Sickness Behavior in Honey Bees

Abstract

During an infection, animals suffer several changes in their normal physiology and behavior which may include lethargy, appetite loss, and reduction in grooming and general movements. This set of alterations is known as sickness behavior and although it has been extensively believed to be orchestrated primarily by the immune system, a relevant role for the central nervous system has also been established. The aim of the present work is to develop a simple animal model to allow studying how the immune and the nervous systems interact coordinately during an infection. We administered a bacterial lipopolysaccharide (LPS) into the thorax of honey bees to mimic a bacterial infection, and then we evaluated a set of stereotyped behaviors of the animals that might be indicative of sickness behavior. First, we show that this immune challenge reduces the locomotor activity of the animals in a narrow time window after LPS injection. Furthermore, bees exhibit a loss of appetite 60 and 90 min after injection, but not 15 h later. We also demonstrate that LPS injection reduces spontaneous antennal movements in harnessed animals, which suggests a reduction in the motivational state of the bees. Finally, we show that the LPS injection diminishes the interaction between animals, a crucial behavior in social insects. To our knowledge these results represent the first systematic description of sickness behavior in honey bees and provide important groundwork for the study of the interaction between the immune and the neural systems in an insect model.

Costs and benefits of sublethal Drosophila C virus infection

“…Support for the adaptive nature of these ‘sickness behaviours’ has come mainly from vertebrate species challenged with deactivated pathogens or their derived components, which are sufficient to stimulate an immune response without causing pathology (Adelman & Martin, ; Lopes et al ., ). In addition to vertebrates, sickness behaviours including lethargy and anorexia have also been described in insect hosts (Ayres & Schneider, ; Kazlauskas et al ., ; Sullivan et al ., ). However, in the current experiment it is not possible to disentangle the effect of an adaptive sickness behaviour from the direct effect of pathology caused by replicating DCV.…”

How and why do T cells and their derived cytokines affect the injured and healthy brain?

“…In 1988, Hart 81 first argued that sickness behaviour is not a maladaptive response to infection but rather a coordinated behavioural strategy to promote host survival. A more recent hypothesis attributes sickness behaviour to altruism and kin selection 82 ; that is, sickness behaviour provides an evolutionary advantage to survival of the herd 83,84 . Interestingly, it has been reported that, if the infected host does not elicit overt sickness behaviour, they may increase their propensity to aggregate 85 .…”

Peptidoglycan sensing by octopaminergic neurons modulates Drosophila oviposition

“…These phenotypes grouped under the term ‘behavioral immunity’ (de Roode and Lefèvre, 2012) or ‘sickness behavior’ (Hart, 1988) refer to a suite of neuronal mechanisms that allow organisms to detect the potential presence of disease-causing agents and to engage in behaviors which prevent contact with the invaders or reduce the consequences of the infection. Although such microbe-induced behavioral changes have been reported in Lepidoptera and Orthoptera, deciphering the molecular mechanisms involved is experimentally challenging in these insects (Sullivan et al, 2016; Kazlauskas et al, 2016; Adamo et al, 2007; Adamo, 2005). Indeed, such an analysis requires a model organism with genetic tools allowing the manipulation of actors and regulators of both the immune and neuronal systems.…”