Which varroa treatment is best?
Why do you need to use several types?
How do they work anyway?
Will mites become resistant to them?
In this article scientist Dr Pablo German outlines the science-y stuff around how various varroa treatments work, and how likely mites are to becoming resistant to each one.
If you need a quick read, here is my non-science-y summary version first (caveat: always refer to the real deal for the total truth, this is just my layman's version!)
Apivar - works on the stress response of mites, slower acting than the previous, but mites develop resistance, although less than above.
Thymol - works in a few different ways at the same time, not all of which are fully understood, and therefore unlikely for mites to develop resistance, but not impossible.
Formic Acid - works in a few ways including on the mitrochondria of mites, and unlikely for mites to develop resistance.
Oxalic Acid - works by direct contact with the mites in ways that aren't entirely clear, and unlikely for mites to develop resistance.
Sugar Dusting - works physically, not very effective, no resistance likely.
Oil Fogging - only affects mites on bees and probably works physically, needs to be applied often, no resistance likely.
So, the short answer is - you need several different types of treatments to deal to varroa effectively.
Here's the full article:
This article was published in The New Zealand Beekeeper, May 2017, Volume 25, number 4.
VARROA TREATMENTS: MODE OF ACTION AND RESISTANCE
How do the different varroa treatments kill the mites? Why do they kill the mites and do not kill the bees? Can mites become resistant to a particular treatment? Do we care about answering all these questions?
Most beekeepers do care for several reasons. First, we have the natural curiosity of wanting to understand how things work. Second, the more we know about our varroa mite enemy and the weapons we use, the better we will be able to fight against it. Third, we want to understand what secondary effects the treatments may have on the bees. Finally, the mode of action can give clues about the ability of the mites to develop resistance against the treatments.
In spite of the importance of this topic, there are no good summaries on how different treatments affect the mites. There are also unsupported opinions circulating on the Internet.
In this article, I review the scientific literature and summarise the mode of action of different varroa treatments as the knowledge currently stands. Some of the treatments act as the chemicals are absorbed within the body of the mite, others have direct physical effects upon contact, and others stimulate defensive behaviours from the bees.
Figure 1. Tau-fluvalinate.
Figure 2. Flumethrin.
The reason why tau-fluvalinate and flumethrin are such powerful weapons against varroa is that these compounds have a high affinityfor the varroa mite voltage-gated sodium channel. Interestingly, a recent study reported that tau-fluvalinate has even higher affinity for the honey bee voltage-gated sodium channel. The established safety profile of flumethrin in bees suggests that the bees have detoxification mechanisms that prevent the harmful effects. The high affinity for one single target makes tau-fluvalinate and flumethrin very effective at killing the mite, while at the same time being relatively safe for humans.
Unfortunately, this high affinity for one single target also enables mites to become resistant to tau-fluvalinate and flumethrin with a single DNA mutation in the voltage-gated sodium channel. Random mutations occur all the time, so one single DNA mutation in one gene is an event likely to occur when thousands of mites are breeding in one single beehive.
In the presence of tau-fluvalinate and flumethrin, only mites with specific mutations in the voltage-gated sodium channel are able to survive and continue reproducing. The relatively high likelihood of a single mutation in a single gene to occur, explains why resistance to tau-fluvalinate and flumethrin has been broadly reported around the world. In fact, several single mutations in the voltage-gated sodium channel have been identified that produce tau-fluvalinate- and flumethrin-resistant varroa mites.
Figure 3. Amitraz.
A similar stress response occurs in insects and mites when octopamine is released, which binds to the octopamine receptors. Amitraz seems to act by binding to the octopamine receptor(s), which leads to an acute stress response with different effects in insects and mites.
Most beekeepers have noticed that amitraz is slower at killing mites than flumethrin, for example. The reason for this seems to be that by causing this stress response, the mite does not die immediately but its behaviour is completely altered, which leads to death later on. Amitraz is said to act by sub-lethal effects rather than by lethal effects. Humans, and in fact all vertebrates, do not have octopamine receptors, which is the reason why amitraz is relatively safe for humans.
The relatively slow and low onset of varroa mite resistance to amitraz—when compared to resistance to flumethrin for example— seems to indicate that amitraz acts on more targets than just one type of octopamine receptor. Indeed, resistance to amitraz has been reported in fewer cases than the previous two miticides, and studies have shown that the level of resistance is lower as well (the dose of amitraz needed to kill amitraz-resistant mites is not that much higher). In fact, amitraz is still the most effective miticide used in the USA, despite resistance having been reported two decades ago. This seems to point to the fact that one single mutation in one gene is not enough to provide resistance. Although point mutations in amitraz-resistant organisms have been identified, evidence from a cattle tick indicates that resistance to amitraz occurs both by mutations in the octopamine receptor and enhanced metabolism in getting rid of amitraz. In spite of the lower resistance to amitraz by the varroa mite, alternating amitraz with other treatments is still necessary.
Figure 4. Thymol.
The presence of multiple targets for thymol makes it more difficult for resistance to occur. In fact, there are no published reports of mite resistance to thymol. This does not mean that resistance to thymol is impossible. One way in which resistance could arise would be by improvement in the detoxification system of the mite. Therefore, it is still best practice to alternate thymol with other treatments.
Figure 5. Formic acid.
What happens when mitochondria in the mite are disrupted? Mitochondria are present within cells and carry out cellular respiration and energy production. When the mitochondria are disrupted, the cells cannot function. This probably leads to neurotoxic effects by disrupting the mitochondria in the neurons and inhibition of respiration. Formic acid seems to cause mitochondria disruption by the physico-chemical effects of low pH.It has been suggested that the bees have higher metabolic and buffering capacity against the acid, which explains why formic acid affects mites more than bees. This mode of action suggests that resistance is not likely to occur as several changes would be needed in the mite. No mite resistance to formic acid has been reported.
Figure 6. Oxalic acid.
Given that oxalic acid has been shown to affect mitochondria in mammals and that mitochondria are sensitive to acids, it is possible that oxalic acid also affects the varroa mite by disrupting or affecting mitochondrial function. In any case, a physico-chemical mode of action would explain why there have been no reports of mites resistant to oxalic acid.
Food-grade mineral oil
The synthetic chemicals are absorbed by the mite and tend to affect one single protein target, such as the voltage-gated sodium channel (flumethrin and fluvalinate) and octopamine receptors (amitraz). This specificity on single targets makes it highly likely that the mites will develop resistance by mutations in those targets, as has indeed been reported for all of them. In addition, mites can also develop resistance with detoxification enzymes that degrade or get rid of these chemicals from the body.
The organic chemicals act by absorption or direct contact and seem to act by physico- chemical effects on more than one target, making them less specific against varroa mites. This is a logical consequence of the fact that these chemicals are synthesized by plants to fight against different types of insects and pests and not against mites in particular. Indeed, thymol seems to act by affecting octopamine, tyramine, and GABA receptors, formic acid disrupts the mitochondria in cells, perhaps as a consequence of low pH, and oxalic acid may also act by affecting mitochondrial function. The action on more than one target or by physico-chemical effects that disrupt cell structures makes resistance to these treatments less likely. In fact, there are no reports of resistance to these treatments. However, alternation with other treatments is still recommended.
Finally, the less-popular icing sugar and food- grade mineral oil treatments seem to affect the mite by physical effect due to the direct contact and by stimulating bee grooming behaviours. This means that resistance to these treatments is very unlikely to arise.
Complete article with references is available on request from the author at firstname.lastname@example.org.