Pesticide resistance in wild mammals--mechanisms of anticoagulant resistance in wild rodents.
ABSTRACT Warfarin is commonly used worldwide as a rodenticide. It inhibits coagulation of blood by inhibiting vitamin K 2,3-epoxide reductase (VKOR) activity. An inadequate supply of vitamin K blocks the production of prothrombin and causes hemorrhage. It has been reported that repeated or long-term treatments with this drug cause resistance in wild rodents. However, the mechanism of warfarin resistance in rodents is still not known precisely. Recent studies reported and identified the function of the molecule, vitamin K epoxide reductase complex subunit 1 (VKORC1), which is the main unit of VKOR. An amino acid substitution in VKORC1 is one of the supposed mechanisms of warfarin resistance. An accelerated detoxification system involving cytochrome P450 (CYP) could also cause the rodenticide resistance. Administration of SKF-525A, a potent inhibitor for P450, increased the mortality due to reduction of warfarin metabolism in warfarin-resistant rats. Meanwhile, the appearance of warfarin-resistant rodents has led to the development of the more effective and toxic rodenticide superwarfarin, which is widely used in Europe and the USA. However, animals resistant to this second-generation rodenticide have already been reported in Europe. In this review, we focus on the mechanism and the pleiotropic effects of pesticide resistance in wild rodents.
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ABSTRACT: Anticoagulant rodenticide (AR) levels were studied in liver of 401 wild and domestic animals found dead in Spain with evidences of AR poisoning, including 2 species of reptiles (n=2), 42 species of birds (n=271) and 18 species of mammals (n=128). Baits (n=32) were also analyzed to detect the potential use of ARs in their intentional preparation to kill predators. AR residues were detected in 155 (38.7%) of the studied animals and 140 (34.9%) may have died by AR poisoning according to the clinical information, necropsy findings, residue levels and results of other toxicological analysis. Animals considered with sublethal AR exposure had total AR residues (geometric mean with 95% CI) in liver of 0.005 (0.003-0.007)μg/g wet weight (w.w.) and animals diagnosed as dead by AR poisoning had 0.706 (0.473-1.054)μg/g w.w. ARs were detected in 19% of baits illegally prepared to kill predators. In terms of the total incidents studied in our laboratory between 2005 and 2010 (n=1792 animals), confirmed poisonings represented 40.9% of the cases, and 21.1% of these were due to ARs (8.6% of the total sample). Nocturnal raptors (62%) and carnivorous mammals (38%) were amongst the secondary consumers with highest prevalence of AR exposure, especially to second generation ARs (SGARs). On the other hand, granivorous birds showed the highest prevalence of AR exposure (51%), especially to chlorophacinone in a region treated against a vole population peak in 2007. The presence of hemorrhages was significantly associated with AR levels in liver, but some animals (7.2%) with elevated residue levels (>0.2μg/g w.w.) showed no evidence of macroscopic bleeding. The use of accumulative SGARs and the application of baits on surface (i.e. treated grain by spreader machines) should be discontinued in future EU regulations on the use of rodenticides to prevent the poisoning of non-target wildlife species.Science of The Total Environment 03/2012; 420:280-8. · 3.26 Impact Factor
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ABSTRACT: BACKGROUND: Genetically based resistance to anticoagulants has led to increasing difficulties in the control of rodents over recent decades. The possible impact of rodenticide-resistant rats on the infection risk of humans and livestock by zoonotic pathogens is generally unknown. Hence, in a monitoring programme in the German federal states of Lower Saxony and Hamburg, more than 500 Norway rats were analysed for both Tyr139Cys polymorphisms within the VKORC1 gene and zoonotic agents. RESULTS: Evidence of resistance was almost completely restricted to the known resistance area in southern Lower Saxony. Homozygous mutations were only found in urban areas sampled owing to the occurrence of rat control problems and were missing in bycatches of rats by muskrat trappers in rural areas. In more than 25% of the rats, zoonotic bacteria (Leptospira, Salmonella, Yersinia and Coxiella) were detected. There was no obvious correlation between the occurrence of rats carrying zoonotic pathogens and anticoagulant resistance. CONCLUSION: Zoonotic agents and genetically based resistance conferred by the Tyr139Cys polymorphism are both unevenly distributed in Lower Saxony. The study provides the basis for further studies focusing on districts with high levels of pathogens and resistance to assess the potential health risk of their combined occurrence. Copyright © 2012 Society of Chemical Industry.Pest Management Science 05/2012; · 2.74 Impact Factor
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ABSTRACT: The current rapid rate of human-driven environmental change presents wild populations with novel conditions and stresses. Theory and experimental evidence for evolutionary rescue present a promising case for species facing environmental change persisting via adaptation. Here, we assess the potential for evolutionary rescue in wild vertebrates. Available information on evolutionary rescue was rare and restricted to abundant and highly fecund species that faced severe intentional anthropogenic selective pressures. However, examples from adaptive tracking in common species and genetic rescues in species of conservation concern provide convincing evidence in favour of the mechanisms of evolutionary rescue. We conclude that low population size, long generation times and limited genetic variability will result in evolutionary rescue occurring rarely for endangered species without intervention. Owing to the risks presented by current environmental change and the possibility of evolutionary rescue in nature, we suggest means to study evolutionary rescue by mapping genotype → phenotype → demography → fitness relationships, and priorities for applying evolutionary rescue to wild populations.Philosophical Transactions of The Royal Society B Biological Sciences 01/2013; 368(1610):20120090. · 6.23 Impact Factor