Pesticides and pathogens are two categories of environmental stressors that may contribute to the decline of honey bee populations (vanEngelsdorp and Meixner, 2010). However, if their separate impacts on the honey bee are relatively well studied, knowledge on their interactions are somewhat lacking. Pioneer studies on toxico-pathological interactions have been conducted on the association of Nosema and chronic bee paralysis virus (CBPV) with organophosphate, organochlorine and pyrethroid insecticides (Ladas, 1972; Bendahou et al., 1997). These studies focused on the acute exposure to insecticides regardless of their chronic toxicity. However, the introduction of systemic insecticides, such as phenylpyrazoles and neonicotinoids in the mid 1990’s renders more relevant the studies on chronic exposures to pesticides by oral route.
A new laboratory approach to study the chronic toxicity of insecticide has offered the possibility to explore the interactions between pathogens and pesticides during chronic exposures (Suchail et al., 2001). Studies on the joint exposure to Nosema and systemic insecticides have revealed that toxico-pathological interactions may elicit damaging effects on the bees, even when both stressors have no or limited effects on bee mortality (Alaux et al., 2010; Vidau et al., 2011). Two approaches have been used to study the effects of pesticide-pathogen associations. The first carries out simultaneous exposures to the pathogen and the pesticide and is particularly suitable to reveal antagonistic, additive and synergistic effects (Alaux et al., 2010). The second involves sequential exposures to the pathogen and the pesticide and is particularly relevant to investigate the sensitization to one stressor by another (Vidau et al., 2011; Aufauvre et al., 2012).
The toxico-pathological interactions have been observed in laboratory conditions but the few attempts to demonstrate them in field conditions were not always as successful as expected (Wehling et al., 2009; Pettis et al., 2012). However, workers reared in brood frames containing high levels of pesticide residues exhibited a higher sensitivity to Nosema infection (Wu et al., 2012). Hence, since such interactions were observed for humans and other species in their living environment, there is no reason to think that they do not occur in field conditions (Arkoosh et al., 1998; Lewis et al., 2002, Bauer et al., 2012). Thus, in many cases, colony diseases could have been triggered by pollutants in healthy carriers.