It is well known, that one stressor often renders the organism more sensitive to a second stressor thereby resulting in effects larger than the sum of the individual stressors. Recently, an increasing number of studies are reporting such synergistic effects on invertebrate survival after combined exposures to pesticides and pathogens. However, though the number of studies is increasing, investigations of the underlying mechanisms remain limited, and hence these are largely unknown. In the present project we aimed at quantifying the individual as well as interactive effects of host-pathogen, host-pesticide and host-pathogen-pesticide interactions and to identify the most important physiological mechanisms responsible for the interactions. We explored the well-described flour beetle model Tenebrio molitor, two groups of common natural insect pathogens: the entomopathogenic fungi Beauveria bassiana and the tapeworm Hymenolepis diminuta, and two pesticides each belonging to groups of widely used pesticides: the pyrethroid insecticide α-cypermethrin and the azole fungicide propiconazole. The stressors were chosen on the basis of their differences in infection strategies and toxicity, respectively. We hypothesized that the stress resulting from individual exposures as well as their combinations would show vastly different outcomes and give insight into the mechanisms at play during the combined stress. The project was divided into three PhD projects each seeking to answer a specific section of the described aim. The aim of the present thesis was to investigate effects of the individual stressors: α-cypermethrin, B. bassiana and H. diminuta; and the interactive effects of α-cypermethrin and B. bassiana on T. molitor survival, reproduction, detoxification and immune function. Already at the initiation of investigating host-pesticide interactions, our investigations revealed that degrading and/or inhibiting agents produced by T. molitor were released during sample preparation, destroying the cytochrome catalytic cycle and limiting the use of in vitro assays for quantification of enzymatic activities. We developed and optimized an ex vivo method exploiting viable gut tissue that is capable of quantifying the activity of the three major detoxification enzymes in invertebrates: cytochrome P450, esterases and glutathione-S-transferase. This method was used to investigate host response to α-cypermethrin both during single exposure and in combination with infection with B. bassiana. When T. molitor was exposed to α-cy permethrin, the production and/or activation of biotransforming enzymes was stimulated, resulting in faster clearance of the toxic compound. The stimulation of especially cytochrome P450 and esterase activity was important for limiting the damage caused by the toxin. Toxicokinetic modeling of the internal concentrations poorly explained the observed mortality (toxicodynamics) and indicated indirect effect of the exposure (paralysis and starvation) to be the main cause of death. The immune system of T. molitor showed no signs of being affected by α-cypermethrin. Infecting T. molitor with B. bassiana initiated the phenol oxidase cascade within 24 hours clearly indicating host recognition of the foreign intruder The infection further resulted in decreased reproduction and increased host mortality. To the contrary, H. diminuta infection did not elicit a rise in phenol oxidase and further prolonged the lifespan of the infected hosts. Using the concepts of Dynamic Energy Budgets (DEB), analyses suggested that the infection with B. bassiana alters the cost of reproduction, whereas the infection with H. diminuta reduces resource assimilation of the host, and thereby the production of reactive oxygen species (ROS). ROS are cytotoxic compounds that cause damage to e.g. cells and DNA and hence contributes to senescence. Combining chemical (α-cypermethrin) and pathogenic (B. bassiana) stress resulted in synergistic effects on mortality of T. molitor. Investigating the effect of the combined stressors on detoxification and immune response indicated a decrease in activity of biotransforming enzymes (especially esterases) during co-exposure. Further, a co-occurring (non-significant) increase in internal pesticide concentrations was observed 48 hours post exposure. A reduction in biotransformation and excretion of toxic chemical leads to an increase in duration and degree of exposure and hence may increase the toxic effects. Hence, whereas neonicotenoids and organophosphates are believed to interact directly with elements of the immune system, synergy between pyrethroids and pathogens is suggested be caused by alterations in biotransforming systems i.e. a suppression (or prevention of chemically induced up-regulation) of esterase activity. The course of action and whether the chemical or the pathogen triggered the suppression remains unknown. In conclusion, the results presented in the present thesis suggested that interactions between chemicals and pathogens and hence effects on host life history traits, are highly dependent on both the type of chemical and the pathogenicity of the infection. It was suggested that similar host immune responses result in similar synergistic potentials, rather than the synergistic potential being determined by the specificity of the pathogen/parasite species.