eXtension Articles,Faqs- bee health

  • Honey Bee Viruses, the Deadly Varroa Mite Associates

    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

    Introduction

    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. mellifera to 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

    Viruses

    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

    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).

    Summary

    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 apis and Nosema cerana can 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.

    Control

    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.

    References  

    Allen, M. and B.V. Ball. 1996. The incidence and world distribution of the honey bee viruses. Bee World 77: 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 jacobsoni as 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 mellifera L.) 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 jacobsoni Oud. 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 destructorJournal 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 CrithidiaPloS 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 Ecology73(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. Apidologie 38: 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
  • All Bugs Good and Bad 2014 Webinar Series

    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

    Straight Talk About Termites
    Presented by Dr. Xing Ping Hu
    Moderated by Mallory Kelley
     

    APRIL 4, 2014

    Get TickSmart: 10 Things to Know, 5 Things to Do
    Presented by Dr. Thomas N. Mather
    Moderated by Shawn Banks
     

    MAY 2, 2014

    Are Those Itsy Bitsy Spiders Good or Bad?
    Presented by Dr. Nancy Hinkle
    Moderated by Charles Pinkston

     

    JUNE 6, 2014

    Fire Ant Management
    Presented by Elizabeth "Wizzie" Brown
    Moderated by Gerald "Mike" McQueen

     

    AUGUST 1, 2014

    Minimize Mosquito Problems
    Presented by Molly Keck
    Moderated by Christopher Becker

     

    SEPTEMBER 5, 2014

    Kudzu Bug Takes Over the Southeastern U.S and Brown Marmorated Stinkbug -- All Bad
    Presented by Michael Toews and Tracy Leskey
    Moderated by Willie Datcher
     

    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
     


    Download the flyer for the entire 2014 All Bugs Good and Bad Webinar Series:  JPG  PDF


    The 2014 Webinars are brought to you by the following eXtension Communities of Practice:  Imported Fire Ants, Urban IPM, Bee HealthInvasive Species, Gardens, Lawns and Landscapes, and Disasters and by the Alabama Cooperative Extension System.

    Looking for 2013 Webinars?  Click here!

  • Pollination Security for Fruit and Vegetable Crops in the Northeast

    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.

    Upcoming Event: UMass Extension Symposium: Pollinator Health for Agriculture and Landscapes March 26, 2015

    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

     
    Video Segments:

    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

     

     

    Funded by the USDA-NIFA Specialty Crops Research Initiative (SCRI)

     

  • Integrated Crop Pollination

    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 and Protecting Pollinators

    Pollination in agriculture and why it matters.

    Pollination and Protecting Pollinators from WSU CAHNRS Video Production on Vimeo.

    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.

  • Bee Health Contents
  • Frequently Asked Questions
    Two "expert" bee researchers ponder a quandary: "well, what do you think?" Credit: Zach Huang



     

          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.

     

  • 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

  • How do honey bees make wax?


    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

  • How is Nosema disease treated?


    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

  • How do I know whether my bees have Nosema disease?


    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

  • What is Nosema disease?


    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

  • If honey becomes crystallized (solid) has it gone ‘bad’?


    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

  • Does honey have nutritional value?


    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

  • Can a honey bee be born without the aid of a drone?


    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

  • How are queen bees raised and mated?


    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

  • Why do newly installed packages of bees seem to abscond more than well-established hives?


    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

  • What is the basic life cycle of the fungus, Ascosphaera apis that causes chalkbrood disease in honey bee colonies?


    Spores of the fungus are ingested with the honey bee larval food. Larvae are most susceptible if they ingest spores when they are 3 to 4 days old and then are chilled briefly 2 days later, immediately after they are sealed in their cells to pupate. The spores germinate in the hind gut of the bee larva, but mycelial (vegetative) growth is arrested until the larva is sealed in its cell. At this stage, the larva is about 6 or 7 days old. The mycelial elements break out through the gut wall and invade the larval tissues until the entire larva is overcome. This generally requires from 2 to 3 days. Dead larvae are chalky white and usually covered with filaments (mycelia) that have a fluffy, cotton-like appearance. These mummified larvae may be mottled with brown or black spots, especially on the ventral sides, due to the presence of spore cysts or fruiting bodies of the fungus. Larvae that have been dead for a long time may become completely black as these fruiting bodies fully mature. Spores form only when there are 2 different strains (+ and -) of mycelia present and in contact with each other. - Clarence Collison, Mississippi State University

  • Will honey bee swarms in my yard move into a hole in the wall of my house?


    Maybe, especially if bees have occupied the wall before. Bees are attracted by the odor of the other bees. You can prevent their entry by sealing outside openings 3/8th of an inch or larger with caulking or window screen. If the bees enter your wall, they are difficult to remove.

  • What crops do not require honey bee pollination?


    Honey bees improve, or supplement, pollination for most plants they visit. However, honey bees are considered negligible pollinators for the following crops: soybean, peach, field beans, snap beans, tomato, corn, cotton, peanuts, pecans, canola, and alfalfa. In cases like these, the plant is either independent of insect pollination in general or dependent on other pollinators. - Keith Delaplane, University of Georgia

  • The drone has no father but has a grandfather. How is that?


    The queen and workers are female bees with a diploid set of chromosomes. The drones are male with a haploid set of chromosomes. To get a worker, the queen must add sperm to the egg. There must be a male to provide that sperm. To get a male, she does nothing but deposit the egg in a cell. No sperm in needed from a male bee. - Ed Beary

  • Which pesticide formulations are least hazardous to honey bees?

    Different formulations of the same insecticide often vary considerably in their toxicity to bees. Granular insecticides generally are not hazardous to honey bees. Dust formulations (seldom used today on commercial field crops) are typically more hazardous than emulsifiable concentrates because they adhere to the bee's body hairs and are carried back to the beehive. Wettable powder and flowable formulations essentially dry to a dust-like form which foragers can carry to the hives. Likewise, microencapsulated insecticides can be collected by foragers along with pollen and carried back to the beehive. When honey bees are exposed to insecticides that kill foraging bees, honey production is reduced but colonies recover as young bees emerge. Exposure to dust, wettable powder, flowable, and microencapsulated formulations of insecticides can cause severe losses of both foraging bees and hive bees. In the worst cases, toxins may remain active in the hive for several months and prevent colonies from recovering from the injury. - Marion Ellis, University of Nebraska

     

  • What are some good flowering plants to put near a vegetable garden to attract bees to help with pollination?


    Any flowering, pollen-producing plant will attract bees, including your vegetables. Bees also need a source of water, so the addition of a bird bath or something similar can help attract them. The only caution is that some of the flowering annuals will reseed themselves vigorously and can become "weeds" in subsequent gardens.

  • What are wax moths and what kind of damage do they make in a beehive?


    There are two species of wax moth that cause damage to honey bee colonies by consuming beeswax as their larvae develop and in the process of making a pupal cocoon they score the wooden frames that hold the wax combs, weakening the wood. Damage becomes obvious as they produce large quantities of gray-white webbing and dark fecal material as they feed. The larger of the two species (3/4 inch long gray-brown adult), the greater wax moth, Gallaria melonella causes more damage and has a wider distribution while the lesser wax moth, Achroia grisella is more limited to warmer southern states. Wax moths are not a cause of colony death, they come in later after some other factor/malady has reduced the population of honey bees. Strong colonies of honey bees with large worker population can reduce numbers of wax moth to a level where they cause little damage. - John Skinner, University of Tennessee

New In the Forums