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Perhaps someday we will even have the word “beedoctor.”

A Tenet of Medicine: Learn the Normal

Colonies of honey bees living in the wild are prospering in American forests even in the face of myriad stressors that are decimating the managed colonies living in apiaries. We know that both cohorts are exposed to the same parasites and pathogens. How then do wild colonies survive without beekeeper inputs, whereas managed colonies live just one to two seasons if humans do not intervene with various supplements or medicines? In examining this conundrum, we must ask ourselves as bee doctors, working hand‐in‐hand with beekeepers, how we should examine the health of the honey bee? A fundamental tenet of medicine is the need to learn what is normal (regarding anatomy, physiology, or the state of being known as health) before one can understand deviations from this baseline. We contend that the “normal” that bee veterinarians should be concerned about is the wonderfully adapted lifestyle of wild colonies of honey bees. In this chapter, we will highlight the important differences between wild and managed colonies of honey bees and we will suggest ways health professionals can make use of the marvelous tools for health and survival that evolution has bestowed upon Apis mellifera through adaptation and natural selection.

      Declines of the world's pollinators are happening at an alarming rate, and it is predicted that these declines will have adverse impacts on pollinator‐sensitive commodities worth billions of dollars (Morse and Calderone 2000). The threat to the honey bee is perhaps the best understood of the pollinator declines. Its causes are diverse: widespread use of agrochemicals, loss of plant and floral diversity, invasive species, migratory beekeeping practices, and monoculture pollen sources. Furthermore, the stresses created by these environmental stressors are intensified by the honey bee's pests, parasites, and pathogens. Although no single disease agent has been identified as the cause of honey bee colony collapse, pests and pathogens are recognized as the primary drivers of the massive deaths of managed bee colonies worldwide. Many of these agents of disease are vectored by an ectoparasitic mite introduced from Asia, Varroa destructor (Ellis et al. 2010; Ratnieks and Carreck 2010).

      Investigations of honey bee declines have focused primarily on the pathogens themselves and their interactions, which are now understood to be multifactorial (vanEngelsdorp et al. 2009; Becher et al. 2013; Di Prisco et al. 2016). Besides the pathogens, the environments in which honey bees live also profoundly impact colony survival. In this chapter, we will examine honey bee health and the alarming levels of colony mortality from an ecological and evolutionary perspective. We will embrace the logic of natural selection and we will learn important lessons from long‐term studies of honey bee colonies living in nature (Brosi et al. 2017; Seeley 2017b, 2019a; Neumann and Blacquière 2016).

Good Genes Versus Good Lifestyle: The Varroa Story

      We will begin our account of the health and fitness of wild colonies by relating the story of the Varroa mite (V. destructor), a parasite that switched hosts from the Eastern honey bee (Apis cerana) to the Western honey bee (A. mellifera). In order to understand the resistance to Varroa mites that is found in wild honey bee colonies, we must examine more deeply their genes and their lifestyle.

      Beekeepers today rely primarily on commercial queen producers for their bee stock. Most hobby beekeepers, for example, will start an apiary or add colonies to an apiary by purchasing either a “package” of bees shipped in a cage or a nucleus colony (“nuc”) living in a small hive. In North America, packaged bees are shipped from various southern states in the U.S., as well as from California, and Hawaii, so they consist of stock that is not necessarily adapted to the beekeeper's local climate, temperatures, and agents of disease. Furthermore, even though queen bees are also produced and sold across North America – their genetics often traces to just a handful of colony lines. In many places, good colony health can be fostered by the use of locally‐adapted bees.

      From an evolutionary perspective, the observation that wild colonies have rapidly adapted to the Varroa mite, and to the diseases they vector, over a remarkably short timeframe (ca. 10 years), suggests that surviving wild colonies have either good genes (DNA), a good lifestyle, or both (Seeley 2017a).

Good Genes

      The Varroa mite is the leading cause of honey bee health problems on all beekeeping‐friendly continents except Australia. Beekeepers have always experienced colony losses, but it was not until the arrival of this parasitic mite that colony die‐offs became severe in North America. The Varroa mite lies at the heart of poor colony health, because it acts both as a primary stressor (the adult mites feed on the “fat bodies” of adult bees and the immature mites feed on immature bees [pupae]) and as a vector for a myriad of the viral diseases of honey bees (vanEngelsdorp et al. 2009; Martin et al. 2012). If a managed colony of honey bees is left untreated, Varroa mites will kill it within two to three years (Rosenkranz et al. 2010). Remarkably, the wild colonies living in the forests of North America today, plus some notable examples of European honey bees living on islands, are resistant to the mite (De Jong and Soares 1997; Rinderer et al. 2001; Fries et al. 2006; Le Conte et al. 2007; Oddie et al. 2017). How did this resistance evolve? We know that wild colonies in the northeastern forests of North America went through a precipitous population decline in the 1990s, following the arrival of the mite (Seeley et al. 2015; Mikheyev et al. 2015; Locke 2016). Yet, studies show that these wild colonies recovered in the absence of mite treatments without appreciable loss of genetic diversity by evolving a stable host‐parasite relationship with V. destructor.

The genetic bottleneck associated with a precipitous population decline would have devastated most species; cheetahs and Florida panthers, to name two prominent mammalian examples, exhibit extensive disease syndromes from low genetic variability. A. mellifera, however, came through its population decline with remarkable genetic variation intact because polyandry, a breeding strategy whereby the queen mates with 10–20 drones, helps maintain the genetic composition of a population. Polyandry also confers improved fitness through enhanced disease resistance (Seeley and Tarpy 2007); higher foraging rates, food storage, and population growth (Mattila and Seeley 2007); and possibly better queen physiology and lifespan in the colony (Richard et al. 2007). Fitness follows diversity and in honey bee colonies this comes through the multiple matings of the queen. In nature, there must be a trade‐off between the optimal number of drone matings and the time that queens spend on their mating flights, which sometimes extend several miles from a queen bee's home. Delaplane and colleagues (2015) showed that queens artificially inseminated with sperm from 30 to 60 drones, rather than the 12 to 15 drones that are typical for the queens of wild colonies, produced more brood and had lower mite infestation rates relative to control colonies, supporting the idea that resistance to pathogens and parasites is a strong selection pressure favoring polyandry. One hypothesis to explain the high levels of polyandry of queen honey bees is that by mating with many males, the queen captures rare alleles that regulate resistance to pests and pathogens (Sherman et al. 1998; Delaplane et al. 2015). This has been confirmed in several studies in which colonies whose queens had either a high or a low number of mates were inoculated with the spores of chalkbrood (Ascosphaera apis) or American foulbrood (Paenabacillus larvae), and the levels of infection in their colonies were compared (Tarpy and Seeley 2006; Seeley and Tarpy 2007). The higher the number of mates, the lower the level of disease.

      We know that Varroa mites initially killed off many wild colonies living in the forests of New York State, so maternal lines (mitochondrial DNA lineages) were lost (Mikheyev et al. 2015). Fortunately, the multiple mating by queen honey bees enabled the maintenance of the diversity of the bees' nuclear DNA despite the massive colony losses. Today, the density of wild colonies living in forests in the northeastern United States (c. 2.5 colonies per square mile, or 1 per square kilometer) is the same as it was prior to the invasion of the Varroa mites (Seeley et al. 2015; Radcliffe and Seeley 2018), and the survivor colonies possess resistance to these mites. In a comparison of the life history traits of wild colonies living in the forests around Ithaca, NY, between the 1970s (pre Varroa) and the 2010s (post Varroa), Seeley (2017b) found no differences, which implies that the wild colonies possess defenses against the

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