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Anticoagulant rodenticides are commonly used in rodent control because they are economical and have great deployment versatility. However, rodents with Single Nucleotide Polymorphism (SNP) mutations within the Vkorc1 gene are resistant to the effects of anticoagulant rodenticide use and this influences the effectiveness of control strategies that rely on such rodenticides. This study examined the prevalence of rat SNP mutations in Singapore to inform the effectiveness of anticoagulant rodenticide use. A total of 130 rat tail samples, comprising 83 Rattus norvegicus (63.8%) and 47 Rattus rattus complex (36.2%) were conveniently sampled from November 2016 to December 2019 from urban settings and sequenced at exon 3 of Vkorc1. Sequencing analysis revealed 4 synonymous and 1 non-synonymous mutations in Rattus rattus complex samples. A novel synonymous mutation of L108L was identified and not previously reported in other studies. Non-synonymous SNPs were not detected in the notable codons of 120, 128 and 139 in R. norvegicus, where these regions are internationally recognised to be associated with resistance from prior studies. Our findings suggest that the prevalence of anticoagulant rodenticide resistance in Singapore is low. Continued monitoring of rodenticide resistance is important for informing rodent control strategies aimed at reducing rodent-borne disease transmission.

Background We conducted a vitamin K epoxide reductase subcomponent 1 (Vkorc1)-based nonsynonymous Single Nucleotide Polymorphism (nsSNP) screen with focus on the house mouse (Mus musculus domesticus), but that also considered the Norway rat (Rattus norvegicus) and roof rat (R. rattus) in the USA. Results We detected six Vkorc1 nsSNPs underlying the amino-acid polymorphisms Ala21Thr, Trp59Leu, Ile104Val, Val118Leu, Leu128Ser and Tyr139Cys in house mice (average coverage/SNP; n = 182 individuals), two nsSNPs underlying Arg35Pro and Gly46Ser in the Norway rat (n = 93), with the notable absence of Tyr139Cys (n = 179), and one nsSNP underlying Tyr25Phe in the roof rat (n = 27). Inferred resistance frequency is 29.1% for mice (variability of states 0-98.8%), 6.5% (0-33.3%) for the Norway rat, and 39.3% (0-52.6%) for the roof rat based on Tyr25Phe frequencies. Conclusions Resistance detected in the USA in the 1980s likely was the consequence of Vkorc1 mutations in mice (Leu128Ser and Tyr139Cys), Norway rats (Arg35Pro) and roof rats (Tyr25Phe). Patterns of variant sharing between the USA and Europe indicate the importance of convergent evolution and gene flow in spreading resistance. The spread of nsSNPs in mice between continents appears to have been more effective than in Norway rats. We hypothesize that Arg35Pro may have originated in Norway rats in the USA, whereas Tyr139Cys variants originated in Europe. Tyr25Phe is the likely cause for resistance in roof rats. Further genetic testing in the USA is required to close sampling gaps, and population genomic data are needed to study the origin and spread of this adaptive trait.

Anticoagulant rodenticides (AR) remain the most effective chemical substances used to control rodents in order to limit their agricultural and public health damage in both rural and urban environments. The emergence of genetically based resistance to AR worldwide has threatened effective rodent control. This study gives a first overview of the distribution and frequency of single nucleotide polymorphism in the vitamin K epoxide reductase subcomponent 1 (Vkorc1) gene in rodents in Lebanon. In the Mus genus, we detected two missense mutations Leu128Ser and Tyr139Cys, that confer resistance to anticoagulant rodenticides in house mice and a new missense mutation Ala72Val in the Mus macedonicus species, not previously described. In the Rattus genus, we found one missense mutation Leu90Ile in the roof rat and one missense mutation Ser149Ile in the Norway rat. This is the first study to demonstrate potential resistance to AR in Lebanese rodents and therefore it provides data to pest control practitioners to choose the most suitable AR to control rodents in order to keep their efficacy.

Biological invasions are a growing threat to biodiversity. The black rat, one of the worst pest in the world, is responsible for extensive population decline of many autochthonous and endemic species, particularly in island ecosystems. A number of rat eradication campaigns have been conducted, however, such endeavors do not always result in a complete removal of the pest. This may be due to the occurrence of individuals resistant to common rodenticides and/or a re-invasion of the same environment from interconnected areas when appropriate eradication units are not defined before starting an eradication campaign. Our study is a multidisciplinary approach whereby genetic and epidemiological methods were used to provide background information for successful eradication of black rats. We investigated the occurrence of mutations in the VKORC1 gene known to confer resistance to rodenticides and evaluated the spread of zoonoses across three islands of the Pontine Archipelago, an Italian hotspot of endemic Mediterranean biodiversity and a possible mainland source of invasion. As part of an eradication campaign, we also assessed patterns of genetic diversity at 10 microsatellite loci in order to identify eradication units. We recorded a strong population structure and revealed at least two distinct eradication units. Some degree of admixture was recorded on Ponza, the largest island and likely the main source of rats invading the other two islands. We did not record the occurrence of rats resistant to anticoagulants, but we revealed transmission of vector-borne pathogens in commensal habitats of the Archipelago.

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. © 2012 Society of Chemical Industry

Once rats have invaded farm buildings, efficient rat control usually requires the application of rodenti-cides. Efficacy of control measures may be lost by physiological resistance to anticoagulant rodenticides and by behavioural reactions of the target rat population. On a farm within the area of anticoagulant resistance in north-west Germany, two consecutive rodenticide treatments were carried out against rats, using different anticoagulant bait preparations. Bait consumption was monitored in combination with direct individual video-monitoring of bait uptake behaviour. Almost half of the rats survived the first three-week treatment using coumatetralyl bait. This result was ascribed to the high overall degree of anticoagulant resistance prevailing in the rat population. The second treatment of the same population using difenacoum bait totally failed to reduce population numbers. Dietary preferences, neophobia, social interactions and habitat structure are important behavioural parameters determining bait uptake. They are discussed in relation to the results of the treatment and a conceptual model for the factors determining rodent control efficacy is presented. The combined results of the two monitoring techniques applied demonstrate the significance of resistance and bait uptake behaviour for the efficacy of rat control measures and suggest the need for adapted rat-control strategies to reduce hygienic problems and the risk of non-target poisoning hazards for livestock and wildlife. This can be achieved if the choices of bait base and active ingredient as well as the methods of bait positioning are adapted to the behavioural peculiarities of the rats and the specific structural conditions on each farm.

The brown rat (Rattus norvegicus) is a relatively recent (VKORC1gene previously associated with resistance to anticoagulant rodenticides. We show that the populations were structured to some degree, but that this was only apparent in the microsatellite data and not the mtDNA data. We discuss various reasons why this is the case. We show that the population as a whole appears not to be at equilibrium. The relative lack of diversity in the mtDNA sequences examined can be explained by founder effects and a subsequent spatial expansion of a species introduced to the UK relatively recently. We found there was a geographical distribution of resistance mutations, and relatively low rate of gene flow between populations, which has implications for the development and management of anticoagulant resistance.

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.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.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.

Since anticoagulant rodenticide resistance was first discovered in the United States in 1971, it has become apparent that the phenomenon is widespread. In cooperation with the Center for Disease Control, a nationwide surveillance program was initiated in 1977 to obtain statistically valid samples of rats from federally funded projects of the Urban Rat Control Program. A summary is given of the basic sampling, testing, and analysis components of this study. Problems encountered in all aspects of the first three years of the program are discussed along with results from the 40 completed samples. The 16 cities with significant Anticoagulant Resistance Problem Areas are distinguished from those in which resistance has merely been observed. Levels of resistance in various rat populations are discussed and recommendations are made in support of integrated pest management programs. Recent findings from retesting resistant rats, half of which die, are presented with regard to application of the surveillance program.

While the problem of anticoagulant resistance in commensal rodents has been well-documented from certain areas of northern Europe in recent years, this paper describes its first known occurrence in North America in 1971. Over a rural area of about 5 square miles in Johnson County, North Carolina, it was noted that attempts to control Norway rats using typical warfarin rodenticide bait were increasingly ineffective. Diphacinone was alternated with warfarin with no success. On one farm, 200 lbs of bait had been used in bait boxes in a single month. Laboratory trials on rats captured at this location demonstrated resistance. It was concluded that at this location, intensive use of anticoagulants (mostly warfarin) over a decade, in the absence of adequate sanitation and building maintenance, provided the selective agent to develop resistant populations. This likely will be repeated elsewhere in the U.S.

Between 2003 and 2010 two 3-year screening periods (I and II) were conducted to monitor the brown rat resistance to rodenticides in Flanders. Resistance was assessed by means of genetic mutations. The aim of the study was to estimate the degree of resistance in Flanders, to test whether there are differences between the 12 river basins, and whether the resistance is increasing over time. Multiple rats per location were caught.Several statistical analyses were performed on these data. On the one hand, aggregated results per location (presence/absence of resistance, defined in several ways) were analysed using logistic regression (glm), while on the other hand, mixed model logistic regression (glmm) was used on the rat-level to incorporate correlations between rats from a single location.The level of resistance differed strongly between river basins, some being almost completely resistant, while in others resistance was nearly zero. Correlation was strongest between rats within a location, but variograms also showed a strong correlation between nearby locations (The number of locations (resp. rats) per river basin ranged from 2 to 54 (resp. 2 to 151) for screening I, and from 4 to 65 (resp. 11 to 110) for screening II. Due to these small numbers, the estimate of resistance was inaccurate for some river basins. Also, evolution of resistance over time was not analysed, since data collection in both screening periods was not comparable. A more balanced follow-up monitoring program, with enough rats and locations per river basin, has been designed to answer all questions more accurately in the future.

Mutations in Exon 1, 2 and 3 of the vitamin K epoxide reductase complex subunit 1 (Vkorc1) gene are known to lead to anticoagulant rodenticide resistance. In order to investigate their putative resistance in rodenticides, we studied the genetic profile of the Vkorc1 gene in Turkish black rats (Rattus rattus) and brown rats (Rattus norvegicus). In this context, previously recorded Ala21Thr mutation (R. rattus) in Exon 1 region, Ile90Leu mutation (R. rattus, R. norvegicus) in Exon 2 region and Leu120Gln mutation (R. norvegicus) in Exon 3 region were identified as “missense mutations” causing amino acid changes. Ala21Thr mutation was first detected in one specimen of Turkish black rat despite the uncertainty of its relevance to resistance. Ile90Leu mutation accepted as neutral variant was detected in most of black rat specimens. Leu120Gln mutation related to anticoagulant rodenticide resistance was found in only one brown rat specimen. Furthermore, Ser74Asn, Gln77Pro (black rat) and Ser79Pro (brown rat) mutations that cause amino acid changes in the Exon 2 region but unclear whether they cause resistance were identified. In addition, “silent mutations” which do not cause amino acid changes were also defined; these mutations were Arg12Arg mutation in Exon 1 region, His68His, Ser81Ser, Ile82Ile and Leu94Leu mutations in Exon 2 region and Ile107Ile, Thr137Thr, Ala143Ala and Gln152Gln mutations in Exon 3 region. These silent mutations were found in both species except for Ser81Ser which was determined in only brown rats.

Anticoagulants are a major component of rodenticides used worldwide, which function by effectively blocking the vitamin K cycle in rodents. The rat Vitamin K epoxide Reductase Complex (VKORC) subunit 1 is the enzyme responsible for recycling vitamin K, and five substitution mutations (Tyr139Cys, Tyr139Ser, Tyr139Phe and Leu128Gln and Leu120Gln) located in the VKORC1 could result in resistance to anticoagulant rodenticides. This study carried out a VKORC1-based survey to estimate the anticoagulant rodenticide resistance in three Rattus species (R. losea, R. norvegicus, and R. tanezumi) collected in Hong Kong. A total of 202 rats captured in Hong Kong between 2017 and 2021 were analysed. Sequencing of molecular marker cytochrome c oxidase subunit 1 (COX1) was carried out to assist the species identification, and the identities of 52 lesser ricefield rats (R. losea), 81 common rats (R. norvegicus) and 69 house rats (R. tanezumi) were confirmed. Three VKORC1 exons were amplified from individuals by PCR followed by Sanger sequencing. A total of 47 R. tanezumi (68.1%) contained Tyr139Cys mutation in VKORC1 gene, and half of them were homozygous. None of the collected R. losea and R. norvegicus were detected with the five known substitutions leading to anticoagulant rodenticides resistance, and previously undescribed missense mutations were revealed in each species. Whole genome sequencing was further carried out on some individuals, and single nucleotide polymorphisms (SNPs) were also identified in the introns. This is the first study investigating the situation of anticoagulant rodenticide resistance in the rats collected in Hong Kong. Given that the efficacy of rodenticides is crucial for effective rodent management, regular genetic testing as well as population genomic analyses will be required to both monitor the situation and understand the adaption of different rat haplotypes for integrated pest management. Susceptibility tests for individual rodenticides should also be conducted regularly to assess their effectiveness on local species.

Anticoagulant rodenticides are commonly used in rodent control because they are economical and have great deployment versatility. However, rodents with Single Nucleotide Polymorphism (SNP) mutations within the Vkorc1 gene are resistant to the effects of anticoagulant rodenticide use and this influences the effectiveness of control strategies that rely on such rodenticides. This study examined the prevalence of rat SNP mutations in Singapore to inform the effectiveness of anticoagulant rodenticide use. A total of 130 rat tail samples, comprising 83 Rattus norvegicus (63.8%) and 47 Rattus rattus spp. (36.2%) were conveniently sampled from November 2016 to December 2019 from urban settings and sequenced at exon 3 of Vkorc1. Sequencing analysis revealed 4 synonymous and 1 non-synonymous mutations in Rattus rattus spp. samples. A novel synonymous mutation of L108L was identified and not previously reported in other studies. Non-synonymous SNPs were not detected in the notable codons of 120, 128 and 139 in Norway rats, where these regions are internationally recognised to be associated with resistance from prior studies. Our findings suggest that the prevalence of anticoagulant rodenticide resistance in Singapore is low. Continued monitoring of rodenticide resistance is important for informing rodent control strategies aimed at reducing rodent-borne disease transmission.

Rodents are mostly controlled by using anticoagulant rodenticides to minimise adverse effects along the food production chain. Genetic resistance to anticoagulant compounds occurs in populations of Norway rats ( Rattus norvergicus ) and other rodents throughout the world. This can be problematic for control operations and put predators and scavengers at risk because resistant prey individuals carry high anticoagulant loads. Single nucleotide polymorphisms (SNPs) in the vitamin K reductase complex subunit 1 (VKORC1) gene that are associated with rodenticide resistance are related to several pleiotropic effects including increased vitamin K requirement. The uptake of dietary vitamin K available from food sources present on farms including corn silage and garden herbs may mitigate such effects. We tested the preference for food rich in vitamin K1/3 in Norway rats susceptible or resistant to bromadiolone due to the homozygous amino acid variant Tyr139Cys. We also studied the effect of vitamin K consumption from several food sources on blood clotting in bromadiolone resistant and susceptible Norway rats. There was no general preference of rats for food sources rich in vitamin K. Surprisingly, there was no effect of vitamin K uptake on blood clotting times. However, the consumption of 4 of 5 corn silages prevented the rise in blood clotting times that otherwise occurred in vitamin K deficient bromadiolone resistant rats. This seemed to be due to substances with vitamin K activity present in silage and may contribute to the sustaining and spreading SNPs that are related to rodenticide resistance. As corn silage is becoming increasingly available to rats due to the expansion in generating bio-energy from corn silage, there may be a future increase in the occurrence of anticoagulant resistant Norway rats and associated problems in agro-ecosystems.

Roof rats (Rattus rattus) are common invasive pests in both urban and agricultural sites as well as a significant public health threat. The use of anticoagulant rodenticides to help control the rodent population poses a risk of developing resistance to these products. Several reports have associated the non-synonymous Single Nucleotide Polymorphism (nsSNP) Tyr25Phe (Y25F) of the vitamin K epoxide reductase subcomponent 1 (Vkorc1) gene to anticoagulant rodenticide resistance (Diaz et al. 2021). We conducted a nsSNP screen in the population of Rattus spp. in Orange County to determine the prevalence of the Y25F nsSNP in the sampled rodents. Thirty-seven live rat traps were set throughout the county and the species of each trapped rat was determined by sequencing the cytochrome oxide I (COI) gene using primers previously described in Goulois et al. (2015). Twenty specimens were identified as R. rattus and 12 as R. tanezumi (Asian house rat); the other five specimens were non-Rattus species. To further evaluate the rat species, we used tree-based methods using sequence alignments for three mitochondrial DNA regions, cytochrome b, COI, and non-coding displacement (D) loop using a different set of primers used by Robins et al. (2007). Sequences were aligned by Geneious Prime (v.2020.2.4), and maximum-likelihood phylogeny using 1,000 bootstrap replications was constructed using Mega (10.2.6). Sequences were compared to reference sequences in Robins et al. (2007) and Rattus norvegicus (Norway rat) was used to root the tree. Phylogenetic analysis confirmed the presence of R. tanezumi in our collected samples as well as two haplotypes of R. rattus. In addition to the concatenated data set, each gene was examined individually, and all phylogenetic trees generally agreed on topology. The Y25F nsSNP was present in both R. rattus (40%; 8 of 20) and R. tanezumi (16.67%; 2 of 12). Further genetic testing in Orange County and other areas of Southern California are needed to determine the extent of these Rattus populations and their hybridization as well as the presence of this adaptive trait.

Stefan Endepols, Bayer CropScience-Environmental Science and Chairman of the Rodenticide Resistance Action Committee (RRAC), describes the work of the RRAC in establishing rodenticide resistance management strategies.

Current reactive pest management methods have serious drawbacks such as the heavy reliance on chemicals, emerging genetic rodenticide resistance and high secondary exposure risks. Rodent control needs to be based on pest species ecology and ethology to facilitate the development of ecologically based rodent management (EBRM). An important aspect of EBRM is a strong understanding of rodent pest species ecology, behaviour and spatiotemporal factors. Gaining insight into the behaviour of pest species is a key aspect of EBRM. The landscape of fear (LOF) is a mapping of the spatial variation in the foraging cost arising from the risk of predation, and reflects the levels of fear a prey species perceives at different locations within its home range. In practice, the LOF maps habitat use as a result of perceived fear, which shows where bait or traps are most likely to be encountered and used by rodents. Several studies have linked perceived predation risk of foraging animals with quitting-harvest rates or giving-up densities (GUDs). GUDs have been used to reflect foraging behaviour strategies of predator avoidance, but to our knowledge very few papers have directly used GUDs in relation to pest management strategies. An opportunity for rodent control strategies lies in the integration of the LOF of rodents in EBRM methodologies. Rodent management could be more efficient and effective by concentrating on those areas where rodents perceive the least levels of predation risk. © 2017 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Background Due to the risk of spreading epizootic diseases through rodents, pest control is mandatory in pig farming in European countries. However, there is limited research focused on rodent control practices, usage of anticoagulant rodenticides, and the acceptance of Pest Control Operators (PCOs) in pig farming in Germany. Therefore, the present study aims to investigate current control practices in pig holdings and to analyze the potential of a financial support on the implementation of professional pest control. Results Data were collected from monitoring records of PCOs and personal interviews with farmers and PCOs. 33 of 47 farmers, who were offered the possibility to outsource rodent control to PCOs supported by financial contribution of the North Rhine-Westphalian Animal Disease Fund (TSK) for a period of 2 years, joined the project. Despite the widespread opinion that the professional would not be beneficial – the authors figured out that farmers could financially benefit in time saved and by improved rodent control measures from the work of the PCOs. Costs of pest control measures per operation on average did not differ significantly between costs incurred by employment of PCOs (1.310 € per year) and calculated costs that arise by farmers themselves (1.217 € per year). All PCOs used Difenacoum and Brodifacoum against pest infestations. In doing so, the infestation with rodents was reduced and most of the participating farmers assessed the project as successful and employ the PCOs permanently. However, mapping the farm locations to resistance areas of the Rodenticide Resistance Action Committee (RRAC) shows that Brodifacoum was frequently used in areas which are marked as areas that are at low risk or rather have no risk for resistance. The environmental risks, however, are increased in these areas. Conclusion The instrument of temporal start-up financing professional pest control allows ensuring the continuous engagement of PCOs after the project period. This could possibly lead to long-term effects on the individual farm hygiene and on disease prevention. Nevertheless, important research questions with regard to the application of anticoagulant rodenticides of farmers and PCOs in livestock farming and with regard to risk mitigation measures were generated, meriting further investigation. Electronic supplementary material The online version of this article (10.1186/s40813-018-0099-0) contains supplementary material, which is available to authorized users.

Rats (brown- or Norway- and black: Rattus norvegicus and Rattus rattus , respectively) are very invasive rodents. They are originated from Southeast Asia and are present now everywhere in the world, exploiting their extraordinary capacity to proliferate in close contact with human populations. Rats, and particularly the brown rat, take advantage of conditions raised by overpopulation in cities, lack of hygiene and poverty. Beside the significant damage caused by their presence in rural and urban ecosystems, rats are also dangerous carriers of numerous pathogens transmissible to humans. Among these pathogens, leptospira and hantaviruses (particularly Seoul virus or SEOV) are the most important. Seoul virus belongs to the virus family Bunyaviridae and genus Hantavirus, has a worldwide distribution, and causes haemorrhagic fever with renal syndrome (HFRS) in humans. Leptospira and particularly Leptospira interrogans , serogroup Icterohaemorrhagiae, are zoonotic bacteria very frequently borne and excreted by rats and cause severe disease - leptospirosis - both in humans and domestic animals. Next-generation sequencing confirmed that rats can carry many other microbes and parasites for which the zoonotic capacity is not always determined. The importance of rats as pests and carriers of numerous pathogens demands the fight against their proliferation, especially in urban environments. The use of rodenticides such as anticoagulants is one pillar of prevention. However, increasing levels of rodenticide resistance can often render this means of control as ineffective. The second and absolutely necessary pillar of prevention involves the control of all environmental factors, which favour the establishment and proliferation of rats: age of housing, density of dwellings, defective drains/sewers, poor structural maintenance, proximity to food sources and poor hygiene.

Author(s): Why, Adena M.; James, David K; Gay, Robert B. | Abstract: The County Service Area (CSA) 1984-1 for Vector Control was established in June 1984 to serve the public’s needs for providing a comprehensive vector control program throughout Alameda County. In 1987, the City of Oakland recognized that it had a severe rat problem emanating from the sanitary sewers, and in an effort to control them the voters approved a supplemental assessment. For thirty years the CSA has implemented an urban rodent surveillance program focusing on monitoring and controlling commensal rats (Norway and roof rats) and mice in residential, commercial, and business properties. In 2017, the CSA received 2,917 Requests for Service from the public about domestic rodents (2,282 re: rats and 635 re: mice), representing 38.9% of overall service requests. Those 2,917 rodent service requests had staff biologists performing 16,722 field services operations related to rodents. The field service operations included performing smoke and dye tests of sewer lines for breaks; field and residential surveys for rodent activity; recommendations and follow-up evaluations of rodent control measures; and assistance with enforcement actions. In 2017, a total of 8,150 sewer inspections and 1,531 applications of Contrac rodenticide bait were made in the City of Oakland. The CSA is now looking at incorporating rodenticide resistance testing, GIS data analysis, pulse-baiting strategies, and disease surveillance as part of an Integrated Pest Management program as improvements in 2018.

The County Service Area (CSA) 1984-1 for Vector Control was established in June 1984 to serve the public’s needs for providing a comprehensive vector control program throughout Alameda County. In 1987, the City of Oakland recognized that it had a severe rat problem emanating from the sanitary sewers, and in an effort to control them the voters approved a supplemental assessment. For thirty years the CSA has implemented an urban rodent surveillance program focusing on monitoring and controlling commensal rats (Norway and roof rats) and mice in residential, commercial, and business properties. In 2017, the CSA received 2,917 Requests for Service from the public about domestic rodents (2,282 re: rats and 635 re: mice), representing 38.9% of overall service requests. Those 2,917 rodent service requests had staff biologists performing 16,722 field services operations related to rodents. The field service operations included performing smoke and dye tests of sewer lines for breaks; field and residential surveys for rodent activity; recommendations and follow-up evaluations of rodent control measures; and assistance with enforcement actions. In 2017, a total of 8,150 sewer inspections and 1,531 applications of Contrac rodenticide bait were made in the City of Oakland. The CSA is now looking at incorporating rodenticide resistance testing, GIS data analysis, pulse-baiting strategies, and disease surveillance as part of an Integrated Pest Management program as improvements in 2018.

Anticoagulant resistance was first discovered in UK Norway rats (Rattus norvegicus Berk.) in 1958 and has been present ever since. The possible detrimental impact of resistance on effective rodent control was quickly recognised, and, for almost three decades, extensive research was conducted on the geographical distribution and severity of anticoagulant resistance in UK rats. Various schemes for the eradication of resistant rats were also implemented. At first, surveys showed resistance only to the first-generation anticoagulants, such as warfarin, chlorophacinone and coumatetralyl, but, later, resistance to the more potent second-generation anticoagulants, such as difenacoum and bromadiolone, was also discovered. Unlike some European countries, where only one or two resistance mutations occur, virtually all known rat resistance mutations occur in the United Kingdom, and five (Leu128Gln, Tyr139Ser, Tyr139Cys, Tyr139Phe and Leu120Gln) are known to have significant impacts on anticoagulant efficacy. Little is currently known of the geographical extent of anticoagulant resistance among Norway rats in the United Kingdom because no comprehensive survey has been conducted recently. At an operational level, anticoagulants generally retain their utility for Norway rat control, but it is impossible to control resistant rats in some areas because of restrictions on the use of the more potent resistance-breaking compounds. This paper reviews the development of resistance in Norway rats in the United Kingdom, outlines the present situation for resistance management and introduces a new resistance management guideline from the UK Rodenticide Resistance Action Group.

The aim of this study was to develop a quick, simple and inexpensive anticoagulant rodenticide resistance test method. The blood clotting response (BCR) test for resistance to chlorophacinone-Na in Mongolian Gerbils was prepared using small-volume blood samples. The normal Prothrombin time for Mongolian Gerbils was 9.92 ± 0.96 s using MDC Haemostasis thromboplastin-s (ISI: 1.86) reagent. Percent coagulation activity (PCA) calibration curves fitted the S curve and the PCA of 17% was found to correspond to a coagulation time International Normalized Ratio of 2.5. Dose–response baselines for BCR were obtained using susceptible Mongolian Gerbils and the ED99 values estimated for a quantal response were 0.27710 mg kg−1 for males and 0.26228 mg kg−1 for females. Based on the BCR test for resistance in wild Mongolian Gerbils from Zhenglanqi, Zhengxiangbaiqi, Kezhen in the Inner Mongolia Autonomous Region, we found that the populations of three areas have developed chlorophacinone-Na resistance populations with r...

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.

Central Eastern Asia, foremost the area bordering northern China and Mongolia, has been thought to be the geographic region where Norway rats (Rattus norvegicus) have originated. However recent fossil analyses pointed to their origin in southern China. Moreover, whereas analyses of fossils dated the species' origin as ∼ 1.2-1.6 million years ago (Mya), molecular analyses yielded ∼ 0.5-2.9 Mya. Here, to study the geographic origin of the Norway rat and its spread across the globe we analyzed new and all published mitochondrial DNA cytochrome-b (cyt-b; N = 156) and D-loop (N = 212) sequences representing wild rats from four continents and select inbred strains. Our results are consistent with an origin of the Norway rat in southern China ∼ 1.3 Mya, subsequent prehistoric differentiation and spread in China and Asia from an initially weakly structured ancestral population, followed by further spread and differentiation across the globe during historic times. The recent spreading occurred mostly from derived European populations rather than from archaic Asian populations. We trace laboratory strains to wild lineages from Europe and North America and these represent a subset of the diversity of the rat; leaving Asian lineages largely untapped as a resource for biomedical models. By studying rats from Europe we made the observation that mtDNA diversity cannot be interpreted without consideration of pest control and, possibly, the evolution of rodenticide resistance. However, demographic models explored by forward-time simulations cannot fully explain the low mtDNA diversity of European rats and lack of haplotype sharing with their source from Asia. Comprehensive nuclear marker analyses of a larger sample of Norway rats representing the world are needed to better resolve the evolutionary history of wild rats and of laboratory rats, as well as to better understand the evolution of anticoagulant resistance.

We report on a genome-wide scan for introgression between the house mouse (Mus musculus domesticus) and the Algerian mouse (Mus spretus), using samples from the ranges of sympatry and allopatry in Africa and Europe. Our analysis reveals wide variability in introgression signatures along the genomes, as well as across the samples. We find that fewer than half of the autosomes in each genome harbor all detectable introgression, whereas the X chromosome has none. Further, European mice carry more M. spretus alleles than the sympatric African ones. Using the length distribution and sharing patterns of introgressed genomic tracts across the samples, we infer, first, that at least three distinct hybridization events involving M. spretus have occurred, one of which is ancient, and the other two are recent (one presumably due to warfarin rodenticide selection). Second, several of the inferred introgressed tracts contain genes that are likely to confer adaptive advantage. Third, introgressed tracts might contain driver genes that determine the evolutionary fate of those tracts. Further, functional analysis revealed introgressed genes that are essential to fitness, including the Vkorc1 gene, which is implicated in rodenticide resistance, and olfactory receptor genes. Our findings highlight the extent and role of introgression in nature and call for careful analysis and interpretation of house mouse data in evolutionary and genetic studies.

The action necessary for resistance management is specified and compared with what has actually been done, with reference to executive, extension and research activities and to the role of rodenticides and rodenticide development. Some obstacles to resistance management are discussed. To account for the fact that no plausible programme to manage resistance has been developed over the last 36 years, the hypothesis is examined that resistance management is injurious to the parties concerned and, hence, that resistance is perceived not as a problem but as an exploitable asset. If correct, this hypothesis yields the prediction that the action necessary for resistance management will be taken when such action is judged to be economically efficient. The establishment of the Rodenticide Resistance Action Committee indicates that this time may be approaching.

BACKGROUND: Nucleotide polymorphisms in the VKORC1 gene can be linked to anticoagulant rodenticide resistance in Norway rats (Rattus norvegicus Berkenhout). This provides a fitness advantage to rats exposed to anticoagulant actives, but may also cause fitness costs. The vitamin K requirement and reproductive parameters of bromadiolone-resistant rats (Westphalian resistant strain; VKOR variant Tyr139Cys) and bromadiolone-susceptible Norway rats were compared. RESULTS: At vitamin K deficiency, blood clotting times increased in all homozygous resistant males within 8 days and in 80% of homozygous resistant females within 15 days. There was little effect on blood clotting in heterozygous males and no effect in heterozygous females and VKOR wild-type individuals. Litter size was about 20% higher in sensitive pairs compared with resistant pairs. Testes growth, male gonad weight, sperm motility and testis cell concentration were unaffected by the mutation. CONCLUSIONS: The VKOR variant Tyr139Cys causes considerable physiological cost in Norway rats in terms of vitamin K requirement and reproduction. This may affect the distribution and spread of resistant individuals in the wild. Decreased litter size of resistant parents seems to be due to lowered female reproductive performance, as there was no significant effect of the mutation on any aspects of male reproduction considered, but this requires further study

Procedures are described which have been developed by the New York State Department of Health for evaluating anticoagulant rodenticide resistance in project cities of the U.S. Urban Rat Control Program. After several years of preliminary study, it has become necessary to set more rigorous standards for the manner in which rats are collected for testing. The statistical background is described in conjunction with the guidelines for planning the trap-sampling program to be used by the project cities. The procedures are designed specifically for accumulating data on urban rat populations in a statistically sound manner. That is, the rats will be trapped in sufficient numbers and in a well-distributed fashion, so as to be representative of the greater urban rat populations from which they come. Additional details are given concerning the basic statistical analysis of the data obtained from the sampling procedures. The methods described should be easy to follow and are generally applicable to the assessment of anticoagulant resistance in rodents in urban areas throughout the world.

Author(s): Frantz, Stephen C.; Madigan, Constance Padula | Abstract: Roughly 50 years ago, the Wisconsin Alumni Research Foundation developed warfarin, the first anticoagulant rodenticide. This product was something close to that desired elusive "magic bullet" of pest management. Warfarin effectively killed rats and mice, required multiple feedings, and had a good margin of safety for non-target species. The widespread adoption of anticoagulants somewhat changed the conduct of rodent control with a shift in interventions toward toxicants and away from education and physical measures. The discovery of warfarin resistance in the United States in Rattus norvegicus in 1971, and later in Mus musculus and Rattus rattus, heralded in another shift in rodent pest mitigation. This shift was the development of more toxic anticoagulant products capable of killing with one or a few feedings and with concomitantly greater risks to non-target species. Development of the more toxic products both anticoagulant and non-anticoagulant continues today, although there is an increasing trend favoring comprehensive approaches (i.e., integrated pest management [IPM]) which: emphasize educating clients and reducing causative conditions; diminishing the role of toxicants; and, when necessary, using products of the least practical toxicity. In this paper, the concept of counteracting anticoagulant resistance is blended with the sometimes necessary use of anticoagulant rodenticides as part of IPM. Nationwide data from the former New York State Department of Health Rodent Control Evaluation Laboratory (in cooperation with the Centers for Disease Control’s former Urban Rat Control Program) are examined regarding warfarin resistance in Rattus norvegicus. In samples from two dozen project cities, population resistance levels ranged from 1.6% to 76.2% using the standard World Health Organization (WHO) testing criteria. However, most survivors (i.e., resistant rats) of the initial test succumbed upon one or more re-exposure(s) to warfarin using the same WHO testing protocol. The results are surprising and have implications on interpreting the phenomenon of anticoagulant rodenticide resistance and on the pragmatic designing of rodent management programs.

Background Bartonella spp. are vector-borne pathogens transmitted to humans via blood-sucking arthropods. Rodents such as the black rat (Rattus rattus) and Norway rat (R. norvegicus) are thought to be the main reservoirs. An infection with rodent-associated Bartonella spp. may cause severe symptoms in humans such as endocarditis and neuroretinitis. The current knowledge of Bartonella prevalence in rats from western Europe is scarce. Methods Rats and a few other rodent by-catches were trapped in the context of a rodenticide resistance study at different sites in Flanders, Belgium. During dissection, biometric data were collected, and spleen tissues were taken. DNA was extracted from spleen samples and tested for Bartonella spp. by conventional generic polymerase chain reaction (PCR). To determine the Bartonella species, a selected number of amplicons were sequenced and compared with GenBank entries. Results In total, 1123 rodents were trapped. The predominate species was R. norvegicus (99.64%). Other rodents trapped included: two water voles (Arvicola amphibius, 0.18%); one colour rat (R. norvegicus forma domestica, 0.09%); and one muskrat (Ondatra zibethicus, 0.09%). PCR analysis of 1097 rodents resulted in 410 (37.37%, 95% CI: 34.50–40.31%) Bartonella spp. DNA-positive samples. Bartonella tribocorum (94.68%, 95% CI: 88.02–98.25%) was the most frequently detected Bartonella species, followed by B. grahamii (3.19%, 95% CI: 0.66–9.04%) and B. doshiae (1.06%, 95% CI: 0.03–5.79%). An uncultured Bartonella species occurred in one water vole (1.06%, 95% CI: 0.03–5.79%). There was a significantly higher Bartonella prevalence in older rats compared to juveniles and a significant difference in Bartonella prevalence concerning the localisation of trapping sites. In contrast, there was no statistically significant difference in Bartonella prevalence regarding sex, degree of urbanisation and season. Conclusions Based on the high prevalence found, we conclude that the Norway rat seems to be a key reservoir host for zoonotic B. tribocorum in Belgium.

In the Norway rat, Rattus norvegicus, anticoagulant rodenticide resistance is mainly associated with mutations in the third exon of the Vitamin K epoxide reductase complex subunit 1 (VKORC1). Identification of the resistant wild populations is very important to improve the control practices and to limit the damages due to inadequate use of the anticoagulant rodenticide. In this study, we determined the distribution of the third exon mutations in poorly investigated areas of Africa, Europe and the Middle East. In particular, we investigated the phenomenon for the first time in the Italian peninsula. We obtained sequences of the third exon for 133 Norway rats from 37 localities in Africa, Europe and the Middle East. For additional analysis, we retrieved information in literature on amino acid substitution in 1136 third exon sequences of Norway rats from Europe, the Far East, North America and South America. However, we found third exon mutations only in Europe and the Far East with the Y139F mutation shared between the two areas. Europe has the higher number of mutant individuals and Y139C mutation prevails. In Italy, we found a single missense mutation (I123S) in a Venetian locality. This homozygote mutation, is not know in literature to be associated with resistance, but it is very similar to a mutation that confers resistance in humans (I123N). This similarity and its high local frequency makes it a good candidate for future testing. Our results provide useful data to better understand the resistance phenomenon and to plan targeted control actions.