Camilo Barbosa, Dr. rer. nat.
University of Michigan, Ann Arbor
from September to December 2022
Born in 1988 in Bogotá
Studied Evolutionary Biology at Kiel University (CAU) and the Max Planck Institute for Evolutionary Biology
John Maynard Smith Prize-Fellow
Population Genetic Determinants of Antibiotic Resistance Evolution in the ClinicWe live in a bacterial world. For billions of years, bacteria have been thriving in our world, adapting, and diversifying in a myriad of environments. They now play a pivotal role in the environment, forming intricate relationships with all sorts of living beings, including humans. In fact, our bodies harbor, on average, as many bacterial as human cells. While most of our interactions with “our” bacterial cells (microbiome) are positive and necessary, there are often cases in which opportunistic bacteria can bypass our innate natural defenses and cause harm. The latter is further aggravated when these opportunistic bacteria find ways to evade and counteract the effects of the chemical defenses we use against them, antibiotics. Better understanding the process by which bacteria evolve resistance against antibiotics has been the central aim of my scientific career.
The main hypothesis of my long-term project stems from the observation that antibiotic resistance evolution is pervasive but somehow limited – why does resistance evolve in some but not all cases, despite bacteria being exposed to similar selective pressures? To approximate this question, I aim to quantify the capacity of pathogens to generate genetic diversity within a population. Bacteria can typically achieve this in one of two ways. The first one is the driving force of diversity and evolution, mutation. In large populations, mutations arise with the potential to confer an advantage to better survive in a given environment. If the intrinsic capacity of a population to generate mutations is high, then that population has a higher likelihood of adapting faster. The second mechanism is bacteria’s ability to acquire foreign genetic material, a process known as horizontal gene transfer (HGT). Through HGT, bacteria essentially amplify their genetic capacity by incorporating genetic elements into their own genome. These genetic elements often include genes that confer resistance to antibiotics, and whether a population can acquire, sustain, and exploit these elements can have a dramatic impact on how bacteria adapt to antibacterial treatments. Ultimately, I aim to better understand and quantify how mutation and HGT determine the likelihood of evolving resistance in genetically close, but distinct bacterial populations.
Barbosa, Camilo, Vincent Trebosc, Christian Kemmer, Philip Rosenstiel, Robert Beardmore, Hinrich Schulenburg, and Gunther Jansen (2017). “Alternative Evolutionary Paths to Bacterial Antibiotic Resistance Cause Distinct Collateral Effects.” Molecular Biology and Evolution 34: 2229–2244. https://doi.org/10.1093/molbev/msx158.
Barbosa, Camilo, Roderich Römhild, Philip Rosenstiel, and Hinrich Schulenburg (2019). “Evolutionary Stability of Collateral Sensitivity to Antibiotics in the Model Pathogen Pseudomonas aeruginosa.” eLife 8: e51481. https://doi.org/10.7554/eLife.51481.
Zhou, Shiwei, Camilo Barbosa, and Robert J. Woods (2020). “Why Is Preventing Antibiotic Resistance So Hard? Analysis of Failed Resistance Management.” Evolution, Medicine, and Public Health 2020: 102–108. https://doi.org/10.1093/emph/eoaa020.