We aim to understand how different reproductive strategies affect drug resistance evolution in bacteria, fungi, and helminths. We want to take advantage of the generality of the evolutionary process while still accommodating important differences between the studied organisms. Therefore, we will develop a modular model that can be tailored to individual species (1).  

In parallel,  we will extract, collect and catalogue as many relevant pharmacokinetic and pharmacodynamic data as possible  (2). This will allow us to map the landscape of known pharmacodynamic parameter values, pointing out gaps and investigating overlaps. The mined data will be analyzed for trends and patterns, exploring their distributions and ranges, which will help us to come up with reasonable estimates of values that are yet unavailable  (2).

Combining the modular model with a large amount of pharmacodynamic data will allow us to model concrete species, investigate specific scenarios, and shed light on the importance of reproductive strategy, ploidy, and lifestyle} in the studied taxa (3). In collaboration with empirical biologists studying these taxa, we will develop testable hypotheses and develop predictions that can be verified experimentally.

In addition, we will review the literature, identifying temporal and spatial trends and patterns in drug resistance evolution in the studied taxa (4). If there are any differences in the observed trends between species, we will investigate whether these can be at least partially explained by the differences in reproductive strategy and associated aspects, e.g., ploidy or lifestyle.