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Dave Black

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  1. Everyone knows honeybee females (queens) mate at the beginning of their adult life and are then unable to mate again. A queen mates with many males (drones), often on a single occasion but sometimes after multiple flights in successive days. The mating is very quick, not more than 5 seconds and perhaps no more than one or two seconds, after which the male is paralysed and dies. Competition between males in a mating congregation occurs, mostly as a result of size and power, and some selection operates seemingly on the basis of flight altitude, different strains favouring different heights. A single drone congregation area might contain more than 20,000 drones from potentially hundreds of colonies, and the chance of an individual male being able to mate more than once would be very low. In honeybees therefore it’s not surprising a male expends his entire effort mating with a single queen, and not surprising that probably his best chance of improving his reproductive success is posthumous sperm competition. Queens, at least during mating, appear to have very little ability to choose the paternity of her offspring, but there are good reasons to suppose her interest is in being able to produce a sizeable range of genetic characteristics. Variation is good for managing conflict in a social group, protecting the colony from diseases and environmental change, and providing progressive, adaptable worker performance. Especially in honeybees, as she can never mate again, she has a particular interest in actually opposing or counteracting individual males’ reproductive success, negating sperm competition and choosing diversity. This ‘choice’ is said to be ‘cryptic’, because it is hidden from the male (Eberhard, 1996). Queens are estimated to lay about 200,000 eggs each year; something like 1.0 – 1.6 million fertilised eggs in her 5 – 8 year lifetime. Some hymenoptera (species of ants) do better by a significant margin, producing 8 million workers fertilised by sperm stored for decades. Much more sperm are stored in the spermatheca (in the order of 5 million) than will be needed. Drones will produce between 2 million and 12 million spermatozoa each, and at the end of a mating flight a queen might contain 200 million or so temporarily housed in her oviducts, vagina, and bursa copulatrix. Only around 2.5% of the sperm she acquires during mating is stored, and even less are actually used (think an average two per egg over her lifetime). Spermatozoa can be stored for many years and retain viability. Paternity studies have shown it is completely mixed and used equitably. Discovered in 1905 the key to this remarkable economy of sperm use is something called a Bresslau sperm pump. This structure sits between the spermathecal and the spermathecal duct, a valve in muscular tissue that, if you like, ‘reaches in’ and grabs a constant volume of spermathecal fluid (containing sperm) and transports it out to the eggs. (After mating it ‘pumps’ in the opposite way, filling the spermatheca). While the fluid volume is replaced and always stays the same, the density of spermatozoa it contains gradually declines. The Bresslau sperm pump is also found in ants. With the instruments available nowadays it’s actually possible to count sperm on eggs. Just how bees, wasps and any are able to keep spermatozoa alive for so long eludes a complete explanation, but in short, by an extreme conservation of energy and reduction in oxidative stress. Both seminal fluid and spermathecal fluid must have a role in providing a habitat that nourishing the cells, reduces oxidative stress, and protects them from pathogens, but it’s most likely spermathecal fluid evolved to maximise their long-term viability. Studying spermathecal fluid from virgins and mated queens shows they do differ, but also have some functional similarity with some elements in seminal fluid. Drones too store sperm, although not for as long. In a process that takes at least 40 hours it appears that the storage ‘environment’ is gradually changed from semen to a receptive queen’s spermathecal fluid, to a mated queen’s spermatheca. Spermatozoa in the spermathecal fluid ‘acclimatise’ to their new environment and begin to metabolise very, very slowly, essentially ‘outsourcing’ some of their vital functions to the female environment. In particular, while spermatozoa are able to metabolise aerobically, in storage there is evidence to suggest they switch to anaerobic energy production using a partly metabolised product in spermathecal fluid to limit the release of damaging Reactive Oxygen Species (ROS). As well, the spermatheca is a bead-like organ with two spermathecal glands situated outside a hard sclerotized wall impervious to oxygen. By comparison to other organs the spermatheca has significantly lower oxygen concentrations inside. Spermathecal fluid is also known to contain many highly-active antioxidant enzymes, and these increase if we compare virgins with mated queens. It's become well documented in many species that males don't just transfer spermatozoa during copulation but include a complex mixture of molecules, anti-oxidants, ions and cells other than spermatozoa, including sometimes pathogenic micro-organisms. These male compounds have a variety of functions. Some directly affect the sperm’s survival in the female’s reproductive tract, providing nutrition, pH and osmotic buffering, and defences against oxidizing agents. Other products have important effects on the physiology and behaviour of the female, such as promotion of sperm transport, and inducing ovulation or oviposition. We are now beginning to realise that seminal fluid contains molecules that have a demonstrable effect on gene expression, and that a number of proteins cross the vaginal wall into haemolymph where they can bind to receptors on neurons directly affecting nerve signalling. A somewhat surprising example, consistent with other insect studies and earlier work, establishes a (short-term) loss of visual ability in queens linked to a peptide transferred in male semen. The effect is that queens are less inclined to undertake further mating flights (because they can’t see properly), but with the consequence that the queen tries to fly earlier if she can, before the loss becomes too debilitating. Males have no interest in queens flying to mate with more males. The scientists used RNA-sequencing to look at the changes in gene expression following artificial insemination, comparing them with naturally inseminated queens and queens inseminated with a saline control. They were able to identify the changed genes as ones known to be associated with functions that mostly enable vision. They then carried out a similar exercise, but this time measured the actual performance of the eyes (all of them!), things like their response to different light frequencies, and sensitivity to visual contrast. Last, they used RFID tags to monitor natural flight activity (and queen loss) after the same set of treatments (insemination, mock insemination etc). Each set of experiments indicated that queen’s visual performance deteriorated 24 – 48 hrs after receiving seminal fluid, and they were more likely to be lost on subsequent mating flights. The same effect has been observed in other studies of fruit flies, a parasitoid wasp, and in the bumble bee Bombus terrestris, suggesting that this ability to manipulate female mating using components of seminal fluid could be widespread or even universal amongst Hymenoptera and perhaps all insects. Further reading Boris Baer, Sexual selection in Apis bees. Apidologie 36 (2005) 187–200, INRA/DIB-AGIB/ EDP Sciences. DOI: 10.1051/apido:2005013 Boris Baer, Jason Collins, Kristiina Maalaps & Susanne P. A. den Boer. Sperm use economy of honeybee (Apis mellifera) queens. Ecology and Evolution 2016; 6(9): 2877–2885 doi: 10.1002/ece3.2075 Laura M. Brutscher, Boris Baer, and Elina L. Niño. Putative Drone Copulation Factors Regulating Honey Bee (Apis mellifera) Queen Reproduction and Health: A Review. Insects 2019, 10, 8; doi:10.3390/insects10010008 G Koeniger et al (1988) Assortative mating in a mixed population of European honeybee Apis mellifera ligustica and Apis mellifera carnnica. Insectes Sociaux, Paris Vol36, No2, pp.129-138 Liberti et al. Seminal fluid compromises visual perception in honeybee queens reducing their survival during additional mating flights eLife 2019;8:e45009. DOI: https://doi.org/10.7554/eLife.45009 Boris Baer et al, Insights into female sperm storage from the spermathecal fluid proteome of the honeybee Apis mellifera. Genome Biology 2009, 10:R67 (doi:10.1186/gb-2009-10-6-r67) Ellen Paynter, A. Harvey Millar, Mat Welch, Barbara Baer-Imhoof, Danyang Cao & Boris Baer. Insights into the molecular basis of long-term storage and survival of sperm in the honeybee (Apis mellifera). Scientific Reports, (2017) 7:40236, doi: 10.1038/srep40236 Niño EL, Malka O, Hefetz A, Tarpy DR, Grozinger CM (2013) Chemical Profiles of Two Pheromone Glands Are Deferentially Regulated by Distinct Mating Factors in Honey Bee Queens (Apis mellifera L.). PLoS ONE 8(11): e78637. doi:10.1371/journal.pone.0078637 J. Woyke (1983) Dynamics of Entry of Spermatozoa into the Spermatheca of Instrumentally inseminated Queen Honeybees, Journal of Apicultural Research, 22:3, 150-154, DOI: 10.1080/00218839.1983.11100579 Aldo Poiani, Complexity of seminal fluid: a review. Behav Ecol Sociobiol (2006) 60: 289–310. DOI 10.1007/s00265-006-0178-0 Eberhard, William. (1996) Female Control: Sexual Selection by Cryptic Female Choice. Princeton University Press, ISBN 0-691-01084-6
  2. A honey bee nest and its enclosure provides a rich and stable range of ecosystems where we might expect an abundance of microbe populations to thrive, constantly replenished through its interface with the phyllosphere that surrounds it. We know a great deal about the harmful micro-organisms that cause disease; foulbrood bacteria, chalkbrood and nosema, even virus infections, but very little about beneficial micro-organisms that maintain health. Despite a contemporary obsession with prophylactic ‘probiotics’ and gut health there is actually not much known about the contribution from microbes to honeybee fitness, and still less about what the effects of antibiotics and fungicides from pollutants or veterinary treatments might be on the microbiotic environment ‘bees share. There are two ‘communities’ of bacteria here that are particularly interesting, that associated with the pollen collected and stored for food, and that inhabiting the ‘bee gut itself. Pollen provides the bulk of proteins, vitamins and lipids for colony growth. It is also a warm, moist and sugar rich source of food, albeit acidic, and arrives with its own collection of microorganisms, some well able to exploit it for their own purpose. While it has always been believed pollen stored as ‘bee-bread’ is a pre-digested store of food (similar to honey) closer study show this is probably not true. We find ‘bees prefer pollen less than three days old, that is, they weren’t waiting for some process (akin to fermentation) to occur before eating it. In addition the bacteria counts from collected pollen were low and declined rather than increased. That’s not what we’d expect if the store was supporting the microbes. The populations were so low that it was implausible there were enough to have any effect; the estimate was one microbe for every 2,500 pollen grains. Using microscopy the mostly intact grains did not appear to have been altered in any way by storage, and the bacteria found did not have the characteristics of a stable microbiome but were adapted for survival in acidic, antimicrobial environments. The bacteria in stored pollen are very different from those in the hind gut where pollen is being digested, and where they are present in hundreds or thousands per grain of pollen. It appears then that stored pollen is in a state for preservation rather than conversion, and that actually the true ‘store’ of nutrients is the ‘bees themselves. We often talk about pollen (fresh or stored) being digested in a ‘communal stomach’. What we mean is that pollen is eaten by a fairly limited group of young bees and fed to everyone else in the colony. These ‘nurse’ bees consume pollen and from glands in their head then secrete a semi-liquid food, This can be pooled in honeycomb cells to feed larvae or shared directly, ‘mouth to mouth’, with the queen and other members of the colony. As nurse bees age and become guard or forager bees they gradually lose the ability to digest pollen and have to be fed by a new generation of nurses. How these ‘bees extract nutrients from pollen grains is not fully understood, but it’s possible microbes play their part. Scanning electron microscope observations of pollen passing through the digestive tract show a range of states, depending on far along the gut you look and, presumably, on the type of pollen grain and its construction. Some are fully ruptured, perhaps because of osmotic shock, others seem more or less intact but empty, the contents removed gradually through the germination pores in the grain. Another interesting line of research has considered the inevitability of bees consuming the yeasts, bacteria, and fungi that naturally associate with pollen (or nectar) and suggest that this would mean bees are actually omnivorous. Using native (solitary) bees and examining isotopes of carbon and nitrogen in the amino acids glutamic acid and phenylalanine that were consumed the research was able to show the bees were assimilating both microbial and plant proteins. In another study they demonstrated a decline in biomass and increased development time in larvae fed a diet progressively increasing in sterilised pollen, indicating the microbes were an essential part of the diet. This is analogous to leaf-cutter ants growing and consuming fungi grown on the leaf substrate they collect, rather than eating the leaves. We talk about the bee ‘gut’ as though it was all one homogenous organ, but in reality it is a series of blended zones or organs each with distinct functions and correspondingly different environments and inhabitants. Looking at the microbes in these ‘zones’ is tricky. Older methods rely on culturing bacteria on a growth media, but it possible to miss or underestimate microbes that are unexpected or difficult to culture. Later methods use PCR amplification and genetic makers, but that too has some limitations so that at the moment the most accurate information comes from studies that use and compare both methods, what’s called culture-dependent and culture-independent methods. Working out where these microbes belong is also tricky, some, not adapted to live in a particular environment, may just be passing though and do not form the stable biofilms bacteria flourish in. Newly emerged ‘bees have no, or only a couple of types, of gut bacteria. ‘Bees acquire bacteria that inhabit their gut from their foraging environment, but also from each other when food is shared. Plainly bacteria in the phyllosphere are present, mostly in the crop, but this is an inhospitable temporary haunt because its contents change so often. It seems unlikely there is a permanent ‘core’ group of bacteria associated with this region, and little evidence for one. The mid-gut and hind-gut do have lasting ‘core’ groups of bacteria and the highest bacterial counts are found here, with most actively growing and reproducing biofilms in the hind gut. The communities have quite different inhabitants from those found in pollen, ‘beebread’ or honey and remain consistent across seasons and geographical regions. When we look closely enough we find that although a gene sequence can indicate a close physiological relationship to other organisms, when it comes to bacteria even closely related species can display remarkable differences in their functional genes. Perhaps surprisingly this simple set of perhaps eight or so core bacteria types are found only amongst eusocial bees, and appear to have diversified to occupy particular niches and perform functions that only apply in groups of honeybees or bumblebees, and that are conserved by their sociality. Long-standing co-evolution has produced functionally unique strains adapted to a symbiotic existence with each other and their bee family, possibly unique even at colony level. L. M. Klungness, Ying-Shin Peng, Scanning electron microscope observations of pollen food bolus in the alimentary canal of honeybees (Apis mellifera L.) Canadian Journal of Zoology, 1984, Vol. 62, No. 7 : pp. 1316-1319 https://doi.org/10.1139/z84-189 Anderson KE, Sheehan TH, Mott BM, Maes P, Snyder L, et al. (2013) Microbial Ecology of the Hive and Pollination Landscape: Bacterial Associates from Floral Nectar, the Alimentary Tract and Stored Food of Honey Bees (Apis mellifera). PLoS ONE 8(12): e83125. doi:10.1371/journal.pone.0083125 Anderson KE, Carroll MJ, Sheehan T, Mott BM, Maes P, Corby-Harris V. 2014 Hive-stored pollen of honey bees: many lines of evidence are consistent with pollen preservation, not nutrient conversion. Mol. Ecol. 23, 5904–5917. (doi:10.1111/mec.12966) Steffan S, Dharampal P, Danforth B, Gaines-Day H, Takizawa Y, Chikaraishi Y. (2019) Omnivory in bees: elevated trophic positions among all major bee families. Am. Nat.vol. 194, no. 3. doi:10.1086/704281 Dharampal PS, Carlson C, Currie CR, Steffan SA. 2019 Pollen-borne microbes shape bee fitness. Proc. R. Soc. B 286: 20182894. http://dx.doi.org/10.1098/rspb.2018.2894 Philipp Engel, Vincent G. Martinson, and Nancy A. Moran Functional diversity within the simple gut microbiota of the honey bee. 11002–11007 PNAS July 3, 2012 vol. 109 no. 27. https://www.pnas.org/content/109/27/11002
  3. Not helpful that the paper sits behind a pay-wall, but I do have a copy. In brief the proposal is that several studies have shown Varroa breeding tanks in high humidity (@ >80%) so modify beehives to be more like natural nests where the humidity (apparently) is high (@80%). Mitchell has done some interesting work modeling airflow in hives (search the Forum) so it's an idea that should be taken seriously, but should still be discussed critically. Most of you probably have an entirely different idea about the value of humidity in a beehive, so that's probably the place to start. BTW Derek Mitchell's work is mentioned in Tom Seeley's new book, but it deals with temperature control, not humility control.
  4. There would be a Trade Descriptions case against this if anyone could be bothered. As the UK will be practically lawless shortly they'd better be quick.
  5. @derekm A few initial thoughts; 1. I knew when I got to the word 'tuple' this read was going to take some effort! 2. This might be the nail in the coffin for the 'heating varroa' advocates. 3. Have there been actual measurements (rather than modeling) of humidity a) in natural nests and b) in the putative 'ideal' man-made nest and do they compare with modeling? 4. I need to read it a few more times.
  6. @Sofia L Yes this a field of interest here, with some very good work being done. Have a look here. https://is.gd/8bjK3Q
  7. @yesbutI don’t really have the time or inclination to read through this, surprisingly acrimonious, thread. Another one to evolve way beyond its remit. I had a skim through the RIRDC document, a pretty conventional one from a reputable government body and all the sections you’d want if submitting to a peer-reviewed journal. I don’t really think it’s reasonable to suggest it’s not written well enough to allow a ‘scientific’ assessment. It hasn’t been peer reviewed perhaps, but while I support the peer review process it hasn’t proved to be the blue tick of all things wise and true. It adds to a body of knowledge. I don’t think it’s credible to argue that dogs can’t be a part of the solution. They are good enough to be trusted with the nation’s biosecurity after all. However, in legal circles tracker dogs and sniffer dogs are known to have a significant error rate and are not infallible ‘evidence’ for a court. Doesn’t make them useless. I don’t see that ApiNZ argue that you can’t use dogs either, but you do also have to satisfy the terms of your DECA. In short then, there seems to be ample room for a quick, negotiated solution here. As the body responsible for ‘enabling’ progress I’d expect ApiNZ and not the Management Agency to do much better here, I see it as their job to facilitate how, not throw up barriers. That said, solving the AFB problem is ultimately up to Beekeepers, not the organisations they create to carry the blame. Pragmatism rules. That will be all.
  8. Discuss. Abstract: Failure of the queen is often identified as a leading cause of honey bee colony mortality. However, the factors that can contribute to “queen failure” are poorly defined and often misunderstood. We studied one specific sign attributed to queen failure: poor brood pattern. In 2016 and 2017, we identified pairs of colonies with “good” and “poor” brood patterns in commercial beekeeping operations and used standard metrics to assess queen and colony health. We found no queen quality measures reliably associated with poor-brood colonies. In the second year (2017), we exchanged queens between colony pairs (n = 21): a queen from a poor-brood colony was introduced into a good-brood colony and vice versa. We observed that brood patterns of queens originally from poor-brood colonies significantly improved after placement into a good-brood colony after 21 days, suggesting factors other than the queen contributed to brood pattern. Our study challenges the notion that brood pattern alone is sufficient to judge queen quality. Our results emphasize the challenges in determining the root source for problems related to the queen when assessing honey bee colony health. Kathleen V. Lee, Michael Goblirsch, Erin McDermott, David R. Tarpy, and Marla Spivak (2019). Is the brood pattern within a honey bee colony a reliable indicator of Queen Quality? Insects 10, 12; doi:10.3390/insects10010012 (Open Access)
  9. We used to diagnose tracheal mites (acarine) in the field with a hand lens, a cork and a few pins. Pull or flick the head, first pair of legs, and first segment of the thorax off with forceps or a blade and with the lens and look for a pair of quite large white tubes heading down into the thorax towards the wing muscles. If they are discoloured from clean white opalescent tubes and show brown staining chances are it’s mites inside blocking the tube. Of course a lab can do it neatly, and expose the individual mites to look at too, but there you go… I doubt it's mites; all the varroa-killing magic we put in hives is probably killing all the Acari.
  10. Physics provides a lens that focuses on our honeybee colonies in interesting new ways and a recent paper from Derek Mitchell at Leeds University’s School of Mechanical Engineering does just that. The mathematics is a bit challenging if you’re anything like me, but it’s possible to get through that, and he also has some worthwhile observations we can apply to polystyrene hives. Mitchell’s current interest (Computational Fluid Dynamics (CFD); his thesis was about differences in heat transfer between natural and man-made honeybee nests using CFD) also has something useful to say about that beekeeping perennial, top vs bottom entrances. This is not the first application of CFD to beekeeping, the Forum has a discussion from a couple of years back about polystyrene hives, and Cory Thompson (with others) studied airflow in Langstroth hives using the method. The results are always interesting, but as important are the assumptions, simplifications and limitations used when devising a workable model. Honeybees harvest nectar to provide a source of a carbohydrate solution in periods of dearth, typically in the winter, but also during drought periods when flowers may not produce any. In order to store this food effectively they concentrate it to reduce the space it occupies and to prevent spoilage. This concentration is accomplished by doing two things. By adding the enzyme invertase the nominally sucrose nectar is converted to contain smaller sugars, mainly fructose and glucose. Fructose is much more soluble in water (even hygroscopic) and not easy to crystalise; a saturated solution of each of the three sugars (at 25C) will contain 81% fructose, 51% glucose, and 67% sucrose. In addition, a solution containing more than 60% fructose can contain much more glucose than a more dilute fructose solution. In almost all cases honey is a super-saturated fructose solution containing glucose. The other thing done to concentrate the volume is to remove most of the water. Typically nectar containing perhaps 80% water is reduced to honey, containing less than 20% water, by evaporation. Any change of state, in this case the liquid to gas transition, requires energy. We call this energy ‘latent heat’; the temperature of the body (the solution, the water) remains constant but the added energy changes its volume, from a fluid to a loosely packed gas of excited molecules. To find out how much energy we can just look it up on Wikipedia J, for water it is 2,260kJ/kg (depending on temperature and pressure). This is actually quite a lot, and even more if you think about the quantity of water involved. A colony could evaporate more than 400kg of water in a year, using almost one gigajoule of energy, or nearly 300 kilowatt-hours. Thirty litres of petrol to you. So where does all that energy come from? A little might come from the warmth of the sun, (and a tiny bit from the invertase chemistry), but given that the ‘bees operate in an enclosed, shaded wooden tree or box a more plausible answer, especially if you can visualise what the ‘bees actually do, is that it is metabolic energy, and it comes from the food itself – nectar. Besides all the other things honeybees do with the energy they harvest; fly, dance, grow, brood, even, waste it, evaporating water might be a very significant one. It’s reasonable to argue that the survival of the colony depends on the efficiency (energy efficiency) of foraging (the colony must gather more energy that it expends or it dies) but we don’t tend to think about the cost (in energy) of storing and making that food energy available. It must be said that the people and (biological) disciplines that study honeybees aren’t experts in physics or engineering, and may not be the best people to think about things like energy or materials. In this study, as a starting point, Mitchell considers the model system to be bounded by the nest enclosure, which constantly loses heat to its environs, and the journey to and from the flower patch where the nectar source is at a fixed distance. The nest enclosure does not change (the hive isn't 'supered'). It excludes the honeybee time spent in flower to flower transport energy (which is assumed to be replaced in the flower patch) and flower nectar depletion or dilution. For the sake of simplicity there is assumed to be no variation in energy consumed due to in-flight changes in insect weight or wind speed, nor does it consider significant activities for the honeybees like water and pollen collection or the nest consumption of honey to fuel brood rearing. The model focuses on the Thermal Energy Efficiency (TEE) as determined by the honey ripening rate, nectar concentration, ambient temperature, airflow inside and outside and any behaviour that controls it, and the thermal conductance of the nest (heat lost). It shows the energy used for nectar conversion is significant, from 20% to 60% of the total energy recovered by nectar foraging. Typical values show that over 50% of the delivered energy may be used in the process of honey ripening and even in exceptionally favourable circumstances for temperate climates, do not use less than 25%. The energy consumption of nectar desiccation limits the maximum foraging distance of honeybees and also changes the energy return for a given nectar source, as well as which nectar sources are viable. The TEE limits nectar conversion so that honeybees can profitably retrieve and refine nectar from either a weaker nectar source or from a greater distance, but not both. A colony that collects nectar at distances, concentrations and TEE outside the break-even line will not add to its honey reserves and may not survive. That much is supported by observations in other studies. As well, improvements in TEE would require less nectar, so less foraging flights, less fanning, and less wing wear. If you're looking for a 'take-away message', Mitchell is suggesting that thermal conductance of hives, previously thought to be only a consideration for winter, has been shown to be a major factor during the nectar collecting periods of the year, and consequently beekeepers should improve thermal efficiency by changing their hives to ones which lose less heat, and facilitating honeybee behaviours that have the same goal, for example, only using bottom entrances. Mitchell D. (2019) Thermal efficiency extends distance and variety for honeybee foragers: analysis of the energetics of nectar collection and desiccation by Apis mellifera. J. R. Soc. Interface 16: 20180879. http://dx.doi.org/10.1098/rsif.2018.0879 Mitchell, D. (2017) Honey bee engineering: Top ventilation and top entrances. American Bee Journal, 157 (8). pp. 887-889. ISSN 0002-7626 EPS vs Wooden Boxes (2017), https://www.nzbees.net/forums/topic/8664-eps-vs-wooden-boxes/ Sudarsan R, Thompson C, Kevan PG, Eberl HJ. (2012) Flow currents and ventilation in Langstroth beehives due to brood thermoregulation efforts of honeybees. J Theor Biol. 1;295:168-93. doi: 10.1016/j.jtbi.2011.11.007. Epub Nov 25 2011.
  11. The quick answer in the books is that foraging ceases with wind speeds over 15mph (24km/h), assuming flight activity is not limited by light or temperature, and honeybees fly at up to 21-28km/h (28km/h is 7.8m/s). The question deserves a little more thought though. Adrian Wenner did some work measuring flight speed in the ‘60s, calculating flight speeds of 7.0 -7.8m/s for laden and un-laden ‘bees. He looked at wind towards and against the direction travel, but not really at cross-winds, and understood that the height at which you measure the wind speed matters. Honeybees reduce altitude as wind speed increases, and they also don’t travel as far. Foragers that work close to home come in to play, the long-distant team stay at home. Nectar sugar concentration becomes more important. Sustained wind at hive sites can aggravate drifting, increase forager mortality, and change the energy budget for a colony, usually making things less favourable, even lethal for unmanaged colonies. How much all that matters, and at what point that begins to matter, only experience will tell.
  12. 'Old' bees in 'spring' might be four months old, but in the absence of precision maybe it's just a matter of which bees are stinging. Can't say I've ever noticed a seasonal effect at all.
  13. We know venom potency is related to bee age. I'd probably expect 'spring' hives to have proportionally more old bees, with more potent venom, for a while. So it might come down to how we define 'spring'.
  14. 1. Introduction 2. Venom Biochemistry 3. Minimising the dose 4. Treating the sting 5. Topical treatments 6. Systemic, toxic, and anaphylactic responses 7. Ocular stings 8. Beekeepers 9. Caring for others 10. References Introduction New Zealand is fortunate to have very few stinging insects. These are members of the hymenoptera in which the ovipositor has been modified into a sting delivering venom and are known collectively as Aculeata. There are 29 native solitary hunting wasps, most of which hunt spiders as food for their offspring and are not known to be aggressive towards people. The native solitary bees amount to 18 species of Leioproctus, seven Hylaeus species and four species of Lasioglossum. All these solitary insects, evolved to use their venom in small amounts for subduing other insects, (not mammals) or in a limited defensive effort. It is the introduced social species from the Aculeata that are mainly responsible for stings to humans. These insects manage a communal defensive effort directed specifically at mammalian predators (like people) and so employ toxins and strategies that are effective against mammals, sometimes fatally so. These introduced animals include four species of wasp, a similar variety of bumblebees, and the honeybee. The honeybee is unique in that an individual can only sting once, and then dies. A wasp or a bumblebee is able to sting repeatedly. All of them defend their nest sites by deploying many individuals to attack the aggressor. Insect repellants (like DEET) are not effective on hymenoptera. The incidence of stings varies with your location and the season. Wasps’ stings are the most numerous, particularly in the late autumn when they actively hunt at picnics and barbeques, dive into soft drink tins, rubbish, and consume the sweet saps from garden plants and trees. Honeybee stings are less numerous and more common in the spring, but it depends on the setting (urban, rural, orchards etc). Bumblebee stings are infrequent, often in mid to late summer when the nests are disturbed as a result of being bigger and more obvious, or because it’s a ‘tidy-up’ time for people and their gardens. The reporting of incidents leaves a little to be desired. Fortunately wingless wasps that look like ants don’t figure in the statistics. Most people are unable to tell a ‘wasp’ from a ‘bee’. A few can identify a bumblebee (there are several kinds), and only the most studious could distinguish a ‘paper wasp’ (either of them) from one of the vespulae. Many claim not to have seen what ‘bit’ them in any case. In some respects the venoms from the three are very similar, and how an individual will react, or needs to be treated, can also very similar. An allergic response to one can mean the individual will be allergic to the others. However, it’s not a rule; there are also significant differences between them. Honeybee (Apidae: Apis) venom has been collected for centuries and is consequently the most studied. Mellitin, Apamin, and a peptide that degranulates mast cells are unique to honeybee venom. Wasp (Vespidae/Polistinae) venom contains different phospholipases, and a unique antigen. Bumblebee (Apidae: Bombus) venom is different from both of these, but has some similarity. Consequently there are separate preparations available for testing hypersensitivity or desensitizing. Almost all reactions to stings are allergic responses, even though we don’t commonly use the phrase. Venom biochemistry Bee venom is a blend of components including two peptides, several acids, histamine, dopamine, noradrenaline, tryptophan, sulphur, some minerals,oils, and enzymes. Fifty percent of the dry weight of honey bee venom is mellitin. Mellitin is a chemical that is unique to bee venom and is cytolytic, which means that it bursts cells (the little red ‘dot’ at the sting site is burst red blood cells). Mellitin also dilates blood vessels, leading to low blood pressure. Twelve percent of honey bee venom is Phospholipase A2 (the most potent allergen). Phospholipases are enzymes that help mellitin destroy cell membranes. Apamin is also unique to bee venom (3%) and is a neurotoxin. Hyaluronidase (2%) is an enzyme that breaks down hyaluronic acid, which is one of the components of the tissue in between your cells that hold them together. Hyaluronidase contributes to the “spread” of the reaction. Mast cell degranulating peptides cause the special ‘mast’ cells in your body (part of your immune response system) to release the many biochemicals (including more histamine) in their granules. Histamine causes ‘leaky’ capillaries and contributes to the slightly raised red area that itches in sensitive individuals. In wasp venom the major unique components are phospholipase A1 and B, antigen5, acetylcholine, and serotonin. Many of these proteins are also recognized as foreign by the human immune system (antigens) and lead to a response from the body’s immune system. The ‘first responders’ are the lymphocytes. Lymphocytes come in different types. Their surfaces recognize things that belong and things that don’t and they respond in two ways to things that don’t. They will release antibodies which ‘label’ the foreign matter so that some action can be taken against it, and they will produce more lymphocytes which are there as a form of ‘memory’ of the event. A ‘normal’ response produces immunoglobulinG (IgG); an allergic response produces ImmunoglobulinE (IgE).The mast cells too play an early role. Mast cells are covered in immunoglobulinE antibodies and come ‘pre-loaded’ with histamine, serotonin, protein-destroying enzymes, the anticoagulant heparin, and slow acting leukotrienes, prostoglandins, and cytokines. In response to IgE mask cells disintegrate, liberating their contents. People all produce different amounts of IgG or IgE in response to different ‘invaders’, and what the antibodies ‘recruite’ to aid their effort varies between individuals, so the range of response is very different and depends on the venom, the dose, the site, the individual’s physiology, and even their psychological state. The venom from a sting therefore has a direct physical effect on surrounding tissue, but also causes a response in the body that may or may not magnify that effect. For example, the venom itself will destroy mast cells and release their contents to have a local effect, but the body’s immune system can also start to produce immunoglobulins that will degranulate mast cells remote from the venom site and create a system-wide (systemic) effect. The table below shows the range of possible reactions to a sting. Reactions Reacting Immunoglobulins Onset Times Clinical Manifestations Local IgG 4-48 hours Painful, pruritic, & oedematous sting lesions, 2.5-10cm in diameter. Systemic IgE 12-24 hours Headache, fever, nausea, vomiting, diarrhea. Toxic IgE ½-1 hour Systemic symptoms, syncope, seizures, hemolysis, rhabdomyolysis, acute tubular necrosis with renal failure. Allergic IgG 12-24 hours Initial wheal & flare response at sting sites, followed by painful, pruritic indurated lesions. Anaphylactic IgE 10-20 min up to 72 hours Generalized urticaria, angioedema, dysnpea, bronchospasm, inspiratory stridor, wheezing, chills, fever, apnea, respiratory failure, hypotension, cardiovascular collapse, rarely disseminated intravascular coagulation. Delayed (Apis only) IgG 2-14 days Headache, malaise, low-grade fever, generalized lymphadenopathy, polyarthralgias, serum sickness & thrombotic hrombocytopenic purpura possible, rarely peripheral neuropathy. (After Diaz, 2007.) Minimising the dose There is a basic difference between honeybee stings and the others in terms of the construction of the ‘apparatus’. A wasp or bumblebee’s stinger has no barbs. This means that the insect can withdraw her stinger, and is able to sting again. In contrast, a honeybee can not withdraw her sting. The sting consists of two barbed lancets and a stylet, and the venom gland discharges into a space in between the lancets and stylet, and venom can only travel down this shaft as movement in the opposite direction is prevented by valves. The venom sac has no musculature; the muscle associated with the sting is attached to plates which drive each lancet in turn forward with respect to the stylet, the stylet supporting each using a sort of ‘monorail’ connection. Once the sting has become caught in the skin the bee can’t escape without it becoming dislodged from her body, and as that happens, the Dufour and Koschevnikov glands are torn out and remain with the trapped sting. The later gland produces isopentyl acetate, the ‘banana’ scented pheromone beekeepers are familiar with. This marks the site and stimulates other bees to sting. The lancets meanwhile, are driving themselves, one by one, deeper into the skin and continue to dispense venom. Do not overlook the fact that the most important response to stings from wasps or bees defending their nests should be to get away from the vicinity of the nest. Getting to safety is more important than removing stings immediately, but stings should removed as soon as possible once a person is away from the area. The method of removal does not affect the quantity of venom received by the subject. Much of the advice commonly given regarding the immediate treatment of bee stings derives from a misunderstanding of the structure of honey bee stings. Conventional wisdom says to scrape bee stingers away from the skin because pinching the venom sack could push extra venom into the victim. In fact, how fast you get the stinger out is much more important than how, and in a small number of cases, the scrape treatment results in breaking the sting lancets from the rest of the sting, with the lancets remaining in the subject’s flesh. The method of removal is irrelevant, but even slight delays in removal caused by concerns over performing it correctly (or getting out a knife blade or credit card) are likely to increase the dose of venom received. The advice is to simply emphasize that the sting should be removed, and as quickly as possible, within a couple of seconds. A fingernail is the most convenient tool; just scrape or flick the sting away. If you think you can get your credit card out that quickly, ‘lets do lunch’. The exception to this advice is in the case of a sting to the eyeball or eyelids. A sting to the eyeball should only be removed using microscopy, by an expert; and sting to the eyelid can be removed but must be examined in the same way to ensure remnants do not damage the eye’s surface. If the sting is followed by severe symptoms, or if it occurs on the neck or mouth, seek medical attention immediately because swelling in these areas of the body can cause suffocation. Stings directly into blood vessels can cause a very rapid cardiopulmonary escalation and systemic response. Occasionally, someone can be stung many times before being able to get away. Depending on the number of stings, the person may just hurt a lot, feel a little sick, or feel very sick. Humans can be killed if stung enough times in a single incident. With honey bees the toxic dose (LD50) of the venom is estimated to be 19 stings per kilo of body weight. Obviously, children are at a greater risk than are adults. In fact, an otherwise healthy adult would have to be stung over 1,000 times to be in risk of death, but half that can make you very sick. Most deaths caused by multiple stings have occurred in victims who were known to have poor cardiopulmonary function. A second, potentially life-threatening result of multiple stings occurs days after the incident. Proteins in the venom act as enzymes: one dissolves the ‘cement’ that holds body cells together, while another perforates the walls of cells. This damage liberates tiny tissue debris that would normally be eliminated through the kidneys. If too much debris accumulates too quickly, the kidneys become ‘clogged’ and the patient is in danger of dying from kidney failure. It is important for people who have received many stings in one event to discuss this secondary effect with their doctors. (Wasp stings are as potent in this respect as bee stings.) Patients should be monitored for a week or two following an incident involving multiple stings to be certain that no secondary health problems arise. Treating the sting Most reactions are local and confined to the general area of the sting with pain and a swollen itch, but over 24 – 48 hours they can develop into a much larger area (sometimes the entire extremity. A few hours after the sting more redness, oedema (swelling), and itching develop. Over 12 – 48 hours, the area can become quite swollen, painful, and may also have some associated bruising. The swelling generally begins to resolve after two days, but the site may remain tender (and continue to itch) for a few more days. The total reaction lasts 4 – 7 days. Large locals around the face and mouth or on the hands may cause temporary disability. The large local is IgE-mediated, and therefore is an allergic response. Treatment of local reactions includes ice and elevation with non-aspirin containing analgesics (Ibuprofen), both H1 and H2-receptor blocking antihistamines (diphenhydramine, (Benadryl), famotidine, ranitidine, and non-sedating ones, such as fexofenadine (Allegra), loratidine (Claritin), and ceterizine (Zyrtec), and, occasionally, systemic corticosteroids, such as methylprednisolone, or prednisone, in doses tapered over 2-3 days. Aspirin-containing analgesics should be avoided because both bee and wasp stings may be complicated by local subcutaneous hemorrhage. Taking anti-histamine or a leukotriene-receptor antagonist very soon after the sting may decrease the late phase reaction. Leukotriene-receptor antagonists’ montelukast (Singulair) and zafirlukast (Accolate) block the leukotriene receptors on mast cells and eosinophils and both have peak activity 3 – 4 hours after taking them. In one study of six allergic beekeepers, the skin within their large local reaction and their blood and urine were analyzed 2 hours after a bee sting. Three of them had high histamine levels and the other three had high leukotriene levels, suggesting that allergic beekeepers either have high histamine release or increased leukotriene production, but not both. This implies that about half of beekeepers who have large local reactions might benefit from the immediate administration of a leukotriene inhibitor, whereas the other half would benefit from anti-histamines before or very soon after the sting Oral steroids are useful in treating large locals to stings around the face and hands. The small blisters sometimes formed on the sting wound should be left alone. It is possible to infect the wound if bits of the sting shaft remain or if adequate cleanliness is not observed. Topical treatments Many local and traditional remedies have been recommended for initial management of local hymenopteran stings including the topical applications of tobacco poultices, vinegar, baking soda and salt, aluminum sulfate, and papain, or meat tenderizer. As a rule the clinical activity of all topical treatments for hymenopteran stings (other than ice) is poor, or absent. The more popular ones include; Antihistamines. Histamine is one of the main mediators of the inflammatory response so treatment with antihistamines is indicated. Several topical products containing antihistamines are available for treating the pain, itching and inflammation caused by bites and stings. However, topical antihistamines have been criticized as not being very effective. They are also liable to cause sensitisation so should not be used more often than two or three times a day for up to three days. Oral antihistamines are more likely than topical preparations to bring sustained and effective relief. Hydrocortisone. This has anti-inflammatory activity and hydrocortisone cream is available for treating itching caused by insect bites. However, its usefulness is limited by the directive to limit use to two applications daily, as more frequent application may be necessary to sustain relief. It is not appropriate for use in children under 10 years of age. Once again, oral administration of a corticosteroid, say, prednisone (by prescription), is a more effective treatment. Calamine and zinc oxide. Calamine is made from zinc carbonate with ferric oxide, which is what gives it the characteristic pink colour. It is mildly astringent and its soothing anti-itching action is due to the large surface area and porous nature of its particles, which promote the evaporation of water to cool the skin. Calamine Lotion BP also contains 0.5 per cent phenol which has a local anesthetic action. Calamine has been used for generations for treating hives and itching from many causes, including insect bites. It is cheap and there are few restrictions on its use. Zinc oxide has similar properties. Ammonium sulphate solution (Stingose). This has been claimed to have a de-naturing effect on the proteins introduced by bites and stings, but the claim dates back to one academic paper in 1980 and should be treated with considerable skepticism. There is little or no objective evidence of its effectiveness (except, perhaps, for stings in the marine environment from jelly fish nematoblasts) nor is there a credible explanation of how it would work in the case of subcutaneous terrestrial stings. Systemic, toxic and anaphylactic responses A systemic reaction can be mild and manifest as purely cutaneous (skin) responses like hives (but distant from the sting site) and typically involves the trunk or scalp, and/or a rapidly-developing swelling of the face. Gastrointestinal symptoms may also occur, and include a metallic taste, nausea, vomiting, diarrhea, and abdominal cramps. Attendant neurologic symptoms include light-headedness, dizziness, (which can also have a cardiovascular cause) and tremor. “Systemic and toxic reactions to stings should be managed with supportive care, including oxygen and intravenous fluid therapy, and pharmacotherapy with intravenous analgesics, H1- and H2-receptor blocking antihistamines, and corticosteroids. Anaphylactic reactions must be managed promptly with immediate airway and circulatory support, including subcutaneous and intravenous vasopressors, specifically adrenalin, and intravenous fluid resuscitation.” That’s another way of saying “You need to be in hospital.” All patients at high risk of any systemic allergic reaction to hymenopteran stings, even those who have undergone successful venom immunotherapy, should carry an emergency kit containing pre-filled adrenalin syringes while outdoors and wear a medical alert identification bracelet or tag. Adrenalin must never be injected intravenously, and preferably, not subcutaneously, only intramuscularly. Patients must be cautioned against injecting adrenalin solutions into their fingers, which could result in ischemic distal digital necrosis, over superficial veins, which could result in rapid vascular up-take, or near the sciatic nerve in the upper, lateral quadrant of the buttocks. A study done in Canada showed that adrenalin for first-aid treatment of anaphylaxis in infants using the ampoules/syringe/needle method is not practical. Most parents were unable to draw up an infant adrenalin dose rapidly or accurately. Someone operating under stress is also unlikely to be able to give the correct dose, but an adult body mass will be more tolerant of small mistakes. Fortunately anaphylaxis is a rare event. In the US about 80-90 people a year are killed by lightening (in NZ it’s less than one), and around 40 people die from insect stings (less than half are honeybee stings). In the general population somewhat less than one per cent are likely to be hypersensitive. The prevalence of hypersensitivity reported is not adjusted for climatic differences between regions or countries, and doesn’t account for the temporal or geographical distribution of Hymenoptera. Ocular stings Sting injuries have long been recognized as a significant source of eye trauma. Sting injuries can affect a variety of ocular structures, and patients typically present with an acutely painful red, watery, swollen eye. The area may be indurated (firm and nodular) around the site of sting, and the retained stinger may be visible. In addition to the immunological and toxic effects the eye can suffer significant mechanical harm. The stinger is composed of hard chitin. As noted, the honeybee’s sting is barbed and cannot be withdrawn, and while wasps and bumblebees do not possess a barbed stinger, portions of this structure may occasionally break off and remain in the tissue. Direct injuries to the lid may involve penetration of the tarsus, in which case not only will there bee a reaction to the venom, but also the disembodied stinger may damage the corneal surface. Sting injuries to the ocular structures therefore often result in a puncture wound and infection from a foreign body. Ocular complications include a retained foreign body, conjunctivitis, corneal swelling or perforation, bleeding, uveitis, blistering of the conjunctiva (chemosis), painful corneal inflammation, pupil dilation, optic nerve swelling and damage, including acute and irreversible demyelination of the optic nerve, cataract formation (notable with wasp stings), and deformation of the lens iris and cornea. Retained stingers should be removed carefully and the area should be cleaned. Removal of the stinger with a jeweler’s forceps under biomicroscopy is the only sure way. Cold compresses may be helpful in limiting the secondary inflammatory response. Ice (wrapped in cloth to avoid freezing the skin) should be applied for no more than 20 minutes every hour. Oral antihistamines and anti-inflammatory agents help control associated itching and pain. In addition, more frequent administration of potent steroids for treating uveitis aggressively and proactively has been recommended to help prevent long-term effects, like cataracts, iris atrophy and glaucoma. In particular, for victims with toxic optic neuritis, early intervention with a three-day course of intravenous methyl-prednisone followed by a tapered dose of oral prednisone over seven additional days has been shown to help patients recover their sight following this type of trauma. Beekeepers Beekeepers have a significantly higher probability of being stung, and a far greater exposure to bee-related antigens than the general population. They have a greater risk of allergy and anaphylaxis; various studies have suggested rates of allergy between 17-43%. In a study of German beekeepers 4.4 % reported systemic reactions to bee stings (allergic reactions), 75.6 % reported mild local reactions, and 18.6 % had no reactions to bee stings. Curiously, 25.3 % of the beekeepers reported more severe reactions to bee stings in spring than in later months. There are few studies, but this one also tried to determine what factors might explain the range of values and the risk factors that appear to predict allergy. This analysis revealed that the most significant factors, in descending order of importance, were symptoms of upper respiratory allergy while working with beehives, susceptibility to allergies in general, time spent as a beekeeper, fewer than ten stings per year, and more severe non-allergic reactions to bee stings in spring. In addition, age, and body mass (but not sex), were inversely correlated with the probability of a systemic reaction, but could not be used as a predictive factor. Using the main factors identified by the study the researchers could correctly classify the allergic reactions in 85.2% of the cases. When comparing studies, much of the variance in the incidence of allergy reported could be successfully explained by the age of the beekeepers used by the different studies. To put all this another way, if you are a new beekeeper, young and skinny with a history of other allergies, and develop respiratory or skin problems when handling bee equipment and haven’t been stung much, then your risk of having a systemic reaction one day is much greater compared to the big crocodile-skinned old geezer who hasn’t worn gloves in years and drinks too much beer (but it should decline as you become a crocodile-skinned…). It might be wise to make sure someone knows when and where you are working with bees About 25 % of beekeepers have high anti-bee venom IgE levels, and all beekeepers have increased anti-bee venom IgG. Despite this, anaphylaxis to bee stings only occurs in a minority of these individuals and we don’t know why. Repeated exposure to the venom leads to a change in the way the lymphocytes in the immune system react to the particular offending antigen. The cells switch antibody production from allergic IgE to non-allergic IgG which cannot cause mast cell activation, and there is no subsequent anaphylaxis. Controlled venom immunotherapy is very successful at ‘de-sensitising’ individuals who have become hypersensitive. Even without considering immunology, being stung is, at best, irritating. In the case of stings to the face they can be debilitating, and especially around or on the eyes, permanently disabling. Mass stinging events can be life threatening. Beekeepers use several methods to mitigate the risk, avoidance (by good technique), evasion (planning an escape route), and physical protection (Personal Protective Equipment - PPE). Beekeepers are able to breed strains that show a considerable difference in their propensity to sting and generally select calm, peaceable populations to work with. The most essential of these strategies is to use a well designed veil; we have seen how dangerous a sting to the eye can be. Consider that dark glasses will make the face and eyes a target. Bees that get in under the veil, or get tangled in hair, are best dispatched between finger and thumb. If a lot of bees get in (not just one or two), walk away, if possible cover your eyes and face with your hands and remove the veil to let the bees out. Clothing fulfills various needs (not just protection), and should be practical, comfortable, washable, and light-coloured, and should not trap bees in the fabric or on the inside! Knowledge of bee behaviour allows a beekeeper to anticipate how bees react to visual cues and scents so that, for example, movements are conducted with finesse, and colours, perfumes and smells that disturb the bees are not used or masked. Gentle techniques, and the act of timing hive manipulations favourably, develop with experience. Stings and any squashed bees are best removed and the site smoked so that guarding bees are not encouraged to sting. Hive design and construction, and position, the weather, bee-forage, and the seasonal life-cycle of the colony and its neighbours all contribute to the need for a colony to heighten or lower its defensive response to a beekeeper’s attentions. It is unwise try to ‘work though’ a situation where stinging or robbing is getting out of hand. Caring for others Plan and prepare your response in advance. Communication, transport, supervision, etc. After a sting… Get you and the victim away to a safe area Remove the sting as quickly as possible Relieve the local symptoms with ice, calamine, ibuprofen and liquid/tablet antihistamine as required/available. Observe, and take action if you see · Stings to the eye, mouth or throat · Swelling of lips, neck, face, or eyes when they have not been stung · Hives or welts · Abdominal pain, vomiting ACTION · Stay with patient and call for Ambulance · Give medications if prescribed (eg. Antihistamines) · Locate EpiPen® or EpiPen® Jr if prescribed · Contact emergency contact/parent/carer WATCH FOR SIGNS OF ANAPHYLAXIS (severe allergic reaction) · Difficulty / noisy breathing · Swelling of tongue · Swelling / tightness in throat · Difficulty talking and / or hoarse voice · Wheeze or persistent cough · Loss of consciousness and / or collapse · Pale and floppy (young children) DO NOT GIVE YOUR PRESCRIPTION MEDICINES TO SOMEONE ELSE References Arcieri, Enyr Saran M.D.; França, Edimar Tiago M.D.; de Oliveria, Hailton Barreiros M.D.; De Abreu Ferreira, Lizane M.D.; Ferreira, Magno Antônio M.D.; Rocha, Flávio Jaime M.D., Ocular Lesions Arising After Stings by Hymenopteran Insects, Cornea, April 2002 - Volume 21 - Issue 3 - pp 328-330. James H. Diaz, Hymenopterid Bites, Stings, Allergic Reactions, and the Impact of Hurricanes on Hymenopterid-Inflicted Injuries, (2007), J La State Med Soc VOL 159. B.J. Donovan, Anaphylactic shock and strong cardiac stimulation caused by stings of the bumble bee Bombus terrestris (Hymenoptera: Apidae), The New Zealand Entomologist, 1978, Vol.6,No.4, pp385-389. Buddy MarterreMD., Bee stings, immunology, allergy and treatment, American Bee Journal (Aug 2006). K Münstedt, M Hellner, D Winter, R von Georgi, Allergy to Bee Venom in Beekeepers in Germany, J Investig Allergol Clin Immunol 2008; Vol. 18(2): 100-105. Hiten G Sheth, and Timothy J Sullivan, Optic neuropathy and orbital inflammatory mass after wasp stings, J R Soc Med. (2004) September; 97(9): 436–437. P Kirk Visscher, Richard S Vetter, Scott Camazine, Removing bee stings, (1996), The Lancet, Volume 348, Issue 9023, Pages 301-302. Dave Black (2013)
  15. Is it even possible to make things worse? The legal definition of mānuka honey could change, if new evidence shows the chemical makeup of the honey is different in Northland, MPI says. https://www.radionz.co.nz/news/national/385953/devastated-northland-manuka-honey-producers-seek-chemical-markers-definition-review-from-mpi
  16. Humanity. Humility. Something like that. Man you're getting a fan club. I'm going to beat my chest now and pour a whisky. That will be all.
  17. Social insects like honeybee living in close proximity have a higher risk of spreading diseases and poisons among nestmates, so we would expect to find mechanisms that mitigate this. One of these systems is an innate immune system that provides an antimicrobial film on their exoskeleton, a hostile gut environment, a peritrophic membrane and gut epithelium, and effective cellular and humoral defences. These secrete antimicrobial chemicals, engulf or entomb foreign materials, and provide enzymes that degrade or destroy pesticides and pathogens. The genetic precursors for all this are ancient, common to invertebrates and invertebrates, and consequently fairly well understood. If we compare honey bees to other solitary insects we find that, relatively, honey bees have about a third as many of the genes known to be associated with disease immunity. Partly that is likely to be because they are targeted by fewer, more specialist pathogens, and live in a very stable nest environment, but it’s also because they use a highly developed strategy that combines behavioural traits that together provide a social immunity. Collectively, they construct or maintain nests using antimicrobial materials, keep their young in hygienic, homeostatic, sterile nurseries, create a ‘fever’ in response to disease, functionally exclude foraging bees from parts of the nest, groom, exhibit ‘altruistic’ suicide, and delegate risk-taking to expendable members of the group. These behavioural traits seem particularly important and yet we know very little about them, how they work, and how they are inherited, even after decades of ‘trial & error’ field research has shown that they are highly effective and highly inheritable. A group of researchers in Canada are involved in a long-running project studying the basis for inheritance of this social immunity. The scale and duration of the study differentiates it from most. Their most recent paper was just published last month. For this study they created two selected populations (of 100 colonies each) that express hygienic behaviour (using freeze-killed brood) across three generations relative to a ‘baseline’ 100 colony population (control). They used genome sequencing to identify genetic ‘loci’ that were associated with the variation in behaviour. The genome sequencing allowed them to consider 2,340,950 SNPs. (Think of SNPs as alterations in DNA sequences – a person will have four to five million SNPs in their genome). The researchers identified regions in the genome that differed between the study and control group down the generations, homing in on 10,140 SNPs, and then compared their candidates to six other, independent studies which at first zeroed in on 2,058 SNPs in 99 regions in the genome, and they then refined that to 73 protein-coding genes that looked to be the most significant in terms of hygienic behaviour. Usefully, perhaps surprisingly, 85-90% of these genes were not unique to honey bees but are shared with other hymenoptera and insects in general. These genes are already all known to be associated with the functioning of features of the neurological system, for example in nerve growth and signal transmission, and olfaction. Rather than novel genes being responsible for hygienic behaviour, it seems that existing genes and gene networks are conserved and ‘repurposed’ during adult development or maturation, perhaps by a difference in the regulation of a pre-existing ‘tool-kit’. But keep that 73 genes in mind. The authors also claim that the ancient genetic ancestry of their selected, hygienic genes had much more in common with C-lineage (Central European) Apis bees (ligustica; carnica) than M-lineages (mellifera) or O, A, Y (Mid-East, Africa, or Yemen, Saudi). This is interesting because many other studies (six are mentioned) have independently come to the same conclusion, that C-lineage bees (carrying C-lineage genes) have superior hygienic abilities. This is the fourth paper in this vein from this group so far. They began (2010) by looking for signs of local adaption in honey bees, establishing and comparing populations from within Canada, but also including some from Chile, California, Hawaii, and Hawkes Bay, because that was where they were buying queens and packages from. They were interested in seeing what trade-offs were being made, if any, by the necessary import of, possibly, mal-adapted stocks. They were able to show distinct metabolic adaptions that related to the geographical source; in some respects, metabolically, NZ bees had more in common with Chilean bees that with Canadian bees. In their words, “The populations studied… may represent separate geographical ecotypes, where metabolic control and protein synthesis/folding mechanisms has been finely tuned to confer fitness to local environmental pressures such as climate, food resources, predation and diseases.” The second paper released (2015) used a subset of the same bee population (without the NZ bees as far as I can tell) to see if it would be possible to use molecular markers rather than behavioural tests to select more disease resistant stock, since that would be faster. They suggest biomarkers in the form of the expression of a particular set of proteins would be a better tool than conventional Marker-Assisted-Selection (They looked specifically at odorant-binding proteins in antennae that correlated with hygienic behaviour). The third paper (2017) has a more detailed demonstration of an ‘expression marker’ as they call it, successfully testing the idea against AFB and varroa in a selection and breeding programme lasting three years. This is how they sum up that paper; “[Marker Assisted Selection - MAS] has the potential to be more precise and more robust to external influences; it has been widely used in certain plants and animals. To date, however, the markers used have been genomic loci exclusively...undoubtedly due, in part, to the availability of efficient genetic approaches for finding such markers. It is also a matter of focus: researchers have spent more time looking for genetic loci than for expression markers... Here we have shown that expression markers can be used to select for a very complex, polygenic trait. (Remember the 73 genes?) Even in this proof-of-principle with a first-generation panel of markers, MAS was as efficient at enriching disease-resistance as Field Assisted Selection [FAS] methods: bees bred using marker-assisted selection could resist levels of disease that would typically kill 70% or more of unselected colonies. The data presented here have implications beyond bees: this is the first demonstration of marker-assisted selection in livestock using expression markers and it enables molecular diagnostic approaches for selecting complex polygenic traits that are recalcitrant to genetic mapping methods. After three generations of selection, the resulting marker-selected stock outperformed an unselected benchmark stock in terms of hygienic behaviour (sic), and had improved survival when challenged with a bacterial disease or a parasitic mite, similar to bees selected using a phenotype–based assessment for this trait. This is the first demonstration of the efficacy of protein markers for industrial selective breeding in any agricultural species, plant or animal.” Just because I can - it seems to be a major topic of discussion at the moment, I’m going to note how all this was funded; a muti-site, international, nine year project using several hundred colonies and some expensive, novel, lab work. Here is a list of the bill-payers; Genome British Columbia, the British Columbia Honey Producers Association, the Canadian Honey Council and Canadian Association of Professional Apiculturists through the Canadian Bee Research Fund, the British Columbia Blueberry Council, the British Columbia Cranberry Marketing Association, Agri-Food Canada’s Advancing Canadian Agriculture and Agri-Food (ACAAF) program, Ontario Genomics, a Discovery Grant from the Natural Sciences and Engineering Council (NSERC) of Canada, Genome British Columbia, Genome Alberta, the University of British Columbia, the University of Manitoba, and the US Department of Agriculture. I haven’t included odd scholarships or research grants supporting the tenure of individuals. Food for thought. Brock A. Harpur, M. Marta Guarna, Elizabeth Huxter, Heather Higo, Kyung-Mee Moon, Shelley E. Hoover, Abdullah Ibrahim Andony P. Melathopoulos, Suresh Desai, Robert W. Currie, Stephen F. Pernal, Leonard J. Foster, and Amro Zayed. (2019) Integrative genomics reveals the genetics and evolution of the honey bee’s social immune system. Genome Biol Evol. 2019 Feb 15. doi: 10.1093/gbe/evz018 Guarna MM, et al. 2017. Peptide biomarkers used for the selective breeding of a complex polygenic trait in honey bees. Scientific Reports 7: 8381. Guarna MM, et al. 2015. A search for protein biomarkers links olfactory signal transduction to social immunity. Bmc Genomics 16: 63. doi: 10.1186/s12864-014-1193-6 Parker R, Melathopoulos AP, White R, Pernal SF, Guarna MM, Foster LJ. (2010) Ecological adaptation of diverse honey bee (Apis mellifera) populations. PLoS One. 2010;5(6):e11096.
  18. This is interesting, in a sort of 'Law of unexpected consequences' kinda way. See here, https://www.nzbees.net/forums/topic/7757-entomopathogenic-fungi/?tab=comments#comment-119565 and here, https://www.nzbees.net/forums/topic/11756-fungi-and-non-chemical-treatment-of-varroa-and-other-illnesses/?tab=comments#comment-185124 Summary Honeybee colonies are under the threat of many stressors, biotic and abiotic factors that strongly affect their survival. Recently, great attention has been directed at chemical pesticides, including their effects at sub-lethal doses on bee behaviour and colony success; whereas the potential side effects of natural biocides largely used in agriculture, such as entomopathogenic fungi, have received only marginal attention. Here, we report the impact of the fungus Beauveria bassiana on honeybee nestmate recognition ability, a crucial feature at the basis of colony integrity. We performed both behavioural assays by recording bee guards’ response towards foragers (nestmate or non-nestmate) either exposed to B. bassiana or unexposed presented at the hive entrance, and GC-MS analyses of the cuticular hydrocarbons (CHCs) of fungus-exposed versus unexposed bees. Our results demonstrated that exposed bees have altered cuticular hydrocarbons and are more easily accepted into foreign colonies than controls. Since CHCs are the main recognition cues in social insects, changes in their composition appear to affect nestmate recognition ability at the colony level. The acceptance of chemically unrecognizable fungus-exposed foragers could therefore favour forager drift and disease spread across colonies. Federico Cappa, Iacopo Petrocelli, Francesca Romana Dani, Leonardo Dapporto, Michele Giovannini, Jeferson Silva-Castellari, Stefano Turillazzi & Rita Cervo. (Feb.2019) Natural biocide disrupts nestmate recognition in honeybees, Nature Scientific Reports, 9:3171, https://doi.org/10.1038/s41598-019-38963-3
  19. All Hymenoptera have haploid males.
  20. This would be a topic for Nelson, @npomeroy Well most of your suppositions seem to me correct, both 'bees feed and 'poop' under the same conditions, mostly on the wing, outside, but sometimes in your hand, in a petrie dish, or on a flower or leaf. I would say bumblebee's poo is more watery, less waxy, but that's about the extent of the difference as far as I've seen. And yes, people do collect it in a petrie dish - to look for pollen or parasite DNA. An area that's not clear to me is what queens do when they are incubating on their own early on, and later when they no longer leave the nest. I think it unlikely that they contribute to your neighbour's decorations simply because there aren't enough of them, they fly lower, and don't have the same consistent, shared flight-path. If you want to think a bit more about bumble bees, how about wondering about how queens, and workers develop. Royal Jelly doesn't seem to be a bumble bee 'thing'!
  21. These reports are published annually on the Forum; have been since 2009.
  22. I can't see what the set up has to do with not liking QXs, but put that to one side. Can you explain why you think that bees 'naturally' work downwards?
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