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Disease resistance (defined as the host capacity to limit systemic infection intensity) and disease tolerance (defined as the host capacity to limit infection-induced damage) are 2 complementary defense strategies that help the hosts maximize their survival and fitness when infected with pathogens and parasites. In addition to the underlying physiological mechanisms, the existing theory postulates that these 2 strategies differ in terms of the conditions under which each strategy evolves in the host populations, their evolutionary dynamics, and the ecological and epidemiological consequences of their evolution. Here, we explored if one or both of these strategies evolve when host populations are subjected to selection for increased postinfection survival. We experimentally evolved Drosophila melanogaster populations, selecting for the flies that survived an infection with the entomopathogen Enterococcus faecalis. We found that the host populations evolved increased disease resistance in response to selection for increased survival. This was despite the physiological costs associated with increased resistance, the expression of which varied with the phase of infection. We did not find evidence of any change in disease tolerance in the evolved host populations. [ABSTRACT FROM AUTHOR]

This article explores the relationship between antibiotic resistance mutations and their fitness benefits in different contexts. It emphasizes that the expression of traits is influenced by both genetic factors and the environment. The study specifically focuses on rifampicin-resistant Escherichia coli mutants and shows that the level of resistance to rifampicin can vary depending on the conditions of the experiment. The authors caution against making broad generalizations about antibiotic resistance and stress the importance of considering the environment when studying and addressing antimicrobial resistance. The article includes a list of references covering various aspects of antibiotic resistance, including the evolution of antibiotic treatment for tuberculosis, the role of genotype-by-environment interactions in shaping resistance, the limitations of certain metrics for measuring antibiotic response, and the significance of understanding the infectious microenvironment. These references provide diverse perspectives on antibiotic resistance and highlight the need for further research in this field. [Extracted from the article]