Review: Rüppell et al. (2007). Current Biology, 17: 274-275. Written: August 6, 2007 Posted: 08/11/07 Word count: 690     Question: Do honey bee workers age “normally”?   Answer: No, because mortality and performance are decoupled   Aging and senescence are important aspects of biology, and their very existence has puzzled scientists since the beginning of human thought. Why do all living things eventually decline in performance and die? Why do some organisms live for very short periods of time, while others can live for centuries?   Leaving the “why” question to the metaphysical (at least for now), another more proximate question is “how”. In what manner do individuals age? The conventional wisdom defines senescence as an age-dependent increase in mortality. Moreover, this increased risk of dying is associated with a corresponding decline in performance. It is generally believed that these two phenomena (increased mortality and decreased performance) are causally linked; aging causes a decline in important body functions, leading to a decrease in performance, which in turn leads an increase in mortality. As a result, the coupling of mortality and performance has been shown in most organisms, including humans.   Honey bees, however, are notorious for defying all sorts of rules when it comes to aging. The classic, and perhaps most obvious, example is the difference in lifespan between workers and queens. Workers, at least during the active season, live for an average of 6-8 weeks. Queens, however, live an average of 2-3 years (at least as long as they are properly mated and fully viable). The genetic difference between workers and queens is zero; any young female larva can develop either into a worker or queen. Rather, the difference in their development is how the female is fed during the larval stage: fed a “bread and water” diet of honey and pollen, it develops into a worker; fed the sugar- and protein-rich diet of royal jelly, it develops into a queen. No wonder people have been eating royal jelly for centuries in the hopes that it is the fountain of youth!   A recent paper by UNC-Greensboro researchers, lead by Olav Rüppell, tested whether or not mortality and performance are coupled in honey bee workers. Specifically, they followed numerous cohorts of foragers (aged between 26 and 52 days old) and recorded their mortality rates as well as their performance. Mortality was measured quite easily, by calculating the percentage of foragers in each age cohort that lived to the end of the experiment. Performance, however, was measured using several bioassays. First, they looked at their responsiveness to light (with the idea that a decreased in performance would show older workers not able to see as well—sound familiar to anyone?). Second, they measured their responsiveness to sucrose, the major sugar in most nectars (such that a decrease in performance would show that older workers would have a less effective sweet tooth). Third, they quantified the ability of the workers to learn—their ability to associate a stimulus (usually an odor) with a reward (usually sucrose) by sticking out their tongues (probosces) just like Pavlov’s dogs salivating at the ring of a bell.   What they found was very interesting. They showed a clear increase in mortality of workers as they aged; the older forager cohorts had a much higher probability of dying than foragers in the younger cohorts. Not all that surprising. However, they didn’t find any corresponding decrease in worker performance among the different age groups: light sensitivity actually increased with age, their sweet tooth never wavered, and their ability to learn remained constant. This clearly shows that honey bees have decoupled the “normal” relationship between performance and mortality.   These findings are very interesting to the social structure and dynamics of honey bee colonies. To the beekeeper, it means that older foragers are just as effective as younger foragers (even though they may die sooner). This line of research may help also even help us learn more about the process of aging in general, which could benefit all of us in our golden years.     Reference   Rüppell, O., S. Christine, C. Mulcrone, and L. Groves. (2007). Aging without functional senescence in honey bee workers. Current Biology, 17: 274-275.         Review: Oldroyd (2007). PLoS Biology, 5: 1195-1199 Written: July 2, 2007 Posted: 07/02/07 Word count: 920     Question: What’s killing American honey bees?   Answer: Still no clear answers, but add one more hypothesis to the list   It has been about six months now since the initial media blitz about Colony Collapse Disorder, or CCD, hit the nation’s headlines. There has been lots of discussion, congressional testimony, and endless speculation about the potential causes and consequences of the dying honey bees, but unfortunately we are no closer to the definitive answer than we were half a year ago.   For those of you who may not have heard about CCD, it is largely unknown problem that honey bee colonies have been experiencing where the entire adult population seemingly disappears. What is left behind in the hive is sometimes a small fist-sized cluster of young bees with the queen (but not always), a large area of brood (suggesting that the colony collapse occurs in a short time interval; how can a few hundred bees raise eight frames of brood?), and ample food stores of honey and pollen. Curiously, robbing bees from neighboring colonies, wax moths, and small hive beetles all seem to keep their distance from empty hives from these collapsed colonies, at least for a period of several weeks. For a single colony, this collection of symptoms may be curious but not all that alarming. But when it happens to hundreds of colonies in the same area all at the same time, it is quite obvious something strange is going on. Indeed, hundreds beekeepers across the nation have reported anywhere from 30% - 80% of their colonies collapsing in this way.   A recent review paper by Ben Oldroyd, one of Australia’s eminent honey bee researchers, does a very nice job at summarizing a lot of the main issues that have been circling around Colony Collapse Disorder. Here are some of the main points he concludes in his review as to the possible causes.   Diseases and parasites: honey bees, as most beekeepers are keenly aware, are hosts to a litany of nasty bugs and parasites. Much emphasis by CCD researchers has been placed on finding something new about an existing pathology (for example, a novel interaction between a virus and varroa mites) or possibly a yet-unknown new disease that may be associated with the disorder. As yet, there is no current “front runner” that seems to be associated with CCD.   Environmental contaminants: Oldroyd briefly reviews both in-hive chemicals, mainly those used to control varroa mites, as well as agricultural insecticides that bees may pick up from their external environment. There is much concern about potential poisoning of the bees, since there are many different and varied sources of such chemicals. CCD researchers are currently testing comb samples from colonies afflicted by CCD, as well as healthy colonies in the same apiary as a control group. If they can find certain pesticide residues in the CCD colonies that are absent in the non-CCD colonies, that will provide strong circumstantial evidence toward a particular contaminant. Currently, however, there is no such smoking gun.   Nutritional stress: the changing face of modern-day beekeeping has caused a significant shift in management practices. In particular, placing hives in or near certain agricultural crops may deplete them of foraging resources that the bees need for healthy and proper development. Transporting colonies thousands of miles and into multiple, nutritionally poor crops per year may therefore be taking its toll. This, too, is a research priority for CCD researchers.   Genetically modified crops: there has been some concern about genetically modified organisms (GMOs) being used in agriculture, particularly those of staple crops like corn, cotton, canola, and soybeans whose genomes have been artificially modified to express protein insecticides from bacteria to keep damaging herbivorous insects at bay. The question arises, however, as to the secondary effects that these novel properties may have on beneficial insects such as honey bees. Several researchers, prior to the headlines of colony collapse disorder, tested the potential effects of GMO pollen on bees and found little if any negative effects, but we would all benefit from additional studies.   Lack of genetic diversity: there is emerging evidence that the overall genetic pool for honey bees in the United States is not as deep as it once was. This is probably not surprising, as much of the feral population has been decimated by varroa mites and other diseases. Oldroyd makes a strong argument that because commercial queens do not have as many unrelated drones to mate with as they did in the past, the decreased genetic diversity within the colonies may make them more vulnerable to disease. CCD researchers are involved in several experiments investigating this possibility as well.   Cool brood: Several researchers, including Oldroyd and his collaborators, have previously shown that bees which develop at sub-optimal temperatures have difficulty learning and foraging. As such, chilled colonies may produce workers that fly from the hive and not return, a symptom that is similar to what happens with CCD. This is a new hypothesis that has yet to be considered, but should be readily testable.   The take-home message: CCD is likely a combination of several of these factors, which will make it difficult to really pin down. Hopefully, honey bee researchers will be able to do so sooner rather than later.       Reference   Oldroyd, B. P. (2007). What’s killing American honey bees? PLoS Biology, 5: 1195-1199.           Review: Torto et al. (2007). Proceedings of the National Academy of Sciences, 104: 8374-8378 Written: May 31, 2007 Posted: 06/05/07 Word count: 689     Question: What attracts small hives beetles?   Answer: Honey bee alarm pheromone, and not just from the bees!   The small hive beetle (SHB), Aethina tumida, was first discovered in South Carolina in 1996. In the spring of 1998 in Fort Pierce, Florida, this beetle was determined to be a destructive pest in beehives, at which point it was positively identified as the small hive beetle (SHB). Prior to its discovery in the U.S., the only record of this insect was in the southern regions of Africa.   During the summer of 1998, the beetle was blamed for the loss of over 20,000 colonies in Florida. The beetles spread quickly, and that same year beetles were also reported in Georgia, South Carolina, and North Carolina. Since that time, the beetle has become established in most counties in North Carolina as well as across much of the United States. This demonstrates the beetle’s remarkable ability to disperse by flight and human transport.   There are several means for control and prevention of SHB. The only approved treatment inside the beehive is a coumophos plastic strip  (CheckMite+TM) cut in half and attached to a small piece of cardboard placed on the bottom board. The adult beetles will hide beneath the cardboard and contact the pesticide, which kills them. The only approved treatment outside the hive is a pemethrin soil drench (GuardStar®), a liquid treatment that is mixed with water and applied to the ground around the hive to kill the beetles pupating in the soil. There are several in-hive traps on the market, which can assist in prevention of SHB outbreaks. However, these traps are passive; they work by filling a resevoir with vegetable or mineral oil, so as the adult beetles enter and look for a hiding spot, they fall into the oil and drown. As such, it would be very helpful to find an effective chemical lure that will attract large numbers of beetles to these traps and therefore greatly minimize SHB damage.   A recent report in the prestigious Proceedings of the National Academy of Sciences provides some information that may help develop a chemical lure for small hive beetles. The researchers investigated what chemicals within a hive is attractive to beetles. To test this, they used gas chromatography (GC), a chemical analysis machine, and electroantenograms (EAG) of SHB adults, which measures the electrical stimulation of antennae to various smells. Based on previous work, they found that SHB adults are attracted to isopentyl acetate, 2-heptanone, and methyl benzoate. These three chemicals comprise about 75% of the honey bee alarm pheromone, strongly suggesting that the beetles are “homing in” on colonies that are disturbed in some way. Moreover, based on their EAG findings, they found that adult SHB are even more sensitive to honey bee alarm pheromone than the honey bees are!   Perhaps what is even more intriguing is that they found that the adult bees are not the only source of these chemicals in the hive. They discovered that SHB adults carry with them certain species of yeast. One in particular, Kodamaea ohmeri, produces the same blend of chemical compounds as honey bee alarm pheromone when it grows on pollen within the hive. This is a very interesting find, as it suggests that beetles can enter a hive, inadvertently inoculate it with this yeast, and cause a positive feedback loop where more adult beetles are attracted to the hive.   This is a very exciting finding, and one that could potentially lead to the development of an active—rather than passive—in-hive, or even external, trap for SHB. It also suggests that minimizing colony disturbance may help reduce the likelihood of SHB invasion. We will have to see in the coming months and years if this technology will benefit beekeepers.       Reference   Torto, B., D. G. Boucias, R. T. Arbogast, J. H. Tumlinson, and P. E. A. Teal. (2007). Multitrophic interaction facilitates parasite–host relationship between an invasive beetle and the honey bee. Proceedings of the National Academy of Sciences, 104: 8374-8378.           Review: Pankiw and Garza (2007). Apidologie, 38: 156–163 Written: May 9, 2007 Posted: 05/09/07 Word count: 673     Question: Is the higher reproduction rate in AHB intrinsic or environmental?   Answer: While partially controlled by the environment, it is also an intrinsic trait   There are many different reasons why the Africanized honey bee has been so ecologically dominant over the last half century. One reason is that some of their more notable characteristics, such as defensive behavior, are genetically dominant. Studies have isolated several regions of the genome, known as quantitative trait loci or QTL, that explain a large percentage of how honey bees respond to intruders and pursue them for long distances from the hive. Using backcrossing techniques, the same studies have shown that bees hybrid bees—those with both African and European parents—tend to be more defensive like their African parent. Another reason is that AHB has outcompeted EHB is that they produce small, parasitic swarms that can invade and take over a European nest. This causes an immediate genetic turnover of the colony from European to African.   But perhaps the largest reason the AHB have been so successful is because of their increased reproduction. It has long been estimated that a standard European honey bee colony issues 1-2 swarms per year. On the other hand, African colonies issue as many as 16 swarms per year. The shear numerical advantage of African colonies in a given area had lead to the complete displacement of the European population by African bees. The conventional wisdom holds that this increased reproduction rate is because African bees are adapted to the tropics and therefore need not store large amounts of honey and pollen for periods of dearth, since there is almost always nectar and pollen available in the tropics. If so, then what controls what: does the environment dictate the reproductive rate of AHB, or are the AHB intrinsically more reproductive?   A recent paper by Texas A&M researchers investigated the mechanisms that govern reproduction in honey bees to answer this question. They used an important signal in the regulation of colony reproduction, brood pheromone. Created by developing larvae, brood pheromone is a complex mix of certain chemicals that create a certain bouquet that, among other things, inhibits queen rearing and worker ovary development. The researchers used worker ovary development as a proxy for how responsive they are to colony reproductive cues, such as brood pheromone. They tested several hypotheses to get to the bottom of this question. First, does brood pheromone from EHB have the same effect as brood pheromone from AHB? Second, is the effect of brood pheromone dose-dependent? (That is, does increasing the amount of brood pheromone decrease the amount of worker ovary development?) And third, does the genetic composition of bees (mixtures of AHB and EHB) affect the influence of brood pheromone on ovary development?   The researchers found that the different racial extracts of brood pheromone did not differentially affect worker ovary development, suggesting that the signal of AHB is effectively the same as EHB. However, the effective concentration of brood pheromone that caused worker ovary development was 16 times higher in AHB workers compared to EHB workers. In other words, AHB workers needed much more brood pheromone to inhibit their ovary development, suggesting that they are intrinsically “more reproductive” than EHB workers. Finally, this difference in worker ovary development was not influenced by whether the workers were all AHB, all EHB, or a mixture of both types.   The results suggest that the increased reproductive rate of AHB colonies is also reflected in an increased reproductive rate of AHB workers. In other words, while the environment obviously affects reproduction in honey bees, Africanized honey bees are “turned up” for reproduction. These findings are further evidence at why the AHB has been such a successful invasive pest, and it may even help researchers find ways to minimize their unwanted behaviors.     Reference   Pankiw, T. and C. Garza. (2007). Africanized and European honey bee worker ovarian follicle development response to racial brood pheromone extracts. Apidologie, 38: 156–163.             Review: Meikle et al. (2007). Journal of Economic Entomology, 100: 1-10. Written: April 1, 2007 Posted: 04/02/07 Word count: 772     Question: Is there a potential for biocontrol of varroa mites?   Answer: Possibly, by using entomopathogenic fungi, but unfortunately not with overwhelming results   Biocontrol for pest organisms is a means of controlling one organism with another. Examples abound in agriculture. Lady beetles are beneficial in home gardens because they eat the eggs of many pest insects, reducing their number and therefore the damage they cause to flowers and shrubs. Parasitic wasps lay their eggs in (or on) caterpillars that feast on various crops, eventually killing them so they do far less damage. Phoretic flies have been released in the US to try and control the invasive red imported fire ant.   One main benefit of using biocontrol to reduce pest numbers is that the pest has a much harder time coming up with ways to survive, at least compared to other means of control. For example, pesticides usually contain only one active ingredient that kills or otherwise controls the pest. That single mechanism of control can eventually be overcome by the pest; that is, the pest can eventually develop a resistance to the chemical (through behavioral means such as avoidance, or physiological means such as detoxification enzymes). For pests to develop resistances to other species, they must simultaneously develop a wide variety of resistance mechanisms, something that is much less likely to happen.   Another important benefit of biocontrol is the persistence and sustainability of many such systems. Releasing predatory mites into a field to control an insect pest needs to be done only once, since the mites will increase their numbers and continue to reproduce on the very pest species that you are trying to control. Needless to say, that can be very beneficial not only for control of the pest population, but because repeated applications are not always necessary.   Given the many benefits of biocontrol as a means to keep pest numbers in check, several researchers have been searching for a biological agent that will kill varroa mites but have no averse effect on honey bees. Unfortunately, there is no parasitic wasp or predatory mite that preferentially attacks varroa mites. However, there are several different species of fungus that have been shown to infect varroa but are completely harmless to bees. Consequently, there has been much speculation and optimism that perhaps one of these entomopathogenic fungi may be used to control varroa in beehives.   A recent study by a French scientific team isolated one such strain of fungus to see how well it controls varroa in field colonies. Their earlier tests, performed in the laboratory, demonstrated that the fungus Beauveria bassiana significantly decreased the lifespan of an adult varroa mite by about 70-80%. They then used this fungal isolate in the field and measured both treated and untreated (control) colonies for mite drop (using sticky boards), adult bee population, and brood area. They also measured whether or not the dead mites developed the fungal infection, suggesting that they died from the fungus rather than another means.   The good news is that they found significantly more dead mites dying from fungal infections in the treatment colonies compared to control colonies. This suggests that the mites were indeed dying from the biocontrol agent, demonstrating its potential for use as a means of controlling varroa mites. The bad news is that the effect was neither pronounced or prolonged. They found significantly higher mite drop in treatment colonies 6 and 8 days after applying the fungal spores, but not at levels that would reduce the mite populations below an acceptable level. Moreover, the persistence of the fungus was not very pronounced, as they estimate the amount of fungi within the hives dropped below the level needed to cause infection within about one week after application.   This study differs from previous studies performed in the US, since it tested an entirely different fungus. However, the two lines of research are similar to each other in that they both demonstrate only modest control of varroa mites in field colonies. While efforts towards a biological control of varroa should certainly continue, as the current findings are very tantalizing for the possibility of using fungi for mite control, researchers have yet to demonstrate that biocontrol is a viable option for beekeepers to keep their pests under control.     Reference   Meikle, W. G., G. Mercadier, N. Holst, C. Nansen, and V. Girod. (2007). Duration and spread of an entomopathogenic fungus, Beauveria bassiana (Deuteromycota: Hyphomycetes), used to treat varroa mites (Acari: Varroidae) in honey bee (Hymenoptera: Apidae) hives. Journal of Economic Entomology, 100: 1-10.           Review: Seeley (2007). Apidologie, 38: 19–29. Written: March 8, 2007 Posted: 03/12/07 Word count: 740     Question: How are feral bees able to cope with varroa mites?   Answer: Because the mites are less virulent, not because the bees are resistant   Parasites are among the most successful life forms on the planet. Why? Because they don't have to work as hard for their food and other resources. Rather, they tap into the resources they need from other life forms (their hosts). But there are limits to how much they can take from their host—if they take too little, they might not be able to survive and reproduce themselves; if they take too much, they run the risk of killing their host and, oftentimes, themselves. Consequently, natural selection tends to balance the degree to which parasites steal from their hosts.   The same holds true for the parasite-host relationship between the varroa mite (Varroa destructor) and honey bees (Apis mellifera). The mites run the risk of killing themselves, by killing the bee colony, if they reproduce more than the colony can handle. In a feral or "wild" setting, this would select for avirulent mites since the best way they would be able to infest a new colony is to allow their current host to reproduce through swarming (called vertical transmission). In a managed setting, however, the risk of mites killing themselves is virtually negated. With beehives spatially clumped so that the likelihood of drifting is increased, beekeepers exchanging frames of brood among hives, and dead-out colonies being robbed by neighboring bees, there is little to no risk for the mites to parasitize as much as they can (i.e., become increasingly virulent) since they can easily switch hosts to another colony (called horizontal transmission). As such, the means by which we tend to keep bees can actually select for nastier mites.   So perhaps it was surprising that Tom Seeley at Cornell University discovered a population of feral honey bees, all infested with varroa mites, living in a nature preserve in upstate New York. While it was generally assumed that varroa mites have wiped out the feral bee population, Dr. Seeley discovered just as many, if not more, colonies living in tree cavities ("bee trees") than he did in the late 1970Õs before the mites were introduced to North America. So the question was: were these bees resistant to the mites, or were the mites less virulent?   He tested this hypothesis by setting out five hives in the spring to capture feral swarms, and he was able to establish three new colonies. He then measured mite levels in the hives using sticky boards over the course of the summer, and showed that the number of mites remained relatively low over time (maximum mite drop of 21 mites in 24 hours, well below the suggested threshold for treatment). While this did not determine whether the bees were resistant or the mites were avirulent, it did demonstrate that the two were able to coexist in a stable relationship.   Next, Dr. Seeley raised new queens from one of the captured feral colonies and let them mate in the forest. He then transferred them back to his research station and placed them along side an equal number of hives headed by commercially produced queens. He then measured each of the six pairs of "Arnot Forest" hives and "New World Carniolan" hives for mite levels every month, again using sticky boards. He showed that mite levels increased over the course of the summer, and they did so similarly in both types of colonies in each pair. These results strongly suggest that the feral bees were not resistant to the mites in some way, but rather that the mites are more virulent in a managed setting compared to a feral setting.   This study should be very encouraging for beekeepers. Rather than view varroa mites as an embittered enemy ("the only good mite is a dead mite"), we should view the varroa-honey bee relationship as one that can reach a happy medium without beekeeper interference. For the time being, it may be difficult to reconcile our current management practices with selection of avirulent mites, but it introduces the possibility that we may be able to coexist with a parasite that has caused so many problems.     Reference   Seeley, T. D. (2007). Honey bees of the Arnot Forest: a population of feral colonies persisting with Varroa destructor in the northeastern United States. Apidologie, 38: 19–29.           Review: Higes et al. (2006). Journal of Invertebrate Pathology, 92: 93-95. Written: February 4, 2007 Posted: 02/06/07 Word count: 729     Question: What are the new disease threats to honey bees?   Answer: There are two: a new, more virulent nosema and an unknown condition known as "colony collapse disorder"   Honey bees are hosts to more parasites and pathogens than any other social insect, with a record of 72 documented so far. Many of the most economically important ones, including varroa mites, have resulted from introductions of foreign exotic pests. In biology, this is known as a "host shift", where a parasite from one species jumps ship and starts to parasitize another species. In the case of varroa, the mites shifted hosts from the Eastern honey bee (Apis cerana) to our Western honey bee (Apis mellifera). Because our bees had not evolved any natural defenses against varroa, the mites are highly virulent; that is, our bees succumb very quickly to them (at least compared to their original hosts).   Well, it looks as if history is repeating itself, as another parasite seems to have shifted hosts from A. cerana to A. mellifera. This time, it is not an ectoparasitic mite but rather an internal microsporidian that infests the hind gut of adult bees. We are already familiar with such a parasite, Nosema apis, which causes nosema disease. The typical symptoms of nosema include unusually high defecation rates in and around the hive, lethargic bees, and swollen abdomens. While the disease can cause problems for colony productivity, our bees usually don't succumb to nosema and can be easily and readily treated with antibiotics (fumigilin) fed through sugar syrup. However, A. cerana has its own version of nosema, N. ceranae, which is slightly different from N. apis.   A recent report out of Spain verifies that A. ceranae has been infecting honey bees in Europe. While N. apis and N. ceranae are not visually distinguishable under the microscope, they are distinct genetically. Mariano Higes and colleagues used modern genetic techniques to confirm that bees collected in Spain have this new version of Nosema. Moreover, the symptoms are different from N. apis, where they do not seem to defecate inside the hive. Nonetheless, honey production is very low and colonies can collapse very readily (particularly over winter). While the parasite is still susceptible to antibiotics, colonies seem to collapse before feeding fumagillin can rescue them.   There are unconfirmed reports that N. ceranae has been found in the U.S. A paper due out in the Journal of Invertebrate Pathology will soon report the findings of a preliminary survey of this new nosema, at which point we will see if it is indeed a problem for our beekeepers and just how widespread it may be.   This potentially new disease is apparently different from another problem our beekeepers have been experiencing, termed "colony collapse disorder" (or CCD), where colonies across the nation have dwindled and inexplicably died. Quoting a recent report, "Initial studies on bee colonies experiencing the die offs has revealed a large number of disease organisms present in the dying colonies, with most being "stress related" diseases and without any one disease being supported as the "culprit" underlying the deaths. The magnitude of detected infectious agents in the adult bees suggests some type of immunosuppression. Case studies and questionnaires related to management practices and environmental factors have identified a few common factors shared by those beekeepers experiencing the CCD; but no common environmental agents or chemicals were easily identified by these surveys. The search for underlying causes has been narrowed by the preliminary studies, but several questions remain to be answered."   While it has been speculated that the new nosema might be the culprit behind this phenomenon, the internal symptoms of CCD appear to be quite different, making it very unlikely that this is the case. Several working groups have been formed to try and get to the bottom of CCD, and we hope to have some answers by the end of this upcoming season.   I'm sure you'll be hearing a lot about these two new threats to the beekeeping industry, so keeps your ears open for suggestions and treatments. For the time being, more information about CCD can be found at http://maarec.cas.psu.edu/.       Reference   Higes, M., R. Mart’n, A. Meana. (2006). Nosema ceranae, a new microsporidian parasite in honeybees in Europe. Journal of Invertebrate Pathology, 92: 93-95.           Review: McMullan and Brown. (2006). Apidologie, 37: 471-479 Written: 12/21/06 Posted: January 2, 2007 Word count: 707     Question: Which is more important for tracheal-mite resistance, temperature or grooming?   Answer: While temperature is important, grooming is more so.   Tracheal mites are internal parasites of honey bees, living in their breathing tubes (called trachea). They were discovered and described as the causative agent of "winter disappearing disease". It is now known that if a colony has more than 30% of its adult bees infested with tracheal mites, winter mortality significantly increases even if the hive has sufficient food reserves. It has long been known, even before the mites were discovered, that some honey bee colonies are more likely to succumb to "disappearing disease" than others; that is, there is variation among bees for their resistance to tracheal mites, to the point where certain strains can be selected for mite tolerance (such as the Buckfast strain developed by Brother Adams).   Much research has gone into identifying the mechanism of tracheal-mite resistance. There are two potential means of resistance: physiological and behavioral. Since a bee's development often has important impacts on its physiology, prior research has investigated the link between the temperature during pupal development and mite infestation. Such tests have found that bees raised at 30oC as pupae become infested with tracheal mites more readily than bees raised at the normal temperature of 34oC. Moreover, knowing that mites actively migrate from one bee to another, it is also possible that resistance can stem from the disruption of horizontal transmission of mites within a colony. Research has shown that autogrooming—or a bee grooming itself—can be very effective at reducing mite levels. So, the question becomes: which is more important, temperature or grooming?   It is this question that John McMullan and Mark Brown at Trinity College in Ireland posed in a recent study. They obtained bees from two sources: a "low susceptibility" colony (derived from an apiary where the bees had never become infested with tracheal mites) and a "high susceptibility" colony (derived from a yard where the colonies had, in the past, become infested with tracheal mites). Capped brood frames from these two sources were raised in an incubator at either 30oC or 34oC. Once they matured, newly emerged—or callow—adult bees from each of these sources and temperature treatments were placed into plastic containers in an incubator. In some of the cages, both mesotarsi ("middle feet") of the adult bees were surgically removed to prevent effective autogrooming, while in the remaining cages the bees were left intact. Finally, each container was "inoculated" with foreign bees from another colony containing a large percentage of tracheal mites, and then the test bees were collected and measured for the number of tracheal mites they were infested with.   At the end of the experiment, the researchers were able to compare the levels of tracheal mites as a function of genetic susceptibility (low vs. high), developmental temperature (reduced vs. normal), and grooming behavior (restricted vs. unrestricted). They found that susceptible bees were not significantly affected by either temperature or grooming; in other words, all susceptible bees became equally infested with tracheal mites. In the mite-tolerant bees, however, they found that grooming had little effect on mite levels in bees raised at a reduced temperature, but that grooming had a very large effect on mite levels in bees raised at a normal temperature.   These results suggest that grooming ability of bees is the main means by which they are able to withstand tracheal mite infestations, but only if the bees are able to develop at brood-nest temperatures. This means that it is important for "winter" bees to develop in a well-populated colony so that the brood nest does not become overextended and the brood become chilled as the colony goes into winter. Moreover, the findings further suggest that autogrooming assays, much like those performed for hygienic behavior, should be incorporated into queen-production programs to help alleviate the levels of tracheal mites within our colonies.     Reference   McMullin, J. B. and M. J. F. Brown. (2006). The role of autogrooming in the differential susceptibility to tracheal mite (Acarapis woodi) infestation of honeybees (Apis mellifera) held at both normal and reduced temperatures during pupation. Apidologie, 37: 471-479.       Review: Weinstock, G. M. et al. (2006). Nature  443: 931-949. Written: November 20, 2006 Posted: 12/04/06 Word count: 718     Question: What can knowing the honey bee genetic sequence do for beekeepers?   Answer: In the long run, plenty—and the sky's the limit   The art of beekeeping is literally an ancient practice, and much of what we do in the bee yard has not changed much since Langstroth revolutionized bee management in the mid 1800s. Honey bee science, on the other hand, has changed dramatically over the years as new technologies have been developed in the biological sciences. Apiculture and honey bee science is currently experiencing a quantum leap forward with the completion of the honey bee genome sequence. This is a project supported by numerous beekeeping groups and research programs across the nation. Collectively known as the Honeybee Genome Sequencing Consortium, the project involved 170 researchers (two of them, by the way, members of the NC Honey Bee Research Consortium) from 64 institutions in 15 countries, and has resulted in over 50 scientific publications. Implemented by Baylor College of Medicine in Texas, they have taken the DNA from honey bees and transcribed the millions of individual letters of the four-letter alphabet that encodes the molecule of life.   The way this process works is quite complicated yet elegant in design. The DNA is isolated from bees; easy enough. That DNA is then literally cut into thousands of small fragments. Those little snippets, then, are inserted into bacteria, which are allowed to grow and replicate these small pieces of bee DNA, creating what is known as a 'DNA library' that researchers can repeatedly access and reference to. Each little fragment is then read to transcribe the sequence of A's, T's, G's, and C's that constitute the entire DNA code of the honey bee.   The difficulty, of course, is putting all of the little snippets back together. This entire process is very much like something that the Beatles producer George Martin did on the Sgt. Peppers album. Taking a long section of tape at the end of the song "For the Benefit of Mr. Kite" (where John Lennon was improvising on the organ), he cut the tape into many foot-long sections, threw them into the air, and told his editor to pick them off the recording booth floor and piece them back together. The final result is a random progression of organ music in the closing part of the song. The process of assembling the honey bee genome is just like that, only the geneticists have to put the little fragments of DNA back in the correct order!   The genetic code of a bee's DNA is used to make proteins, those proteins are then assembled to make a bee, and those bees come together to make a colony. The honey bee genome, therefore, provides a road map for geneticists to locate regions of this long DNA sequence that encode particular traits of interest at the gene, bee, or colony level. Thus we are poised over the next few decades to make tremendous advances in bee science and management by understanding the genetic underpinnings of a wide range of topics. Here are just a few things that the Honeybee Genome Sequencing Consortium has learned so far:   ¯         Conservatively, honey bees have at least 10,000 genes, which is lower than other insects. By contrast, humans have between 20,000-25,000 genes. ¯         The honey bee genome shows greater similarities to vertebrate (including human) genomes than other insect models (such as fruit flies) for many common Òhouse-keepingÓ genes, making the honey bee an excellent model system to investigate certain human diseases and behavioral disorders. ¯         The western honey bee, Apis mellifera—the species that we use—evolved in Africa rather than Asia, where all the other honey bee species are native. Moreover, they seem to have been introduced to Europe on two separate occasions, once through Eastern Europe and once directly to Western Europe via the Iberian peninsula. ¯         Honey bees have about two-thirds fewer genes for immunity than do other insects. This suggests that honey bees are poorly defended against pathogens at the individual level but rely more on social mechanisms of disease resistance. This can have important ramifications for understanding disease transmission and management.   In short, we are entering a new era of honey bee research: the genomic era. With time, it should yield tremendous benefits for bees and beekeepers.     Reference   Weinstock, G. M. et al. (2006). Insights into social insects from the genome of the honeybee Apis mellifera. Nature  443: 931-949.       Review: Chen et al. (2006). Applied and Environmental Microbiology, 72: 606–611. Written: October 24, 2006 Posted: 11/05/06 Word count: 626     Question: Are mites the only way that viruses are spread within a colony?   Answer: No; queens can also directly pass on viral infections to their eggs   There is increasing evidence that viruses may play a much greater role in decreased colony health than we previously thought. The likely reason that we don't immediately think of viruses as a leading culprit of colony ill-health is because they are invisible, difficult to detect, and infected individuals are often asymptomatic. Research over the last few years has clearly indicated, however, that varroa mites are excellent transmitters of numerous viruses, such as deformed wing virus (DWV) and Kashmir bee virus (KBV), both of which have clear (but subtle) negative effects on colonies. As one apiculture researcher put it, "pretty soon we'll be saying that mites don't kill your colonies--mites pass on viruses that kill your colonies."   Understanding how a disease is transmitted, therefore, is an important aspect of understanding how we can minimize its impact. There are two general ways that disease can be transmitted. The first is the "typical" way we think disease is transmitted, from bee to bee. This is known as horizontal transmission, between members of the same generation. Horizontal transmission is the way that varroa mites pass along viruses to brood and adult bees, colonies can spread numerous diseases to each other (particularly through robbing and, to a much lesser extent, though drifting), and beekeepers can transmit any number of pathogens to other colonies by swapping diseased frames between hives. The second means of transmission is known as vertical transmission, spreading disease from one generation to the next. One obvious example of this process is by parent colonies passing along their diseases to their daughter colonies during the process of swarming.   A recent study by USDA researchers in Beltsville have identified another means of vertical transmission of certain bee viruses. Judy Chen and her colleagues have demonstrated that queens infected with certain viruses can actually pass them along to their offspring by directly infecting the eggs when they are laid. To determine this, they sampled queens to determine if they were infected with acute bee paralysis virus (ABPV), black queen cell virus (BQCV), chronic bee paralysis virus (CBPV), deformed wing virus (DWV), Kashmir bee virus (KBV), and/or sacbrood bee virus (SBV). They then sampled the colonies for eggs, larvae, pupae, and adult bees. Using the modern technique of reverse-transcription PCR, they were able to detect the presence and relative abundance of each of these viruses in various tissues of the queens and offspring. They found a very strong correlation between them, such that brood of all stages always had the virus(es) that the queen was infected with. Moreover, if queens were infected with either BQCV or DWV, their offspring were only infected with these viruses and no others. Given that horizontal modes of transmission, such as varroa mites, cannot pass along viruses to eggs or young larvae, this demonstrates a unique vertical mode of transmission for these diseases: from mother to daughter.   This finding is important, but we're still a long way from being able to address viral infections in our colonies as no antibiotic or pesticide can be applied to alleviate the problem. Currently, the best approach to minimizing viruses in our hives is to reduce the numbers of varroa mites that horizontally transmit them. However, with additional research on viral transmission within colonies, we may also be able to determine ways that we can prevent their vertical spread.       Reference   Chen, Y. P., J. S. Pettis, A. Collins, and M. F. Feldlaufer. (2006). Prevalence and transmission of honeybee viruses. Applied and Environmental Microbiology, 72: 606–611.       Review: Connor (2006). Increase Essentials. Wicwas: New Haven. Written: September 16, 2006 Posted: 10/02/06 Word count: 712     Question: What is the best way to counter winter losses?   Answer: Learn how to make strong, healthy colonies through increases   It may be hard to believe, but there was a time where a honey bee colony was expected to survive the winter as long as it has sufficient honey stores. Today, it is not unusual for beekeepers to see one-third to one-half of their colonies die during the winter, even if they were adequately provisioned. The leading culprits that are blamed for such drastic losses are, of course, varroa and tracheal mites, although the latter is probably not given as much credit as the former (even though it make be more deserving). But other factors, such as poor fall honey flows, prolonged winters, Indian summers (where the bees start rearing brood too early and waste their precious stored resources), and overstressed colonies can really stack the deck against a colony making it through the winter dearth.   It seems curious that if beekeepers lose up to half of their colonies every year, they why doesnÕt the honey bee population quickly dwindle to nothing? While there has been a slow and steady decline in the number of managed hives over the past 20 years, there hasnÕt been a total extinction of honey bees. Why? Because every year beekeepers grow new colonies of bees to try and replace the ones that died out. There is a real art to this practice, one that can take a lot more care and subtlety than one might think. Making new colonies from existing ones is the basis for a new book titled Increase Essentials by Larry Connor.   This is a book written for the experienced beekeeper, particularly for the larger, non-commercial or semi-commercial sideliner with enough hives and colonies to make the advice worthwhile. Beginners or strict hobbyists would probably not get as much from it, other than perhaps an optimistic enthusiasm for the art of beekeeping and possibly even an incentive to make their operations into larger ones.   The topic is quite straight forward (split one large colony into two or more smaller colonies), but surprisingly complex when all of the details are laid out. The author, however, does a very nice job at introducing and integrating the various topics as they apply to making splits, raising queens, and replacing colonies. Some of these issues include: swarming, initial worker and brood populations, ecology and seasonal timing, supplemental feeding and honey stores, and genetic quality. He provides just enough biological background to place each issue into a larger context, and then outlines some very practical advice without giving over-simplified (and therefore likely erroneous) step-by-step instructions on how to establish new colonies.   At its core, the practice of making splits requires that the initial unit is optimized for both size and timing. Using some simplistic (and therefore comprehendible) computer models, Dr. Connor illustrates why starting a colony that is too small or too large, or too early or too late, will produce sub-optimal colonies. Colonies started with too few resources or too late will struggle to grow their population and not be able to take advantage of the spring nectar flow. Colonies started with too many resources or too early may build up too quickly and swarm during the nectar flow. The propensity of bees to grow depends on both their genetics and the environment in which they are located, so understanding both is vital to make the most out of making increases (in short, know your bees and your backyard). The take-home message: make moderately sized splits with brood in early spring, maintain strict control over queens and genetic stock, and stay vigilant over the growth and development of the colony.   In the end, this book provides exceedingly helpful advice in the artistic application of bee management in an effort to propagate honey bee colonies through splits and divides. In doing so, the author makes a cogent argument that this is a powerful means of keeping a healthy population of honey bees, and one that pretty much any beekeeper, at any scale, can accomplish.     Reference   Connor, L. J. (2006). Increase Essientials. Wicwas Press: New Haven CT, 128 pp.     Review: Branco et al. (2006). Apidologie, 37: 452-461. Written: August 21, 2006 Posted: September 6, 2006 Word count: 887     Question: How accurate are varroa sampling techniques?   Answer: About 92% accurate, so they are good tools for mite management   It is a tricky business, keeping on top of those pesky varroa mites. This time of year, beekeepers are particularly concerned with these parasites: their populations are usually at their highest because theyÕve been able to increase their numbers all summer long, the surplus honey supers have been or in the process of being taken off and extracted, and steps are taken to treat those colonies that have unacceptably high mite levels. Estimating this latter number can be laborious and time consuming, but it is critical for proper beekeeping management in the post-modern era.   There are a number of methods to estimate mite levels in beehives, but they generally fall into two categories. The first is an estimation of the mite load of a colony, usually performed by the Ôsticky boardÕ test. This method employs a paper or plastic sheet covered with a glue-like substance, which is placed beneath the hive to capture any mite that falls off of their host bee. Sticky boards are left in the hive overnight or up to several days, but the standard measure is a 24-hour mite drop. In essence, this method samples the natural death rate of the mites in a hive as a proxy of the total number of mites. The second method is an estimation of the mite intensity within a colony, performed by any number of techniques, by sampling brood or adult bees and calculating the percentage of them that have mites. One popular technique that estimates percentage infestation is the Ôsugar shakeÕ method, where 200-300 adult bees are taken from the brood nest, placed in a jar, and covered with powdered sugar. The mites are then shaken through a wire-mesh screen to estimate the number of mites per adult bee. Similar methods include the ether roll, alcohol wash, and drone-brood sampling techniques.   Each of these methods has their merits and drawbacks. Sticky boards donÕt require opening or manipulating a hive, but they donÕt give an immediate answer (not to mention going half blind from counting dozens or even hundreds of little dead mites). Sugar shakes give you an immediate answer, but it can take some work (not to mention the risk of inadvertently sampling the queen!). But one drawback that each of these measures has in common is that they derive estimates from only a sample of the mites in the colony, not the whole number. This means you can repeatedly measure mite levels using the exact same technique, but the precise estimate might be different each time. This is a statistical issue known as sampling error, where shear chance can actually cause your estimates to vary (for example, you just happen to collect bees from a varroa Òhot spotÓ in the hive, inflating your estimate of varroa intensity). So the question is: which, if any, of these sampling procedures gives an adequate estimate of all the mites in a particular hive?   This is what a recent study, published in the journal Apidologie, attempted to answer. A Welsh research team, led by Manuela Branco, sampled 22 beehives for varroa mites using three methods. First, they sampled natural mite mortality using the sticky board assay as described above. Second, they estimated infestation level of adult bees by sampling about 200 adult workers from the brood nest area and washing the mites from them. Additionally, they sampled wo