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normal bee weight gain, an effect which can be attributed to regulation of endocrine signaling of important bee hormones. The microbiome increases the levels of vitellogenin and juvenile hormone in worker bees, and these regulate the nutritional status and the development of their social behaviors, so it is likely that the state of the bees' microbiomes affects the health of the whole colony. Bee microbes are also implicated in modulating the worker bee's immune system (Zheng et al. 2018).
Alterations in the microbiota of the bee gut have been linked to disease and reduced fitness of the bee host. The use of tetracycline – an antibiotic commonly used to treat American foulbrood and European foulbrood, and often given prophylactically – reduces both the number and the composition of normal bacteria in the bee gut. Raymann and colleagues (2018) found that Serratia marcescens, a known pathogen of honey bees and other insects, normally inhabits the bee gut without eliciting a host immune response. However, bee disease occurs when this pathogen is inoculated into a bee's hemolymph through the bite of a Varroa mite or when the gut microbiome is disturbed with antibiotic use. Researchers studying Colony Collapse Disorder observed a shift in gut pathogen abundance and diversity, and proposed that such shifts within diseased honey bees may be a biomarker for collapsing colonies (Cornman et al. 2012). See Chapter 9 for more details on the bee microbiome.
Part 2: Epidemiology for Bee Health: How Lifestyle Impacts Disease Spread
The preceding comparison of the environments of honey bee colonies living in the wild versus in apiaries sets the stage for reviewing the host–parasite interactions that ultimately define colony health. Let us now compare the impacts of disease on colonies living in the differing settings in which honey bee colonies now find themselves. Compared to organisms that do not live in large and complex eusocial societies (i.e. ones with a reproductive division of labor and overlapping generations) honey bees have far greater complexities in their host–pathogen and host–parasite relationships.
Ecological Drivers of Disease
Living in crowded communities of thousands of individuals, honey bees interact closely through regular communication behaviors, grooming activities, and the trophallactic transfer of food and glandular secretions. This complex group living provides abundant opportunities for pathogens to spread and reproduce. Moreover, the high temperature and high humidity of a honey bee colony's home makes it a perfect environment for disease outbreaks. It comes as no surprise, then, that many of the protective mechanisms that honey bees have evolved to control the spread of disease operate at the level of the whole colony, the superorganism. The members of a colony work together closely to achieve a social immunity: they groom themselves and one another (allogroom); they work as undertakers to remove dead and diseased bees; they collect antibiotic enriched pollen and nectar; and they practice miticidal and hygienic behaviors by biting off the body parts of mites and by removing infected bee larvae and pupae from their nests (Fries and Camazine 2001). Relatively few mechanisms of disease resistance have evolved at the level of the individual bee. These include individual immune system functioning and filters in the proventriculus (the valve between esophagus and stomach) that remove spores of American foulbrood. Most of these protective mechanisms limit intra‐colony transmission of disease agents, and they work well. What is probably the primary driver of disease problems for honey bees at present, however, is inter‐colony disease transmission.
A Critical Distinction: Vertical vs. Horizontal Disease Transmission
The method by which a disease is transmitted from colony to colony is a fundamental determinant of pathogen virulence. Vertical transmission (the spread of disease from parent to offspring) favors the evolution of avirulence whereas horizontal transmission (the spread of disease among unrelated individuals) favors the evolution of virulence (Lipstich et al. 1996). This is because pathogens and parasites that spread vertically need their host to stay healthy to produce offspring, whereas those that spread horizontally do not have this need. Although numerous other host factors (i.e. host longevity, density, population structure, and novel hosts) and pathogen factors (i.e. vector availability and pathogen replication potential) also influence virulence, we will focus on how the mode of honey bee pathogen and parasite transmission within and among colonies impacts the evolution of the virulence of these agents of disease.
Vertical Transmission: Swarming
In honey bees, one way that a colony achieves reproductive success is by swarming: an established colony casts a swarm to produce a new colony. The other way that a colony achieves reproductive success is by producing drones; even though weak colonies can propagate their genes by producing drones, this does not create another colony. If a pathogen or parasite that is transmitted vertically (from parent to offspring) weakens its host and so hampers it from producing offspring (which for honey bee colonies equates to casting swarms) then it reduces its own reproductive success. In short, the natural mode of colony reproduction in honey bees favors the evolution of avirulence in most of its pathogens and parasites. The two exceptions to this generalization are American foulbrood and Varroa destructor, both of which are easily transmitted horizontally when one colony robs honey from another.
Swarming also helps inhibit the reproduction of Varroa mites (and other agents of brood diseases) by creating a natural break in brood production, which forces the mites to likewise suspend their reproduction (Seeley 2017b). Once a daughter queen emerges to replace the mother queen that has left in a swarm, this daughter queen must leave the hive to fly to a drone congregation area, where she will mate with multiple drones before returning to the hive to commence egg laying. This transition from mother queen to daughter queen creates a period without sealed brood (needed for mite reproduction) that can last from 7 to 14 days. This imposes a break in the reproduction of the Varroa mites. Furthermore, with each swarming event a sizable fraction (approximately a third) of the colony's mite population is exported with the departing workforce: the fraction of mites shed can be readily calculated since about half of the female breeding‐age mites are on the workers in a colony at any given time, and nearly three‐quarters of these workers depart in the prime swarm (Rangel and Seeley 2012). In a six‐year study of the life‐histories of wild honey bee colonies living in a forest in the northeast US, Seeley (2017b) found that most (~87%) swarmed each summer.
In contrast to the relatively small nest cavities of wild honey bee colonies, the colonies kept by beekeepers occupy large hives, and they are less apt to produce swarms (Oliver 2015). The swarm control methods of beekeepers include transferring sealed brood to the top of the hive and queen exclusion (the Demaree method), cutting out queen cells, preventing the filling of cells around the brood nest with nectar (possibly a cue for swarming) by providing empty combs above the brood nest, reversing the brood boxes and inserting empty combs in the brood nest, and reducing the worker populations of colonies by splitting them. All of these methods weaken the stimuli that trigger swarming, but only one helps control the Varroa mites: the removal of bees. We propose instead controlled colony fission by making “splits” to mimic the beneficial effects of swarming on mite control (Loftus et al. 2016).
Horizontal Transmission: Bee Drift, Robbing, Forager Contact, and Contamination
Fries and Camazine (2001) outline three distinct things that a pathogen must do to reproduce and disperse to a new honey bee colony. A pathogen must: (i) infect a single honey bee; (ii) infect multiple honey bees; and (iii) infect another colony. Of these, it is the spread to another colony that should most concern beekeepers and bee doctors:
In terms of fitness, the successful transfer of a pathogen's offspring to a new colony is a critical step in its life history. If a parasite or pathogen fails to achieve a foothold in another host colony, the parasite will not increase its reproductive fitness, regardless of how prolific it has been within the original host colony. Thus, hurdles #1 and #2 (intra‐individual and intra‐colony transmission) are important aspects of pathogen fitness only to the extent that they contribute to more efficient inter‐colony transmission
(Fries