Describing Common Honey Bee Viruses Affecting Albertan Colonies – Part 1
The Three-Part Honey Bee Virus Series
By Nicole McCormick, Alberta Tech Transfer Program Technician
Let’s talk about honey bee viruses!
The battle with viral infections is becoming constant within the honey bee industry, and it’s more crucial than ever that beekeepers know the identification, transmission, and management of bee-related viruses. Some common viruses present in Alberta, of which I will focus on throughout this series, include: Deformed Wing Virus (DWV), Varroa Destructor Virus (VDV), Chronic Bee Paralysis Virus (CBPV), Black Queen Cell Virus (BQCV), and Sacbrood Virus (SBV). While all these different viruses can have detrimental colony and bee health effects, they tend to hide in the shadow of other bee pathogens, such as American foulbrood, European foulbrood, Nosema, and the major threat to apiculture, Varroa mites. When present on their own, viral levels have historically been undetectable, causing no major harm to colony health1. However, when present in conjunction with other diseases, viruses have the opportunity to flourish, and potentially cause bigger problems over time.
One of the major linkages between bee-related viruses and other bee pathogens is high Varroa mite infestation, leading to increased viral levels1. Varroa mites function as vectors for viral diseases, as they can be a source of mechanical transmission for most viruses and facilitate viral replication for viruses such as DWV and VDV1. Furthermore, mites can cause bee immunosuppression making colonies more susceptible to infection when exposed to viral pathogens1.
The goal of this three-part series on honey bee viruses is to help you identify, understand, and manage viruses, and ultimately, help Alberta’s honey bee population and industry thrive. The first part of this series will focus on laying the foundation for understanding honey bee viruses. It’s important to be able to identify signs of viral infection, as infected colonies tend to ‘appear’ asymptomatic until it’s too late. Throughout this article you will be provided with a description of the common viruses, highlighting important clinical signs, factors leading to infection, effects on productivity, and much more.
Deformed Wing Virus
Deformed wing virus (DWV) is considered to be one of the most significant viruses affecting colony health2. Due to its close linkage to Varroa destructor, its distribution has become worldwide, making it one of the most common viruses observed by beekeepers3. As a result, the seasonality of DWV-infection tends to follow that of varroa mites; increasing levels from the spring to the fall1.
Deformed wing virus attacks the eggs, larvae, pupae, and adult bees within the colony4. While DWV infection can affect bees during all life stages, high viral levels are most prevalent in the pupal stage, most likely due to their weaker immune system in comparison to adult bees1. Clinical signs that can be observed in symptomatic adult bees include: bees emerging with deformed or shrunken wings, reduced body size, and discoloration causing infected bees to appear lighter and ‘washed-out’ (Fig. 1)1. One of the main effects of this virus on worker bees is a shortened lifespan. This has been observed in workers with deformed wings (symptomatic) that were infected during the pupal or adult stage, and also those that are asymptomatic4,1. In addition to having a shorter lifespan, symptomatic worker bees are also less likely to contribute to hive activities during their lifetime4. At the colony level, studies have shown that DWV-infected hives have less brood and a decreased adult bee population, likely due to the effect of this virus on individual bees (i.e., premature death and decreased performance in hive activities)4. Furthermore, queens have also been observed with deformed wings; however, it was found that DWV infection has no effects on their behaviour or health4.
Deformed wing virus has become a chronic issue of honey bees due to its low pathogenicity4. More clearly, its ability to cause a serious threat upon infection is minimal, as bees infected with DWV do not instantly die. Instead, replication of the virus within the bee happens slow, but constant, and the bee maintains the infection during its lifespan1. As a result, DWV is able to persist within a colony at low levels without causing major health issues. However, increases in colony stress can change this outcome3. This includes: lack of essential resources (i.e., nectar, pollen, and water), increased pathogen and parasite pressure, and unfavorable weather conditions1. Among all stressors, the most relevant to increased DWV infection potentially leading to colony death, is Varroa destructor infestation1. Deformed wing virus replicates within the mite and then is physically transmitted to worker bees within the colony via mite attachment, making infection quicker and potentially more lethal1.
Varroa Destructor Virus
Varroa destructor virus (VDV) is a relatively new variant of DWV, also considered to be one of the most prevalent viruses of honey bees1. This virus was first identified in the varroa mite but has now been found in both worker bees and queens5. Clinical signs of VDV infection are very similar to those of a DWV infection. These include wing deformities in newly emerged bees, pupal mortality, shortened lifespan, and overwinter mortality6.
While signs of VDV infection can be very similar to DWV, the former has shown to be more virulent, meaning that disease infection can progress more quickly and cause more harm to the colony6. This is due in part to the fact that VDV replicates at a much faster rate, compared to DWV, in both the varroa mite and the honey bee6. Over the past 10 years, VDV levels have increased significantly and has become more widespread2. Due to this, it is predicted that VDV will become the dominant DWV variant and one of the main predictors of overwinter colony losses2,7. High levels of both VDV and DWV have been observed simultaneously within a colony, indicating that competition between the two viruses is not likely to exist, but rather a mutualistic relationship where the presence of the two variants may help induce greater infection2.
Chronic Bee Paralysis Virus
Chronic bee paralysis virus (CBPV) is an emerging viral disease that has a worldwide distribution, with instances of CBPV recently increasing in North America8. CBPV can be found in all stages of the bee life cycle5. However, it mainly affects adult bees, causing paralysis, abnormal trembling, reduced flight, hairless black bees (Fig. 3), and k-wing4. It takes about 6 days for infected bees to develop clinical signs, with symptomatic bees usually dying within a week5,8. Those that survive will often die in the field, weak, unable to return to the colony5. As a result, colonies experiencing high viral levels can collapse due to the loss of infected nurse and forager bees. At the colony level, one of the major signs of a highly infected colony is mounds of dead bees in front of the entrance8. These are usually infected bees that have been removed from the colony, or bees that were unable to crawl back into the colony due to paralysis8.
Chronic bee paralysis virus is most commonly within the colony as a covert infection – this is when bees are able to keep the virus infection under control, with minimal signs of infection or effects to colony performance and health1. However, covert infections can turn into overt infections – infections that present clinical signs and have detrimental effects on the colony1. Some inducers of overt CBPV infections are scarcity of food resources, severe winters, or adverse weather conditions1. All these factors increase bee confinement, which is one of the main causes of higher viral load as the virus is spread through tight clustering and rubbing together of infected and healthy bees5. Colonies that are heavily infected can become very weak, reducing the hives ability to pollinate and produce honey8.
Black Queen Cell Virus
Black queen cell virus (BQCV) affects colonies around the world by persisting as asymptomatic infections in worker bees and brood, leading to the infection of developing queens5. During the capped-cell phase of queen development, the virus will begin to replicate and eventually cause queen pupal death9. The diseased pupa will begin to turn pale yellow and develop a tough sac-like skin, similar to that of sacbrood virus. Once the pupa has died, it will turn dark brown in color and the outside of the queen cell will become dark brown/black.5 These clinical signs have also been observed in drone pupae5. Previous studies have shown that BQCV infections in adult bees is positively associated with Nosema spp (Fig. 4) load5. This positive relationship is likely due to adult bees with a previous Nosema spp. infection presenting a compromised midgut cell line, allowing for easy viral infection and replication5. Adult bees that are co-infected with Nosema spp. and BQCV are found to have shorter lifespans than those only infected with Nosema spp.5 Due to this link between BQCV and Nosema spp., there is an increase in viral levels mainly in the spring and early summer as this is, historically, when Nosema levels are high1. At the colony level, reduced adult bee population due to shorten lifespan and queen death can have negative effects on colony strength and productivity throughout the season1.
Black queen cell virus poses a big threat to queen breeders5. Newly grafted queens can become infected with BQCV, and the virus can easily spread between queen cells, potentially resulting in a poor queen hatch9. In the spring, when breeders are extensively raising queens for the upcoming season, Nosema levels tend to be high5. This puts breeders at an even higher risk during this time of the year due to the relationship between Nosema and BQCV-infection in adult honey bees.
Sacbrood virus (SBV) was the first virus to be detected in honey bees, and it’s one of the most common viruses of honey bees today10. Sacbrood virus is not considered to be a major threat to colony health as it does not typically cause colony loss and is usually a consequence of colony expansion in the early spring5,10. This virus can affect the brood and adult bees; however, larvae that are approximately 2 days old tend to be the most vulnerable to SBV infection10. Upon infection, the larvae will turn greyish yellow in colour and develop a tough skin-like outer layer, holding the larvae in a sac that can be removed whole from the cell (Fig. 5)9. The larvae will continue to develop until the capped phase, when infected cells will then be uncapped by worker bees5. Uncapped larvae will be seen laying straight on the side of the cell, with the head pointing towards the top. At this point, worker bees will often remove infected larvae from the colony9. Adult bees infected with SBV will often have a greater preference for nectar while foraging10. As a result, nutritional deficiencies within the colony can arise due to lack of pollen, reducing worker life expectancy10.
It is important to note that common brood diseases such as American Foulbrood (AFB) and European Foulbrood (EFB) can appear very similar to SBV. Therefore, knowing how to differentiate these diseases is an important skill to ensure that the proper management is employed. Unlike AFB-infected larvae or scales, SBV-infected larvae are easily removed from the cell in one whole piece10. Additionally, following death SBV-infected larvae are odourless, unlike AFB/EFB infected brood10.
Identifying viral infections within honey bee colonies is an important first step to understanding, managing, and reducing viral loads. To learn more about what to do next, follow along with the Three-Part Honey Bee Virus Series. Next month’s edition of the Bee News will have “Part 2- Identifying Viral pathways of Transmission”, where we will go through all the pathways viruses infect and amplify within honey bee colonies.
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