Kalyn Bickerman is a Ph.D. student at the University of Maine under the supervision of Dr. Frank Drummond and works on investigating the health of native bumblebees in Maine's lowbush blueberry fields. Before arriving at UMaine, Kalyn completed a Bachelor of Arts degree in Biology at Bowdoin College in Brunswick, ME, as well as a Master of Arts degree in Conservation Biology at Columbia University in the City of New York.
Although her Master's work focused on the health of loggerhead sea turtles in the Pacific, Kalyn has been able to transfer her knowledge of, and her interest in, pathology and disease ecology to doing her Ph.D. work with Maine's bumblebees. Beyond looking for common parasites and pathogens in the bees, Kalyn also has done some work looking at pesticides and how they affect colony development, along with how well individual bees are able to detoxify themselves when faced with pesticide exposure.
Lowbush blueberries are one of Maine's most important exports and bumblebees are instrumental in their pollination for successful fruit production. Therefore, it is vital to protect our native pollinators, particularly in a time when our managed pollinator, the honeybee, is facing such grave declines. Although she traveled and has lived in different cities since graduating college, Kalyn (a Maine native) always knew she wanted to return to Maine to begin her professional career. She is very happy that her work not only helps protect the bees, but also the agricultural economy of her home State.
European foulbrood (abbreviated EFB) is a bacterial disease that effects honey bee larvae before the capped stage. European foulbrood disease is characterized by dead and dying larvae which can appear curled upwards, brown or yellow, melted, and/or dried out and rubbery. The causative bacteria, Melissococcus plutonius is ingested by honey bee larvae after which the bacterium competes for food inside the larvae. If the bacteria out-competes the larva, the larva will die before the cell is capped. Alternatively, the bee may survive until adulthood if the larvae has sufficient food resources. European foulbrood should not be confused with American foulbrood (AFB), which is caused by a different bacteria that produces different symptoms and control requirements.
European foulbrood disease is considered to be more problematic in situations where forage nectar is sporadic, or other situations that result in fewer nurse bees in colonies to feed larvae. At the onset of nectar flow in early spring, forage recruitment of house bees may increase rapidly resulting in few bees in colonies to feed honey bee larvae. Often, when the nurse bee to larvae ratio stabilizes later in the season, or remains stable throughout a season, symptoms disappear. However, this disease can occur throughout a season and will sometimes not clear up on its own. In severe cases, colony death can occur. Also, yearly reoccurrence of EFB from contaminated combs and equipment can occur. The bacteria that causes EFB does not produce spores, but combs contaminated with the bacteria can still reinfect honey bees in subsequent years.
European foulbrood is caused by the bacterium Melissococcus plutonius. G. F. White is credited with first identifying the correct bacterium that causes European foulbrood in 1908, naming it Bacillus Y which he later renamed Bacillus pluton (Baily 1983). The bacterium was subsequently renamed by several scientists after it became clearly linked to the disease. Baily (1956) isolated the bacterium and, based on morphology, called it Streptococcus pluton. Baily and Collins (1981), later re-classified the bacterium as Melissococcus pluton based on additional culture and chemical knowledge. This was then tweaked due to nomenclature rules to Melissococcus plutonius meaning "pertaining to Pluto or the underworld" instead of M. pluton which means "Pluton, Greek god of the underworld'" (Truper and de Clari 1998).
As if the changing nomenclature is not enough to confuse, several other bacteria that are only found in association with M. plutonius were at times credited with causing EFB. This is at least partially due to the fact that these bacteria can overgrow M. plutonius and sometimes seem to improve its growth in lab conditions (Baily 1983). These secondary, infective bacteria present with M. plutonius include; Paenibacillus alvei, Achromobacter (Bacterium) eurydice, and Bacillus laterosporus Laubach (Shimanuki 1997). These bacteria are sometimes considered symbiotic and may cause some of the differences in smell and appearance in infected larvae (Baily 1981). There is suspicion that some of these bacteria may have some causal relationship to symptom onset, but this has never been clearly established (Shimanuki 1997).
Life cycle of European foulbrood
Larvae become infected with European foulbrood when they consume brood food that contains the bacteria M. plutonius (Shimanuki 1997). There is also some evidence that transmission may occur from bites of the parasitic mite, Varroa destructor (Kanbar and Engels 2003). Inside infected larva, the bacterial populations concentrate in the food mass in the midgut and the gut peritrophic membrane interface (McKee et al. 2004) where the bacteria then reproduces (Bailey 1983). Depending on the level of infection, and possibly the amount of available food, the infected larva will either survive or die.
The degree of larval mortality, measured in one experiment, was directly related to the duration or amount of bacteria that was fed to the larva. Larvae were found to be more likely to die as increasing amounts of bacteria were fed (McKee et al. 2004). The larvae that survive go on to defecate and pupate, which leaves bacteria on the combs that can be infective for years, even though this bacteria does not produce spores (Baily 1981, 1983). Surviving larvae will become adults with generally lower weight and delayed pupation when compared to their uninfected counterparts, supporting the idea that infection creates higher energy demands (Baily 1960, Mckee et al. 2004). It is noted that an increased food supply from adequate numbers of nurse bees can reduce larval death and observed symptoms. With adequate amounts of food, larvae are more likely to survive (Baily 1983). This may explain why expression of the disease can change sporadically year to year, and season to season, depending on the balance of nurse bee to larvae ratio and thus, the amount of brood food made available to the larvae.
Symptoms of European foulbrood
It is important to not confuse European foulbrood with American foulbrood. These are two very different diseases that require different management and treatment routines. Both are however bacterial brood diseases. Use the table below as an overview to tell the difference between European foulbrood and American foulbrood.
European foulbrood American foulbrood
- Can be slightly ropey with threads less than 1.5cm, but usually not ropey.
- Odor: sour or none
- Scale: brown to black, rubbery
- Stage of Brood: before capped
- Appearance: twisted, dull to yellow to dark brown, tracheal tubes often visible
- Coffee color, ropey with a fine thread about 2.5cm
- Odor: sulfurous, “chicken house”
- Scale: brown to black, brittle
- Stage of Brood: after capped
- Appearance: chocolate brown to black, perforated cappings
Fig.3: Table from Shimanuki and Knox (2000) and Delaplane (1998), Ropey length from Shimanuki (1997), American foulbrood photo by Williams, USDA.
A "spotty brood pattern" (Fig. 4) in a honey bee colony can often be the first sign of a wide variety of problems, including EFB. A spotty brood pattern can occur when some larvae die in their cells from a disease, while others survive and become capped resulting in a spotty or shotgun appearance of the capped stage of brood. Many other conditions and situations can cause a spotty brood pattern. For example, an inbred queen can produce a spotty brood pattern when the alleles at the sex locus become homozygous. This produces fertilized, diploid males which are then consumed by worker bees. Although not unique to hives affected with EFB, a spotty brood pattern is a common symptom of EFB.
In hives infected with EFB, dying and dead larvae can become yellow and then brown. A sour, fishy odor may be present or not. Tracheal tubes can become more apparent as the larvae flattens or 'deflates'(Fig.2). The larvae can also twist as they die and can die curled upwards (fig.1). Other times they melt in their cells and will generally be mushy. The remains can be slightly ropey with threads less then 1.5cm long (Shimanuki 1997). To test if the remains are ropey, a toothpick, match, or small stick can be probed into the cell and removed (fig.5). Once dried, a rubbery scale remains.
Diagnosis of infection with European foulbrood should begin with visual inspections of the above symptoms. Beekeeper's inexperienced with EFB would likely benefit from confirmation of diagnosis before taking action, in case the infection is another bacteria, virus, chilled brood, or some other situation. Confirmation could occur through their state sponsored apiary inspection program, if available, or by the use of an inexpensive and easy to use diagnostic test kit, or sending a sample to the USDA Beltsville Bee Research Laboratory for testing.
Diagnostic field validation kits for EFB are based on monoclonal antibodies of M. plutonius (Tomkies et al. 2009). Samples sent to the USDA Beltsville Bee Research Laboratory for diagnosis will be examined microscopically for the presence of M. plutonius or one of the associated bacteria, which have often eliminated M. plutonius (Smith 2009). Other methods to confirm M. plutonius include: Enzyme-linked immunosorbent assays (ELISA), (Pinnock and Featherstone 1983), a hemi-nested PCR assay (Djordjevic et al. 1998), and quantitative real-time PCR (Roetschi et al. 2008).
For additional information on diagnosing European Foulbrood, see the following two pages.
Occurrence and distribution
European foulbrood occurs on all continents where honey bees are kept (Shimanuki 1997). During the early 1980's in the U.S., it was historically severely problematic in New Jersey during the spring cranberry and blueberry pollination season. This created some suspicion that low nutrition in pollination fields were having an effect on EFB occurrence, but this did not seem apparent in trials conducted by the USDA (Herbert and Shimanuki 1984). This regional outbreak in New Jersey pollination fields was not consistent. Herbert et al. (1987) reported that in 1986-87, European foulbrood could not be found in the New Jersey, USDA test colonies, while previous to 1986 the disease was a serious problem.
Baily (1983) explains the occurrence of EFB as having the propensity, "...to remain inapparent, then to appear, sometimes in a very severe form, and then frequently to disappear spontaneously, especially after midsummer...". Thompson and Brown (2001 see summary) indicate that yearly recurrence of the disease in infected apiaries is particularly problematic in the UK.
In Switzerland, incidences have increased in recent years (Forsgren et al. 2005). In that country, PCR techniques were used to detect European foulbrood in colonies with and without symptoms, (Belloy et al. 2007 see summary). It was found that in colonies without symptoms in apiaries where other colonies were symptomatic, 90% of the adult bees carried the bacteria. In apiaries without symptoms, but near symptomatic apiaries, 30% of the colonies carried the bacteria, and in apiaries far from symptomatic apiaries, the bacteria could not be detected. This means that it is possible that the bacteria may not be present in regionally isolated areas.
There are limited options for possible cultural control of this disease. However, as noted above, treatment may not always be necessary in all cases if conditions change that result in disappearance of the disease. Control is sometimes necessary though. Re-queening the colony may have some benefit, due to a break in the brood cycle, and supplying a queen that is more prolific (Shimanuki 1997). There is some evidence of genetic resistance towards the disease (McKee et al. 2004, Shimanuki 1997), but there are no known lines/breeds that are resistant to EFB, including lines bred for hygienic behavior (Spivak per comm). Hygienic lines are however clearly resistant to American foulbrood.
Due to the infectious activity of the bacteria on contaminated combs, moving combs and equipment should be expected to cause cross contamination. In some countries, destruction or sanitation of infected combs and equipment is required. As of 2008 in Switzerland, European foulbrood is a notifiable disease which requires sanitation of apiaries, without the use of antibiotics. This includes the process of burning every infected and weak colony. In a Swiss study, Roetschi et al. (2008 see summary) showed that this process was not very effective as 5 out of 8 sanitized apiaries were reinfected one year later. However, destroying contaminated equipment has proven effective in another study (see "Chemical control").
In the US, as of this writing 2009, the antibiotic Oxytetracycline HCL soluble powder (OTC), trade name Terramycin is the only product labeled for the control of European foulbrood. Various concentrations are available. This means that users of this product should pay particular attention to the product label to deliver the correct dose, or contact their local state beekeeping inspector or extension specialist for assistance.
Terramycin is also registered for the use in controlling American foulbrood, although it has been established that American foulbrood is expressing resistance to this drug in the U.S. (Miyagi et al. 2000). An equivalent study on whether or not European foulbrood is expressing resistance to Terramycin in the U.S. could not be found. There is a study that investigated European foulbrood OTC resistance in the U.K. and it found that resistance was not occurring (Waite et al. 2003b see summary). However, use of Terramycin in the U.K. is greatly different then in the U.S., so this may not give any indication to its effectiveness in the U.S. Use of Terramycin as a precautionary, or prophylactic, method to prevent European foulbrood in non-symptomatic colonies, even in infected apiaries, is not recommended (Thompson and Brown 2001 see summary).
A promising method for controlling European foulbrood has been developed in the U.K., which involves the combination of removing contaminated equipment with the "shook swarm" method along with the use of antibiotics (Waite et al. 2003a see summary). As mentioned above, recurrence of the disease can be a major problem. This method seems to help control recurrence the following year, in addition to disease control the year implemented. See the research summary, Shook Swarm and OTC Antibiotics for European Foulbrood Control for more information. A trial of this method in the U.S. was not found.
Research Publication Summaries:
- Distribution of European Foulbrood in Apiaries With and Without Symptoms
- Infection of European Foulbrood Before and After Apiary Sanitation
- Antibiotic Treatment Study Summaries:
- Shook Swarm and OTC Antibiotics for European Foulbrood Control
- Assessment of Precautionary Antibiotic Treatments for European Foulbrood in Infected Apiaries
- Resistance Trial of European Foulbrood to OTC
- Baily, L. (1956). Aetiology of European foulbrood; a disease of larval honeybee. Nature 178: 1130.
- Baily, L. (1960). The epizootiology of European foulbrood of the larval honey bee, Apis mellifera Linnaeus. Journal of Insect Pathology 2: 67-83.
- Bailey, L. (1981). Honey Bee Pathology 124p.Academic Press Inc. (London) LTD.
- Bailey, L. (1983). Melissococcus pluton, the cause of European foulbrood of honey bes (Apis spp.). Journal of Applied Bacteriology 55: 65-69.
- Bailey, L. (1985). Melissococcus pluton and European foulbrood. Bee World 66: 134-136.
- Baily, L. and Collins, M. D. (1981). Reclassification of Streptococcus pluton (White) in a new genus Melissococcus, as Melissococcus pluton nom. rev.; comb. nov. Journal of Applied Microbiology 53(2): 215-217.
- Belloy, L., Imdorf, A., Fries, I., Forsgren, E., Berthoud, H., Kuhn, R., Charriere, J. (2007). Spatial distribution of Melissococcus plutonius in adult honey bees collected from apiaries and colonies with and without symptoms of European foulbrood. Apidologie 38: 136-140. Read summary here
- Delaplane, K. (1998). Strictly for the hobbyist: European foulbrood and its control. American Bee Journal 138(10): 736-737.
- Djordjevic, S. P., Noone, K., Smith, L, and Hornitzky, M. A. Z. (1998). Development of a hemi-nested PCR assay for the specific detection of Melissococcus pluton. Journal of Apicultural Research 37(3): 165-174.
- Forsgren, E., Lundhagen, A. C., Imdorf, A., and Fries, I. (2005). Distribution of Melissococcus plutonius in honeybee colonies with and without symptoms of European foulbrood. Microbial Ecology 50: 369-374.
- Herbert, E. W., Chitwood, D. J., and Shimanuki, H. (1987). Chalkbrood research at Beltsville. American Bee Journal 127: 488-491.
- Herbert, E. W. and Shimanuki (1984). An update on European foulbrood research in New Jersey. American Bee Journal 124(6): 472-473.
- Hornitzky, M. A. Z. and Smith, L. A. (1999). Sensitivity of Autralian Melissococcus pluton isolates to oxytetracycline hydrochloride. Australian Journal of Experimental Agriculture 39: 881-883.
- Kanbar, G., and Engels, W. (2003). Ultrastructure and bacterial infection of wounds in honey bee (Apis mellifera) pupae punctured by Varroa mites. Parasitology Research 90: 349-354.
- Lehnert, T., and Shimanuki (1980). European foulbrood disease control in honey bee colonies used for blueberry and cranberry pollination. American Bee Journal 120: 429-430.
- McKee, B. A., Goodman, R. D., and Hornitzcky, M. A. (2004). The transmittion of European foulbrood (Melissococcus plutonius) to artificially reared honey bee larvae (Apis mellifera). Journal of Apiclutural Research 43(3): 93-100.
- Miyagi, T., Peng, C. Y. S., Chuang, R. Y., Mussen, E. C., Spivak, M. S., and Doi, R. H. (2000). Verification of oxytetracycline-resistant American foulbrood pathogen Paenibacillus larvae in the United States. Journal of Invertebrate Pathology 75(1): 95-96.
- Morse, R., A. and Nowogrodzki, R. editors (1990). Honey Bee Pests, Predators, and Diseases 474p. Cornell University Press. Second edition.
- Pinnock, D. E. and Featherstone, N. E. (1984). Detection and quantification of Melissococcus Pluton infection in honeybee colonies by means of enzyme-linked immunosorbent assay. Journal of Apicultural Research 23(3): 168-170.
- Roetschi, A., Berthoud, H., Kuhn, R., Imdorf, A. (2008). Infection rate based on quantitative real-time PCR of Melissococcus plutonius, the causal agent of European foulbrood, in honeybee colonies before and after apiary sanitation. Apidologie 39: 362-371. Read summary here.
- Shimanuki, H. 1997 Bacteria, Chapter 3 from Morse, R., A. and Flottum, K. editors. Honey Bee Pests, Predators, and Diseases 718p. A. I. Root Company. Third edition.
- Shimanuki, H. and Knox, D. A (2000). Diagnosis of honey bee diseases. USDA-ARS Agriculture Handbook Number 690 : 61p.
- Shimanuki, H., Knox, D., and Feldlaufer, M. (1992). Honey bee disease interactions: The impact of chalkbrood on other honey bee brood diseases. American Bee Journal 132(11): 735-736.
- Smith, B. (2009). Lab Diagnosis of European Foulbrood. http://extension.org/pages/Lab_Diagnosis_of_European_Foulbrood
- Thompson, H. M. and Brown, M. A. (2001). Is contact colony treatment with antibiotics an effective control for Europan foulbrood? Bee World 82(3): 130-138. Read summary here.
- Tomkies, V, Flint, J., Johnson, G., Ruth, W., Wilkins, S., Danks, C., Watkins, M., Cuthbertson, G., Carpana, E., Marris, G., Budge, G., and Brown, M. (2009). Development and validation of a novel field test kit for European foulbrood. Apidologie 40: 63-72.
- Truper, H. G. and de Clari, L. (1998). Taxonomic note: erratum and correction of further specific epithets formed as substantives (nouns) 'in apposition'. International Journal of Systematic Bacteriology 48: 615.
- Waite, R. J., Brown, M. A., Thompson, H. M., Bew, M. H. (2003a). Controlling European foulbrood with the shook swarm method and oxytetracycline in the UK. Apidologie 34: 569-575.Read summary here.
- Waite, R., Jackson, S., and Thompson, H. (2003b). Preliminary investigations into possible resistance to oxytetracycline in Melissococcus plutonius, a pathogen of honeybee larvae. Letters in Applied Microbiology 36: 20-24.Read summary here.
Page Authors: Michael Wilson and John Skinner, University of Tennessee. 2009.
Photographs by: Michael Wilson, except American foulbrood USDA photo noted above.
Acknowledgments: We appreciate the excellent review and editing provided by Dr. Dewey M. Caron, Affiliate Professor OSU and Dr. Jeff Harris, USDA.
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What is Integrated Crop Pollination?
Integrated crop pollination is the combined use of multiple pollinator species, habitat augmentation, and crop management practices to provide reliable and economical pollination of crops. Pollinator species can include managed honey bees, alternative managed bees, and many different types of wild bees. Habitat augmentation refers to adding floral and nesting resources to farms (e.g. wildflower strip, meadows, and hedgerows). Crop management practices that support pollination include modifying pest management practices to reduce risks to pollinators, using conservation tillage, and allowing cover crops to bloom. Reliable and economical pollination may come from honey bees alone or from a combination of different pollinators. It all depends on the crop, on the farm situation, and the economics of different approaches.
Factsheets on crop pollination for specialty crop growers
- 4 Ways to Help Bees Help You!
- Almond Pollination (California)
- Apple Pollination (Michigan)
- Apple Pollination (Pennsylvania)
- Blueberry Pollination (British Columbia)
- Blueberry Pollination (Florida)
- Blueberry Pollination (Michigan)
- Blueberry Pollination (Vermont)
- Cane Fruit Pollination (Oregon)
- Cherry Pollination (Michigan)
- Pumpkin Pollination (Pennsylvania)
Resources for extension professionals
Researchers with the Integrated Crop Pollination Project surveyed specialty crop growers to determine pollination practices and grower perspectives on crop pollination. Access the regional and crop specific reports below.
Watch recorded webinars on the following topics:
Ensuring almond pollination
Presented by Theresa Pitts-Singer, USDA-ARS/Utah State University
Pollinating highbush blueberries: bees bring bigger berries
Presented by Rufus Isaacs, Michigan State University
Pollinating apples and cherries East of the Rockies
Presented by Julianna Wilson, Michigan State University
On-farm pollinator benefits for watermelon pollination
Presented by Neal Williams, University of California, Davis
Ensuring pumpkin pollination
Presented by Shelby Fleischer, Pennsylvania State University
How to manage solitary orchard bees for crop pollination
Presented by: Theresa Pitts-Singer, Utah State University
The Integrated Crop Pollination Project
Members of the Integrated Crop Pollination Project Team are investigating the performance, economics, and farmer perceptions of different pollination strategies in various fruit and vegetable crops.This project is supported by USDA-NIFA Specialty Crop Research Initiative Grant (#2012-51181-20105). To learn more go to the project website at projecticp.org or read the project brochure click here.
- Identify economically-valuable pollinators and the factors affecting their abundance.
- Develop habitat management practices to improve crop pollination.
- Determine performance of alternative managed bees as specialty crop pollinators.
- Demonstrate and deliver ICP practices for specialty crops.
- Determine optimal methods for ICP information delivery and measure ICP adoption.
- Economics and modeling of pollination ecosystem services.
Project Advisory Panel:
This project is advised by a diverse group of stakeholders with interest in crop pollination. The project’s advisory panel includes representatives from the organizations listed below.
- American Fruit Grower Magazine
- California Almond Board
- Cardno J.F. New
- Crown Bees
- MBG Marketing
- Orchard Bee Association
- Oregon State University Extension
- Peerbolt Crop Management
- University of Reading
- University of Minnesota
- USDA-Farm Service Agency
- USDA-Natural Resource Conservation Service
Project team contributing to materials on this page
- Rufus Isaacs, Michigan State University, East Lansing, MI
- Kelly Garbach, Point Blue Conservation Science, Petaluma, CA
- Eric Lonsdorf, University of Minnesota, Minneapolis, MN
- Keith Mason, Michigan State University, East Lansing, MI
- Theresa Pitts-Singer, USDA-ARS Pollinating Insects Research Unit, Logan, UT
- Taylor Ricketts, University of Vermont, Burlington, VT
- Mace Vaughan, The Xerces Society, Portland, OR
- Neal Williams, University of California - Davis, Davis, CA
- Derek Artz, USDA-ARS Pollinating Insects Research Unit, Logan, UT
- Mary Bammer, University of Florida, Gainesville, FL
- David Biddinger, Pennsylvania State University, University Park, PA
- Natalie Boyle, USDA ARS Pollinating Insects Research Unit, Logan, UT
- Claire Brittain, University of California - Davis, Davis, CA
- Josh Campbell, University of Florida, Gainesville, FL
- Jim Cane, USDA ARS Pollinating Insects Research Unit, Logan, UT
- Jaret Daniels, University of Florida, Gainesville, FL
- Elizabeth Elle, Simon Fraser University, Burnaby, British Columbia, CA
- Jamie Ellis, University of Florida, Gainesville, FL
- Shelby Fleischer, Pennsylvania State University, University Park, PA
- Jason Gibbs, Michigan State University, East Lansing, MI
- Bob Gillespie, Wenatchee Valley College, Wenatchee, WA
- Larry Gut, Michigan State University, East Lansing, MI
- George Hoffman, Oregon State University, Corvallis, OR
- Jennifer Hopwood, The Xerces Society, Portland, OR
- Neelendra Joshi, Pennsylvania State University, University Park, PA
- Karen Klonsky, University of California-Davis, Davis, CA
- Insu Koh, University of Vermont, Burlington, VT
- Claire Kremen, University of California-Berkeley, Berkeley, CA
- Emily May, The Xerces Society, New Haven, CT
- Sujaya Rao, Oregon State University, Corvallis, OR
- James Reilly, Rutgers University, New Brunswick, NJ
- Nikki Rothwell, Michigan State University, Traverse City, MI
- Cory Stanley-Stahr, University of Florida, Gainesville, FL
- James Strange, USDA-ARS Pollinating Insects Research Unit, Logan, UT
- Katharina Ullmann, The Xerces Society, Davis, CA
- Kimiora Ward, University of California - Davis, Davis, CA
- Julianna Wilson, Michigan State University, East Lansing, MI
- Rachael Winfree, Rutgers University, New Brunswick, NJ
Funding for the Integrated Crop Pollination Project was provided by USDA-NIFA Specialty Crop Research Initiative Grant (#2012-51181-20105).
This webinar series will provide an overview of pollination requirements and strategies to ensure pollination of different specialty crops. Farmers and gardeners rely on crop pollinators, including honey bees, alternative managed bees like the blue orchard bee, and wild bees. Pollination experts will discuss how to support these pollinators in almond, blueberry, tree fruit, pumpkin, and watermelon. Webinars will take place on selected Tuesdays at 11a.m. Pacific time, noon Mountain time, 1 p.m. Central time, 2 p.m. Eastern time. Registration required for these free webinars. Click on the title below for more information about each webinar. All webinars moderated by John Skinner (University of Tennessee) and Katharina Ullmann (Xerces Society).
JANUARY 24, 2017
JANUARY 31, 2017
Title Pollinating highbush blueberries: bees bring bigger berries
Presented by: Rufus Isaacs, Michigan State University
Register here: https://extension.zoom.us/j/892630181
FEBRUARY 7, 2017
Title Providing habitat for wild bees on organic farms (organized by eOrganics)
Presented by Elias Bloom (Washington State Universtiy (WSU)), Rachel Olsson (WSU), Bridget McNasser (Oxbow Farm and Conservation Center)
Register here: https://attendee.gotowebinar.com/register/2124436063988236545
FEBRUARY 14, 2017
Title Pollinating apples and cherries East of the Rockies
Presented by Julianna Wilson, Michigan State University
Register here: https://extension.zoom.us/j/940545278
FEBRUARY 28, 2017
Title On-farm pollinator benefits for watermelon pollination
Presented by Neal Williams, University of California, Davis
Register here: https://extension.zoom.us/j/619691844
MARCH 21, 2017
MARCH 28, 2017
Title How to manage solitary orchard bees for crop pollination
Presented by: Theresa Pitts-Singer, Utah State University
Register here: https://extension.zoom.us/j/239662773
Download the flyer for the entire 2017 Ensuring Specialty Crop Pollination Webinar Series: 2017 Bee Health and Pollination Webinar Series
The 2017 Webinars are brought to you by the Bee Health eXtension Community of Practice; the Integrated Crop Pollination Project; and by Michigan State University, University of California,Davis, Pennsylvania State University, the Xerces Society, and University of Tennessee. Series Coordinators: John Skinner and Katharina Ullmann. Funding provided by USDA-NIFA Specialty Crop Research Initiative Grant (#2012-51181-20105) except for webinar titled "Providing habitat for wild bees on organic farms".
Image credits: Katharina Ullmann (Xerces Society), Emily May (Xerces Society), Logan Rowe (MSU)
Honey Bee Health Coalition Varroa Management
Honey Bee Health Coalition Unveils Videos to Help Beekeepers Combat Devastating Parasites
Videos Complement Coalition’s Tools for Varroa Management Guide, Provides Step-By-Step Demonstrations of Utilizing an Integrated Pest Management Strategy of Monitoring and Treatment
KEYSTONE, CO, Nov. 28, 2016 — The Honey Bee Health Coalition released a series of videos today to help beekeepers promote colony health and combat costly and destructive Varroa mite (Varroa destructor) infestations. The videos can be found on the Coalition website at www.honeybeehealthcoalition.org/Varroa and provide detailed step-by-step instructions on how to monitor hives for varroa and when levels get too high, safely treat. The videos complement the Coalition’s wildly popular Tools for Varroa Management Guide.
“The Honey Bee Health Coalition’s Tools for Varroa Management Guide has provided beekeepers in the US and Canada with invaluable tools and techniques to confront destructive Varroa mite infestations,” said Mark Dykes, Apiary Inspectors of America. “These videos will show beekeeper real world application techniques that will help them correctly apply treatments.”
The videos provide helpful visual aids and step-by-step directions on how beekeepers can monitor and control Varroa mites through an Integrated Pest Management strategy. The videos cover a range of strategies and tools, including the uses of formic acid, essential oils, and other synthetic miticides.
“Healthy bees support our world’s food supply and farmers everywhere. A single untreated colony can transmit Varroa mites to other nearby hives and threaten honey bee health across large geographic regions,” said Danielle Downey, Project Apis m. “Beekeeping is becoming very popular, and often keeping the bees healthy is a mysterious learning curve. These important 'how to' videos bring the Coalition’s Tools for Varroa Management Guide to life — and will amplify its impact in the United States, Canada, and around the globe.”
The Coalition’s Tools for Varroa Management has given beekeepers the tools they need to measure Varroa mite infestations in their hives and select appropriate control methods. The guide, which has been downloaded more than 5,500 times since its release, has been updated 4 times with continued refinements and details.
About the Honey Bee Health Coalition
The Honey Bee Health Coalition brings together beekeepers, growers, researchers, government agencies, agribusinesses, conservation groups, manufacturers and brands, and other key partners to improve the health of honey bees and other pollinators. Its mission is to collaboratively implement solutions that will help to achieve a healthy population of honey bees while also supporting healthy populations of native and managed pollinators in the context of productive agricultural systems and thriving ecosystems. The Coalition is focusing on accelerating collective impact to improve honey bee health in four key areas: forage and nutrition, hive management, crop pest management, and communications, outreach, and education.
Through its unique network of private and public sector members, the Coalition fosters new partnerships, leverages existing efforts and expertise, and incubates and implements new solutions. The Coalition brings its diverse resources to bear in promoting communication, coordination, collaboration, and investment to strategically and substantively improve honey bee health in North America.
A list of Honey Bee Health Coalition members can be found at www.honeybeehealthcoalition.org.
Authors: Philip A. Moore, Michael E. Wilson, John A. Skinner
Department of Entomology and Plant Pathology, the University of Tennessee, Knoxville TN
Originally Published: August 4, 2015
The honey bee tracheal mite (Acarapis woodi) was first described in 1921 by Rennie, who believed the mite was the cause of the Isle of Wight Disease, after dissecting infected honey bees (Apis mellifera)from colonies on the island off the coast of England (Henderson and Morse 1990). Between 1905 and 1919, 90 percent of colonies on the island were killed in one of the most infamous honey bee epidemics in history (Adam 1968). Although the causative agent or complex of agents was never specifically identified, tracheal mites and Nosema are commonly cited (vanEnglesdorp and Meixner 2010). The disease spread to the mainland United Kingdom and continental Europe, which initiated a ban on imports of live bees into the United States in 1922 (Phillips 1923).
In 1980, tracheal mites were discovered in Mexico. By 1984, bees from a commercial beekeeping operation in Weslaco Texas tested positive for the parasite. In spite of efforts to restrict the distribution of the pest, including the destruction of 43,367 colonies, tracheal mites reached all major beekeeping states in less than five years (Mussen 2001). Exceedingly high colony losses reported by beekeepers in many parts of the US in 1986-1989 were attributed to tracheal mites (Furgala et al 1989, Bailey 1981). For example, when the pest first reached Pennsylvania, beekeepers with infested colonies lost 31 percent of their colonies overwinter, compared to their non-infested neighbors who lost just 11 percent (Frazier et al 1994). Tracheal mites have now been spread throughout Europe, Asia, parts of Africa and North and South America. It is not known whether Australia, New Zealand, or Scandinavian countries contain the pest (Denmark et al 2000; Hoy 2011).
Figure 1: Tracheal mite as seem in a scanning electron micrograph (SEM). Credit: The Food and Environment Research Agency (Fera), Crown Copyright
Tracheal Mite Life History
Tracheal mites are oval shaped, between 125-174 micrometers long and 60-81 micrometers wide with a semi glossy white color, numerous setae (bristle like hairs), three sets of legs, and a long piercing mouthpart for feeding (Delfinado-Baker and Baker 1982). They are primarily found in the adult honey bee respiratory system that is composed of a network of tracheae tubes and have also been found in the air sacks of the abdomen and head (Giorani 1965) and externally at the base of the wing (Royce and Rossignol 1991). The tracheae initiate in large trunks at the spiracles (openings for air passage) and progressively branch out into smaller tracheoles that serve to carry air into and out of the honey bee, connecting to all tissues of the body. Female mites enter the first set of spiracles of adult bees and lay eggs in the large initial section of tracheae.
Figure 2: Tracheal mite eggs inside a trachea tube. Credit: The Food and Environment Research Agency (Fera), Crown Copyright
The female mite will lay 5-7 eggs over 3-4 days (Morgenthaler 1931). After 3-4 days the eggs hatch and progress from larva to nymph, and into the adult stage. Males develop to adulthood 11-12 days after hatching, while females develop in 14-15 days. Mating occurs in the same trachea in which it developed. All mite instars live within the tracheae, except for the brief period when a mated female disperses to find a new host. Female mites disperse when the bee host is at least 12 days old, typically between 15 to 25 days (Pettis and Wilson 1996), most often dispersing at night when the older foraging bees are in close contact with young bees (Pettis et al 1992). Mites exposed outside of the host will die within a few hours and therefore do not persist on comb or other colony and environmental components (Sammataro and Needham 1996; Sammataro et al. 2000).
The mated female leaves the tracheae by emerging from the spiracle and adhering to the tip of a hair on the bee’s thorax. Once another bee’s hair brushes against the original host, the mite attaches to the passing bee (Hirschfelder and Sachs 1952). Mites are attracted to the exhausted air of the spiracle and to specific hydrocarbons from the bee’s cuticle (Phelan et al 1991; McMullan et al 2010). Female mites are less attracted to older bees and rarely enter bees older than 4 days (Gary et al 1989). These older bees may not live long enough in the summer for the mite to complete its lifecycle.
Because of the time lag of invading a host, laying eggs, mite development, mating and the new reproductive females’ emergence, foraging workers bees (who contain the reproductive female mite) must contact young worker bees for successful transmission. Foraging worker bees rarely encounter young bees, due to division of labor and physical separation of tasks in the hive, except at night or periods when weather does not permit leaving the hive (Bailey and Perry 2001). When workers are unable to forage, such as during poor weather, mites are more able to find young bees and the rate of transmission increases (Bailey and Perry 2001).
Tracheal Mite Prevalence in the United States
Figure 3: USDA-ARS bee diagnostic lab percentage of tracheal mite infestation of all submitted samples for pest or disease analysis by year.
Figure 3 displays the prevalence of tracheal mites in diagnostic samples sent to the USDA-ARS bee lab in Beltsville Maryland. This shows a decline in tracheal mite prevalence since introduction into the US. This may indicate that current control and resistance techniques are effective in reducing the pest population or that the pest population is declining for some other reason. However, this data is not from a systematic sample and may contain sampling bias by location, reasons for sampling, or other unknown factors. It is therefore not completely representative of US honey bee colonies, but does indicate a reduction in prevalence of samples submitted for diagnosis to the USDA-ARS Beltsville bee lab, and reflects a decline in prevalence seen in other studies and observations. Current systematic honey bee pest surveys by USDA-APHIS do not measure tracheal mite prevalence.
Damage Caused by Tracheal Mites
Tracheal mites feed on bee hemolymph (fluid of the circulatory and lymphatic system similar to blood), which they access by piercing the wall of the trachea with their sharply pointed stylets (mouthpart). The mite then sucks the hemolymph through a short tube into the pharynx (Hirschfelder and Sachs, 1952). These mites, unlike Varroamites, have not been shown to transmit other microorganisms through feeding. Individual bees are thought to die because mite populations build up in the tracheae, limiting or preventing air flow, or by damaging the tracheae during feeding (Shimanuki et al 1992).
Figure 4. Mortality spiral on a moderately infested colony during the winter/early spring period. Credit: McMullan and Brown 2009
Heavy mite population affects bee metabolism, and the ability of the winter cluster to regulate temperature (Skinner 2000). Tracheal mites can cause diminished brood area, smaller adult bee populations, loose winter clusters, increased honey consumption, which all combine to cause colony death (Figure 4; McMullan and Brown 2009; Komejli et al 1989). When over 30 percent of bees in a colony become infected, honey production is reduced and winter survival decreases (Furgala et al 1989). Bees confined over winter cause increased mite populations in the winter cluster. Colonies with greater than 40 infection frequently die over winter in the US and Canada (Furgala et al 1989; Otis and Scott-Dupree 1992). The colder and longer the winter, the more likely an infested colony will die.
Tracheal mites can infect all castes of adult honey bees. Drones have been found to harbor more mites than workers (Royce and Rossignol 1991; Darwicke et al. 1992). However since workers are available all year, they are the primary host. Queens infected with tracheal mites weigh less, although the effect on reproductive ability is not well understood (Camazine et al 1998). Commercially reared queens have commonly been found with tracheal mites, although the most recent survey of US queen producers found that only one of the twelve producers surveyed had some tracheal mite infected queens (Delaney et al 2010).
There are no reliable indicators or symptoms of mite infestation. Tracheal mites shorten the lifespan of adult bees and have been associated with disjointed “K” wings and bees crawling on the ground near a hive, unable to fly. Unfortunately, these symptoms are also associated with Nosema infection (Fries et al. 2013) and some viruses (de Miranda et al 2013). The only way to diagnose a tracheal mite outbreak is to examine honey bees for mites.
Detection of Tracheal Mites
Diagnosis of tracheal mite infestation is accomplished through microscope examination of the tracheae. The timing of sampling is important because the population of tracheal mites varies with the season. The greatest likelihood of detection is the late fall, winter, or early spring when bee populations are at the lowest and a high proportion of old bees are present, which have allowed for mites to reproduce. Infestation decreases in the summer when large bee populations dilute the mite population and bee turn over limits mite reproduction.
Bee age influences the detection of tracheal mites, therefore the location of sampling should be considered. Collect 50 bees from the frames of honey supers, the inner cover, or hive entrance, where older bees congregate. Drones tend to have higher mite abundance and should be collected as well, when available. Bees can be collected with a hand held modified insect vacuum or by scooping up bees directly into a wide mouth jar. Add the sample to a wide mouth jar and label the jar with the colony identity and date. Add 70% ethanol or freeze the jar to kill the bees (examination of tracheae is easier with no alcohol present). Bees should not be stored in alcohol for a long period because this will darken the tissue and obscure the tracheae.
If the bees are to be sent to the Beltsville Maryland USDA-ARS lab for diagnosis, the samples must be wet in alcohol. To ship through the postal service, samples are treated as if for Varroa. Collect 100 recently dead, dying, or older bees, and soak in 70% alcohol (ethyl, methyl, or isopropyl). Prior to shipping, pour off excess alcohol because postal services will not accept packages containing alcohol and pack into a leak proof container. For more information on submitting a sample for analysis see here. If a dissecting and compound microscope is available, dissection of the bees and examination of the tracheae is possible.
Dissection for Tracheal Mites
All 50 bees do not necessarily need to be sampled. A sequential sampling technique allows one to classify a low infestation (<10%) and high infestation (>10%), which will help determine the decision to treat with an acaricide (miticide). If the first 3 out of 7 bees sampled are infested, there is a high infestation and should be treated. If less than 3 bees are infested, continue sampling until 17 bees have been examined. After examining 17 bees, if only one is infested, the colony has a low infestation and does not need to be treated. If 5 of 17 bees are infested, then the colony is highly infested. If 2-4 bees are infested, continue sampling. In general, infestations lower than 20% do not require treatment, but that varies depending on the length and severity of winter (Frazier et al 2000).
Figure 4: Honey bee tracheae as seen after removing the head, first set of legs, and collar. Credit: Zach Huang
There are many techniques for examining bees for tracheal mites. The classical technique is to place the bee on its back and secure with a pin. Then, under a dissecting microscope, use a scalpel or razor blade to remove the bee’s head and first set of legs. The first ring of the thorax, called the collar, is then removed with forceps. This exposes the tracheal trunk. Using a fine pair of forceps and probe, remove the tracheae and carefully place it onto a microscope slide with a drop of glycerol or 85% lactic acid and cover slip.
Place the slide on a compound microscope. The tracheae of severely infected bees may have brown blotches or be black, obscured by numerous mites. Healthy tracheae will be cream or white. However, trachea may not always be discolored when mites are present, and discolored tracheae do not always contain mites. To view a video on this technique click here.
Figure 5: Healthy and infested tracheae tubes. Credit: The Food and Environment Research Agency (Fera), Crown Copyright
Treatment for tracheal mites includes vaporizing menthol crystals and chemical miticides. Cultural control measures include resistant lines of bees, grease patties made from vegetable shortening and sugar, and proper apiary location. No biological controls currently exist. Be aware that some miticides marketed for Varroacontrol also control tracheal mites. However if treatments for Varroa are discontinuing or switched to a different chemical product, the beekeeper may no longer be treating for tracheal mites as well. Since miticides are often only tested for efficacy against Varroa, the effectiveness of a given chemical control against tracheal mites may be unclear and will not be present on the product label.
Honey bees show considerable variation in phenotypic susceptibility to tracheal mites (Gary and Page 1987, Gary et al. 1990, Page and Gary 1990, Milne et al. 1991, Szabo et al. 1991, Otis and Scott-Dupree 1992, Danka et al. 1995, Lin et al. 1996, Guzman et al. 1998, Nasr et al 2001). Among commercially available bee strains, Buckfast bees have shown resistance to tracheal mites (Milne et al. 1991, Danka et al. 1995, Lin et al. 1996) as have Russian bees (de Guzman et al 2002; de Guzman et al 2005).
Resistance to tracheal mites is heritable and can be passed from one generation to the next (Nasr et al 2001) and is likely brought about through grooming behaviors of bees. Both grooming between bees and self grooming by dancing in particular are associated with mite resistance (Pettis and Pankiw 1998; Danka and Villa 1998). Another possibility is that resistance is achieved by some bees being less attractive to mites due to their odor (Phelan et al. 1991; van Engelsdorp 1995). It is likely that a combination of host recognition by mites and removal of mites through grooming both translate into fewer mites entering the tracheae of resistant bees compared to susceptible bees.
Grease patties are made from mixing two parts white granulated sugar to one part hydrogenated vegetable shortening by volume. A four ounce (113 g) patty is placed on the top bars at the center of the broodnest where it is most likely to contact the most bees. The shortening appears to disrupt the questing female mites as they search for a new host (young bees) (Sammataro and Needham 1996; Sammataro et al. 1994). Because young bees are emerging continually, the patty must be present for an extended period. Application should be made in fall and early spring when mite levels are increasing.
Because heat is associated with mite mortality (Harbo 1993), placing hives in direct sunlight may limit mite population growth and shading tends to accelerate it (de Guzman unpublished data; vanEngelsdorp and Otis 2001).
As of this writing, the organic chemical formic acid (Mite Away II™) is registered for tracheal mite control. Other widely used treatments against Varroamites may also be affective against tracheal mites, but are not labeled for tracheal mite control since their primary target for study was Varroamites.
Based on research by Giordani (1977), menthol was tested and registered for use in the US and Canada. Menthol is extracted from the mint plant Mentha arvensis and is sold as crystals inside of a nylon mesh sac, which is placed on the top bars of frames, as the labeled product, Mite-A-Thol™. This application is temperature dependent with too cool temperatures resulting in reduced volatilization and a too high temperatures forcing bees out of the colony. If bees are hanging outside of the colony entrance in treated colonies, the crystals should be removed until temperatures drop.
Tracheal mites are a wide spread and serious pest of western honey bees. Current genetic resistance and control of the pest appears to be effective in the US. However high winter loss rates in the last decade and limited infection data leaves conclusions of the current damage caused by tracheal mites to be unknown. Unfortunately, laboratory diagnosis is the only way to determine if a colony is infested. A vigilant beekeeper should not become complacent; do not assume tracheal mites are under control or do not exist in apiaries if an effective monitoring protocol is not in place.
Bailey, L., B. V. Ball. 1991. Honey bee pathology. Academic Press; London UK
Camazine, S., I. Cakmak, K. Cramp, J. Finely, J. Fisher, M. Frazier. 1998. How healthy are commercially-produced US honey bee queens? American Bee Journal138: 677-680
Danka, R. G. and J. D. Villa. 1998. Evidence of autogrooming as a mechanism of honey bee resistance to tracheal mite infestation. J. Apic. Res 39–46. 37.
Danka, R. G., J. D. Villa, T. E. Rinderer, and G. T. Delatte. 1995. Field test of resistance to Acarapis woodi (Acari: Tarsonemidae) and of colony production by four stocks of honey bees (Hymenoptera: Apidae). J. Econ. Entomol 584–591. 88.
Dawicke, B.L., G. W. Otis, C. Scott-Dupree, M. E. Nasr. 1992. Host preference of the honey-bee tracheal mite (Acarapis woodi (Rennie)). Experimental and Applied Acarology15: 83-98
de Guzman, L. I., T. E. Rinderer, G. T. Delatte, J. A. Stelzer, G. Beaman, V. Kuznetsov. 2002. Resistance to Acarapis woodi by honey bees from Far-eastern Russia. Apidologie 33(4): 411-415
de Guzman, L. I., T. E. Rinderer, M. Bigalk, H. Tubbs, S. J. Bernard. 2005. Russian honey bee (Hymenoptera: Apidae) colonies: Acarapsis woodi (Acari: Tarsonemidae) infestations and overwintering survival. Journal of Economic Entomology 98 (6): 1796-1801
de Miranda, J. R., L. Bailey, B. V. Ball, P. Blanchard, G. Budge, N. Chejanovsky, Y. P. Chen, L. Gauthier, E. Genersch, D. de Graff, M. Ribiere, E. Ryabov, L. de Smet. J.J.M. van der Steen. 2013. Standard methods for virus research in Apis mellifera. In V. Dietman, J. D. Ellis, P. Neuman (Eds.) The Coloss Beebook, volume II: standard methods forApis mellifera pest and pathogen research. Journal of Apicultural Research 52(4)
Delaney, D. A., Keller, J. J., Caren, J. R., & Tarpy, D. R. (2010). The physical, insemination, and reproductive quality of honey bee queens (Apis mellifera L.).Apidologie.
Delfinado-Baker, M. 1984. Acarapis woodi in the United States. American Bee Journal. 124:805-806.
Delfinado-Baker, M. E. W. Baker. 1982. Notes on honey bee mites of the genus AcarpisHirst (Acari: Tarsonemidae). International Journal of Acarology 8: 211-226.
Denmark, H.A., H.L. Cromroy, M.T. Sanford. 2000. Honey bee tracheal mite, Acarapis woodi (Rennie) (Arachnida: Acari: Tarsonemidae). SPI Entomology Circular, 267. University of Florida, IFAS Extension.
Eckert, J.E. 1961. Acarapis mites of the honey bee, Apis mellifera Linnaeus. Journal of Insect Pathology 3: 409-425
Fries, I., M. P. Chauzat., Y. P. Chen, V. Doublet, E. Genersch, S. Gisder, M. Higes, D. P. McMahon, R. Martin-Hernandez, M. Natsopoulou, R. J. Paxton, G. Tanner, T. C. Webster, G. R. Williams. 2013. Standard methods for nosema research. In V. Dietman, J. D. Ellis, P. Neuman (Eds.) The Coloss Beebook, volume II: standard methods forApis mellifera pest and pathogen research. Journal of Apicultural Research 52(1)
Furgala, B., Duff, S., Aboulfaraj, S., Ragsdale, D., & Hyser, R. (1989). Some effects of the honey bee tracheal mite (Acarapis woodi Rennie) on non-migratory, wintering honey bee (Apis mellifera L.) colonies in east central Minnesota. American bee journal (USA).
Furgala, B., S. Duff, S. Aboulfara, D. Ragsdale, R. Hyser. 1989. Some effects of the honey bee tracheal mite (Acarapis woodiRennie) on non-migratory, wintering honey bee (Apis melliferaL.) colonies in east central Minnesota. American Bee Journal 129: 195-197.
Giordani, G. 1961. Recherches au laboratoire suyr Acarapis woodiRennie, agent de l’acariose des abeilles (Apis melliferaL) Note 1. Bulletin Apicole,V: 33-48.
Giordani, G. 1961. Recherches au laboratoire suyr Acarapis woodiRennie, agent de l’acariose des abeilles (Apis melliferaL) Note 4. Bulletin Apicole,VII: 159-175.
Gary, N. E. and R. E. Page. 1987. Phenotypic variation in susceptibility of honey bees, Apis mellifera, to infestation by tracheal mites, Acarapis woodi. Exp. Appl. Acarol 291–305. 3.
Gary, N. E., R. E. Page, R. A. Morse, C. E. Henderson, M. E. Nasr, and K. Lorenzen. 1990. Comparative resistance of honey bees (Apis mellifera L.) from Great Britain and United States to infestation by tracheal mites (Acarapis woodi). Am. Bee J 667–669. 130.
Guzman, L. I de, T. E. Rinderer, and G. T. Delatte. 1998. Comparative resistance of four honey bee (Hymenoptera: Apidae) stocks to infestation by Acarapis woodi (Acari: Tarsonemidae). J. Econ. Entomol 1078–1083. 91.
Harbo, J. 1993. Field and laboratory tests that associate heat with mortality of tracheal mites. Journal of Apicultural Research 32 (3-4): 159-165
Hoy, M. A. 2011. Agricultural acarology: introduction to integrated mite management. CRC Press; Florida, USA. 303-308
Lin, H., G. W. Otis, and C. Scott-Dupree. 1996. Comparative resistance in Buckfast and Canadian stocks of honey bees (Apis mellifera L.) to infestation by honey bee tracheal mites (Acarapis woodi (Rennie)). Exp. Appl. Acarol 87–101. 20.
McMullan, J. B., & Brown, M. J. (2009). A qualitative model of mortality in honey bee (Apis mellifera) colonies infested with tracheal mites (Acarapis woodi). Experimental and Applied Acarology, 47(3), 225-234.
McMullan, J.B., R. D’Ettorre, M. J. F. Brown. 2010. Chemical cues in the host-seeking behavior of tracheal mites (Acarapis woodi) in honey bees (Apis mellifera mellifera). Apidology41: 568-578
Milne, C. P., G. W. Otis, F. A. Eischen, and J. M. Domaier. 1991. A comparison of tracheal mite resistance in two commercially available stocks of honey bees. Am. Bee J 713–718. 131.
Nasr, M. E., Otis, G. W., & Scott-Dupree, C. D. (2001). Resistance to Acarapis woodi by honey bees (Hymenoptera: Apidae): divergent selection and evaluation of selection progress. Journal of economic entomology, 94(2), 332-338.
Otis, G. W. and C. D. Scott-Dupree. 1992. Effects of Acarapis woodi on overwintering colonies of honey bees (Hymenoptera: Apidae) in New York. J. Econ. Entomol 40–46. 85.
Otis, S. W., C. D. Scott-Dupree. 1992. Effects of Acarapis woodion overwintering colonies of honey bees (Hymenoptera: Apidae) in New York. Journal of Economic Entomology 85: 40-48
Page, R. E. and N. E. Gary. 1990. Genotypic variation in susceptibility of honey bees (Apis mellifera) to infestation by tracheal mites (Acarapis woodi). Exp. Appl. Acarol 275–283. 8..
Pettis, J. S. and T. Pankiw. 1998. Grooming behaviour by Apis mellifera L. in the presence of Acarapis woodi (Rennie) (Acari: Tarsonemidae). Apidologie 241–253. 29.
Pettis, J. S. W.T. Wilson, F. A. Elschen. 1992. Nocturnal dispersal by female Acarapis woodi in honey bee (Apis mellifera) colonies. Experimental and Applies Acarology15:99-108
Pettis, J. S., W. T. Wilson. 1996. Life history of the honey bee tracheal mite (Acari:Tarsonemidae). Arthropod Biology 89 (3): 368-374
Phelan, P. L. Smith, A. W., G. R., Needham. 1991. Mediation of host selection by cuticular hydrocarbons in the honey bee tracheal mite Acarapsis woodi (Rennie). Journal of Chemical Ecology17:463-473.
Phelan, P. L., A. L. Smith, and G. R. Needham. Mediation of host selection by hydrocarbons in the honey bee tracheal mite Acarapis woodi (Rennie). J. Chem. Ecol 463–473. 17.1991.
Phillip, E. F. 1923. The occurance of diseases of adult honey bees. II.US Department of Agriculture #287
Royce, L. A., Rossignol, P.A. 1991. Sex bias in tracheal mite [Acarapis woodi (Rennie)] infestation of honey bees (Apis melliferaL.) Bee Science1: 159-161
Sammataro, D. Needham, G.R. 1996. Host-seeking behavior of tracheal mites (Acari:Tarsonemidae) on honey bees (Hymenoptera: Apidae). Experimental and Applied Acarology 20: 212-136
Sammataro, D. U. Gerson, G. R. Needham. 2000. Parasitic mite of honey bees: life history, implications and impact. Annual Review of Entomology45:519-548
Skinner, A. J. 2000. Impacts of tracheal mites (Acarapis woodi(Rennie)) on the respiration and thermoregulation of overwintering honey bees in a temperate climate. Masters Thesis. University of Guelph; Guelph, Ontario, Canada. 186p
Szabo, T. L., L. P. Lefkovitch, and K. J. Clark. 1991. Comparative resistance of honey bees from a closed population to infestation by tracheal mites. Am. Bee J 643–645. 131.
van Engelsdorp, D. 1995. A field evaluation of nine genetic lines of honey bees for tracheal mite resistance and other economically important traits. M.S. Thesis, University of Guelph, Guelph, Ontario, Canada.
vanEngelsdorp, D. Otis, G.W. 2001. Field evaluation of nine families of honey bees for resistance to tracheal mites. Canadian Entomology133:793-803.
Researchers and other knowledgeable individuals commonly give presentations on their area of expertise, either at conferences or other smaller meetings. We try to record these seminars whenever possible to allow the widest audience for the presentation. Overtime some of the links to a seminar may be broken and unrecoverable, we will attempt to maintain an up-to-date list of our video content. Webinars and seminars that are recorded, archived online, and available for free can be found below. Other videos can be found on our YouTube channel.
- 2017 Bee Health Webinar Series: Ensuring Crop Pollination in US Specialty Crops
- Seminars Web-Cast from UC Davis
- Proceeding of the American Bee Research Conference 2010
- A New Assay to Measure Mite Grooming Behavior
- Pesticide in Pollen Trapped from Honey Bee Hives in Connecticut
- A Test for Sub-acute Effects of Some Commonly Used Bee Hive Chemicals
- Pests Pathogens and Queen Losses in Commercial Migratory Operations
- Apis mellifera Proteomics of Innate Resistance
- Variability and Correlations Among Five Traits Associated with American Foulbrood Resistance in a Canadian Breeding Population
- Effects of a Miticide on Honeybee Memory - is the Cure Worse than the Disease
- Nosema ceranae in North America Nasty Nice or Neither
- Beneficial Microflora in Honey Bee Colonies
- Molecular Diagnostics of Nosema ceranae and apis from Honey Bees in New York
- Nestmate Recognition in the Honey Bee Apis mellifera
- Effects of Varroa Mites and Bee Diseases on Pollination Efficacy of Honey Bees
- Effect of Transportation on Honey Bee Physiology
- Disinfection of Nosema ceranae Infected Comb by Irradiation Acetic Acid and Heat
- Interactions Between Nosema Microspores and a Neonicotinoid on Honey Bees
- Pesticide Analysis at the Stationary Apiaries
- Bee Health at eXtension
- Drug Interactions Between In-hive Miticides and Fungicides in Honey Bees
- Bee CAP Overview and Stationary Apiaries
- Preference of Phoretic Mites for Young Bees Increase Varroa Fitness
- Varroa Sensitive Hygiene and Mite Reproduction
- Safe Exchange of Honey Bee Germplasm
- Proceeding of the American Bee Research Conference 2011
- The Good the Bad and the Ugly Varroa Mite Control Strategy
- The CAP Stationary Apiary Project: A Synopsis of Colony Strength and Preliminary Statistical Modeling 2009-20010
- Varroacide Effects on Honey Bee Queens
- Bees Under Surveillance: Using Video-Tracking to Monitor Honey Bee Activity After Sublethal Exposure to Pesticides
- Evaluation of Honey Production and Varroa Mite Load in Russian and VSH Bees
- Broodmapper: Developing a Web-Based Game to Detect Pesticide Effects in Honey Bee Brood
- Report on Pesticides Found in Pollen and Bee Bread in Colonies Placed in California Almond Orchards
- A Primer on Pesticide Formulation ‘inerts’ and Honey Bees
- Challenges for Developing Biopesticides Against Varroa
- Relay Effect in Landscape Learning in Honey Bees and its use for Detecting Subtle Effects of Pesticides.
- Examination on the Reproductive Success of Re-invading Varroa Mites
- Determining the Botanical Origins of Plant Resins Collected by Apis mellifera with Metabolic Fingerprinting Analysis
- Location Location Location How Landscape Quality Affects Honey Bee Health
- Bee Communities at Crop Flowers and Bee Food Plots
- Identifying Candidate Genes for Honey Bee Mite-Grooming Behavior Using Fine-Scale Linkage Mapping
- If Flowers are Restaurants to Bees, Then What Are Bees to Flowers?
If your bees have Varroa, your bees have viruses.
Authors: Philip A. Moore, Michael E. Wilson, and John A. Skinner
Department of Entomology and Plant Pathology, the University of Tennessee, Knoxville TN
Originally Published: August 21, 2014
Varroa mites (Varroa spp.) are a ubiquitous parasite of honey bee (Apis spp.) colonies. They are common nearly everywhere honey bees are found, and every beekeeper should assume they have a Varroa infestation, if they are in a geographic area that has Varroa (Varroa mites are not established in Australia as of spring 2014). Varroa mites were first introduced to the western honey bee (Apis mellifera) about 70 years ago after bringing A. melliferato the native range of the eastern honey bee (Apis cerana). Varroa mites (Varroa jacobsoni) in eastern honey bee colonies cause little damage. But after switching hosts and being dispersed across the world through natural and commercial transportation of honey bee colonies, Varroa has became a major western honey bee pest since the 1980’s. Varroa mites (Varroa destructor) are now the most serious pest of western honey bee colonies and one of the primary causes of honey bee decline (Dietemann et al. 2012). A western honey bee colony with Varroa, that is not treated to kill the pest, will likely die within one to three years (Korpela et al. 1993; Fries et al. 2006).
Varroa Life History
Varroa mites attack honey bee colonies as an external parasite of adult and developing bees, by feeding on hemolymph (fluid of the circulatory system similar to blood), spreading disease, and reducing their lifespan. Evidence suggests that Varroa and their vectored viruses affect the immune response of honey bees, making them more susceptible to disease agents (Yang and Cox-Foster 2005). For more information on this topic see here. Mature female Varroa mites survive on immature and adult honey bees (worker, drone, and rarely queen), are reddish brown, and about the size of a pin head. Male mites are a smaller size and tan color, do not feed on bees, and are only found inside brood cells (Rosenkranz et al. 2010).
Varroa have two life stages, phoretic and reproductive. The phoretic stage is when a mature Varroa mite is attached to an adult bee and survives on the bee’s hemolymph. During this stage the mite may change hosts often transmitting viruses by picking up the virus on one individual and injecting it to another during feeding. Phoretic mites may fall off the host, sometimes being bitten when bees groom each other, or it may die of old age. Mites found on the bottom board of the hive or that fall though a screen bottom board are called the “natural mite drop”. But these mites that fall off of bees represent a small portion of the total mite population because the reproductive mites are hidden under cell cappings.
Image 1: Reproductive Varroa mite on a developing pupa (reddish oval) and two immature Varroa (opaque ovals). Credit: Abdullah Ibrahim (arrows added for emphasis)
The reproductive life stage of Varroa begins when an adult female mite is ready to lay eggs and moves from an adult bee into the cell of a developing larval bee. After the brood cell is capped and the larva begins pupating, the mite begins to feed. After about three days from capping, the mite lays its eggs, one unfertilized egg (male) and four to six fertilized (female) eggs (Rosenkranz et al. 2010). After the eggs hatch, the female mites feed on the pupa, mate with the male mite and the surviving sexually mature female mites stay attached to the host bee when it emerges as an adult. It takes six to seven days for a female mite to mature from egg to adult and it can live two to three months in the summer and five to eight months in the fall. Only mature female mites can survive outside of a brood cell (the phoretic stage), and on average a mite will produce 1.2 viable mature female offspring per worker cell invaded (Schulz 1984; Fuchs & Langenbach 1989). However, since the development time is longer for drone brood, the average viable offspring for a mite in a drone cell increases to 2.2 per cell invaded (Schulz 1984; Fuchs & Langenbach 1989). For more on Varroa life history see here.
One of the serious problems caused by Varroa is the transmission of viruses to honey bees which cause deadly diseases. Viruses found in honey bees have been known to scientists for 50 years and were generally considered harmless until the 1980’s when Varroa became a widespread problem. Since then, nearly twenty honey bee viruses have been discovered and the majority of them have an association with Varroa mites, which act as a physical and or biological vector (Kevan et al. 2006). Therefore controlling Varroa populations in a hive will often control the associated viruses and finding symptoms of the viral diseases is indicative of a Varroa epidemic in the colony. Viruses are however, the least understood of honey bee diseases. Emerging information of honey bee viruses continue to alter our understanding of the role viruses play in honey bee colonies (Genersch and Aubert 2010).
Viral Life History
Viruses are microscopic organisms that consist of genetic material (RNA or DNA) contained in a protein coat. Viruses do not acquire their own nutrients or live independently, and can only multiply within living cells of a host. An individual virus unit is called a virus particle or virion and the abundance of these particles in a host is called the virus titer. A virus particle injects itself in to a host cell and uses the cells’ organelles to make copies of itself. This process will continue without obvious change to the cell, until the host cell becomes damaged or dies, releasing large amounts of infective virus particles. All forms of life are attacked by viruses and most are host specific.
Honey Bee Viruses
Viruses of the honey bee typically infect the larval or pupa stage, but the symptoms are often most obvious in adult bees. Many of these viruses are consumed in pollen or the jelly produced by nurse bees that are fed to developing bees. Many viruses are also transmitted by Varroa. Varroa, when feeding on the hemolymph transfer the viruses directly into the open circulatory system, which reaches every cell in the insect body.
Honey bee viruses are not limited to honey bees. Honey bee viruses have been found in other non-Apis bee species, other colony inhabitants like small hive beetle, and in pollen and nectar (Andersen 1991; Bailey and Gibbs 1964; Genersch et al. 2006; Singh et al 2010). For more on honey bee pathogens found in native bees see here. Transfer of honey bee viruses from infected colonies to non-infected individuals or colonies can occur during foraging on common flowers or through robbing of weak or collapsed colonies (Singh et al 2010).
Identification of a virus is difficult due to the small size of particles. Expensive and often uncommon laboratory equipment is required for accurate diagnosis. However, symptoms of some viral diseases are more visible, especially with overt infection. A lack of symptoms does not rule out the presence of a virus. Viruses can remain in a latent form within the host, acting as a reservoir of infection, complicating diagnosis and control, and only becoming an outbreak when conditions are right.
Viral Prevalence in the United States
The USDA-APHIS National Honey Bee Pests and Diseases Survey has taken samples from honey bee colonies in over 27 states since the year 2009. Data from these surveys and other data are complied into a database with the Bee Informed Partnership and used to determine baseline disease level, determine the absence of exotic honey bee pests that have not yet been found in America, and to gauge the overall health of U.S. honey bee colonies. Results of virus presence from the 2013 survey are below (Figure 1). Deformed wing virus (DWV) and Black queen cell virus (BQCV) were present in over 80% of sampled colonies. Other viruses were much less common, but still present in 10-20 percent of colonies sampled. Of the viruses tested for presence, only slow bee paralysis virus (SBPV) was not found in the U.S
Figure 1: 2013 USDA-APHIS National Honey Bee Pests and Diseases Survey, Virus Prevalence Results (Virus abbreviations: BQCV=Black queen cell virus; DWV= Deformed wing virus; LSV2= Lake Sinai virus 2; ABPV= Acute bee paralysis virus; KBV= Kashmir bee virus; IAPV= Israel acute paralysis virus; CBPV= Chronic bee paralysis virus; SBPV= Slow bee paralysis virus)
Sacbrood, a disease cause by a virus, was the first honey bee virus to be discovered in the early 20th century and now has a recognized widespread distribution. It is perhaps the most common honey bee virus (Shen et al. 2005). This disease has been found in adult, queen, egg, and larval bees, in all forms of food, and in Varroa mites, suggesting a wide range of transmission routes. Although it is commonly found without serious outbreak, sacbrood is more likely to cause disease when the division of labor is less defined, in the early parts of the year before the nectar flow, or during prolong dearth (Bailey 1981). It often goes unnoticed since it usually infects only a small portion of brood, and adult bees will usually detect and remove infected larvae.
Image 2: Sacbrood infected pupa. Credit: Michael E. Wilson
The disease causes larvae to fail to shed their final skin prior to pupation, after the larva has spun its cocoon. Infected larvae remain on their back with their head towards the cell capping. Fluid accumulates in the body and the color will change from pearly white to pale yellow, with the head changing color first. Then, after the larva dies, it becomes dark brown with the head black (Image 2). Larvae that have ingested sufficient quantities of sacbrood in their food die after being sealed in their comb.
Sacbrood multiplies in several body tissues of young larvae but these larvae appear normal until cell capping. Each larva that dies from sacbrood contains enough virus particles to infect every larva in 1000 colonies (Bailey 1981). But in most instances, diseased larvae are quickly removed in the early stages of the disease by nurse bees. The cell cappings are first punctured to detect the disease, which a good sign of infection for the beekeeper look for (Image 6). Then, young worker bees remove the diseased larvae from the colony. Adult bees, although not susceptible to infection, become a harbor as the virus collects in the bee’s hypopharyngeal glands, which are used to produce larval jelly (Bailey 1981). These infected adult bees, however, cease to eat pollen and soon stop tending larvae. They will become foragers more quickly in life than usual and tend to collect nectar instead of pollen (Bailey 1981). Nectar that contains the virus becomes diluted in the colony when mixed with nectar from other foragers. Whereas pollen, is collected and compacted into the “pollen basket” and deposited intact into a cell. Dilute virus containing nectar is less likely to cause infection than when the virus is concentrated in a pollen pellet. Therefore use caution when transferring frames with pollen among colonies. Little is known of the other transmission routes: through Varroa mites, between workers, from bee feces or through transovarial transmission (from queen to egg). Sacbrood usually subsides in late spring when the honey flow begins, but if symptoms persist, requeening with hygienic stock is recommended (Frazier et al. 2011).
Deformed Wing Virus (DWV)
Deformed wing virus is common, widely distributed, and closely associated with Varroa mites. Both the virus titers and prevalence of the virus in colonies are directly linked to Varroa infestations (Bowens-Walker et al. 1999). In heavily Varroa infested colonies, nearly 100 percent of adult workers may be infected with DWV and have high virus titers even without showing symptoms (de Miranda et al. 2012). DWV is strongly associated with winter colony mortality (Highfield et al 2009; Genersch et al 2010). Control of DWV is usually achieved by treatment against Varroa, After treatment a gradual decrease in virus titers occurs as infected bees are replaced by healthy ones (Martin et al 2010). DWV can be found in all castes and life stages of honey bees and will persist in adults without obvious symptoms. DWV is also transmitted through food, feces, from queen to egg, and from drone to queen (de Miranda et al. 2012).
Image 3: Adult bees with deformed wings resulting from DWV. Credit: Katherine Aronstein
Acute infections of DWV are typically linked to high Varroa infestation levels (Martin et al 2010). Covert infections (a detectable level of virus without damaging symptoms) can occur through transovarial transmission (Chen et al. 2004), and through larval food (Chen et al. 2006). Symptoms noted in acute infections include early death of pupae, deformed wings, shortened abdomen, and cuticle discoloration in adult bees, which die within 3 days causing the colony to eventually collapse. Not all mite infested pupae develop these symptoms, but all adult honey bees with symptoms develop from parasitized pupae. Bees infected as adults can have high virus titers but do not develop symptoms. DWV may also affect aggression (Fujiyuki et al. 2004) and learning behaviors of adult bees (Iqbal and Muller 2007). DWV appears to replicate in Varroa, making it a biological as well as physical vector. Infection of pupae may be dependent on DWV replication in Varroa prior to transmission. Winter colony mortality is strongly associated with DWV presence, irrespective of Varroa infestation. This suggests that Varroa infection should be reduced in a colony far in advance of producing overwintering bees, to ensure reduction in DWV titers. DWV is closely related to Kakugo Virus and Varroa destructor Virus 1, which together form the Deformed Wing Virus Complex (de Miranda et al. 2012).
Black Queen Cell Virus (BQCV)
Black queen cell virus is a widespread and common virus that persists as asymptomatic infections of worker bees and brood. Although generally understood as being asymptomatic in adult bees, Shutler et al. (2014) found BQCV to be associated with the symptom K-wing, where the wing pair is disjointed and more perpendicular to one another. Queen pupae with symptoms display a pale yellow sac-like skin similar to sacbrood. The pupae rapidly darken after death and turn the wall of the queen cell dark brown to black. Symptomatic drone pupae have also been observed. Unlike other viruses that are associated with Varroa, BQCV is strongly associated with Nosema apis and little evidence supports its co-occurrence with Varroa, although, BQCV has been isolated from Varroa (Ribière et al. 2008). Nosema disease affects a bee’s mid gut, increasing susceptibility of the alimentary tract to infection by BQCV. BQCV can be orally transmitted to adults only when Nosema has co-infected (Ribière et al. 2008). It can also be transmitted by injection to pupae. BQCV has a seasonal relationship similar to Nosema, with a strong peak in spring. Because of the seasonal occurrence with Nosema, queen rearing operations who produce queens in the spring are susceptible to BQCV (Ribière et al. 2008).
Image 4: Dysentery on the front of a hive is a symptom but not indicative of Nosema disease. Credit: Michael E. Wilson
Chronic Bee Paralysis Virus (CBPV)
Chronic bee paralysis virus was one of the first honey bee viruses to be isolated. It is unique among honey bee viruses in that it has a distinct particle size and genome composition. It is also the only common honey bee virus to have both visual behavior and physiological modifications resulting from infection. Symptoms of the disease are observed in adult bees displaying one of two sets of symptoms called syndromes (Genersch & Aubert 2010). Type 1 symptoms include trembling motion of the wings and bodies of adult bees, who are unable to fly, and crawl along the ground or up plant stems, often clustering together. The bees may also have a bloated abdomen, causing dysentery and will die within a few days after displaying symptoms.
Type 2 symptoms are greasy, hairless, black adult bees that can fly, but within a few days, become flightless, trembling, and soon die (Image 5). Both of these syndromes can occur within the same colony. Severely affected colonies, often the strongest in an apiary (Ribiere at al. 2010), quickly lose adult workers, causing collapse and often leaving few adult bees with the queen on unattended comb (Bailey & Ball 1991). These symptoms, however, are similar and often confused with other honey bee maladies including Nosema apis,colony collapse disorder (CCD), tracheal mites, chemical toxicity, and other viruses.
Image 5: Bees with CBPV type 2 symptoms: greasy and hairless. Credit: The Food and Environment Research Agency (Fera), Crown Copyright
Transmission of the virus primarily occurs through direct body contact, although oral transmission also occurs but is much less virulent. Direct body transmission happens when bees are either crowded or confined within the hive for a long period of time (due to poor weather or during long-distance transportation) or when too many colonies are foraging within a limited area, such as a monoculture of sunflower with high honey bee colony density (Genersch & Aubert 2010). In both instances, small cuts from broken hairs on an adult bee’s cuticle and direct contact with infected adult bees spreads the virus through their exposed pores; if this occurs rapidly and enough adult bees are infected, an outbreak with colony mortality will occur. Feces from infected bees within a colony can also spread the disease, and other transmission routes are still being investigated, including possible Varroa transmission. The virus is widespread and an outbreak can occur at any time of year. Spring and summer are the most common seasons for mortality from the virus, but it will persist in a colony year-round without displaying any overt symptoms (de Miranda et al. 2012).
Two new viruses related to CBPV with no yet described symptoms are Lake Sinai virus 1 (LSV1) and Lake Sinai virus 2 (LSV2)(Runckel et al. 2011). New molecular tools have allowed researchers to identify the presence of these and other new viruses and their seasonality in test colonies. Little else is know of the Lake Sinai viruses, including its pathogenic or epidemiological significance. Other described honey bee viruses that were discovered before the advent of molecular techniques have no genomic data to reference; therefore newly discovered viruses may in fact be the already discovered viruses of the past such as Bee virus X and Y, Arkansas Bee Virus or Berkeley Bee Virus(Runckel et al. 2011).
Acute Bee Paralysis Virus Complex
Acute bee paralysis virus (ABPV), Kashmir bee virus (KBV), and Israel acute paralysis virus (IAPV) are a complex of associated viruses with similar transmission routes and affect similar life stages. These viruses are widespread at low titers and can quickly develop high titers due to extremely virulent pathology. Frequently associated with colony loss, this virus complex is especially deadly when colonies are heavily infested with Varroa mites. (Ball 1989; Genersch 2010, Genersh et al. 2010). These viruses have not been shown to cause symptoms in larval life stages, but show quick mortality in pupae and adult bees.
Acute Bee Paralysis Virus (ABPV)
Acute bee paralysis virus was accidentally discovered when CBPV was first isolated. ABPV displays similar symptoms as CBPV however the acute adjective describes a bees’ more rapid mortality compared to CBPV. Unlike CBPV, ABPV virulence is directly related to Varroa infestation. APBV is transmitted in larval jelly from asymptomatic infected adult bees to developing larva or when vectored by Varroa mites to larvae and pupae. ABPV is common and typically cause covert infections (no obvious symptoms) when transmitted orally from adult to developing bee. It takes about one billion viral particles to cause death via ingestion, but when vectored by Varroa and directly injected into the developing bee’s hemolymph, only 100 virus particles will cause death (Genersch & Aubert 2010). When the virus is picked up by Varroa, the transmission rate to pupae is between 50 and 90 percent. The longer the feeding period of Varroa, the greater the transmission rate will become. (Genersch & Aubert 2010). Pupae infected with ABPV die before emerging, making the appearance of paralysis symptoms less obvious. The decline in emerging bees causes a colony to dwindle towards collapse. A colony infected with an ABPV epidemic will die within one season (Sumpter and Martin 2004).
Kashmir Bee Virus (KBV)
Kashmir bee virus has widespread distribution and is considered the most virulent of honey bee viruses under laboratory condition (Allen and Ball 1996). When KBV is injected in to adult bee hemolymph, death occurs in just 3 days (de Miranda et al. 2012). KBV does not cause infection when fed to developing bees, but does persist in adult and developing bees without any obvious symptoms. When Varroa mites transmit the virus, it becomes deadly to all forms of the bee lifecycle but displays no clearly defined symptoms. Even with moderate levels of mite infestation, KBV, like ABPV, can kill colonies (Todd et al. 2007). Control of Varroa mites is necessary to prevent colony losses from KBV.
Israeli Acute Paralysis Virus (IAPV)
Symptoms of IAPV are similar to ABPV and CBPV including: shivering wings, darkened hairless abdomens and thoraxes, progressing into paralysis and death. IAPV is found in all life stages and castes of bees. IAPV and other viruses were found to be strongly associated with colony collapse disorder (CCD) in the United States, but no direct relationship between the viruses and CCD has yet been shown (Cox-Foster et al. 2007). IAPV is extremely virulent at high titers, as when vectored by Varroa and is covert at low titers.
Slow Bee Paralysis Virus
In contrast to ABPV, which produces symptoms in a few days after infection, SBPV induces paralysis after 12 days, and only on the two fore (anterior) legs. SBPV persists as a covert infection and is transmitted by Varroa to adults and pupae. The disease will kill adult bees and eventually the entire colony (de Miranda et al. 2012). Prevalence of the virus is limited. It has not been found in the U.S., but has been found in England, Switzerland, Fiji and Western Samoa and only in Britain has SBPV been associated with colony deaths (Carreck et al. 2010).
Most pathogens invade the digestive system through oral ingestion of inoculated food. These pathogens infect the mid gut epithelial cells, which are constantly being replaced and are protected by membranes and filters which confine the pathogen to gut tissues. Parasites that infect gut tissue like Nosema apisand Nosema ceranacan create lesions in the epithelium that allow a virus like BQCV to pass into the hemolymph and infect other cells in the body. In contrast the external parasite Varroa destructor feeds directly on bee hemolymph providing an opening in the cuticle for viruses to enter. Most virus infections rarely cause infection when ingested orally, but only a few virus particles are necessary to cause infection when injected directly into the hemolymph. Many viruses can be directly transmitted by Varroa mites, such as: DWV, those in the acute bee paralysis virus complex, and slow bee paralysis virus. Other viruses, like sacbrood, have been detected in Varroa mites but Varroa has not been shown to directly transmit the virus. Some viruses, like DWV, have been shown to directly multiply in Varroa mites, however in most cases we don’t know the exact relationship of Varroa mites to viruses or enough about how transmission occurs from mites to bees. Knowledge about the presence, role, and transmitting routes of these viruses in native bees, and other potential non-Varroa transmission routes is also lacking in detail, complicating recommendations for control. Research does show viruses clearly affect honey bee health and warrant attention from the beekeeper and researcher alike.
Viruses persist in normal, healthy colonies, only to explode during times of stress. Many viruses are only damaging when in combination with another stressor like Varroa or Nosema. Active, integrated management of Varroa and other stressors is essential to minimizing virus titers. To learn more about reducing stressors with best management practices see here.
Routinely inspect your colonies for possible disease. Have a thorough knowledge of symptoms and identify when colonies are slow to build up or have sporadic brood patterns, indicating brood has been pulled out and removed (Image 6). If you suspect you have a disease, take a sample and send it to be identified. For more information on submitting a sample for diagnosis see here.
Image 6: Punctured cell cappings that indicate adult bees have detected a brood disease (note DWV infected adult bee). Credit: The Food and Environment Research Agency (Fera), Crown Copyright (Arrows added for emphasis)
Other future avenues of control include breeding hygienic bee strains that detect brood diseases and remove infected individuals from colonies or breeding of resistance to Varroa infestation. Specific resistance to viruses are not yet considered in most breeding programs. There is evidence of specific viral resistance in honey bees, and there has been at least some attempt to breed resistance to IAPV. For more on this topic see here.
Another promising research area for controlling honey bee viruses in the use of gene silencing called RNAi. The private bee research company Beeologics, as well as public and private university researchers are developing this method and a consumer product may be available in the near future as RNAi technology continues to become more efficient and inexpensive. For more on this topic see here.
Allen, M. and B.V. Ball. 1996. The incidence and world distribution of the honey bee viruses. Bee World77: 141-162.
Anderson DL (1991) Kashmir bee virus - a relatively harmless virus of honeybee colonies. Am. Bee J. 131: 767–770.
Bailey, L. 1981. Honey bee pathology. Academic Press. London. 9-25.
Bailey, L. and B. V. Ball. 1991. Honey bee pathology(2nd ed.). Academic Press. London
Bailey L, Gibbs AJ (1964) Acute infection of bees with paralysis virus. J. Insect Pathol. 6: 395–407.
Ball, B. V. 1989. Varroa jacobsonias a virus vector. In Present Status of Varroatosis in Europe and Progress in the Varra Mite Control.Proc. Meeting, Undine, Italy, 1988. Cavalloro, E. (Ed.) EC-Experts Group, Luxembourg. pp. 241-244.
Bowen-Walker, P. L., S. J. Martin, & A. Gunn. 1999. The Transmission of Deformed Wing Virus between Honeybees (Apis melliferaL.) by the Ectoparasitic Mite Varroa jacobsoni Oud. Journal of invertebrate pathology 73(1), 101-106.
Carreck, N. L., D. V. Ball, & S. J. Martin. 2010. Honey bee colony collapse and changes in viral prevalence associated with Varroa destructor. J. Apic. Res. 49(1), 93-94.
Chen, Y. P., J. S. Pettis, A. Collins, & M. F. Feldlaufer. 2006. Prevalence and transmission of honeybee viruses. Applied and environmental microbiology 72(1), 606-611.
Chen, Y., J. S. Pettis, J. D Evans, M. Kramer, & M. F. Feldlaufer. 2004. Transmission of Kashmir bee virus by the ectoparasitic mite Varroa destructor. Apidologie 35(4), 441-448.
Cox-Foster, D. L., S. Conlan, E. C. Holmes, G. Palacios, J. D. Evans, N. A. Moran, P. Quan, T. Briese, M. Hornig, D. M. Geiser, V. Martinson, D. vanEngelsdorp, A. L. Kalkstein, A. Drysdale, J. Hui, J. Zhai, L. Cui, S. K. Hutchinson, J. F. Simons, M. Egholm, , J. S. Pettis, W. I. Lipkin. 2007. A metagenomic survey of microbes in honey bee colony collapse disorder. Science 318(5848), 283-287.
Dietemann, V., J. Pflugfelder, D. Anderson, J. D. Charrière, N. Chejanovsky, B. Dainat, J. de Miranda, K. Delaplane, F. Diller, S. Fuch, P. Gallman, L. Gauthier, A. Imdorf, N. Koeniger, J. Kralj, W. Meikle, J. Pettis, P. Rosenkranz, D. Sammataro, D. Smith, O. Yañez, P. Neumann. 2012. Varroa destructor: research avenues towards sustainable control. Journal of Apicultural Research 51(1): 125-132
Evans, J. D., & R. S. Schwarz. 2011. Bees brought to their knees: microbes affecting honey bee health. Trends in microbiology 19(12), 614-620.
Francis, R. M., S. L. Nielsen, & p. Kryger. 2013. Varroa-virus interaction in collapsing honey bee colonies. PloS one 8(3).
Fujiyuki, T., H. Takeuchi, M. Ono, S. Ohka, T. Sasaki, A. Nomoto, & T. Kubo, 2004. Novel insect picorna-like virus identified in the brains of aggressive worker honeybees. Journal of virology 78(3), 1093-1100.
Fraxier, M., C. Dewey, & D. vanEngelsdorp. 2011. A field guide to honey bees and their maladies. Ag Communications and Marketing # AGRS-116. The Pennsylvania State University.
Fries, I, A. Imdorf,P. Rosenkranz. 2006. Survival of mite infested (Varroa destructor) honey bee (Apis mellifera) colonies in a Nordic climate. Apidologie 37: 564-570
Fuchs, S. & K. Langenback. 1989. Multiple infestation of Apis mellifera L. brood cells and reproduction of in Varroa jacobsoni Oud. Apidologie, 20, 257–266.
Genersch, E. 2010 Honey bee pathology: Current threats to honey bees and beekeeping. Appl. Microbiol. Biotechnol.87, 87-97.
Genersch, E., W. von der Ohe, H. Kaatz, A. Schroeder, C. Otten,R. Büchler... & P. Rosenkranz. 2010. The German bee monitoring project: a long term study to understand periodically high winter losses of honey bee colonies. Apidologie 41(3), 332-352.
Genersch, E., & M. Aubert. 2010. Emerging and re-emerging viruses of the honey bee (Apis mellifera L.). Veterinary research 41(6), 54.
Genersch, E., C. Yue, I. Fries, & J. R. de Miranda. 2006. Detection of Deformed wing virus a honey bee viral pathogen, in bumble bees ( Bombus terrestris and Bombus pascuorum) with wing deformities.Journal of invertebrate pathology 91(1), 61-63.
Gochnauer, T. A. 1978. Viruses. In Morse, R. A., & Nowogrodzki, R. (Eds.) Honey bee pests, predators, and diseases,(2nd ed). Cornell University Press.
Highfield, A. C., A., El Nagar, L. C. Mackinde, M. L. N. Laure, M. J. Hall, S. J. Martin, & D. C. Schroeder. 2009. Deformed wing virus implicated in overwintering honeybee colony losses. Applied and environmental microbiology 75(22), 7212-7220.
Iqbal, J., & U. Mueller. 2007. Virus infection causes specific learning deficits in honeybee foragers. Proceedings of the Royal Society B: Biological Sciences 274(1617), 1517-1521.
Kevan, P. G., M. A. Hannan, N. Ostiguy, & E. Guzman-Novoa. 2006. A summary of the Varroa-virus disease complex in honey bees. Am. Bee J. 146 (8), 694-697.
Korpela, S. A. Aarhus, I. Fries, H. Hansen. 1992. Varroa jacobsoniOud. in cold climates: population growth, winter mortality and influence on the survival of honey bee colonies. Journal of Apicultural Research 31: 157-164.
Martin, S. J., B. V. Ball, & N. L. Carreck. 2010. Prevalence and persistence of deformed wing virus (DWV) in untreated or acaricide-treated Varroa destructor infested honey bee (Apis mellifera) colonies. Journal of Apicultural Research 49(1), 72-79.
de Miranda, J. R., B.Dainat, B. Locke, G.Cordoni, H. Berthoud, L. Gauthier,... & D. B.Stoltz. 2010. Genetic characterization of slow bee paralysis virus of the honeybee (Apis mellifera L.). Journal of General Virology 91(10), 2524-2530.
de Miranda, J. R., L. Gauthier, M. Ribiere, and Y. P. Chen. 2012. Honey bee viruses and their effect on bee and colony health. In D. Sammataro & J. Yoder (Eds.) Honey bee colony health: challenges and sustainable solutions. CRC Press. Boca Raton. 71-102.
Ribière, M., B. Ball, & M. Aubert. 2008. Natural history and geographical distribution of honey bee viruses. In M. Aubert (Ed.) Virology and the honey bee.European Communities, Luxembourg, 15-84.
Ribière, M., V. Olivier, & P. Blanchard. 2010. Chronic bee paralysis: A disease and a virus like no other? Journal of invertebrate pathology 103, 120-131.
Rosenkranz, P., P. Aumeier, & B. Ziegelmann. 2010. Biology and control of Varroa destructor. Journal of invertebrate pathology 103, 96-119.
Runckel, C., M. L. Flenniken, J. C. Engel, J. G. Ruby, D. Ganem, R. Andino & J. L. DeRisi. 2011. Temporal analysis of the honey bee microbiome reveals four novel viruses and seasonal prevalence of known viruses, Nosema, and Crithidia. PloS one 6(6).
Schulz, A. 1984. Reproduktion und Populationsentwicklung der parasitischen Milbe Varroa jacobsoni Oud. in Abhänkgigkeit vom Brutzyklus ihres Wirtes Apis mellifera L. Apidologie 15, 401–420.
Shen, M., L. Cui, N. Ostiguy, & D. Cox-Foster. 2005. Intricate transmission routes and interactions between picorna-like viruses (Kashmir bee virus and sacbrood virus) with the honeybee host and the parasitic Varroa mite. Journal of General Virology 86(8), 2281-2289.
Shutler, D., Head, K., Burgher-MacLellan, K. L., Colwell, M. J., Levitt, A. L., Ostiguy, N., & Williams, G. R. (2014). Honey Bee Apis mellifera Parasites in the Absence of Nosema ceranae Fungi and Varroa destructor Mites. PloS one,9(6), e98599.
Singh R, Levitt AL, Rajotte EG, Holmes EC, Ostiguy N, et al. (2010) RNA Viruses in Hymenopteran Pollinators: Evidence of Inter-Taxa Virus Transmission via Pollen and Potential Impact on Non-Apis Hymenopteran Species. PLoS ONE 5(12).
Sumpter, D. J., & S. J. Martin 2004. The dynamics of virus epidemics in Varroa‐infested honey bee colonies. Journal of Animal Ecology, 73(1), 51-63.
Todd, J. H. J. R. de Miranda, and B. V. Ball. 2007. Incidence and molecular characterization of viruses found in dying New Zealand honey bee (Apis mellifera) colonies infested with Varroa destructor. Apidologie38: 354-367.
Yang, X. and D.L. Cox-Foster. 2005. Impact of an ectoparasite on the immunity and pathology of an invertebrate: Evidence for host immunosuppression and viral amplification.Proceedings of the National Academy of Sciences of the United States of America 102(21): 7470-7475.
Thank you to Jay Evans (USDA-ARS) for review of this article
Please join us for this webinar series for information you can use about good and bad insects. Topics will include how you can help good insects like bee pollinators and how to control insects we think of as bad, like fire ants, termites, and new invasive insects. Spiders and ticks aren't actually insects, but we will talk about them too. Webinars will be on the first Friday of each month at 2 p.m. Eastern time. Click on the title for information on how to connect to the webinar.
2014 Webinar Series: All Bugs Good and Bad
FEBRUARY 7, 2014
If Flowers are Restaurants to Bees, then What Are Bees to Flowers?
Presented by Dr. John Skinner
Moderated by Danielle Carroll
MARCH 7, 2014
APRIL 4, 2014
MAY 2, 2014
JUNE 6, 2014
AUGUST 1, 2014
SEPTEMBER 5, 2014
OCTOBER 3, 2014
Alien Invasions, Zombies Under Foot, and Billions of Decapitated Fire Ants
Presented by Dr. Sanford Porter
Moderated by Nelson Wynn
NOVEMBER 7, 2014
Where Have All the Honey Bees Gone? Hope for the Future
Presented by Dr. John Skinner
Moderated by Sallie Lee
The 2014 Webinars are brought to you by the following eXtension Communities of Practice: Imported Fire Ants, Urban IPM, Bee Health, Invasive Species, Gardens, Lawns and Landscapes, and Disasters and by the Alabama Cooperative Extension System.
Looking for 2013 Webinars? Click here!
- Researchers work to make crop pollination sustainable in the Northeast
Editor:Philip Moore, The University of Tennessee
Last Edited: January 15, 2015
The pollinator security project was initiated in 2011 to address a gap in knowledge with respect to pollinator communities in northeastern cropland.
Reports of declining native pollinators, decreased availability of honey bee rental colonies, and general public misunderstanding led to the creation of this working group to produce a sustainable pollination strategy for stakeholders.
The goal is to contribute to long-term profitability of fruit and vegetable production and the outcome is this webpage along with other farm training and publications to increase knowledge and adoption of practices that protect pollinator communities.
One component of this project is video segments which highlight aspects of fruit or vegetable production in the Northeast.
Part One: Commercial Blueberry Pollination in Maine's Blueberry Barrens
Part 1:Commercial Blueberry Pollination in Maine's Blueberry Barrens
Part 2: Lowbush Blueberry in Maine, Native Plants and Native Bees in a Modern System
Part 3: Pollinator Plantings (The Bee Module) for Maine Lowbush Blueberry
Part 4: Landscape Ecology in Maine's Blueberry Growing Region
Part 5: How to Estimate Native Bee Abundance in the Field
Part 6: Economics of Lowbush Blueberry in Maine
Part 8: Research Topics in Lowbush Blueberry Pollination
Part 9: Pollinator Habitat Enhancement in Cranberries
Part 10: UMass Cranberry Station, Reducing Pesticides, Helping Bees
Part 11: Pollination Requirements of Heritage and Hybrid Cranberries
Specific objectives of this project are to :
1. Determine the contributions of pollinator communities and identify which site characteristics have the greatest influence on pollinator effectiveness in apple, lowbush blueberry, cranberry, and cucurbit.
2. Develop hypotheis-driven model based on factors shown to affect pollination deficits.
3. Quantify pesticide residues in pollen and relate to crop and management strategies, and estimated risk to the bee community.
4. Assess shared parasite load between introduced and native pollinator communities.
5. Analyze the economics of pollination services and determine the value of pollination service.
6. Heighten our understanding of the grower community to understand why farmers accept innovation and to increase adoption of pollinator conservation measures.
7. Facilitate knowledge transfer allowing growers to both assess and improve pollination security.
This content is produced by a group of researchers from across the northeast:
Anne Averil, The University of Massachusetts
Frank Drummond, The University of Maine
Kimberly Stoner, The Connecticut Agricultural Experiment Station
Bryan Danforth, Cornell University
John Burand, The University of Massachusetts
Brian Eitzer, The Connecticut Agricultural Experiment Station
Aaron Hoshide, The University of Maine
Cyndy Loftin, The University of Maine
Tom Stevens, The University of Massachusetts
John Skinner, The University of Tennessee
Dave Yarborough, The University of Maine
Tracy Zarrillo, The Connecticut Agricultural Experiment Station
Kalyn Bickerman, The University of Maine
Eric Asare, The University of Maine
Shannon Chapin, The University of Maine
Eric Venturini, The University of Maine
Sam Hanes, The University of Maine
Kourtney Collum, The University of Maine
Michael Wilson, The University of Tennessee
Philip Moore, The University of Tennessee
Take an integrated approach to crop pollination
Specialty crop growers depend on pollinators to ensure pollination and to achieve marketable yields. Integrated crop pollination is an integrative approach to pollination management that can help specialty crop growers receive reliable, economical crop pollination. There are two main components to integrated crop pollination: (1) diversifying crop pollination strategies (e.g. using a combination of honey bees, alternative managed bees and/or wild bees) and (2) using farm practices that support pollinators. Pollinators require food (pollen and nectar), nesting habitat, and a safe environment protected from pesticide exposure. Farmers can support pollinators by using practices that provide these habitat requirements. Learn more about integrated crop pollination by watching this video.
Video produced by Emily May (Xerces Society) for the Integrated Crop Pollination Project. The Integrated Crop Pollination Project is supported by the USDA-NIFA Specialty Crop Research Initiative Coordinated Agricultural Project (Award #2012-51181-20105).
Pollination in agriculture and why it matters.
Honey bees are the most important pollinator in the United States and worldwide. Pollination is essential and a critically important process in producing much of the food we eat. Without pollinators, such as the honey bee, we would have few fruits, vegetables, nuts and many other types of food we depend upon. This 52-minute video gives an overview of the pollination process, the value of bees and the benefit humans gain from this relationship. It also provides insight into the complexity and challenges of the beekeeping industry. Most importantly, it presents a balanced perspective on the many factors associated with the decline of honey bees. The video concludes with an overview on some of the research currently underway at Washington State University in support of honey bee health and things we all can do to help bees and other pollinators.
Beekeepers are almost by definition curious individuals. The nature of beekeeping, as with any environmental relationship, is complex. Even some of the most experienced beekeepers are confounded by the mysteries of a bee hive. That is what makes honey bee research a rewarding and never-ending journey.
Below is a list of commonly asked questions and links to the best answer at the time it was asked. As more information becomes available, perceptions shift, and may render a formerly correct answer invalid. The following list is only a starting point and one should always seek a second opinion on any difficult or important subject. Local knowledge is especially important as geographical variables cannot be resolved in this universal forum. If your question is not listed below, consider using the Ask an Expert function.
- Are there plants that produce nectar that is poisonous to either honey bees or humans?
- How can bees make honey from nectar that is poisonous to them?
- What is the life cycle of the bumble bee?
- How can farmers, gardeners, and applicators reduce risks of honey bee injury from pesticide application?
- What steps can beekeepers take to protect their colonies from pesticide injury?
- How can I tell the difference between small hive beetle larvae and wax moth larvae?
- What are wax moths and what kind of damage do they make in a hive?
- How many bee hives do I need to pollinate a crop?
- What causes purple brood?
- What is a "pollen bee" or a "non-apis" bee?
- Has research been done on comparing 5.4 mm comb cell size with 4.9 mm?
- What are small hive beetles and where did they come from?
- What is the best way to introduce a queen into a colony?
- What plants in my vegetable garden attract or need bees?
- What are some suggestions for keeping bears out of active beehives?
- What is causing the decline of honey bee populations?
- What is a toxic reaction to bee stings?
- What is the difference between a normal reaction to a honey bee sting and an allergic abnormal reaction?
- How long do worker honey bees live?
- Which pesticide formulations are least hazardous to honey bees?
- How many times does a queen honey bee mate?
- The drone has no father but has a grandfather. How is that?
- What crops do not require honey bee pollination?
- Why is honey different colors?
- I have bees in my house. How can I get rid of them without killing them?
- I have honey bees in a tree. Can I remove them and keep the bees?
- Will honey bee swarms in my yard move into a hole in the wall of my house?
- What is the basic life cycle of the fungus Ascosphaera apis that causes chalkbrood disease in honey bees colonies?
- Why do newly installed packages of bees seem to abscond more than well-established hives?
- How do honey bees use pheromones to communicate?
- How are queen bees raised and mated?
- Can a honey bee be born without the aid of a drone?
- Does honey have nutritional value?
- If honey is crystallized (solid) has it gone bad?
- What is Nosema disease?
- How do I know whether my bees have Nosema disease?
- How is Nosema disease treated?
- How do honey bees make wax?
- What are some ways to reduce the population of Varroa mites in honey bee colonies, without the use of pesticides?
- What is raw honey?
It is assumed that raw honey is neither heated nor filtered. As there is no official or legal definition of raw honey, it is possible that a product labeled raw honey may have been heated or filtered. - Nancy Ostiguy, Pennsylvania State University
What are some ways to reduce the population of Varroa mites in honey bee colonies, without the use of pesticides?
Mite-resistant Bees. In response to development of resistance to chemical miticides, and in order to provide more sustainable mite management, honey bees have been selectively bred for resistance to, or tolerance of, Varroa. There are two known mechanisms of resistance: hygienic behavior and suppression of mite reproduction (SMR). Hygiene is the removal of diseased (including mite-parasitized) brood by workers; SMR is the reduction in reproduction of female mites within brood cells. Types of resistant queens include; Minnesota Hygienic, the Russian and the SMR. The Minnesota Hygienic, as the name implies, has been selectively bred to be hygienic against diseases such as American Foulbrood and against mite parasitism. Russian bees, originated from far-eastern Russia, where developed by the USDA, and are resistant to Varroa. SMR bees, also developed by the USDA, reduce Varroa numbers by interfering with reproduction, although host factors affecting mite reproduction are not well understood. Open Bottom Boards. The use of open bottom boards takes advantage of the natural fall of Varroa from the colony to reduce mite numbers by exclusion. Mites continually fall from bees and when exiting capped cells. Many fall to the bottom board where they are likely to re-attach to bees. But if the floor of the bottom board is screened rather than solid, the bees will fall to the ground below where they perish. Open bottom boards have been shown to reduce Varroa numbers by about 15%. And they can enhance the performance of treatments by removing mites that fall from bees during a treatment, but are not killed directly by the treatment. Removal of Drone Brood. The preference of Varroa for drone brood can be used to help delay buildup of mite populations. Wax drone brood foundation, which encourages bees to build larger cells and the queen to lay drone eggs, can be purchased, or empty frames with a starter strip can be given to colonies during drone rearing season. After capping, the entire frame can be discarded, or the brood can be destroyed (with a capping scratcher or by freezing) and the frame can be used again. Drone brood foundation should be inserted in early spring within or directly next to the brood cluster and it must be removed before drones begin emerging. Removing naturally occurring drone brood may not be practical because it is usually scattered throughout the cluster and is not numerous enough to affect Varroa numbers if removed. Apiary Isolation. Even if you are diligent about managing your colonies, they can be re-infested if Varroa-infested colonies are located nearby. Workers with mites can “drift” to other colonies; and workers from stronger colonies can rob weak, mite-infested colonies, and bring Varroa back with them. The greater the distance between apiaries, the less likely re-infestation will occur. This tactic is not always feasible because worker bees may fly several miles from their colony when foraging, and, of course, you probably will have no influence on the management of your neighbor’s colonies. Integrated Management. Reliance on traditional chemical mite treatments may be reduced by using a combination of management tactics. For example, combining resistant bees and open bottom boards may help to maintain Varroa below damaging levels and thereby reduce the number of treatments required. Perhaps the most important component of an integrated management program for Varroa is monitoring. Before development of resistance to Apistan™, few beekeepers considered monitoring mite populations because they knew this product would provide control. Now control is not certain, and monitoring has become a necessity. At the very least, monitoring should be conducted after treating to determine treatment effectiveness. When using control tactics which require more time to affect Varroa numbers, such as open bottom boards or resistant bees, monitoring should be conducted about once a month over the course of a season. Regardless of your management program or mite monitoring schedule, colonies should be sampled for Varroa in late August so that if a treatment is necessary, it can be applied and affect mite numbers before cold weather sets in. -John Skinner, University of Tennessee
Bees produce the beeswax used in the construction of their combs from the four pair of wax glands located on the underside of the abdomen. These glands are most highly developed and active in bees 10-18 days old. The wax appears in small, irregular oval flakes or scales that project between the overlapped portions of the last four abdominal segments. Wax can be secreted only at relatively high temperatures and after a large intake of honey or nectar. -John Skinner, University of Tennessee
Nosema disease can be treated successfully with Fumigillin (trade name Fumidil). Colonies are usually treated in the fall, spring, or both. Follow the directions on the label and feed the correct dosage in 50% sugar syrup (1:1 sugar:water, with antibiotic dissolved in 5-10 ml warm water then mixed into the syrup) in the spring, 66% in the fall. Nosema ceranae also responds to Fumidil treatment, but may require a higher dosage. The antibiotic does not kill the spores, but disrupts vegetative reproduction of the pathogen inside the host cells. Fumidil will not, therefore, completely remove the spore source if colonies are heavily infected because both honey and beeswax can be a reservoir for Nosema spores. - Zachary Huang, Michigan State University
The only way to be sure is to examine bees by microscope. A sample of bees is macerated in a small amount of water, and then a drop of the liquid is examined on a microscope slide at 400 power. Spores appear as ovals, about 3 by 5 microns. One outward indication of Nosema is brown spots (fecal material) on the outside or inside of a hive. The inner cover or top bars can be soiled with feces in a hive that carries Nosema ceranae. However, a hive heavily infested with Nosema ceranae may appear normal otherwise. - Tom Webster, Kentucky State University
Nosema disease in honey bees is caused by two species of pathogens, Nosema apis and Nosema ceranae. Nosema apis was the only known microsporidian honey bee pathogen until 1996, when a second species, Nosema ceranae, was identified from the Asian honey bee. Nosema ceranae appears to be the dominant species in the European honey bee (Apis mellifera) in many parts of the world, including in Europe and the United States. Both of these pathogens cause chronic deleterious effects in the honey bee host. - Lee Solter, University of Illinois
Honey does not spoil. Crystallized honey is caused by the glucose in liquid honey becoming a solid. Honey can be consumed in its crystallized form or you can warm the honey to dissolve the crystals by placing the jar in warm water and stirring until the crystals disappear. Do not boil or scorch the honey. - Nancy Ostiguy, Pennsylvania State University
Honey consists primarily of glucose and fructose (both are carbohydrates) and 17-18% water. Unlike other sweeteners, honey has trace vitamins and minerals including calcium, copper, iron, magnesium, manganese, niacin, pantothenic acid, phosphorus, potassium, riboflavin and zinc. Antioxidants are also found in honey. Flavanoids and phenolic acids found in honey act as antioxidants scavenging and eliminating free radicals. Darker honeys tend to have higher quantities of antioxidants. Honey also makes an effective antimicrobial agent for treating sore throats and other bacterial infections. - Nancy Ostiguy, Pennsylvania State University
Yes and no. A drone's (male bee) purpose is to mate with a queen (female reproductive bee). All other colony activities are performed by worker bees (female bees). To discuss how a bee is born, we can start with when the egg is laid. Generally speaking, if the queen fertilizes this egg with sperm, it will become a worker bee, or another queen. If she does not fertilize the egg, it will become a drone (male). The care and feeding of the larvae that hatches from these eggs are done by worker bees. So you see, in some ways the drone is not required for another drone bee to be born, since sperm is not required for drone bees. Drones are instead required to provide the sperm to fertilize female bees (resulting in genetic recombination), so clearly they are necessary for the species to survive, which is of course required for any honey bee to be born. -Michael Wilson, University of Tennessee
There are many methods of raising queen bees, but the central tenant of queen production is that a fertilized egg may be reared into a queen or worker depending on the food it receives as a larva. In general, a beekeeper specializing in queen production sets up special colonies (e.g., “starter” colonies) that are queenless. Young larvae are transferred, or “grafted,” from selected breeder colonies into man-made queen cell cups. The grafted larvae are placed into the starter colony where the queenless workers feed the queen-destined larvae large amounts of royal jelly. The developing queen larvae may later be transferred to a “finishing” colony where the workers continue to feed and incubate the developing queens, or in some operations, the larvae are maintained throughout development in the starter colony. In all cases, the queens are removed from the colony a day or two before they are due to emerge, or about 10 days after the larvae were grafted into queen cups. Each queen cell is introduced individually into a small, queenless colony called a “mating nuc”. About 5-7 days after the queen emerges from her cell, she takes mating flight(s) over one or sometimes two afternoons and mates with 10-20 drones in a “drone congregation area.” She returns to her mating nuc and after several more days, begins to lay fertilized eggs. When the beekeeper sees eggs and larvae from the newly mated queen, about 2 weeks after the cell was introduced into the mating nuc, the queen is caged and sold. - Marla Spivak, University of Minnesota
The difference between a newly installed package of bees and an established hive has to do with the comb (an established have has drawn the comb out and has stores and brood) and the existence of brood in an established hive. Between the drawn comb and the presence of brood bees are very likely to stay put. Installing a package is usually pretty simple and successful. NC State Cooperative Extension has a series of Beekeeping Notes, one of which is on "How to Install a Package of Bees." You can find all the information notes at www.cals.ncsu.edu/entomology/apiculture and clicking on "Extension," then "Beekeeping Notes," and then scrolling down to the particular note of interest. - Bill Skelton, North Carolina State University