EXPLODING THE VITAMIN K - RODENTICIDE RESISTANCE MYTHOLOGY
Sharon Hughes, Rodenticide Development Manager, Sorex
Under the sheer pressure of this season's overwhelming rat populations, it's certainly tempting to blame increased rodenticide resistance problems linked to vitamin K levels in animal feeds and pet foods for less than ideal control.
However, a detailed investigation of the science and the results of our latest research clearly shows that the vitamin K found in the overwhelming majority of alternative food sources to which even farm rats may have access can have no significant effect on the potency of modern anticoagulant baits.
The theory that additional dietary vitamin K could allow rats and mice to overcome the effects of second generation anticoagulant rodenticides like difenacoum, brodifacoum and bromadiolone is entirely plausible. After all, they have long been recognised as working by disrupting the normal recycling of vitamin K. And vitamin K continues to be used as a successful antidote to anticoagulant rodenticide poisoning in human and veterinary medicine.
Major differences in the type and level of the vitamin concerned, however, makes the suggestion that vitamin K in animal feeds could be having a negative effect on the potency of anticoagulants extremely unlikely.
To start with the vitamin K used with great effect in overcoming accidental rodenticide poisoning in pets and humans is vitamin K1 (2-methyl-3-phytyl-1, 4,naphthoquinone) which occurs naturally in green plants.
In marked contrast, the similar but different synthetic form, vitamin K3 (2-methyl-1,4, naphthoquinone) used to supplement animal feeds has been proven to be far less effective in combating rodenticide poisoning and of no practical value as an antidote.
Equally, treatment with even the valuable antidote, vitamin K1 at rates of 5 mg/kg (5 ppm) or more over a prolonged period is necessary to combat rodenticide poisoning. Yet analysis of modern pig and poultry feeds shows typical levels of the less effective vitamin K3 at under 0.05 and 1.0 mg/kg (0.05 – 1.0 ppm) respectively despite original inclusions of 5 mg/kg – primarily due to losses during processing. And cattle and sheep feeds are not supplemented at all because ruminants obtain sufficient vitamin K from a combination of green forages and their own bacterial manufacture.
Even so, CSL studies by MacNicoll in the late ‘Eighties and early ‘Nineties continue to be used as the basis for suggesting a link between vitamin K levels in animal feeds and poor rodenticide efficacy.
These studies actually showed vitamin K3 had absolutely no effect on the survival of
anticoagulant susceptible rats or either susceptible or resistant house mice.
What is more, they only showed an increase in the apparent survival of resistant strains of Norway rats when fed at fully 5 mg/kg in the diet. No increases in the survival of even these strains were evident at less extreme supplementary vitamin K3 rates of either 1 or 2 mg/kg.
It was against this background that we recently undertook a series of studies with both second-generation anticoagulant tolerant and susceptible rates to establish the extent of any relationship between vitamin K availability and difenacoum potency.
We used male and female rats from a known second-generation anticoagulant tolerant strain and anticoagulant susceptible males housed in wire cages to prevent them obtaining any supplementary vitamin K from consuming their own faeces. At the end of the trial period, we took blood samples and measured their clotting times under a standard protocol for assessing rodenticide potency.
To examine any antidotal effect of dietary vitamin K we supplemented the rations of the
rats with 5 mg/kg vitamin K3 for three days before and three days after treating them with difenacoum.
As in the earlier CSL studies, the vitamin supplementation had no effect on the potency of the rodenticide in the susceptible rats. Although clotting times were reduce slightly, even at the lowest doses of difenacoum used (5.0 mg/kg in males and 7.5 mg/kg in females) we could measure no significant effect from vitamin K3 supplementation in anticoagulant resistant rats either.
These findings reinforce University of Reading investigations by Hussain showing no detectable effect of vitamin K3 on either susceptible or resistant rats treated with warfarin or bromadiolone unless at levels of anticoagulant intake so low as to be sub-lethal anyway. And this at vitamin supplementation levels far in excess of those ever likely to be consumed by rats even if fed exclusively on animal feeds containing the highest stated vitamin K3 inclusions.
We also examined the extent to which vitamin K deficiency might affect the potency of difenacoum in a separate study with the same anticoagulant tolerant and susceptible rat strains by denying them both vitamin K1 and vitamin K3 for three days before and after difenacoum treatment.
Interestingly, we found the withdrawal of all vitamin K enhanced the potency of difenacoum in both the male and female anticoagulant tolerant rats, more obviously in the males – presumably as a result of their lower inherent reservoirs of the vitamin. Difenacoum potency was also increased by vitamin K deficiency in the anticoagulant susceptible rats but to a much lesser extent.
Our findings dispel the notion that vitamin K in animal feeds could have any effect on the potency of anticoagulant rodenticides in practice, showing that even at levels far above those typically present in the feeds there is no significant diminution of the effect of difenacoum.As well as finding pig and poultry diets far lower in actual vitamin K3 levels than typical inclusion rates would suggest, our analysis of the standard laboratory diet used as a control
in these studies established an actual vitamin K3 content of just 0.66 mg/kg as fed compared with a nominal content of 30 mg/kg. This reinforces the extent to which feed production processes – especially pelleting – reduce the content of relatively easily degraded vitamins.
The results from our vitamin K withdrawal study are consistent with the understanding that second-generation rodenticide resistant rats have a greater requirement for vitamin K in their diets than susceptible populations; a weakness that might usefully be exploited in achieving more complete control in some cases.
Equally, they support the observation that female rats in anticoagulant tolerant populations appear to have greater resistance to rodenticides than males by virtue of a greater ability to store vitamin K.
So if vitamin K is not to blame for the increase in apparent treatment failures found by many over the past winter in particular, what is causing it.
It could, of course, be due to an increasing number of resistant populations. However, the fact that second-generation anticoagulant resistance has remained confined to a relatively small number of specific areas of England since it was first reported 30 years ago suggests a sudden upsurge in physiological resistance is most unlikely. Especially so given the fact that resistant individuals are known to be less competitive as a result of lower growth rates and increased susceptibility to vitamin K deficiency.
Instead, we must look to the most common causes of reported treatment failure we invariably find in practice, including large populations overwhelming bait supplies, insufficiently palatable or potent baits, abundant alternative food sources, and re-invasion from adjacent areas.
The sheer pressure of rat infestations seen by many this season as a result of the poor control achieved in the very mild winter of 2006/7 and substantial population growth over the warm spring and summer will undoubtedly have compounded any deficiencies in rodenticide treatment practice.
For instance, bait takes in many places have been so much higher than normal that, unless topped up every week, many baiting points are likely to have been depleted before all the individuals in a population have had a chance to consume lethal rodenticide doses. And we know that under favourable conditions survival rates of only 20% allow treated populations to re-establish themselves in little more than a month.
We also know that the very best way of combating resistance development is to pay scrupulous attention to the very best, behaviour-led control practices based on the most appealing and reliable baits, and the most effective and consistent baiting.
<< Back to Rodent NewsPrint this page