These contrasting results suggest that when animals are stressed, living in large groups can be energetically disadvantageous, while when animals are not stressed living in groups is energetically beneficial. For example, nutrient availability under laboratory conditions could reduce cannibalism within nests affecting nest density, but this idea remains to be tested. In the present study we showed that living in large groups impacts on physiological condition of group members depending on the environmental conditions, presumably food availability. Despite energetic body condition being highly sensitive to group size, this was not the case for cuticular antifungal activity, which was not affected by nest density. The permanent pressure of pathogens on spider nests is likely to be responsible for the low plasticity of cuticular antifungal expression; if investment in Praeruptorin-B pathogen protection needs to be constant, it can explain why energetic condition is compromised if resources are scarce. Future studies should formally evaluate the physiological basis of a potential trade off between lipid reserves and cuticular antifungals, and evaluate the importance of protective defense in the evolution of sociality. The number of multidrug resistant bacteria has increased steadily over the past decades, and the associated problems gain more and more importance with regard to infections, especially in hospitalized patients. Every year the number of 6-gingerol patients dying from MRSA-infections in the US almost outnumbers those dying from AIDS, tuberculosis, and viral hepatitis combined. The consequence is not only an enormous rise of health care costs, but also a significantly higher mortality. Enterococci are currently the second most common cause of nosocomial infections in the US. In Europe, incidences of vancomycin-resistant enterococcal infections are increasing too. Enterococcus faecalis is the third most common cause of prosthetic valve endocarditis and despite steadily improved antibiotic strategies the incidence of bacterial endocarditis remained stable throughout the last 40 years. The ability to produce biofilm plays a crucial role in foreign body infections, such as prosthetic valve endocarditis. Nevertheless, the underlying mechanisms of biofilm formation and maintenance still need to be further investigated, especially in enterococcus where these mechanisms have not been studied as extensively as in staphylococci. Mutants of enterococcal strains with a reduced ability to produce biofilm have been studied previously by several investigators and in vivo bacteremia, endocarditis and urinary tract infection models could confirm the reduced pathogenicity of those strains. Our previous results demonstrated that elimination of glycolipid synthesis results in a reduced accumulation of biofilm mass rather than in impaired adherence itself. Adhesion of enterococci to colon carcinoma cell-line Caco2 was specifically inhibited by up to 47% through the addition of DGlcDAG, suggesting a role of glycolipids in cellular adherence to gastrointestinal epithelia. To assess if this mechanism is also operative in native valve endocarditis we compared theses mutants with the wild type strain using a rat endocarditis model.