Richard Wooding, a recent biological sciences graduate, studied Varroa for his dissertation
What do many consider to be one of the key drivers of the planet’s concerning honeybee losses? Perhaps Varroa destructor, a parasitic mite that feeds on the haemolymph (basically the blood) of the honeybee. It is now found across honeybee populations globally, with Australia remaining the only country without it.
As Varroa first appeared in more and more colonies across the world, serious disease symptoms were being observed and colonies suffered as a result. Varroa parasitisation of a developing bee pupa or larva can result in the adult bee suffering a range of symptoms, including paralysis and heavily deformed wings (see figure). But are all of these disease pathologies solely because of the Varroa mite? After all, some bees parasitised during development can still emerge as normal, fully functional bees.
It has since been revealed that honeybee viruses may be involved. Even in Varroa-free hives, multiple viruses are normally present, but the majority don’t result in symptoms or severe effects on bee health. However, transmission by Varroa seems to result in symptomatic infections. When Varroa finds a bee host to feed on, not only does it ingest haemolymph, but it can also take in any honeybee viruses that are present. Like a biological syringe, these viruses may then be ‘injected’ into the next bee host that the Varroa mite decides to feed on.
But how does transmission via this vector result in the problematic infections that are contributing towards today’s losses? There are two main schools of thought. First is the potential role of Varroa as a biological vector. Replication of a virus within the mite before transmission and then the injection of a particular amount of virus could cause the infection to result in a bee emerging with deformed wings, for example. The other up and coming idea is that Varroa causes immunosuppression in the bees it feeds on, and may therefore provide the opportunity for viruses to suddenly take hold and develop into overt infections (whether the virus is transmitted by Varroa or even if it was already present in the bee as a latent infection).
As more and more is uncovered about the various complex interactions that exist between bees, Varroa and viruses, attention turns towards how we can control the overall problem. Currently most control methods target Varroa, such as selective breeding of Varroa-tolerant bees or the use of chemical pesticides and biological control agents to kill Varroa. Other research is focusing on the genetic RNAi weapons to silence the problematic viruses. But if Varroa is the ‘trigger’ for the concerning overt viral infections, would it not be best to be focus solely on controlling the mite? Or perhaps a multi-faceted approach would be more effective in such a situation?
That does seem a logical explanation, however, there is evidence from multiple papers showing the scarring and healing over of the Varroa bite wound following feeding. But the bees would obviously be vulnerable to infection up to prior to wound-healing, especially once free from their brood cells and moving around as adults.
While there has been some research into the role of pathogenic infection, especially in conjunction with the likely immunosuppression of the bee larvae by Varroa, there does not seem to be much research in this particular area and it is still mysterious to a large extent. Yang & Cox-Foster (2005) published “Impact of an ectoparasite on the immunity and pathology of an invertebrate: Evidence for host immunosuppression and viral amplification” and concluded listing several examples of genes involved in, the transcription of which are somehow affected by Varroa. Although they do not give many genes that were found to be significantly influenced, it does indeed seem that immunosuppression also plays a role.
Ultimately, the physical innate immune barrier of the exoskeleton is compromised, but it also seems that immune system within is also affected, both making bees more susceptible. However, the likelihood of infection through a bite-wound and the role of immunosuppression both remain largely mysterious it seems.
This now slightly dated paper by Kanbar and Engels touches briefly on the presence of bacteria around bite-wounds and the potential subsequent infection of the bee. It might provide some interesting information: Kanbar, G. & Engels, W. (2003), Ultrastructure and bacterial infection of wounds in honey bee (Apis mellifera) pupae punctured by Varroa mites, Parasitol Res 90, 349-354.
My understanding is that when the Varroa mite bites the host bee larvae, an agent in its saliva prevents the hole from healing. From that point on, the host bee is liable to be infected by any number of viruses or other infections penetrating the bees exoskeleton during its probably shortened lifespan.