Biology subjects

Tekade, K.

Publications and source records attributed to Tekade, K..

2 recordsLinked to original sources

bioRxiv2025

Dose- and outcome-dependent effects of bacterial infection on female fecundity in Drosophila melanogaster

The virulence of a pathogenic infection challenge can manifest in the form of increased host mortality rates and/or reduced host fecundity. Reduced fecundity in infected hosts can result from resource-allocation trade-offs: increased investment in immune defences depletes the common pool of resources, which are also required for reproduction. Alternatively, reduced fecundity may result from damage to host organs, especially reproductive organs, caused by the infection. We infected Drosophila melanogaster females with the bacterial pathogen Enterococcus faecalis at different infection doses and found that increasing the infection dose led to greater suppression of fecundity, without a corresponding increase in mortality rates. We further found that the reduction in host fecundity is contingent on the infection outcome (whether the host lives or dies after being infected), particularly in flies infected with a high dose of bacteria. Interestingly, survivors of the infection challenge had exhibited comparable fecundity irrespective of the dose used to infect them, whereas amongst females that died after infection, a higher infection dose led to a lower fecundity. We therefore propose that our results indicate that fecundity suppression in E. faecalis-infected females is likely caused by host organ damage rather than by diversion of limited resources towards immune function.

evolutionary biology↗

bioRxiv2024

Experimental evolution for improved post-infection survival selects for increased disease resistance in Drosophila melanogaster

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 two 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, existing theory postulates that these two strategies differ in terms of the conditions under which each strategy evolves in 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 post-infection survival. We experimentally evolved Drosophila melanogaster populations, selecting for the flies that survived an infection with the entomopathogen Enterococcus faecalis, and found that the host populations evolved increased disease resistance in response. This was despite the physiological costs associated with increased resistance. We did not find evidence of any change in disease tolerance in the host populations. We have therefore demonstrated that in an experimental evolution set-up, where insect hosts must survive an infection with a pathogenic bacterium, the hosts evolve improved disease resistance but not disease tolerance.

evolutionary biology↗