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Found 17 results

  1. View Offer Nassenheider Proffesional Total height is now 70mm only - therefore it even fits into a feeder, turned upside down! The tank is a bottle - You can fill it under optimal safety conditions in your workshop and transport it closed to the bee yard. The tank capacity is now 290 ml, enough to treat even the biggest hives with formic acid, without the need of filling it up again. The whole Evaporator is a compact item. The horizontal wick lies inside a tray, to save the young brood from the concentrated formic acid-fumes and liquid acid. The evaporator is standing absolutely stabile inside the tray. Innovation: Two drip trays plugged together allow the clean and convenient storage of the evaporator with accessories until the next season. Price 25.00 NZD Submitter Manfred Submitted 08/05/19 Category Commercial Produce For Sale
  2. Total height is now 70mm only - therefore it even fits into a feeder, turned upside down! The tank is a bottle - You can fill it under optimal safety conditions in your workshop and transport it closed to the bee yard. The tank capacity is now 290 ml, enough to treat even the biggest hives with formic acid, without the need of filling it up again. The whole Evaporator is a compact item. The horizontal wick lies inside a tray, to save the young brood from the concentrated formic acid-fumes and liquid acid. The evaporator is standing absolutely stabile inside the tray. Innovation: Two drip trays plugged together allow the clean and convenient storage of the evaporator with accessories until the next season.
  3. This article was originally published in 2015 Everybody needs to look over the fence once in a while, especially beekeepers. Something that caught my eye recently was a study looking at weeds and glyphosate resistance, a study which itself took a glance over the palings at antibiotic resistance in hospitals. Resistance is not a phenomenon unique to beekeeping, it is universal and, at its simplest, just about how organisms adapt and evolve in their environment. From our point of view, when we think about resistance, the aspect that concerns us most often is varroa mites not disappearing after we have treated the hive with a substance that usually kills them, and usually we’re talking about the efficacy of the two synthetic pyrethroids used to treat the pest, Apistan and Bayvarol. Pyrethroids have a long history and it was never in doubt that varroa mites would adapt to the treatment. Pyrethroids are copies of naturally occurring esters from Chrysanthemum flowers. What we call pyrethrins were first used as insecticides in the first century in China. They were used in Europe more than 200 years ago and in commercial production by the mid-19th century. Although effective, they were expensive to produce and quickly degraded by light and air, so by 1924 chemists began making ‘synthetic’ copies which were more stable and better suited to one pest or another, or to different ‘delivery systems’. By the 60s and 70s many variants had been produced, including deltamethrin, at the time the most active insecticide ever produced. Apistan and Bayvarol are different pyrethroids, called tau-fluvalinate and flumethrin respectively, which differ in the construction of one end of the molecule. One of life’s ironies (one of my favourites) finds that the ‘natural’ pyrethrins, the synthetic pyrethroids, and the environmentalist’s bête noire, DDT, are all much the same when it comes to their effect on arthropod pests. All of them affect the normal transmission of nerve impulses along the nervous system by stopping the exchange of sodium and potassium ions across an impermeable membrane through a special ‘channel’. (If you’re interested look up ‘voltage gated sodium channels’). What resistant pests have done is to modify the sodium-channel proteins so the insecticide can’t bind to the site. Different pests have modified different proteins, but resistance is extraordinarily common; whitefly, cockroaches, fleas, lice, mosquitos, flies, aphids, thrips, and many others have all evolved resistance to pyrethroids and DDT, to a greater or lesser extent. Known as ‘knockdown’ resistance (knockdown being the excited but paralysed state caused by the nerve disruption) it was first recognised in 1951 in house flies. When we add a treatment to our hives we alter the environment in the hive, hoping that the bees can still flourish but that the things we don’t want die or can’t reproduce. In this sense varroa mites are analogous to the weeds I mentioned at the start. Weeds, and mites, adapt to pesticides in various ways. Besides changing their behaviour (avoiding the chemical for instance) pests can slow or stop the chemical getting into their body, or store it up where it can’t do any damage; they can use enzymes to destroy the active ingredient, or they can change the site or process the chemical is able to disrupt. It’s important to realise these changes come at a cost, sometimes a very high cost, sometimes a very low cost, and rarely, sometimes with an added advantage. For example, a bacteria may construct a thicker ‘skin’, but it will have to use more resources to do so. As long as it faces a threat from the chemical it’s worth doing that, but in an environment where the threat no longer exists if there is extra ‘effort’ involved it’s wasted, and puts the ‘resistant’ organism at a disadvantage compared with an organism that doesn’t bother. For any particular adaption it’s important to understand the cost of that adaption if we want to understand how long-lived and pervasive that adaption will become. Complex, costly changes are easily lost when they are unnecessary; simple, cheap alterations are likely to remain. The science looking at pyrethroid resistant mites has been able to describe in pretty good detail what genes are involved and what they do to allow make mites less sensitive to the chemical. This type of chemical and it’s mode of action is pretty well understood as it been in widespread use for a long time. Around four amino acid substitutions have been proposed in the case of varroa’s pyrethroid resistance. So far, it looks as though the metabolic cost of this adaption to pyrethroids comes at a very low cost for mites, and no differences in ‘fitness’ (for their environment) has been observed between resistant and non-resistant mites. So far, there is very little evidence that regression to a predominately non-resistant strain occurs within a reasonable period of time if pyrethroid treatments are suspended, and that also suggests the cost of carrying the adaption is relatively low. There is not a lot of data about the incidence and spread of resistant mites. Beekeepers aren’t looking for resistance, even though it is simple to do so, and often the only clue is the unexplained loss of treated colonies. Ascribing the cause of the collapse to resistant mites is a long bow to draw however and so usually the cause is hidden by the many plausible reasons for a colony dying. On the large scale however, we do have a picture, and wherever we have looked we can see that the spread of ‘resistance’ replicates the same route that the original mite invasion took; a slow local spread accompanied by an occasional ‘long-distance’ hop. That’s no surprise, mites can’t survive and travel without a bee host, and so the spread of the resistant variety relies on the movement of bees and their colonies, and the same ineffective phytosanitary regimes that permitted the original spread of the pest. It’s also no surprise because that is what happened with other examples of resistance. We will have to wait for more information about the genes involved in providing resistance, but so far it does not look as though it appears spontaneously from multiple origins, it emerges once or twice, by chance, and the mites carrying the attribute spread. Pyrethroid resistant mites have been reported all over Europe, the US, Israel, and parts of S. America. Resistance to coumaphos has been reported in Italy, and resistance to amitraz has been reported in Croatia, France, and the USA. In October 2009, not quite ten years after varroa was first discovered, resistant mites were reported from a hive in Auckland. In the ensuing discussion speculation suggested resistance was likely present in Northland, Waikato, and the Bay of Plenty, and maybe further south. We do not know if the necessary genetic change arose here and was selected by the prevailing pyrethroid use at the time, or whether we managed to import a resistant strain as easily as the original import had occurred. As we don’t know how varroa entered the country it’s possible the ‘gate was never closed’. However it arose, we know it will gradually spread, just as the non-resistant type(s) have. While the available evidence suggest pyrethroid resistance is not widespread amongst varroa mites in New Zealand we have to add the word ‘yet’. Resistance isn’t anyone’s fault, it’s just the way Nature works, and it was not caused by the injudicious use of the chemicals used to control it; the fact is that the clock was always ticking and at some point luck ran out. Inappropriate pesticide use will ‘fix’ the problem in place though. The challenge is to understand its incidence and find the best strategy to manage resistant mites. That’s why I’m interested in looking over the fence. Everywhere we are faced with similar challenges; super-resistant weeds and antibiotic resistant hospital bacteria are two sides of the same coin. The paper studying glyphosate resistance in Ilinois (Evans et al) used a lot of data to look at the outcome of different management practices, broadly, rotating herbicides with different modes of action (MOA) or mixing different herbicides together. These two divergent strategies are also used to manage bacterial resistance to antibiotics in public hospitals, and in both cases the finding is that mixing, not rotation, is the better (but more expensive) strategy. This appears to be true when the fitness cost of a resistant trait is low, in which case the adaption is fixed even in the absence of the selective agent (the pesticide). Mixing strategies are not reliant on the cost of fitness driving depletion. Instead, mixing depletes any resistance alleles by decreasing survival probabilities of all individuals carrying the relevant alleles. It is an expensive strategy as the pesticides for each MOA must be effective. Ineffective, low-dose mixtures can potentially increase the risk of non-target-site resistance and cross-resistance evolution. I can see very little justification for adopting the strategy as a prophylactic treatment; besides the extra cost it only increases the chance of eventually selecting for cross-resistance. In the conclusion the paper points out; ”Herbicide mixtures are not a permanent solution to the problem of target-site resistance; herbicidal mixtures may delay evolution of resistance, but they do not prevent it…long-term, cost-effective, environmentally sound weed management will require truly diversified management practices… Combining chemical, cultural, physical, and biological tactics can provide cost-effective weed management while reducing reliance on herbicides.” For Evans, “We will encounter resistance evolution repeatedly in natural systems managed for human benefit. Sustainable stewardship of these systems will depend on recognising that we are always applying selective pressures, and that management responses need to grow from our understanding of applied evolution” Can’t help feeling there is a lesson for beekeepers in there. Evans, Jeffrey A., et al, (2015) Managing the evolution of herbicide resistance. Pest Manag Sci, (wileyonlinelibrary.com) DOI 10.1002/ps4009 Martin, Stephen, J., (2004) Acaracide (pyrethroid) resistance in Varroa destructor. BeeWorld 85(4): 67-69. Davis, T.G.E., et al (2007) DDT, Pyrethrins, Pyrethroids, and Insect Sodium Channels. IUBMB Life, 59: 151-162. Lagator, Mato et al (2013) Herbicide mixtures at high doses slow the evolution of resistance in Chlamydomonas reinhardii New Phytologist Vol 198(3): 938-945. DOI 10.1111/nph.12195
  4. You should look at the research being done by Paul Stamels at Washington State Uni with Fungi and non chemical treatment of Varroa and other illnesses.
  5. PhD research shows Varroa are Werewolves not ?‍♂️ Take a look
  6. Hi team. I purchased a nuc 5 days ago. They have an autum queen and everything seems good. They were treated for varroa with bayverol which was removed the day I purchased them (not sure when it was applied). I have fed them 2 liters of sugar syrup (1:1) in a frame feeder. I have attached a photo of the hive. My questions are: 1. After 3 days they haven’t made a dent in the syrup. How quickly would you expense a new hive (5 frames) of bees go through syrup? Do I keep the feed toped up? 2. Do I need to do anything else regarding varroa treatment at the moment? Thanks Dave
  7. Hey guys, I’ve got two hives and both have apivar strips in them until 28th of October. My question is if it’s a good idea to do an alcohol wash after treatment strips are removed to check mite levels? And if I’m not happy can I put in bayvarol strips for a number of weeks until beginning of December? Is it ok to run one strip of apivar and one strip bayvarol in a hive for spring treatment?
  8. Hello. Someone used wormwood tincture for the prevention and treatment of nosematosis and varroa? What do you think about using tinctures in beekeeping? In Ukraine, beekeepers often use wormwood. The ancient doctor Avicenna called wormwood "a panacea for all diseases". Wormwood is considered a poisonous plant, but all medicines are also poisonous in a certain concentration. In Ukraine, beekeepers often use wormwood tincture for the prevention and treatment of nosematosis and varroa. Tincture of wormwood has a normalizing effect on the digestive system, metabolism, eliminates virtually all existing fungal and infectious diseases. Tincture of wormwood works well on varroa mite, but it does not give one hundred percent result. That why it is necessary to use additional means for the prevention and treatment of bees from varroa mites and nosematosis. Tincture of wormwood is added to the syrup at each feeding. Proportion: one tablespoon per one liter of syrup. For 50 colonies, we disperse 5-7 liters of wormwood tincture per year. Wormwood for tincture is harvested during the flowering period. It is dried and then cut into pieces. When cutting, wear a respirator because it produces a lot of dust. You can also buy wormwood in a pharmacy and make her tincture To make the tincture, you need a three-liter bank. At the bottom of the banks we pour a glass of dogrose (if there is no dogrose, you can do not use it). We use dogrose as a source of vitamin C. Then lay wormwood. It needs to be well punched. It is better to use wormwood of different ages in equal proportions. After the wormwood was laid pour vodka or moonshine to the top of the bank. On a three-liter bank we used two and a half liters of vodka. Cover the top of the bank with cellophane and cover with a lid to avoid evaporation. Wormwood insists about two weeks in a dark place. Thank you. Ask questions. Subscribe to our channel.
  9. I did a sugar shake test on my hives yesterday and one of them had a varroa count of 10, but the sample probably had around 400 bees in it. That seems a bit high for this time of the year, but 'Practical beekeeping in NZ' says treat if there are 40 or more, and 'Control of Varroa' has a threshold of 65 mites. What do other people use as a threshold? I could treat now as this hive was split and is rebuilding at the moment, but am unsure if it is necessary.
  10. Hi Team, I've been watching various treatment threats in Diseases & Pests, and I have one question of Beginners. I'm using OA with good success. But my question regards adding MAQS to the regime. I understand the MAQS/Formic acid is a different action and can attack varroa in the brood comb and not so much the varroa on the bees (phoretic) I've seen it's temperature and volume restrictions and the needs for a strong well fed hive. But it says "leave the hive undisturbed for 7days". Now that clearly means, no inspections... no big deal. But does it mean, no concurrent OA treatments? I the reason I ask, is why not do your usual OA treatment then place MAQS. Then continue your OA treatments. This would mean both larval and phoretic varroa will take a hit. I'm thinking of doing this with my autumn treatment, as my spring nucs (now in 10frame FD) are not up to strength yet pp MAQS information) Or is this the overthinking of the well read, but inexperienced newbee. Thoughts?
  11. Hi all. I have a single brood box langstroth hive with plenty of bees and about a frame of brood. It has had varroa treatment (apistan strips x2 correctly positioned in the brood box) it's been in for five of the six weeks. There is evidence of deformed wing virus (12 bees) and looking harder with my reading glasses on, I could see varroa mites on some of the bees. As an emergency measure I replaced the strips with fresh ones from my beebox for the final week of treatment but it looks like this may be grasping at straws. Does anybody have experience of this situation and have any suggestions?
  12. Hi again Beeks, I received my first ever nucs two days ago, on the day I received them I transferred them to there new brood boxes. Yesterday I left them alone to give them some time to recover. Today a friend of my helped me mark the queens. While in the hives we saw a few things that concerned us, could all you experts out there have a look at the following photos and let me know how serious you think they are? I didn't get a good photo of it, but we also noticed a fair number of the bees have deformed or clipped wings.
  13. I opened one of my hives yesterday to find it was basically empty! (I did some experiments on the dozen odd bees that remained and none of them appear to be capable of flying). So I assume the hive swarmed and the non flyers got left behind. The hive definitely did not have AFB/Sack Brood or foul brood. (I got it inspected by a respected member of my local club). It was suffering from a high Varroa population - so I can only assume they swarmed because the Varroa numbers became unmanageable. I had fitted Bayvarol strips a week earlier, but it must have been to little to late. Anyway my question is, what should I do with the now empty hive/frames? I understand that transferring disease is a big concern, but if I know it only suffered from Varroa can I just take steps to deal with all the Varroa - then I could put the drawn out frames in my good hive to save them some work. My understanding is freezing the frames until they are solid (2-3 days) will ensure any remaining Varroa is killed off. Can I then just defrost them and put them in the good hive? My other thought was, if I just close the hive up and treat it with oxalic acid a couple of times over winter, could I then just open it in the spring and wait for a swarm to turn up?
  14. I lost a queen earlier this year in one of my hive, either she left or more likely a clumsy beginner (me) killed her by accident. The hive built a number of queen cells and on advice from a beekeeper I removed all except one. Last week the cell was gone and tomorrow I will be checking for eggs to see if the queen was successful. As there is no sealed brood in the hive I was wondering if this was a good time to do a varooa treatment with ApiGuard?, all the varroa would be exposed meaning that one treatment might do the trick. Or should I go with 2 treatments as per the instructions. Or is a treatment like this the wrong thing to do with a queen that has only just started laying, would the smell get in the way of her pheremones or cause any other disturbance?
  15. Does it make sense to treat a newly caught swarm for varroa before any brood is capped? My thinking is that a varroa treatment will significantly reduce any varroa on the adult bees before the varroa gets a chance to start breeding in capped brood cells.
  16. I found this interesting article online earlier today, and I thought there might be other Bee and Beer lovers that will appreciate the idea that drinking beer could help save the honeybees: Could Beer Save The Honeybees?
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