Not totally bulging at the seams but definitely growing. This is the 2 frame nuc that I have been feeding protein substitutes and sugar syrup all winter. They finally graduated to a second brood box today. By the End of October I think they will be ready to split and add a mated queen to The queenless half. Bam! doubled a hive count instantly and plenty of time to build up for the summer honey flow.
The drawn empty frame I checkerboarded a week or so back has now been populated with eggs and newly hatched larvae, honey and pollen stored as well. There is lots of natural pollen coming in now and the bees have mostly left the pollen patties alone.
As the colony grows there are a couple of older brood frames that will be cycled out to make way for new frames.
For most of us viruses are confusing. Many people are unable to distinguish between viruses and bacteria and expect them to be much the same kind of thing, which they are not. Viruses don’t fit easily in to the various categories of living things we are used to dealing with, and actually whether they even are living organisms is arguable, and how they came to be still more controversial. Which is why there is never a clear answer about how we might kill a harmful virus.
Viruses are not cells and can’t reproduce on their own, and some see them merely as parcels of genetic material (most often RNA) that have just gone rogue, a molecular accident. To coin a phrase ‘bad news in a protein coat’, although, not all viruses are harmful. For others they are an extreme simplification evolved from ancient living cells. At the moment, the former guess seems the more likely.
Part of the reason for that is a growing understanding about how cells communicate. While we have known for a long time the cells can secrete chemicals, it’s only in the last ten years or so that scientists have realised that they do much more. Cells produce small ‘packages’ of molecules, including the RNA that can be translated into proteins or which affect gene expression, in great quantities all the time, and in every body fluid they have tested. These packages are produced as ‘bud’s from the cell wall, or from within the cell contents and released through the cell wall, and many of them are uncannily like viruses in size and structure. Not un-naturally this has led to speculation that maybe extra-cellular vesicles and viruses were two extremes on the same continuum.
The evidence that ‘messenger’ fragments of RNA in extra-cellular vesicles are a form of communication is substantial, and we are beginning to realise how widespread this is, finding it throughout animal and plant kingdoms. What is also becoming clear that part of this communication is involved in the on-going ‘war’ between infectious viral agents and their hosts, facilitating or defending against invasion. Viral RNA communicated to another organism in an extra-cellular vesicle can pre-emptively prepare a response, a non-infectious vesicle-virus ‘inoculating’ a host against the infectious ‘real thing’. Scientists have also found instances where host genetic material and viral genetic material have become intertwined over millennia, not just as junk or contamination, but conferring new functions on the host. Viruses seem to provide a ‘library’ of genetic material, freely used by all other organisms.
Instances of RNA ‘interference’ (iRNA) in honey bee biology have popped up in recent years. It has been suggested that iRNA (or gene ‘silencing’) has a role in determining honey bee castes (worker vs queen) and other epigenetic effects, and that a honey bee virus (IAPV, once talked about as a candidate for causing CCD) can be treated with iRNA from the right dsRNA fed in syrup. An iRNA treatment for varroa mites is the subject of a US patent*. iRNA is now known to be an important response to control viral infections in many insects, not just bees. What the latest paper from Maori et al (who hold the RNA/varroa patent) suggests is that social honey bees have the ability to pass an acquired immune response to each other and to larvae while food sharing, providing long-term, intergenerational, colony level protection circumventing a non-existent hereditary mechanism and boosting a naturally depauperate immune response.
“It is generally agreed that RNAi evolved as a defense mechanism against selfish nucleic acids and further diversified to regulate endogenous gene expression. The presence of differential naturally occurring RNA among worker and royal jellies points towards a potential effect of transmissible RNA on genome function in recipient bees. Indeed, supplementing jelly with endogenous or exogenous miRNAs that are naturally enriched in worker jelly affected gene expression as well as developmental and morphological characters of newly emerged workers and queens. We speculate that bee to-larva RNA transfer could also play a role in epigenetic dynamics among honey bees…”
Esther Nolte-‘t Hoen, Tom Cremer, Robert C. Gallo, and Leonid B. Margolis (2016). Extracellular vesicles and viruses: Are they close relatives? PNAS August 16, 2016 vol. 113 no. 33 9155–9161. www.pnas.org/cgi/doi/10.1073/pnas.1605146113
Knip M, Constantin ME, Thordal-Christensen H (2014). Trans-kingdom Cross-Talk: Small RNAs on the Move. PLoS Genet 10(9): e1004602. doi:10.1371/journal.pgen.1004602
Zhu, K., Liu, M., Fu, Z., Zhou, Z., Kong, Y., Liang, H., Lin, Z., Luo, J., Zheng, H., Wan, P., et al. (2017). Plant microRNAs in larval food regulate honeybee caste development. PLoS Genet. 13, e1006946.
Garbian, Y., Maori, E., Kalev, H., Shafir, S., and Sela, I. (2012). Bidirectional transfer of RNAi between honey bee and Varroa destructor: Varroa gene silencing reduces Varroa population. PLoS Pathog. 8, e1003035.
Eyal Maori, Yael Garbian, Vered Kunik, Rita Mozes-Koch, Osnat Malka, Haim Kalev, Niv Sabath, Ilan Sela and Sharoni Shafir, A transmissible RNA pathway in honey bees (2018). bioRxiv preprint, doi:http://dx.doi.org/10.1101/299800.
Inspection of the nucleus colony today was pivotal in the development of this colony. The queen had all but run out of space to lay. 5 frames had about 80% coverage by attached bees and more out foraging.
Rather than potentially stalling the egg laying through having no empty cells To lay in I made the decision to transfer the colony to a 10 frame box.
Whilst transfering I placed an empty drawn frame 2 frames in from the internal feeder with the thought of providing a new brood frame for the queen to start laying in.
This stimulation process has proved to be effective in growing a small colony over winter and is something I will look to replicate next winter with more colonies.
I will keep posting in this blog throughout the season as the colony grows and moves in to honey production.
Colony is still expanding. Brood area is increasing significantly. Still shot gun pattern although every cell has either a pupae, larvae or egg in it. Some dodgy cappings but all inspection of larvae, pupae come up negative for AFB.
If the laying pattern doesn’t improve by October this queen will be culled and replaced with a new season queen. Which is a shame as the current queen is an April 2018 mated queen.
Getting colonies sorted today for a sale I made, so while in the back yard I checked on the nucleus colonies I have been building up over the past few months.
Nucleus 1 is now covering 4 frames and has 2 frames with brood on both sides, a total coverage of about 1.5 FD frames.
This is excellent and the colony is heading in the right direction. By the end of August I reckon I will be moving them over to a 10 frame box.
Nucleus 2 has done extremely well and today was used to make up a larger colony with the addition of Bees and brood frames from a very strong 2 box colony ( it had Drones in Drone cells and 6 frames of capped worker brood).
Another Nucleus colony that has been part of the experiment was used to requeen a queenless colony. This was done with newspaper over the bottom queenless colony then a queen excluder. The plan is to have the two colonies combine but give the queen a bit of protection until they become a happy family.
Overcast afternoon. Venturing out to the back yard recovering from a migraine.
Over the past month or so I have been feeding a couple of nucleus colonies 1:1 syrup with seaweed extract added. Also 1/3 of a Megabee premade patty.
Nucleus 1 has continued to increase the brood area and there is a continuous emerging of new Bees now, and in turn the population is noticeably getting larger to care for the corresponding increase in brood. I added 1 Apivar strip after adding some bees from a queenless colony that had missed the treatment round. A few dead varroa were noted on the floor of the nuc box.
Nucleus 2 has been treated the same way. This colony started the process with no brood. The colony is smaller than Nuc 1 however the queen started laying with the addition of 1:1 syrup and later pollen substitute was added. Brood area and newly emerged Bees have seen this colony also noticeably increase in size.
Both nucs have brood areas that, when emerged will start to have a significant impact on how the colony functions. They will be getting to a point of criticle mass and will continue to increase in numbers very quickly.
looking good so far -
The promiscuity of honey bee queens generates lots of interesting questions about social insect society, many of which relate to the many different ‘sub-families’ that co-exist within a colony. For example, do individuals within a colony overcome their self-interest to rear the ‘best’ replacement queen in an emergency or do they try to pick their closest relative? Just how far does social co-operation extend? Emerging recent research is starting to suggest that, apart from picking well-fed larvae of the optimum age, workers tend to select larvae from particular ‘royal’ sub-families. If that turns out to be true, we may well have some of our ideas about honey bee queens wrong.
Most of our contemporary ideas about the ‘families’ in a honey bee colony stem from studying the genetics of individuals in the colony. The workers in the hive are all sisters, daughters of one queen ‘mother’, but they have many fathers, depending on which particular sperm fertilised the egg they hatched from. Usefully, the lengths of inherited genetic material we call genes contain non-functioning stretches of repetitive elements that we can look at easily. These are known as ‘microsatellite’ markers, and because they don’t code (for proteins) chance changes in these areas don’t affect protein coding and can accumulate, providing a record of change and relationship we can read. Typically researchers amplify the sections of DNA they are interested in using PCR, at the same time tagging the microsatellites with fluorescent markers. As the repeated sequences have different lengths and masses these can then be seen using (for example) chromatography. Researchers will choose a number of microsatellite markers that are relevant to whatever they are studying, say 3 – 8 different ones, and then group individuals that share common sets of markers.
People looking at this sort of thing will collect lots of workers, analyse the microsatellite markers, and work out the number of different drones there must have been in order to produce the number of different families of worker they have. They have shown that, for a considerable period (many months), the composition of the families remains much the same, suggesting that drone semen is pretty well mixed after mating and used randomly. Over the long term however (up to 4 years) the make-up of the sub-families do change, possibly a consequence of the filling sequence and changing sperm density in the spermatheca, and maybe evidence of ‘cryptic female choice’ or sperm competition in honey bee queens.
Lately, some studies have begun to include queens in the microsatellite analysis, and discovered sets of families that are unique to queens and do not appear if you just examine worker offspring. These ‘extra’ families suggest that queens actually mate with more drones that we thought, rather than 10 – 20 being a ‘normal’ number, 20 – 40 might be more accurate, and actually more in line with that reported for other honey bee species. These ‘royal’ sub-families appear to be quite rare, and stay that way, despite the apparent advantage natural selection would give them if they are more attractive to queen-rearing nurses. That’s likely to be because emergency queen rearing is a relatively rare event so workers seldom get a chance to exercise any preference, and because there are other factors that determine the result in any case. Nevertheless several studies suggest that, in the case of queens raised in an emergency, the choice of which larvae to pick is biased towards particular ‘royal’ subfamilies rather than towards the workers’ own subfamilies.
Withrow JM, Tarpy DR (2018) Cryptic "royal" subfamilies in honey bee (Apis mellifera) colonies. PLoS ONE 13(7): e0199124. https://doi.org/10.1371/journal.pone.0199124
Moritz RFA, Lattorff HMG, Neumann P, Kraus FB, Radloff SE, Hepburn HR. (2005) Rare royal families in honeybees, Apis mellifera. Naturwissenschaften. 2005; 92:488±91. https://doi.org/10.1007/s00114-005-0025-6 PMID: 16151795
Brodschneider, R., Arnold, G., Hrassnigg, N., and Crailsheim, K. (2012) Does Patriline Composition Change over a Honey Bee Queen's Lifetime? Insects 2012, 3, 857-869; doi:10.3390/insects3030857 ISSN 2075-4450
Nucs are going OK with 1-1 1/2 frames of brood and some older brood starting to emerge.
Today I topped up syrup and added another 1/2 of a MegaBee pattie.
Brood area is increasing in all the hives. Nuc #1 has some dodgy looking capping so I have inspected those and a few more cells. All is OK so far but I will remain alert the this in future inspections.
OK so a quick look in the nucs today. Overcast grey skies but relatively warm so lots of bees were out flying and good amounts of pollen on the returning bees. Colours ranged from vivid orange, yellow and a small amount of white.
Todays task was to add about 500ml - 1 litre of 1:1 syrup to each nuc feeder and have a look to see if brood rearing has increased.
Both nucs are chomping through the Megabee pattie and all the syrup add last week has on the whole been consumed with a small amount evident as freshly stored syrup in the empty comb.
#1 nuc has gone through nearly half of the pattie and the other nuc which has a smaller population is consuming it from underneath between the frames.
Surface area of brood in #1 nuc has doubled since last inspection. Nice fat larvae lying in plenty of feed. Fresh eggs obvious in cells as well. Even saw a fairly young Drone, perhaps with sufficient food available they are willing to care for a Drone or two.
Nuc #2 although it is a smaller population has suprised me with a brood area nearly quadrupled since last inspection. Lots of eggs and larvae ranging from 3 days to a week old.
Pretty pleased with how how this is tracking. Stimulating the queens to start laying more seems to have been a success, now we just need to maintain it.
It’s 8.58pm and I am sitting by the fire. To date I have added a pollen patty to all of the 5 frame nucs and fed them copious amounts of syrup to get at least 3 frames of feed in the boxes. So far this has worked. There are a few 3 frame nucs that are house in 3 way boxes. They, apart from only 3 frames of bees are looking happy and the combined warmth from sharing a common hive body seems to be helping them. Each of these 3 way nucs has a 500ml container sitting above on the hive mat. This feeds each colony over a week or two. I will be keeping a close eye on them and look to move them in to 5 frame boxes closer to spring.
Plans are to take pics of the colonies where possible. I will probably focus on 1 or 2 for the photos to show progress or lack of progress where applicable.
I have been experimenting with moisture removal over the last few years and we now have the ability to build machines to remove water at 4 litres p/hr from honey at 35 degrees. If you have fermentation issues or concerns I have been investigating this issue a lot but there is still lots to learn. Always keen to share and learn from others.
Looking for somebody that may have some beehives that they may wish to put on our property that has many fruit trees and a large garden.
We are in the middle of a big residential area that has plenty of food for bees so would be very keen to hear from somebody.
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
The bacterial brood disease American Foul Brood (AFB) occurs worldwide and leads to significant losses of honey bee colonies every year. In several countries, as in New Zealand, AFB is a notifiable disease and infected bee colonies have to be burned to contain the disease. Although it has been under investigation now for more than a century, the underlying characteristics of the host–pathogen interactions on larval level remain elusive. An effective treatment of AFB does still not exist, partly since the progression of the disease following ingestion of spores has only been described superficially.
The bacteria that cause AFB belong to a large group of similar bacteria that can be both extremely useful and highly damaging. In 1988 scientists began to divide the main 'bacillus' classification into smaller, more comparable sub groups based on genetic, phylogenic principles rather than morphology, and one of the initial five sub-groups was 'Paenibacillus'. Literally, 'almost' bacillus. The species known for AFB became Paenibacillus larvae. The continual re-evaluation of the groups has led to the re-naming of some new species and the re-classification of existing species so that the classification continues to grow, and the genus currently has about 200 species. Paenibacillus is still expected to undergo significant taxonomic subdivision as these useful or otherwise relevant Paenibacillus continue to be studied, more are added, and the groups get unreasonably large.
Many species of Paenibacillus produce antimicrobial compounds that are useful to fields like medicine, agriculture, industrial chemistry or bioremediation. Another well-known aspect of Paenibacillus is its role in the spoilage of milk and other dairy products, where its enzymes and metabolic products negatively impact the flavour or texture of dairy products, in, for example, the milk curdling caused by proteases. One of the challenges is that Paenibacillus are 'psychrotolerant' spore-forming bacteria. They form hardy spores, and function well at low temperature. Many Paenibacillus strains grow well in refrigerated temperatures used for storing milk. They represent more than 95% of bacteria in raw milk after 10 days of refrigerated shelf life, while spoilage of pasteurized milk due to Paenibacillus is delayed by the germination process of spores and usually occurs after 17–21 days. Paenibacillus species have also been used as pesticides to kill agricultural pests in a variety of ways. The chitinase enzymes they produce hydrolyse chitin, which is a structural polysaccharide of insect exoskeletons and gut linings. Like other bacteria, Paenibacillus species compete with other micro-organisms through the production of a wide range of antimicrobial compounds. All these general properties of Paenibacillus - curdling proteases, cool temperature range, chitin-destroying enzymes, persistent spores, and antimicrobial activity, are apparent in the symptoms produced by honey bee colonies infected by Paenibacillus.
For beekeepers, we know AFB is caused by strains of Paenibacillus larvae, each identity named after particular gene sequences known as ERIC (Enterobacterial Repetitive Intergenic Consensus) sequences. ERIC I and II are the types typically isolated from hives; ERIC III and IV are not considered to be significant. ERIC II is the most virulent strain, but ERIC I is more prevalent globally, not just because it can infect all honeybee subspecies, whereas ERIC II has been confined to to certain subspecies, but also because, being less virulent, it is more likely to be found. ERIC II will kill larvae in just 6 to 7 days. This strain produces a unique protein which facilitates attachment of the bacteria to part of the honeybee’s midgut. By contrast, ERIC I takes up to 12 days to kill infected larvae. The earlier larvae die the more effectively they can be removed as part of the social immune response of honey bees. By removing the dead larvae quickly during normal brood hygiene fewer bacterial spores are produced and spread in the hive. As a worker larval stage lasts six days ERIC I strains tend to die as pupae, while ERIC II strains can have deaths in open brood which are easily detected and removed by the bees. In one study only around 5% of ERIC II infected larvae died after cell capping, while 27% of the ERIC I infected larvae died after capping.
Reports about the variable behaviour of AFB infections, and of the disappearance of infections in some circumstances, are presumably explained by the different expression of symptoms for each strain, and the variation between different strains and races of honey bee. For example, different species of honeybees produce subtly different royal jelly proteins, and this seems to affect their vulnerability to P. larvae infections. Apis mellifera ligustica’s royal jelly proteins are known to differ from those produced by Apis cerana. Interestingly, this difference in activity may provide Apis mellifera ligustica faster metabolic function and enhanced immune activity, and so the strain is a little more resistant to P.larvae (and A.apis) than is Apis cerana in that larval exposure to the spores results in infection less frequently. This may also help to explain the specificity observed in P. larvae ERIC II infections. Until recently it had been assumed ERIC II was restricted to northern and central Europe, Argentina and Uruguay, but examples have now (2014) been isolated in Canada and New Zealand (Schäfer 2014).
Honeybee larvae are most susceptible to infection by the bacteria's spores within the first 36 hours after egg hatching when larvae are fed with accidentally contaminated food. After metamorphosis bees are not susceptible to infection by the spores. As pupa they are not fed, and as adults they are able to void any spores they ingest. Foul brood eventually kills all the colony's offspring so there are no replacement workers to replace aging and dying individuals and the colony will collapse, often succumbing to robbers that spread the infectious spores in the process. Only a few spores are needed to initiate infection, but the number depends on the age, caste, and genetics of each larvae. As a rule, very young larvae are fed with brood food produced by nurse bee head glands, but as they age this food is progressively diluted by adding some of the honey or nectar content regurgitated by the nurses, increasing the risk of contamination. This is mitigated to an extent by the nurse's proventriculus filtering out spores, and with increasing age the larva's gut environment becomes progressively more hostile to the bacteria. By 48 hours after egg hatching most larvae are no longer vulnerable to the bacteria. The phospholipid lysophosphatidylcholine (LPC) has been identified as an antibacterial compound in honeybee midguts in both naturally developed and artificially reared honeybees. The concentration of LPC in royal jelly was below the limit of quantification, which probably indicates that it is not produced from the head glands. On the other hand, feeding experiments using fluorescent-labelled LPC indicate that it is delivered to young larvae with regurgitated honey stomach content to larvae. Fluorescence was found in middle-aged and older larvae to a higher extent than in young larvae, which corroborates that the delivery route via honey stomach becomes increasingly important with larval age. In older larvae and adults, in addition to a fully-formed peritrophic membrane, LPC is present in honeybee midguts, coexisting with the normal gut microbiota, as a permanently active immune trait representing a first line of defence against AFB and other infections. A healthy (lipid-rich) pollen supply is partly responsible for enabling LPC production.
Spores that have been ingested germinate rapidly in the midgut of infected larvae. Soon after ingestion vegetative bacteria can be found randomly distributed in the midgut cavity or 'lumen' and proliferate in the following days. Four to five days post infection the guts of larvae can be filled with P. larvae, while no bacteria are detected in the body, the midgut epithelium remains intact, and the 'bolus' containing the bacteria is still contained with the insect's peritrophic membrane, protecting the gut lining. This membrane, common to most insects, begins to form in larvae after about 8 hours and is thought to have evolved from the mucus lining the gut cells. It will in time form a barrier to protect the bees from mechanical abrasion and invasion by micro-organisms. As the bacteria multiply in the gut cavity they release compounds that have antibacterial and antifungal properties that kill any and all other species that might compete in the space. Metabolic fingerprinting (tracing carbon use) of P. larvae has revealed that this bacterium is able to use different sugars and sugar derivatives as a carbon source, so that the larval food and chitin containing larval structures can serve as food during this phase of infection. Both strains use chitinases that will degrade the peritrophic membrane for nourishment and once degraded they have access to the midgut lining. They eventually penetrate the midgut epithelium and migrate through the spaces between the cells into the haemocoel using an extensive arsenal of enzymes that destroy the proteins and collagen that bind the cells together, or bind the cells to extracellular matrices. At this point he host larvae dies and the toxins and enzymes produced continue to destroy and homogenise the body contents. When the larva dies a pure culture of P.larvae is present, a mix of both vegetative bacteria and bacterial spores. While we have always thought that the bacteria begins to form long-lived spores as a response to the immanent consumption of its food supply it is now clear that spore formation begins immediately and continues through the entire infection process.
This article is available as a Portable Document (.pdf) here; The bacterial brood disease American Foul Brood.pdf
Photographs 1. An infected and normal pupa, cell cap removed, both 13 days old. The infected lava shows no body differentiation or segmentation and gravity makes it slump or ‘melt’ into the bottom of the cell. (Genersch 2010) 2. An advanced infection, with ragged and perforated and ‘wet’ cell caps, ooze through the cap, and scales forming on the cell floor. Note the brown colour of the exposed pupa. (Bee Informed Partnership) 3. Top/bottom row. Fluorescent markers added to the bacteria highlight the bacteria green against the yellow (or red) body parts. In B the large arrow points to a break in the gut wall. The images in the bottom row are of an uninfected larva. (Yue et al 2008) 4. Electron micrograph of a single P.larvae spore. The germ cell of the spore itself starts at position ‘GW’. The outer coats make it extremely resistant to desiccation, direct heat, chemicals, and antibiotics. (de Guzman et al 2011)
References and Reading
Current knowledge and perspectives of Paenibacillus: a review, (2016) Grady et al. Microbial Cell Factories 15:203 DOI 10.1186/s12934-016-0603-7
Reclassification, genotypes and virulence of Paenibacillus larvae, the etiological agent of American foulbrood in honeybees - a review, (2006) Ainura Ashiralieva, Elke Genersch Apidologie, 37 (4), pp.411-420.
Strain and Genotype-Specific Differences in Virulence of Paenibacillus larvae subsp. larvae, a Bacterial Pathogen Causing American Foulbrood Disease in Honeybees, (2005) Elke Genersch, Ainura Ashiralieva, and Ingemar Fries Applied and Environmental Microbiology, Vol. 71, No. 11 p. 7551–7555. doi:10.1128/AEM.71.11.7551–7555.2005
Rapid identification of differentially virulent genotypes of Paenibacillus larvae, the causative organism of American foulbrood of honey bees, by whole cell MALDI-TOF mass spectrometry. (2014) Marc Oliver Schäfer, Elke Genersch, Anne Fünfhaus, Lena Popping, Noreen Formell, Barbara Bettin, Axel Karger. Veterinary Microbiology Volume 170, Issues 3–4, Pages 291-297 https://doi.org/10.1016/j.vetmic.2014.02.006
How to Kill the Honey Bee Larva: Genomic Potential and Virulence Mechanisms of Paenibacillus larvae, (2014) Djukic M, Brzuszkiewicz E, Funfhaus A, Voss J, Gollnow K, et al. PLoS ONE 9(3): e90914. doi:10.1371/journal.pone.0090914
Paenibacillus larvae Chitin-Degrading Protein PlCBP49 Is a Key Virulence Factor in American Foulbrood of Honey Bees, (2014) Garcia-Gonzalez E, Poppinga L, Funfhaus A, Hertlein G, Hedtke K, et al.
PLoS Pathog 10(7): e1004284. doi:10.1371/journal.ppat.1004284
Fluorescence in situ hybridization (FISH) analysis of the interactions between honeybee larvae and Paenibacillus larvae, the causative agent of American foulbrood of honeybees (Apis mellifera), (2008) Dominique Yue, Marcel Nordhoff, Lothar H. Wieler, and Elke Genersch. Environmental Microbiology 10(6), 1612–1620 doi:10.1111/j.1462-2920.2008.01579.x
Lysophosphatidylcholine acts in the constitutive immune defence against American foulbrood in adult honeybees, (2016) Ulrike Riessberger-Gallé, Javier Hernández-López, Gerald Rechberger, Karl Crailsheim & Wolfgang Schuehly. www.nature.com/scientificreports/ Scientific Reports | 6:30699 | DOI: 10.1038/srep30699.
Honey bee age-dependent resistance against American foulbrood (2001) Karl Crailsheim, Ulrike Riessberger-Galle. Apidologie 32 (2001) 91–103 91.
Response of in-vitro reared honey bee larvae to various doses of Paenibacillus larvae larvae spores, (1998) Camilla J. Brødsgaard, Wolfgang Ritter, Henrik Hansen Apidologie, 29 (6), pp.569-578.
Involvement of secondary metabolites in the pathogenesis of the American foulbrood of honey bees caused by Paenibacillus larvae, (2015) Sebastian Muller, Eva Garcia-Gonzalez, Elke Genersch and Roderich D. Sussmuth The Royal Society of Chemistry Nat. Prod. Rep., 2015, 32, 765.
Radiation inactivation of Paenbacillus larvae and sterilization of American Foul Brood (AFB) infected hives using Co-60 gamma rays, (2011) De Guzman, Z.M., et al Applied Radiation and Isotopes, 69 pp1374-1379 doi:10.1016/j.apradiso.2011.05.032
American Foulbrood in honeybees and its causative agent, Paenibacillus larvae, Elke Genersch, (2010) Journal of Invertebrate Pathology Volume 103, Supplement Pages S10-S19
Checked both hives.
The split hive was fed syrup for the past week to encourage comb-drawing, which has worked very well - the checkerboarded top box has a good amount of uncapped syrup on freshly drawn comb and the queen is busily laying in the middle - no queen cups / cells. Sugar shake tested for varroa from brood frames, no mites fell on the plate. Removed varroa strips and the top feeder, added a honey super above QE. Happier about the stores situation now than I was last week - the bees have put a good amount of syrup / nectar away and there's plenty of pollen around the brood nest, both coming in and stored away.
The other hive was doing well, however saw 2 queen cups with eggs. Not properly drawn, just a play cup shapes...but with an egg in each. Moved emptier frames from the bottom box to the top FD in the middle where the queen is laying to give her space, removed one old frame with mostly drone brood and replaced with an empty frame. Removed varroa strips and added a honey super above QE. I need to keep an eye on this one in the next week to see if I need to take further measures to prevent swarming. Didn't do sugar shake but tore open and inspected a bunch of capped brood from the frame I removed. No varroa seen - either it's a good result and the strips have knocked them back or I'm not very good at spotting the mites...but I've seen them before easily enough so I'm reasonably confident that the treatment was effective.
A pretty disruptive day at the hives - tried to be careful but wasn't 100% sure of where the queens were for some of the time. I hope I didn't roll one by accident.
Went through the hive with the old (failing) queen and the new prolific one. The queens are separated with a QE so I know what's happening with each one. Hive is doing really well in terms of numbers of bees & brood.
In the failing queen FD, the bees had made a supersedure cell from one of the playcups - it had been capped during the week. No swarm cells anywhere - just the one supersedure. My guess is that the nurse bees in that part of the hive couldn't smell the better queen up the top and decided to requeen. It would be a shame to let a perfectly good looking queen cell go to waste, so I split the old failing queen into a new single FD, together with a few frames of brood & bees including the supersedure cell and some stores. I hope the new virgin queen will get mated and replace the old failing one. Plenty of drones in my hive, so I assume others in the area have them too.
This also gave the strong queen more laying space, which she was starting to run low on at the top. I moved her brood nest to the bottom, lifted some frames up and checkerboarded a second FD with stores and foundation frames. The split has obviously weakened the hive a bit just before honey flow and there weren't a lot of stores: I'm feeding 1:1 syrup to both the split and the hive to make sure the bees don't starve and that they have the feed they need to draw out the foundation frames. Hopefully they draw these frames reasonably quickly so I can add supers soon.
The other hive is doing very well with good bee numbers (although not as high as with the 2-queen hive) and heaps of fresh stores, no signs of swarm cells. Varroa strips are coming out next week and then it'll be super time.
Gear & maintenance
I got a couple of extra FD boxes just in case they are needed and slapped some primer sealer on. I'll paint them later in the week and swap them with the current boxes so they can come out for a bit of maintenance.
Last season I was in a rush and got some of those thermowood boxes that supposedly don't need paint...but they are already showing signs of cracking, so I'm not that impressed with those. I'll give them a scrape and a lick of paint and hopefully they'll last a bit better. It would be ideal to have a paraffin dipper of course but that would be overkill for my tiny operation - might find out if ABC has one I could use.
The hive lid designs seem to both be compromises one way or the other. I started with the closed ends lids but they aren't very easy to get on and off after a season of weather so I bought a sprung end lid and have preferred that in terms of ease of use. I got sprung end lids for the father-in-law but now after the winter he is saying they were letting in water on the hive mat. Who knows, didn't happen to me.
I need to start thinking about which kind of honey extractor to buy. It would be nice to just uncap the frames and spin rather than making the bees redraw all those supers every year. It's not a small investment though, even as a shared purchase. A spoon is pretty cheap in comparison.
Both hives checked.
The 2-queened hive is really pumping - having one queen in each FD and placing a QE in between was a great tip, as now I can better see what's going on.
The new queen is laying up a storm - the old one is still laying but not as well. The hive is full of bees and the bees are 'holding hands' big time - they are even hanging below the hivedoctor base. Despite this, there is still space to lay and to store honey. Hopefully checkerboarding emptier frames to the middle will help so that the bees don't do anything silly before the varroa strips are coming out in 2 weeks' time.
There isn't a lot of stores in this hive but there's still pollen, capped and uncapped honey in there and the new grubs look nice and wet so it looks like the build up is being fed from the incoming nectar/pollen. I still have the granulated sugar at the top, which has been taken in but not very fast. If I don't have to feed syrup I'd rather not, as there isn't a lot of room for more build up really - just need to make sure the bees don't starve if we get poor weather. Ideally this hive would just stay this strong but not run out of control for another 2 weeks, at which point a super is going on the top.
Also forked out a few drone pupae to check for varroa & matchstick-poked a few capped brood cells. No varroa found and no ropey goo, so that's good. I saw a few bees with a relatively black-looking (hairless) thorax - they seemed to be acting normally so maybe they are just old and worn out rather having chronic bee paralysis virus...but who knows.
The other hive is doing well at a more measured pace - I guess they only have one queen so it only makes sense. I'm happy with their progress also, though - a good amount of stores, uncapped & capped honey and brood. The top box was getting really full so moved some empties from the bottom FD up to give a bit more space. Again, I mainly want to keep things under control until super time, at which point frame-drawing should keep the girls too busy to even consider swarming (I hope).
Carefully hopeful about how things are going - I certainly have a lot more bees than I did this time last year.
Have you ever wondered about honey, what it is and why it’s like it is? What about quality and honey, what should beekeepers know?
Honey comes from Nectar
Nectar is a solution produced by plants that animals collect for food. Plants have special structures that make this solution usually from water and sap flowing in the plant. Often these are found in flowers and attract animals that pollinate the plant, but that is not always the case, and they can sometimes be found on any parts of the plant above the ground. Nor is nectar always there to facilitate pollination.
The composition of the solution varies, but mostly it’s a solution of sugars in water, with small amounts of minerals and organic molecules. The nectars we are interested in contain something like 10% to 40% carbohydrates, mainly sugars like sucrose, fructose, and glucose. As well as the sugars the plants produce other chemicals that, for example, help the nectar store, make it attractive to a particular animal, or repel animals that might steal it.
Nectar is a very dynamic product. It varies for every type of plant, and for the same type of plant growing in different places. It is presented outside the plant’s tissues, so its properties change with the weather and with time. It is a very expensive product, in terms of energy and raw materials, so it’s highly conserved, even re-absorbed, by the plant. It contains enzymes that gradually change the proportions of sugars in the solution, and these sugars make it hygroscopic.
All sorts of animals use nectar as food, from yeasts and bacteria, to insects and birds. Because nectars have such different properties the relationship between the producing plants and the consuming animals can be very specific, but often are not. For example, the consumer may have special mouth parts that specialise in harvesting liquid of a certain viscosity, or it may rely on a solution that contains lots of amino-acids. These relationships can alter as the secretion of nectar changes over time.
What is honey?
If honey comes from nectar it’s obvious the composition and physical properties of honey originate with nectar, but honey bees alter nectar in two important ways.
As they collect the liquid they add a collection of enzymes, (mostly α-glucosidases, generally referred to as ‘invertase’ or ‘sucrase’) that will split a long sugar into small sugars; each sucrose molecule is split in to two sugars, fructose and glucose. They secrete these enzymes from glands in their head as they imbibe the solution, and ‘swallow’ the mixture into their honey stomach (or ‘crop’). During the intake and expulsion of the nectar it’s likely to be contaminated with pollen grains and spores from the environment. An organ in the crop is able to filter some particulates like this out into the bee’s digestive system where they are digested or excreted.
After they have transported it back to their hive they regurgitate the liquid and then concentrate it by evaporating water. Whereas nectar is mostly water, honey has four to five times as much sugar as water. By splitting most of the sucrose into smaller sugars the ‘bees end up with a warm (about 34oC) fructose solution that has a lot of glucose dissolved in it, and a little sucrose (1-2%). How this solution behaves when it cools depends on the exact mixture of sugars in it, but as a rule some or all the sugars will not remain liquid and the honey will slowly granulate.
The honey will also still contain any of the minerals and organic molecules that were produced in the nectar. The minerals are what gives honey most of its colour, the trace molecules contribute to its flavour, aroma and ‘mouth-feel’. It will now be much ‘thicker’; it has a high viscosity – 200 times that of water, ten times that of an oil. Different densities may have some effect on packaging and container size if sold by weight. Some honeys have such high protein contents they exhibit a property called ‘thixotropy’ and need special handling and packing. As honey it will also absorb water even more quickly that its parent nectar did, which it why ‘bees and beekeepers are careful about exposing it to moist air. And it will contain some (uncertain) quantity of pollen grains and microorganism spores as a result of its natural origin.
So honey is concentrated nectar, but honey is a food, defined in law governed by a principle in an international Codex. The Codex alimentarious defines honey too, and if you’re thinking about honey as a commodity, that’s much more important. To paraphrase what the Codex says, “honey is …an unfermented, sweet substance… produced by honey bees from nectar or secretions from living plants… collected… and transformed in honey combs… without objectionable flavours, aromas, or taints absorbed from foreign matter or during storage… or natural plant toxins in an amount hazardous to health.”
Everything we need to understand about honey quality can be read from the Codex.
The first thing is that it is not fermented. If it’s fermented it’s something else, not honey. What prevents honey from spoiling, and fermenting, is its high sugar concentration. As a result, the amount of water in honey is usually regulated by statute. Above 20% water we know honey is likely to ferment, below 17.0% fermentation is not likely. Between those two points the chance of fermentation depends on the count of yeast spores in the honey. This all assumes the honey is homogeneous – the same throughout.
If honey has begun to crystalise (we call it granulation) clearly it is no longer homogenous. As honey naturally granulates, the possibility of fermentation increases. If we incorporate air into honey, it is no longer homogeneous and the possibility of fermentation increases. If we leave bits of leaf, pollen and dust, and the odd bee’s leg in the honey it’s not homogeneous (and we add to the bacteria/yeast content). Not only will various sorts of foreign material set up concentration gradients that permit fermentation we increase the chance of there being ‘objectionable taints’ and the like in our honey. Particulates in the honey can also ‘seed’ premature crystal formation leading to early granulation, and it’s common to filter out most or all particulates.
The other important part of the Codex is that we should expect honey to be a product of living plants, transformed only by honey bees. It should not contain anything (like chemical pollutants) or be adulterated with products that are not ‘a product of living plants’. It should contain the natural enzymes and biological products that are ‘a product of living plants’, insofar as they are not a hazard to human health. We should not be destroying constituent enzymes by over-heating or processing honey, and in any case, we should be able to tell only honey bees have ‘collected, transformed, and combined’ the nectars to honey. There are many tests in use that can check the integrity of honey, but measuring 5-hydroxymethylfurfural (HMF), one of the main volatile alcohols in any honey, has proved a useful general standard. The compound is produced by sugary solutions at a rate that depends on time and temperature, and the ‘HMF’ quantity has proved to be a good proxy for indicating change in the chemical properties of honey. HMF can tell us whether or to what extent we have ‘transformed’ the honey, and not the ‘bees.
Being true to quality
It is important to adhere to local legislation about trade descriptions, food labelling, and weights and measures. There may be specific regulations that deal with food safety, (in NZ the Tutin regulations are the prime example) or standards that must be met to conform with export regulations and compliance in local or overseas markets. None of these take anything away from the principles in the Codex.
There are also conventions (with varying degrees of ‘authority’) that attempt to define how honey shall be described, especially when trading between countries. For many years honey colour has been described using the ‘Pfund scale’ using a colorimeter, and while there are now more sophisticated spectrophotometric measures the Pfund remains part of the beekeeping vocabulary. Several countries have attempted to standardise the descriptions of the aroma and flavour of honeys using tools like a ‘flavour wheel’ (not New Zealand), and as the interest in ‘varietal’ or ‘gourmet’ honeys has grown these have become widely used to describe and classify the variety of honey available, rather like wine tasting. You can find one you like on the ‘web.
Representing the ‘honesty’ of honey is essential in preparing and describing the product. When preparing honey for consumption and sale seemingly small ‘defects’ create doubt about the provenance and preparation process in the mind of the observer. Are those small bubbles from fermentation or sloppy preparation? Why is there sediment at the bottom of the jar and scum on the top? Worldwide, different consumer groups have different attitudes to filtration, clarity, and shelf-life, some more discerning and selective than others.
It is also important that descriptions, of any kind, are true. Apple blossom pictured on the label of a jar of pasture honey is misleading would not be permitted in some jurisdictions. Putting a sprig of lavender in your lavender honey may not be smart, but putting it in clover honey can be construed as a lie.
As consumers become more discerning your product also characterises how you run your business; “You said it was ‘honey’, not ‘honey with added ‘bee bits’!”. Are the fragments an indication of how roughly you treat your bees, an errant wing an indicator of your insensitive beekeeping? Consumers may regard the possibility of mite treatment residues in the honey you supply as a betrayal. While these details may or may not be part of the regulatory environment, they are part of the ethical framework beekeepers have established over many years. Disregard them at your peril.
The number of kiwifruit blocks covered by a canopy is increasing. These canopies consist of a hail netting supported on rammed posts, and can cover a considerable area, thousands of square meters. Many, but not all, are fully enclosed with netting down to ground level along the sides. From a grower's perspective these provide some substantial benefits. Obviously, given the name, one is protection from hail. Even unnoticed hail damage can cause a significant fall in the return a grower gets for their fruit. Another benefit is an almost total reduction in bird damage to buds and fruit, and any waste due to bird lime. The benefit that may have pushed these constructions 'over the line' is PSA protection. While the canopy may increase winter chilling (a good thing!), it certainly does protect the plants from wind damage. Broken shoots are an important point of entry for the bacteria, so this is why full enclosures are becoming more popular. There is an opinion that, having reduced the level of inoculum inside the enclosure, the canopy helps to maintain a phytosanitary environment within.
Beekeepers are more reluctant to come onto orchards and place hives these days. Access to an orchard at night (when most hives are delivered) is often problematic, and the current phytosanitary requirements do not make it easy for a beekeeper on a tight schedule operating in the dark. It is getting more common for hives to be delivered to a 'dump' site from which they are distributed by the grower, and for the grower to undertake stimulant feeding. This reduces the amount of foreign traffic in the orchard. Beekeepers are particularly unwilling to enter a canopy, either to deliver or feed hives.
But what no one really gave much thought to is how to get the flowers pollinated; at the time; racked with fear about PSA it was perhaps optimistic to think orchardists would figure out honeybees might not fare to well in a cage. In the last three or four years people have realised that pollinating under a canopy isn't, after all, a simple thing, and there is a move to look at how it might be done effectively by resolving the problems honey bees face, or by using some alternative.
The optimum placing of hives inside a canopy has not been determined, but may well be different compared with an uncovered block. There are clues that suggest things are not quite the same. There can be a drift of bees from hives in the centre to the hives on the margins near the netting. The distance between male and female vines may be more significant, within a decline in successful pollination with increasing distance from a male, and some anecdotal doubt about effective cross-pollination. With little information about the density of bees, or the density and distribution of males, it’s difficult to know if these are problems that would have existed anyway and are unrelated to an enclosure. It is also difficult to make a judgement about the stocking rates required. Logically, in a confined space without competing forage, less hives per hectare would be assumed.
Often large numbers of bees are seen flying at the canopy mesh; those that find a way through are unable to return. A bee’s eyes probably only see a featureless, bright, white plane rather than a barrier, and in a more natural setting bees can fly towards and through bright areas. Some trials of black mesh which apparently lessen the problem probably just relocate it. Bees flying inside the canopy appear to have considerable difficulty relocating their hive, possibly because of the uniformity of the geography within.
By far the most serious problem for hives working under cover is bee mortality. In a fully enclosed canopy there is nothing available to sustain large colonies of honeybees. They must be provided with a water source and will have to be fed. A newly delivered pollination unit will have a great need for pollen by design, because we normally want a hive at this stage of growth to maximise the effect it has on pollination. However, it will only contain a few days of pollen reserves (bees do not store large quantities of pollen), and the pollen gathered from the vines in the orchard is poor quality, without the complete set of amino acids the bees require for adequate protein nutrition. Supplementary feeding is possible with manufactured protein supplements and carbohydrates (sugars) but it's important to know these are not replacements for a natural diet. Bee mortality from hives in an enclosure is extremely high. Large numbers of foraging bees may fail to return because of an inability to navigate adequately, and those that do return deliver 'junk food'. A hive starved by both quantity and quality deteriorates very quickly. The loss of bees affects the colony's ability to regulate temperature and care for brood, young bees that normally care for brood begin foraging prematurely, protein deficiency encourages brood cannibalisation, the queen will stop laying eggs that produce new bees, and the hive enters a spiral of decline that takes months to correct. Not only are the hives unsuitable for follow-on pollination work they are incapable of honey production too, effectively rendering them useless for that season. Rather than pollination being priced at a marginal cost, as it is now, a beekeeper would have to attribute the full annual cost of a pollination unit to a 'one-time' use.
Honeybees use a variety of strategies to navigate, and are able to communicate (in distinct dialects) distant locations to nest-mates. They have good memories, understand time, and can measure distance. They are able to use the sun as a compass and compensate for its apparent movement across the sky but, as they cannot actually see the sun itself, it’s probably more accurate to think they are using a combination of brightness, size, UV, and light polarization. When the sun is not visible (to a bee) they use the angle of polarised light in the sky, and there is plenty of evidence to suggest they are sensitive to magnetic fields. Bees also have a good memory for landmarks. These have to be substantial given their visual acuity; patterns have to fairly large or really close to be any use, on a geographic scale lines of trees, the shape of the horizon, shorelines, roads, boundaries, buildings and so on. Close up, bees use their eyesight and olfactory clues (scents), and have good pattern recognition, colour vision peaking at the UV, blue and green end of the spectrum, and fast, accurate odour perception.
It's quite possible that for much of the time the light transmitted through a canopy does not contain the navigational 'data' that bees need, although there doesn't seem to be any studies to either discount or support this assertion. There is evidence of this in the case of some type of greenhouse. [See Tjeerd Blacquière, Jeannette van der Aa-Furnée, Bram Cornelissen & Jeroen Donders. (2006). Behaviour of honey bees and bumble bees beneath three different greenhouse claddings. Proc.Neth.Entomol.Soc.Meet – Vol. 17]. It is also very likely that an enclosure will limit both the aspect and size of navigational 'landmarks' the bees might use, and the height and angle from which they can be viewed. They have no view of any horizon. In the absence of good spatial information they would need to adopt a more 'route-based' strategy and will be looking for 'close-up' features to use for image matching and as waypoints, and may depend on odour trails. These are fairly easy features to provide, various coloured disks nailed to the top of each post for example, or large graffiti on the canopy! No doubt, aids to navigation are better placed above the canopy than below, and some should be associated with the hive location only.
Another thing to consider is whether the current standard for a pollination unit is appropriate for enclosures. Previous trials with honeybees in greenhouses and tunnels suggest it’s probably well worth trying the use of hives that are composed of 'naive' foraging bees, that is, bees that have yet to take their orientation flights. Bees that have already learnt to orient and have to 're-learn' the new location will do so within a pre-existing paradigm, whereas naive bees will learn within the constraints provided by the enclosure. Such hives are fairly simple to provide, but it would be worth experimenting with both queen-right and queen-less versions to understand their foraging capacity, hive density, and so on. There may be advantages combining the use of these hives with dry artificial pollination. Such a system would be comparable to the use of bumblebees, often used in enclosed spaces, but provide greater numbers of foraging bees.
Any enclosed hive is going to need dietary supplements for both pollen and nectar, adding to the burden of maintenance and cost. Liquid protein feeds may be particularly suitable in this instance (eg: Megabee). It's not just the cost of feed and labour. Beekeepers have to be careful about feeding hives at this time of year because any food the bees choose not to consume and store instead invariably ends up in the crop produced at the end of the year. In particular, it is easy to contaminate a honey crop with sucrose sugars that render the product unfit for export. Hives that are supplemented may be set aside for pollination use only, limiting their productivity for the beekeeper and potentially increasing the cost to the orchard. The use of small hives that are less demanding of their foraging force may be appropriate, and lessen the problem of ‘overstocking’ the enclosure given the limited forage inside. They may also better control the risk for the beekeeper, and cost for the grower.
While growers may think it important to place hives as close to the vines as they can, if a sufficient number of units are used there may be no good reason for distributing bee colonies inside the canopy. In blocks where hives are placed by the edge of the covered area (there are no side panels) perfectly adequate pollination has been achieved for the vines inside. This may not always be the case, but beekeepers are much more likely to favour this kind of arrangement as they are more able to keep control of their asset, and the hives are likely to be self-sustaining. Placing hives at a (say) 10m by 6m opening in the canopy side is possible without creating a wind tunnel (the hive between the opening and a matching 10x6 screen, and at this time the sides are not necessary for excluding birds - buds and soft growth are over, their normal food is available, and no fruit is in the orchard. Alternatively (we don’t know the answer yet), placing hives throughout the area, and particularly in corners, may help to ‘mop up’ lost and drifting foragers, giving them a home even if it isn’t the right home.
Are there viable alternatives? Artificial pollination clearly is one, although beyond the scope of the discussion here. However there is no doubt there are high performing orchards where this is the method of choice. There is a current project studying the feasibility of bumble bees as an alternate pollinator (Zespri/Plant & Food). New Zealand is not particularly well-blessed with ‘manageable’ pollinators (that is after all why bees were introduced) but the Bombus bees are worth considering. It’s not clear that the advantages claimed for them apply to kiwifruit, or why in large blocks (rather than greenhouses) they would not suffer from the same navigational issues as their smaller cousins. They are however known for adopting a ‘trap-lining’ strategy when foraging, and this might be an advantage. Perhaps looking at the needs of bumble bees will go some way to re-evaluating the commercial and ecological value of other unmanaged and ‘minimally managed’ pollinators.
Not only kiwifruit growers face challenges. Besides the usual seasonal variation that impacts on honeybee survivability, beekeepers already battle the effects of two invaders, the varroa mite and species of Vespid wasp, and there are more to worry about on the horizon. In the autumn wasps, which arrived in the 1940s and 1970s, can completely destroy a honeybee colony in a few hours, and they seem to have a greater impact each year. Since the turn of the century varroa and its associated viruses necessitate a permanent combination of costly management and medicinal measures to keep colonies in good health or they will die. World demand for honey is high, altering the balance between the competing interests of production and pollination in favour of production, while the local demand for pollination is growing as the new gold variety expands. While the market for services will react to the cost and supply of pollination units it is far better to be proactive and anticipate change, rather than cope with its consequences. It's more important than ever that growers think about and plan their pollination requirement well ahead, and that they keep a communication channel open with their beekeeper, particularly when they are considering changes (like covered blocks) to their growing practices. That way beekeepers will be able to adjust the service, technique, and supply to suit the change in circumstances.