{"id":36991,"date":"2024-03-05T15:37:19","date_gmt":"2024-03-05T04:37:19","guid":{"rendered":"https:\/\/professionalpestmanager.com\/?p=42475"},"modified":"2024-03-19T19:27:00","modified_gmt":"2024-03-19T08:27:00","slug":"rodenticide-resistance-an-overview","status":"publish","type":"post","link":"https:\/\/professionalpestmanager.com\/nz\/rodent-control\/rodenticide-resistance-an-overview\/","title":{"rendered":"Rodenticide Resistance \u2013 An Overview"},"content":{"rendered":"

If a rodent control program fails, is it a case of rodenticide resistance? An overview of rodenticide resistance \u2013 history, incidence, mechanism and more.<\/em><\/p>\n

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As with all pesticide use, the potential for rodent populations developing resistance to rodenticides is very real. But before jumping to a conclusion that the non-performance of a rodent program is due to rodenticide resistance, it is important to exclude other potential factors for non-performance. Are the rodents actually taking the bait? Is enough bait being provided? Are additional rodents entering from outside the treatment area? If all other reasons for treatment failure can be excluded and there is repeated failure of different rodent baits on site, then rodenticide resistance may be a cause. Resistance can only be confirmed through laboratory testing and DNA analysis.<\/p>\n

Here we take a closer look at rodenticide resistance around the world (including Australia and New Zealand).<\/p>\n

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First Generation Anticoagulant Rodenticides (FGARs)<\/strong><\/h2>\n

First generation anticoagulants (warfarin, diphacinone, coumatetralyl and chlorophacinone) became widely available in rodenticide baits in the 1950s. These rodenticides impacted the vitamin K cycle resulting in excessive bleeding and death over a period of days. It is generally necessary for rodents to have multiple feeds on an FGAR bait to ingest a lethal dose. Consequently, it is not uncommon for some rodents in a population to receive a sub-lethal dose, which in turn can aid in the development of rodenticide resistance.<\/p>\n

It was therefore not a surprise that before the end of the 1950s the first cases of resistance in the Norway Rat (Rattus norwegicus<\/em>) were reported in Scotland. Over the following years, reports of resistance to warfarin and the other FGARs increased across Europe.<\/p>\n

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Second Generation Anticoagulant Rodenticides (SGARs)<\/strong><\/h2>\n

The 1970s and 1980s saw the development of the Second Generation Anticoagulant Rodenticides (SGARs). The first SGARs developed were bromadiolone and difenacoum. Although they had the same mode of action as the FGARS, they were significantly more potent. However, reports of resistance to baits containing these actives started appearing in the late 1970s in Europe. However, no resistance to bromadiolone or difenacoum has been reported in Australian or New Zealand.<\/p>\n

The more recent and more potent SGARs, brodifacoum, flocoumafen and difethialone, were introduced later as \u2018resistance breakers\u2019. To date, there have been no reported cases in the field of resistance to rodent baits containing these rodenticides in either Norway rats or house mice.<\/p>\n

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\"Rodent
SGARs were designed to be ‘resistance breakers’<\/figcaption><\/figure>\n

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Mechanism of rodenticide resistance<\/strong><\/h2>\n

The mechanism of resistance to anticoagulant rodenticides is due to a mutation on the gene (Vkorc1) encoding for the vitamin K epoxide reductase (VKOR) enzyme. The VKOR enzyme is essential in activating vitamin K for its involvement in blood coagulation. Anticoagulants bind to this enzyme preventing it activating vitamin K and therefore preventing blood coagulation, which results in excessive bleeding and death. Mutations on the VKOR enzyme present in resistant rodents prevent the anticoagulants binding to the enzyme and therefore still allow the VKOR enzyme to do its job in the blood coagulation process, even in the presence of the anticoagulant rodenticide, rendering them less effective.<\/p>\n

There are a number of different mutations of the VKOR enzyme, each of which confer different levels of resistance.<\/p>\n

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\"Roof
Rodenticide resistance is more likely to occur in areas of high rodenticide use<\/figcaption><\/figure>\n

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Resistance to non-anticoagulant rodenticides<\/strong><\/h2>\n

As is the general nature of pesticide resistance, non-anticoagulant rodenticides \u2013 such as bromethalin, cholecalciferol and zinc phosphide \u2013 remain effective against anticoagulant-resistant rodents. Further, there are no reported incidences of resistance to these actives with their differing modes of action.<\/p>\n

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Measuring resistance and resistance maps<\/strong><\/h2>\n

In cases of suspected rodenticide resistance (i.e. repeated failure of correctly applied baiting programs when baits have been consumed), resistance can only be confirmed through DNA testing. This is typically achieved by the pest manager taking the tip of the tail of a recently deceased rodent and sending it to a suitable laboratory. In a number of countries, especially in Europe, the process for this is well established and laboratories will perform the necessary tests.<\/p>\n

Apart from confirming resistance or otherwise in a particular population, the collection of data allows resistance maps to be generated for individual countries. The Rodenticide Resistance Action Committee (RRAC) \u2013 which is a working group with the framework of CropLife International, and includes the leading global rodenticide companies as participants \u2013 provides rodenticide resistance maps by country. Obviously, the quality of these maps depends on the amount of data generated in each country. Europe certainly has the most rodenticide resistance maps.<\/p>\n

Unfortunately, no such data is available in Australia and New Zealand. However, a recent study<\/a> in Western Australia analysed mouse populations from Perth (where there has been significant rodenticide used over an extended period) and Browse Island (where no anticoagulant rodenticides have been used). Surprisingly, no mutation was found on the gene encoding for the VKOR enzyme in either population \u2013 which indicates no evidence of resistance in these house mouse populations.<\/p>\n

Data on resistance in New Zealand is also somewhat limited, although a 2017 study on invasive rats across 30 sites found at least one species at each site contained gene mutations in the Vkorc1 gene. \u00a0Although only the roof rat, Rattus Rattus<\/em>, contained mutations of the gene that had previously been associated with anticoagulant resistance.<\/p>\n

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Rodenticide resistance by rodent species<\/strong><\/h2>\n

When it comes to rodenticide resistance, the focus is very much on the house mouse and Norway rat. These tend to be the more common rodents in the US and Europe where most of the research occurs. Data on levels of resistance in roof rat populations is very limited.<\/p>\n

The incidence of rodenticide resistance will vary depending on location. Clearly those areas where anticoagulant rodenticides have been used over an extended period will have a higher level of incidence. Urban areas and agricultural areas would be two obvious hotspots. To actual confirm levels of resistance, actual sampling needs to occur, and this is more limited. However, a recent countrywide study in the Netherlands found resistance genes in\u00a038% of house mouse and 15.3% of Norway rat populations.<\/p>\n

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Bait not being eaten? That\u2019s not rodenticide resistance!<\/strong><\/h2>\n

Rodents refusing to feed on baits is not evidence of rodenticide resistance. There are a number of reasons why rodents may not be taking a particular rodent bait, including:<\/p>\n