Anticoagulant resistance in the Norway rat and guidelines for the management of resistant rat infestations in the UK.
In September 2018, the Rodenticide Resistance Action Group released an updated report on the use of rodenticide to manage the Norway rat. The Norway rat is the most prolific and common rat one finds in the UK.
Rodenticide Resistance Action Group is mainly based out of Reading University.
The report can be found here. However below is a brief over view:
anticoagulant have been used successfully since the 1950s.
Took over from acute rodenticide use which could not reach shy and rapid recovery populations.
Key to the success of anticoagulant was how slow it worked on the Norway rat. Allowing rat over a number of days to consume a lethal dose.
The rats achieve surplus or sufficient poison over a longer period of time.
First brand was called Warfarin 1950s along with other first generation anticoagulants including diphacinone, coumatetralyl and chlorophacinone.
Development of resistance from the rat:
Resistance developed in the late 1950s and early 1960s in the Norway rat along with the house mouse.
Second generation poison was developed called: Difenacoum and bromadiolone. Both types needed saturation or surplus baiting techniques.
New baiting techniques needed along with stronger anti coagulants.
Developed pulse baiting of higher toxicity and less frequency of bait applied. The minimum time to death and the average time to death has not changed since the first generation of anticoagulants of between 14 - 28 days.
Higher toxicity of brodifacoum and flocoumafen increased the likelihood of non target species being affected. Thus restricted indoors. Along with difethialone.
Restricting the use of poison indoors drastically reduced the ability to control the infestation.
The types of resistance includes:
Technical resistance – this term is used in cases where resistance tests identify resistance but where resistance factors are low and the resistance has no observable practical effect.
Practical resistance – this term is used in cases where resistance tests identify resistance and resistance factors are sufficiently high so that an acceptable level of control is unlikely to be achieved.
Metabolic resistance – this is a form of resistance not conferred by a mutation in the VKORC1 gene (see table 1). Instead modified enzymes permit animals that possess this resistance to break-down and/or eliminate anticoagulants from the body more quickly.
|Leucine128Glutamine||L128Q†||Scotland, parts of NW and NE England|
|Leucine120Glutamine||Y139C†||Hampshire, Berkshire and else-where|
|Tyrosine139Phenylalanine||Y139F||Kent, Sussex and elsewhere|
| † Known either from field experiments and/or field experience to have a significant practical effect on antico-agulant efficacy.
‡ Known from laboratory experiments to confer warfarin resistance.
* Shown in laboratory experiments to have a significant impact on protein function.
# Unlikely to confer any significant degree of resistance.