Drifting in honeybees

Note This post was first published on The Apiarists’ blog.

During previous research on deformed wing virus (DWV) biology and its transmission by Varroa I’ve moved known Varroa-free colonies (sourced from a region of the UK which the mite has yet to reach and maintained totally mite-free) into apiaries in the countryside. Within 2-3 weeks Varroa was detectable in sealed brood, showing that mite infestation occurs very readily. I know other researchers who have made very similar observations. Where do these mites come from?

They’re not all ‘your’ bees

The obvious source would be the phoretic mites transported on workers ‘drifting’ from nearby infested colonies, or on drones which are known to travel quite long distances and may be accepted by almost any colony. If you want to see how frequent this is try marking a few dozen drones with a dab of paint. To avoid confusion use the colour used to mark queens next year. There are unlikely to be 4+ year old queens in the apiary and the drones will all perish before the end of the current season. Over the next few days and weeks the drones will appear in adjacent colonies, and some will likely leave the apiary and be accepted in your neighbours colonies.

Hives in rows ...

Hives in rows …

Beekeepers are usually aware that colonies at the ends of rows often ‘accumulate’ bees that have drifted when returning to the hive. In shared association apiaries some crafty beekeepers will site their colonies at the ends of rows to take advantage of the ‘generosity’ of other colonies. However, many beekeepers probably do not appreciate the extent to which drifting occurs. Pfeiffer and Crailsheim report (1998) that 13-42% of the population of a colony are ‘alien’ i.e. have drifted from adjacent hives, depending upon the time of season. Remember that drifting occurs in both directions simultaneously, so the overall numbers of bees in a colony may not be adversely affected (or boosted). In other studies Sekulja and colleagues report (2014) that ~1% of marked bees drifted between colonies over a three day observation window. Interestingly, American foulbrood (AFB) infected bees drifted slightly more than uninfected bees. Spread of foulbroods during drifting is one reason the bee inspectors check nearby apiaries when there is an outbreak. These studies were all on workers where drifting primarily occurs during orientation flights before the bees become foragers. Drones drift two to three times more than workers (Free, 1958).

The likelihood of drifting must be closely related to the separation of hives and apiaries. Although workers will forage up to 2-3 miles from the hive I suspect the proportion of bees that drift this distance is small to undetectable. Drones are known to fly up to about five miles to reach drone congregation areas for queen mating and are accepted by all colonies. I’ve regularly found drones appearing in (relatively) isolated mini-nucs. I’m not aware of studies that have formally tested drifting between apiaries (though it is reported in passing in the Sekulja et al., 2014 paper referenced above).

Consequences of drifting

So, your hives contain workers and drones from many nearby colonies, and you can only really be sure that they’re all “your” bees if you live – as the sole beekeeper – on an isolated island. Not only does your neighbour generously exchange bees with you, he or she also kindly shares the phoretic mites those bees are carrying, the viral payload the bees and mites are infected with and – if you’re really unlucky – the Paenibacillus larvae spores responsible for causing AFB infection (and vice versa of course).

There are lessons here that should inform the way we conduct our integrated pest management to maintain healthy colonies. 

This post provides background information for an article (“Viruses and Varroa: Using our current controls more effectively” by David Evans, Fiona Highet and Alan Bowman) in the December 2015 issue of Scottish Beekeeper, the monthly magazine for members of the Scottish Beekeepers Association.

More later …

 

Scottish Beekeepers November meeting

SBA logo

SBA logo

I enjoyed speaking at the Scottish Beekeepers November meeting in Perth last Saturday. This was the first of several specifically Scottish outreach-type events I’m doing over the next few months and it was a great opportunity to meet people I’ve corresponded with online – often via the highly informative SBAi forum – or who my research group are already collaborating with.

Hampshire BK autumn convention

Sparsholt College

Sparsholt College

I’m delighted to be talking at the Hampshire Beekeepers Association autumn convention at Sparsholt College this weekend. This is the first of several ‘winter talks’ to BKAs about our research on deformed wing virus and Varroa. Time permitting I hope to discuss some forthcoming studies on coordinated Varroa control that we’re doing with Alan Bowman (Aberdeen) and Fiona Highet (SASA) and that will shortly be featured in the Scottish Beekeeper. I was invited to talk at this event before accepting a post in St. Andrews … it’s a long way to travel. However, one of the advantages of flying to these events is I can’t be tempted by too many goodies from the trade stands 😉

First occupants

Bees installed ...

Bees installed …

Late last week, in the dark and rain, the first two honeybee colonies were installed in the bee house on our research apiary. The warm(ish) and dry environment will greatly benefit our research by helping us harvest larvae and pupae whatever the weather conditions are outside. In addition, we expect brood rearing by the colony to be extended earlier and later in the season, so enabling us to undertake more extensive studies of the biology of deformed wing virus.

The bee shed has special windows – just about visible in the poor quality cellphone picture – that allows the bees that leave the hive when the roof is removed to ‘escape’ from the shed … they can then re-enter the hive via a tunnel entrance through the shed wall.

PeerJ pre-print on sacbrood virus

We have recently submitted a paper to PeerJ on gene expression changes resulting from deformed wing virus and sacbrood virus infection. A pre-print of this manuscript can be viewed on the PeerJ website.

Manuscript authors and title

Ryabov EV, Fannon JM, Moore JD, Wood GR, Evans DJ. (2015Evolutionarily related Sacbrood virus and Deformed wing virus evoke different transcriptional responses in the honeybee which may facilitate horizontal or vertical transmission of these virusesPeerJ PrePrints 3:e1749

Abstract

Sacbrood virus (SBV) and deformed wing virus (DWV) are evolutionarily related positive-strand RNA viruses, members of the Iflavirus group, which infect the honeybee Apis mellifera, but have strikingly different levels of virulence when transmitted orally. Honeybee larvae orally infected with SBV usually accumulate high levels of the virus, which halts larval development and causes insect death. In contrast, oral DWV infection at the larval stage usually causes asymptomatic infection with low levels of the virus, although high doses of ingested DWV could lead to DWV replicating to high levels. We investigated effects of DWV and SBV infection on the transcriptome of honeybee larvae and pupae using global RNA-Seq and real-time PCR analysis. This showed that high levels of SBV replication resulted in down-regulation of the genes involved in cuticle and muscle development, together with changes in expression of putative immune-related genes. In particular, honeybee larvae with high levels of SBV replication, with and without high levels of DWV replication, showed concerted up-regulated expression of antimicrobial peptides (AMPs), and down-regulated expression of the prophenoloxidase activating enzyme (PPAE) together with up-regulation of the expression of a putative serpin, which could lead to the suppression of the melanisation pathway. The effects of high SBV levels on expression of these immune genes were unlikely to be a consequence of SBV-induced developmental changes, because similar effects were observed in the honeybee pupae infected by injection. We suggest that the effects of SBV infection on the honeybee immunity could be an adaptation to horizontal transmission of the virus. Up-regulation of the expression of AMP genes in the SBV-infected brood may contribute to protection of the SBV virus particles in dead larvae from bacterial degradation. Suppression of the melanisation may also reduce the loss of infectivity of SBV in the larvae. Therefore it is possible that activation of AMP expression and suppression of melanisation could increase ability of SBV to be transmitted horizontally via cannibalization route. We observed no changes of AMPs and the melanisation pathway genes expression in the orally infected larvae with high levels of DWV replication alone. In the injected pupae, high levels of DWV alone did not alter expression of the tested melanisation pathway genes, but resulted in up-regulation of the AMPs, which could be contributed to the effect of DWV on the regulation of AMP expression in response to wounding. We suggest that the effects of single DWV infection on the expression of these immune-related genes could reflect evolutionary adaptations of DWV to vertical transmission. Up-regulation of AMPs is costly and suppression of melanisation may increase susceptibility to infections, therefore these changes may have negative impact on honeybee survival and, consequently, of the survival of DWV.

MSWCC 2015

The Royal Agricutural University, Cirencester

The Royal Agricutural University, Cirencester

I spent Friday and Saturday attending the Midland and South West Counties Convention at the Royal Agricultural University, Cirencester. It was a good venue for a meeting, complemented by an interesting and entertaining programme of talks. I discussed our developing story about the influence of Varroa on the transmission of pathogenic strains of deformed wing virus, together with brief coverage of both high and low-tech solutions that might be useful in controlling the detrimental impact of the mite on the virus population. On the Saturday I donned my beekeepers hat (veil?) and discussed queenright queen rearing methods … lots of stakeholder engagement to keep the funders happy 😉

There were some excellent presentations on the use of pollen in forensic studies (Michael Keith-Lucas) and the use of nucleus hives (Bob Smith). I had to leave early to make sure I caught my cancelled train to Swindon (“too many passengers”), the delayed connection to Paddington (“waiting for staff to turn up”), the slow running Heathrow Express (“engineering work”) and so missed my flight back to Edinburgh … all part of the rich outreach experience.

Pollinator pests and diseases

DWV symptoms

DWV symptoms

One additional output from our Insect Pollinators Initiative has been an LWEC PPN (Living With Environmental Change Policy and Practice Note) on How are pests and diseases affecting bee pollinators? (Note #17, March 2015). This was jointly written with Robert Paxton (Halle, Germany) and Giles Budge (National Bee Unit). Copies should be available from the LWEC website or directly from here.

Tuplin et al., 2015

Recently published

Tuplin, A., Struthers, M., Cook, J., Bentley., K and Evans, D.J. (2015) Inhibition of HCV translation by disrupting the structure and interactions of the viral CRE and 3′ X-tail. Nucl. Acids Res. doi: 10.1093/nar/gkv142

Abstract

A phylogenetically conserved RNA structure within the NS5B coding region of hepatitis C virus functions as a cis-replicating element (CRE). Integrity of this CRE, designated SL9266 (alternatively 5BSL3.2), is critical for genome replication. SL9266 forms the core of an extended pseudoknot, designated SL9266/PK, involving long distance RNA–RNA interactions between unpaired loops of SL9266 and distal regions of the genome. Previous studies demonstrated that SL9266/PK is dynamic, with ‘open’ and ‘closed’ conformations predicted to have distinct functions during virus replication. Using a combination of site-directed mutagenesis and locked nucleic acids (LNA) complementary to defined domains of SL9266 and its interacting regions, we have explored the influence of this structure on genome translation and replication. We demonstrate that LNAs which block formation of the closed conformation inhibit genome translation. Inhibition was at least partly independent of the initiation mechanism, whether driven by homologous or heterologous internal ribosome entry sites or from a capped message. Provision of SL9266/PK in trans relieved translational inhibition, and mutational analysis implied a mechanism in which the closed conformation recruits a cellular factor that would otherwise suppresses translation. We propose that SL9266/PK functions as a temporal switch, modulating the mutually incompatible processes of translation and replication.