The natural environment of host organisms consists of several stress factors which vary from biotic (e.g. predators, pathogens) to abiotic (e.g. temperature, humidity, UVradiation, food). Pathogens and parasites utilize host resources for their own growth and development whereby they negatively affect the fitness of their host. The cost of infection to the host may encompass immune activation, change in host behavior, modification of host fitness parameters, life-history traits and increased risk of mortality of the host. However, hosts are often exposed to multiple stressors in their natural environment and it is therefore relevant to study the effects of combined exposures of pathogens or parasites with other stress factors. Use of anthropogenic stressors such as agro-chemicals increases the risk of exposure of non-target insects to toxic chemicals and the combination of these chemicals with pathogens or parasites might produce a larger effect than what can be predicted from studying their individual effect separately. Chemical toxicants not only interact with pathogens or parasites impact on host fitness but the combination may also alter disease severity as insects serve as host for a broad range of pathogens and parasites. Accordingly, besides toxic effects of agrochemicals, chemical stress can potentially change the disease dynamics of host-pathogen systems .The main aim of the present PhD project was to quantify the individual and interactive effects of the interactions of host-pathogen, chemical-pathogen, and pathogen-chemicalhost and study the mechanisms behind these interactions. A well-described model system was used; the flour beetle Tenebrio molitor and two of its natural pathogens and parasites: the tapeworm parasite Hymenolepis diminuta and the entomopathogenic fungus Beauveria bassiana. The widely used pyrethroid insecticide alpha-cypermethrin was included as the agro-chemical stressor. Besides this, the present study also aimed to further develop this model system to explore host-pathogen-chemical interactions at the level of the whole organisms. For developing the protocol for H. diminuta infection in T. molitor host, it was found that the establishment success of H. diminuta in the T. molitor host as cysticercoids is density-dependent. The establishment success is explained by a non-linear positive relationship within the range of ecologically relevant infection levels. Body condition of the host was found to play an important role in the successful establishment of cysticercoids because long-term starvation of T. molitor decreased the successful establishment of H. diminuta cysticercoids. Also, virgin female beetles showed higher establishment of cysticercoids than female beetles that were mated before infection. When T. molitor was exposed to infections by two organisms, H. diminuta and B. bassiana, with two contrasting host exploitation strategies, the effects on selected lifehistory traits were different. Exposure to low levels of the entomopathogenic fungus B. bassiana killed a proportion of the host population and the surviving host individuals showed a decrease in the offspring quantity (number), but an increase in the quality (size) compared to uninfected control population. Whereas H. diminuta infection was found not to affect offspring quantity and quality, a reduction in offspring number during the development of the parasite was observed. In addition, H. diminuta -exposed female T. molitor produced a significantly higher proportion of female offspring, while B. bassiana infection did not change offspring sex-ratio compared to uninfected control beetles. Trans-generational transmission of life-history traits (i.e. size and fecundity) from pathogen-infected parent female to offspring was not observed. Single or multiple exposures of the insecticide alpha-cypermethrin even at sub-lethal concentrations changed the H. diminuta infection level in T. molitor hosts. Alphacypermethrin exposure before H. diminuta infection decreased cysticercoid load, whereas exposure of alpha-cypermethrin immediately after infection increased the number of established cysticercoids. The interaction of the two stressors (H. diminuta and sequential sub-lethal exposure of alpha-cypermethrin) showed a synergistic effect on host mortality. The mechanism behind this synergy was not identified in this study as measured level of detoxification enzymes in T. molitor did not show any difference between H. diminuta infected, alpha-cypermethrin exposed and combination of these two. In conclusion, this model system proved to be useful for quantifying interactions between different stressors (pathogens, parasites and chemicals) at the whole organism level. The interactions between host and pathogens depends on the pathogen strategy of host exploitation, and the combination of two stressors (pathogen and chemical) can produce a higher effect than predicted from the knowledge of their individual effects. Also, these interactions not only affect the host life-history traits, but they can also increase or decrease the establishment success of the pathogens or parasites of the host, thereby affecting disease dynamics in natural host-pathogen systems.