Honey bee abdominal lipids decline with age, a change thought to be associated with the onset of foraging behavior. Stressors, such as pesticides, may accelerate this decline by mobilizing internal lipid to facilitate the stress response. Whether bees with stressor-induced accelerated lipid loss vary from controls in both the onset of foraging and nutritional quality of collected pollen is not fully understood. We asked whether stressors affect foraging behavior through the depletion of abdominal lipid, and whether stress-induced lipid depletion causes bees to forage earlier and for fattier pollen. We tested this by treating newly emerged bees with one of two pesticides, pyriproxyfen (a juvenile hormone analog) and spirodiclofen (a fatty acid synthesis disruptor), that may affect energy homeostasis in nontarget insects. Bees fed these pesticides were returned to hives to observe the onset of foraging behavior. We also sampled foraging bees to assay both abdominal lipids and dietary lipid content of their corbicular pollen. Initially, spirodiclofen-treated bees had significantly more abdominal lipids, but these declined faster compared with controls. These bees also collected less, yet more lipid-rich, pollen. Our results suggest that bees with accelerated lipid decline rely on dietary lipid content and must collect fattier pollen to compensate. Pyriproxyfen treatment reduced the age at first forage but did not affect abdominal or collected pollen lipid levels, suggesting that accelerated fat body depletion is not a prerequisite for precocious foraging.

Honey bees obtain lipids from pollen or commercial supplements. These supplements do not fully support colony health. We tested the hypothesis that supplements are deficient because they lack essential fatty acids (EFAs). The five supplements we tested had low linolenic (⍵3) acid and were unbalanced (⍵6:⍵3 > 6) compared to natural pollen. We selected two of these supplements for further study because they had different levels of individual EFAs and different ⍵6:⍵3 ratios. Bees from hives fed these different supplements had equivalent tissue EFA levels. In choice assays, hives fed these different supplements were presented with flours with various absolute and relative levels of EFAs. We saw no difference in foraging preference. Rather, all hives preferred flours with small grain size and high protein to lipid ratios. We conclude that bees balance their internal EFAs and that differential colony nutrition does not affect foraging preference. The data also argue for more linolenic (⍵3) acid in commercial supplements.

Varroa destructor is an ectoparasitic mite of immature and adult honey bees that can transmit several single-stranded RNA viruses to its host. Varroa reproduce in brood cells, and mite populations increase as colonies produce brood in spring and summer. Mite numbers also can sharply rise, particularly in the fall, by the migration of varroa into hives on foragers. Colonies with high levels of varroa and viruses often die over the winter. Feeding colonies pollen might keep virus levels low and improve survival because of the positive effects of pollen on immunity and colony growth. We compared varroa and virus levels and overwinter survival in colonies with (fed) and without (unfed) supplemental pollen. We also measured the frequency of capturing foragers with mites (FWM) at colony entrances to determine its relationship to varroa and virus levels. Colonies fed supplemental pollen were larger than unfed colonies and survived longer. Varroa populations and levels of Deformed wing virus (DWV) rose throughout the season, and were similar between fed and unfed colonies. The growth of varroa populations was correlated with FWM in fed and unfed colonies, and significantly affected DWV levels. Increasing frequencies of FWM and the effects on varroa populations might reduce the positive influence of supplemental pollen on immune function. However, pollen feeding can stimulate colony growth and this can improve colony survival.

Recent widespread honey bee (Apis mellifera) colony loss is attributed to a variety of stressors, including parasites, pathogens, pesticides and poor nutrition. In principle, we can reduce stress-induced declines in colony health by either removing the stressor or increasing the bees' tolerance to the stressor. This latter option requires a better understanding than we currently have of how honey bees respond to stress. Here, we investigated how octopamine, a stress-induced hormone that mediates invertebrate physiology and behavior, influences the health of young nurse-aged bees. Specifically, we asked whether octopamine induces abdominal lipid and hypopharyngeal gland (HG) degradation, two physiological traits of stressed nurse bees. Nurse-aged workers were treated topically with octopamine and their abdominal lipid content, HG size and HG autophagic gene expression were measured. Hemolymph lipid titer was measured to determine whether tissue degradation was associated with the release of nutrients from these tissues into the hemolymph. The HGs of octopamine-treated bees were smaller than control bees and had higher levels of HG autophagy gene expression. Octopamine-treated bees also had higher levels of hemolymph lipid compared with control bees. Abdominal lipids did not change in response to octopamine. Our findings support the hypothesis that the HGs are a rich source of stored energy that can be mobilized during periods of stress.