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1.
Sci Rep ; 8(1): 4535, 2018 03 14.
Article in English | MEDLINE | ID: mdl-29540746

ABSTRACT

While resistance to anticoagulant rodenticides is known to occur in many European populations of Norway rat and house mouse, to-date no data is available on the occurrence in Ireland of such resistance. No genetic evidence for the occurrence of resistance was found in 65 Norway rat samples analysed, indicative of an absence, or low prevalence, of resistance in rats in at least the Eastern region of the island of Ireland. The presence of two of the most commonly found amino acid substitutions Leu128Ser and Tyr139Cys associated with house mouse resistance to anticoagulant rodenticides was confirmed. The occurrence of two such mutations is indicative of the occurrence of resistance to anticoagulant rodenticides in house mice in the Eastern region of the island of Ireland.


Subject(s)
Amino Acid Substitution , Drug Resistance , Membrane Proteins/genetics , Rodenticides , Vitamin K Epoxide Reductases/genetics , Animals , Anticoagulants/adverse effects , Ireland , Mice , Rats , Rodenticides/adverse effects
2.
Pest Manag Sci ; 72(6): 1168-77, 2016 Jun.
Article in English | MEDLINE | ID: mdl-26271625

ABSTRACT

BACKGROUND: Little is known about native and non-native rodent species interactions in complex tropical agroecosystems. We hypothesised that the native non-pest rodent Rattus everetti may be competitively dominant over the invasive pest rodent Rattus tanezumi within agroforests. We tested this experimentally by using pulse removal for three consecutive months to reduce populations of R. everetti in agroforest habitat, and assessed over 6 months the response of R. tanezumi and other rodent species. RESULTS: Following removal, R. everetti individuals rapidly immigrated into removal sites. At the end of the study period, R. tanezumi were larger and there was a significant shift in their microhabitat use with respect to the use of ground vegetation cover following the perturbation of R. everetti. Irrespective of treatment, R. tanezumi selected microhabitat with less tree canopy cover, indicative of severely disturbed habitat, whereas R. everetti selected microhabitat with a dense canopy. CONCLUSION: Our results suggest that sustained habitat disturbance in agroforests favours R. tanezumi, while the regeneration of agroforests towards a more natural state would favour native species and may reduce pest pressure in adjacent crops. In addition, the rapid recolonisation of R. everetti suggests this species would be able to recover from non-target impacts of short-term rodent pest control. © 2015 Society of Chemical Industry.


Subject(s)
Forestry , Introduced Species , Pest Control, Biological/methods , Rats , Rodent Control/methods , Animals , Crop Protection/methods , Ecosystem , Female , Forestry/methods , Male , Population Dynamics
3.
Pest Manag Sci ; 70(6): 939-45, 2014 Jun.
Article in English | MEDLINE | ID: mdl-24038791

ABSTRACT

BACKGROUND: Reduction of vegetation height is recommended as a management strategy for controlling rodent pests of rice in South-east Asia, but there are limited field data to assess its effectiveness. The breeding biology of the main pest species of rodent in the Philippines, Rattus tanezumi, suggests that habitat manipulation in irrigated rice-coconut cropping systems may be an effective strategy to limit the quality and availability of their nesting habitat. The authors imposed a replicated manipulation of vegetation cover in adjacent coconut groves during a single rice-cropping season, and added artificial nest sites to facilitate capture and culling of young. RESULTS: Three trapping sessions in four rice fields (two treatments, two controls) adjacent to coconut groves led to the capture of 176 R. tanezumi, 12 Rattus exulans and seven Chrotomys mindorensis individuals. There was no significant difference in overall abundance between crop stages or between treatments, and there was no treatment effect on damage to tillers or rice yield. Only two R. tanezumi were caught at the artificial nest sites. CONCLUSION: Habitat manipulation to reduce the quality of R. tanezumi nesting habitat adjacent to rice fields is not effective as a lone rodent management tool in rice-coconut cropping systems.


Subject(s)
Murinae/physiology , Rats/physiology , Rodent Control/methods , Animals , Cocos , Ecosystem , Oryza , Philippines , Population Dynamics
4.
Pest Manag Sci ; 68(12): 1579-85, 2012 Dec.
Article in English | MEDLINE | ID: mdl-23007948

ABSTRACT

BACKGROUND: The tyrosine to cysteine amino acid substitution at location 139 of the vkorc1 protein (i.e. tyrosine139cysteine or Y139C) is the most widespread anticoagulant resistance mutation in Norway rats (Rattus norvegicus Berk.) in Europe. Field trials were conducted to determine the incidence of the Y139C mutation at two rat-infested farms in Westphalia, Germany, and to estimate the practical efficacy against them of applications, using a pulsed baiting treatment regime, of a proprietary bait (Klerat™) containing 0.005% brodifacoum. RESULTS: DNA analysis for the Y139C mutation showed that resistant rats were prevalent at the two farms, with an incidence of 80.0 and 78.6% respectively. Applications of brodifacoum bait achieved results of 99.2 and 100.0% control at the two farms, when measured by census baiting, although the treatment was somewhat prolonged at one site, possibly owing to the abundance of attractive alternative food. CONCLUSION: The study showed that 0.005% brodifacoum bait is fully effective against Norway rats possessing the Y139C mutation at the Münsterland focus and is likely to be so elsewhere in Europe where this mutation is found. The pulsed baiting regime reduced to relatively low levels the quantity of bait required to control these two substantial resistant Norway rat infestations. Previous studies had shown much larger quantities of bromadiolone and difenacoum baits used in largely ineffective treatments against Y139C resistant rats in the Münsterland. These results should be considered when making decisions about the use of anticoagulants against resistant Norway rats and their potential environmental impacts.


Subject(s)
4-Hydroxycoumarins/toxicity , Amino Acid Substitution , Anticoagulants/toxicity , Mixed Function Oxygenases/genetics , Rats/genetics , Rodent Control/methods , Rodenticides/toxicity , Animals , Cysteine/chemistry , Drug Resistance/genetics , Germany , Mixed Function Oxygenases/chemistry , Sequence Analysis, DNA , Tyrosine/chemistry , Vitamin K Epoxide Reductases
5.
Genetics ; 170(4): 1839-47, 2005 Aug.
Article in English | MEDLINE | ID: mdl-15879509

ABSTRACT

Anticoagulant compounds, i.e., derivatives of either 4-hydroxycoumarin (e.g., warfarin, bromadiolone) or indane-1,3-dione (e.g., diphacinone, chlorophacinone), have been in worldwide use as rodenticides for >50 years. These compounds inhibit blood coagulation by repression of the vitamin K reductase reaction (VKOR). Anticoagulant-resistant rodent populations have been reported from many countries and pose a considerable problem for pest control. Resistance is transmitted as an autosomal dominant trait although, until recently, the basic genetic mutation was unknown. Here, we report on the identification of eight different mutations in the VKORC1 gene in resistant laboratory strains of brown rats and house mice and in wild-caught brown rats from various locations in Europe with five of these mutations affecting only two amino acids (Tyr139Cys, Tyr139Ser, Tyr139Phe and Leu128Gln, Leu128Ser). By recombinant expression of VKORC1 constructs in HEK293 cells we demonstrate that mutations at Tyr139 confer resistance to warfarin at variable degrees while the other mutations, in addition, dramatically reduce VKOR activity. Our data strongly argue for at least seven independent mutation events in brown rats and two in mice. They suggest that mutations in VKORC1 are the genetic basis of anticoagulant resistance in wild populations of rodents, although the mutations alone do not explain all aspects of resistance that have been reported. We hypothesize that these mutations, apart from generating structural changes in the VKORC1 protein, may induce compensatory mechanisms to maintain blood clotting. Our findings provide the basis for a DNA-based field monitoring of anticoagulant resistance in rodents.


Subject(s)
Anticoagulants/pharmacology , Drug Resistance/genetics , Mixed Function Oxygenases/genetics , Mixed Function Oxygenases/metabolism , Mutation , Amino Acid Motifs , Amino Acid Sequence , Animals , Cell Line , Codon , DNA Mutational Analysis , Dose-Response Relationship, Drug , Female , Humans , Male , Mice , Mixed Function Oxygenases/chemistry , Molecular Sequence Data , Protein Structure, Tertiary , Rats , Recombinant Proteins/metabolism , Sequence Analysis, DNA , Sequence Homology, Amino Acid , Tyrosine/chemistry , Vitamin K Epoxide Reductases , Warfarin/pharmacology
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