Living with a Pest, 'Fight the mite' conference, Cardiff, IBRA

October 1996

It is 50 years since the Asian mite Varroa jacobsoni transferred to a new host, Apis mellifera the European honeybee, in Asia. There remains some debate about whether the Apis cerana mite and the A. mellifera mite are the same species but once on the new host the parasite’s spread to Europe and the Americas was assured. Although its introduction into Britain happened almost five years ago it had already been well established in much of Europe for a long time and once it was realised that the mite could have a real effect on the economy of European apicultural systems two things happened. First in many countries there was an concerted effort to stop the spread of the pest using both geographically based quarantine or stand-still orders and by co-ordinated regional treatments with synthetic pyrethroid pesticides. Secondly various research programmes began to look at the biology of the mite and the pathology of this new host-parasite relationship. The difficulty of controlling a pest we didn’t understand cannot be underestimated and now, 25 years on with the research beginning to bear fruit, it’s worth considering the strategies employed once more. At IBRA’s recent ‘Fight the Mite’ conference in Cardiff this October we had the opportunity to do just that.

Like all other European countries Britain seems to have no success in reducing the spread of the mite by restricting the movement of bees. Since 1992 and the discovery of the mite in Devon the restricted area has been extended several times to cover most of England and Wales and there is every prospect of further expansion. Even in a country where migratory beekeeping was not thought to be particularly extensive or essential Varroa has managed to extend its distribution unaffected by any notional border and there is no reason to suppose that ‘irresponsible beekeepers’ have caused this. In a country that can be traversed in a few hours bees and mites have all sorts of opportunities to travel. Treatment of the infestation too has had a rather mixed success. Despite the undoubted efficacy of the chemical recommended, flumethrin as Bayvarol strips from Bayer, a number of problems occurred. First, beekeepers found they were losing colonies even though they followed the treatment programme. Secondly the additional financial and logistical expense of the medicament was a disincentive to treat. Thirdly the danger of resistant mites developing had to be taken seriously with only one chemical being used in a blanket treatment programme regardless of the level of infection. Last, the problem of chemical residues in a natural product, both because the effect of low residual levels on pest resistance was not generally understood and because of the potential effects on the product’s image as of benefit to human health.

For years the anecdotal experience of Varroa has been confusing. Some treated colonies died out while other untreated colonies appeared to be resistant. Mite population estimates inferred by natural death rates were at best an unreliable measure of risk. The problem of reinfestation from feral sources late in the season was said to have been misjudged and late treatments were prejudicing the health of the wintering bees. Deformed bees appeared and disappeared and colonies collapsed in different ways and at different times. Given such unpredictable behaviour no one could be sure how effective the control of the pest was and the potential for unease and misinformation was only exceeded by the actual unease and misinformation. The latest results from the scientific professionals have a great deal to say about these problems. In the UK Dr Steve Martin from the National Bee Unit has been investigating diagnostic and monitoring methods for Varroa so that treatment strategies can be made more effective by understanding the population dynamics of the mite. Brenda Ball from the Insect Pathology Section at Rothamstead Experimental Station has shown that the cause of the colony’s death is not as simple as first thought and not entirely due to the mite. In Europe a great deal of research is being undertaken into types of treatment regimes or into the development of acarcide resistance and chemical residues.

We now seem to be very near to having an reliable model of the population growth of the mite in A. mellifera. There seems to be a direct relationship between the natural mite fall and the changing area covered by the bee’s brood nest so that true mite populations can be estimated using this relationship. We can be reasonably sure that it is the reproduction in drone cells that allows the mite populations to grow and that the number of reproductive cycles achieved, usually two or three, is crucial to the rate of growth. The tolerance shown by the natural host is due to some inbuilt restraint on the mite population. This seems dependant on a number of factors making selection in a breeding programme quite complicated. For example experiments suggest it may be that a substance in the workers pupal body inhibits the female mites’ egg production perhaps because one of A. cerana’s adaptations enables it to detect and remove the reproducing mite in worker cells. The viability of the first haploid male egg is also important. The egg must be laid high in the cell to prevent it being damaged by a still mobile larva and some are lost as part of the mite’s strategy to prevent lethal inbreeding. In A. cerana the male death rate is much higher than in A melifera, (84% vs 24%) possibly because of later mobility of the bee larva disturbing the first egg. It may be that the ‘resistance’ of Africanised A. mellifera bees is also because of a lower mite fertility rate due to factors such as these combined. Management of drone populations and brood stop techniques too would seem to have an enhanced role in the light of this research.

The work at Rothampstead has shown that the main cause of death in Varroa infested colonies has been virus infections. These have all been associated with bee colonies before but the mite has provided a new route for the viral particle’s entry and acts as a vector spreading the infection both within the colony and between colonies. It is highly probable that the variation in the response to Varroa infestations is due to the presence or absence of different types of viral pathogens. It is also possible to detect the viral infection after the Varroa mites have been removed and once established it will remain still causing the death of the colony. The first treatment programmes allowed a mite population to build and then attacked it with a single treatment. At the time it was thought that it was the large population of mites feeding on the bees that was causing the damage. However the direct effect of the mite feeding on the bee’s haemolymph seems minimal and future methods will have to limit the population of mites so that viral infections can’t become established. The symptoms of a viral infection are not clear but death of all stages of brood in midsummer has been noted. These infections are also responsible for the deformed wings and so on that appear in emerged bees. Testing mites for viruses can give an early indication of trouble as they can be detected in the mite as much as three months before they appear in bees.

In Britain the only recommended and registered treatment for Varroa infestations was the synthetic pyrethroid flumethrin supplied as a contact strip (Bayvarol) by Bayer. Although there has been some concern about residual contamination in hive products more often it was the danger of developing resistant mites that was being expressed. The next product likely to be registered and already imported by apiarists for their own use is another pyrethroid, tau-Fluvalinate (Apistan). Unfortunately the two products are essentially the same and once resistance to one synthetic pyrethroid has been established the mite will tolerate any other version too. There is some prospect of a third product becoming available based on the amidine Amitraz (Apivar) and this might enable effective rotation. Resistance to varroacides will depend on some members of the mite population having some chance genetic characteristic that allows them to survive a normally fatal dose of the poison. In Varroa, with the number of reproductive cycles (or generations) produced each year being as many as twelve, the possibility of the surviving resistant gene becoming the norm is high, especially where there is a constant pressure to select survivors. As far as we know the resistance depends on just one gene and this is probably a dominant gene. The best strategy to slow the actual expression of that gene in the whole population is to keep the selection pressure for dominantly resistant mites as high as possible and then remove it altogether. This will allow sensitive individuals to appear in the population again and ‘deselect’ the resistant gene, sensitising the population once more. To deviate from this strategy by using ill-considered or persistent pesticides with an uncertain dosing profile not only creates contamination of the beekeepers products but improves the chances of developing a resistant mite population. Both pyrethriod products have been designed with this strategy in mind but it is generally agreed that some rotation of treatments is a good thing, whether for a different chemical or for some physical (or biological) control, as this will prolong the efficacy of the pyrethroid products.

In both products the contamination of wax has been regarded as negligible but cumulative and the likely transfer to honey inestimably small. On occasions where residual fluvalinate has migrated to honey a different formulation of the product has been responsible. No migration of flumethrin has been shown. Never-the-less many beekeepers would prefer that the problem of residual chemicals be avoided altogether and so a great deal of effort has been put into developing alternative ‘biotechnical’ controls. At the moment of these the most successful of these rely on a physical control of the mite. The methods of applying organic acids as oxidising agents have been refined and provide good control, but rely on careful handling and accurate monitoring if they are to be safe and effective. Drone brood control, trap combs, nucleus formation and the like need a degree of beekeeping skill to use but also work well, especially in conjunction with another treatment. The disadvantage of biotechnical controls is said to be the extra effort involved. To an extent this is true but the significance of the labour cost of these techniques is exaggerated. The majority of British beekeepers, in common with many Europeans, keep less than five hives so small additional increments of time have little effect. A more judicious approach to the use of chemical controls by these beekeepers would slow the development of resistant mites and prolong the effective life of the chemical products for all beekeepers. The use of essential oils is proving to be effective too but its not clear whether by a chemical or a physical activity. If their action is chemical then the same kind of concerns about resistant and residual contamination apply but it can be argued that the products are more benign and less persistent. So far however, especially in a temperate climate, control of the dose has been difficult and strict monitoring of the results is needed. With very little idea about how these oils work most experimentation has been by trial and error. Consequently it’s very difficult to formulate successful treatment methods that are independent of the beekeepers skill or the bees’ environment and produce reliable, consistent, cost effective results. The only commercial essential oil treatment available now is the Italian Apilife-VAR.

Only proper targeting of the treatment and integration of control methods into apiary management can reduce any additional costs incurred as a result of Varroa infestations. The strategy we employ needs to take account of the latest research in order to achieve this. Beekeepers vary enormously, from the experienced commercial men to the one hive novice. The methods used must vary and be appropriate and to recommend one requiring experience and skill which is clearly lacking jeopardises an individual’s bees and threatens the entire control strategy. Our practical experience and the research suggest a continual assault on the mite population is what is effective and that this should consist of permanent physical and chemical restraints on the mite’s reproduction. Such a programme could not be sustained were it not for our ability to change treatments so beekeepers must be familiar with using the full complement of weapons at our disposal.