves et al 1982;MacNicoll and Gill 1987;Johnson 1988) but this can-CXXC motif known from thioredoxin oxidoreductases (Trx) as an electron donor in a variety of reduction not be fully explained by variability in VKORC1 sequence data. It has been suggested that secondary reactions (see Figure 3; Goodstadt and Ponting 2004;Rost et al 2004).…”

Superwarfarins

“…It is more toxic than warfarin but less palatable (IPCS, 1995c). Difenacoum is still effective against many populations of warfarin-resistant rats (Desideri et al, 1979), but resistance may be developing in the United Kingdom (Greaves et al, 1982).…”