This week’s BEACON Researchers at Work blog post is by University of Idaho postdoc Silvia Smith.
Humans, like any other organism, impact their environment as their natural history unfolds. As the result of selection for increased brain size and improved cognitive abilities, we developed a variety of cultural adaptations, the most remarkable (both negatively or positively) being the domestication of animal and plants, starting about 10,000 years ago in the Fertile Crescent. This set of cultural adaptations spread across the sparse nomadic human populations, actually evolving independently in several locations, and resulted in the availability of a constant food supply, which in turn supported an increase in human population size and density. This major shift in subsistence patterns and our newly imposed selective pressures during the process of domestication have resulted in large-scale changes in the target animal and plant species, but also in our pathogens. In fact, as population density increased, so did the likelihood of sustaining and transmitting infectious disease, a shift described as the first epidemiological transition by Armelagos and colleagues (1996). The adoption of domestication also resulted in an increase in the human life span, which was accompanied by an increased likelihood of developing chronic disease; this is also known as the second epidemiological transition. Since the turn of the century, when antibiotic were first discovered, we have seen the emergence of multi-drug resistant pathogens. This is the result of rapid artificial (i.e., human-imposed) selection on organisms with short generation (or doubling) time like bacteria and viruses, and is referred to as the third epidemiological transition.
As a biological anthropologist interested in various aspects of human health and infectious disease, I conducted my dissertation work on the coevolutionary relationships that exist between mycobacteria (among which are the causative pathogens of tuberculosis) and their human host species. I subsequently took a postdoctoral fellowship at the University of Utah School of Medicine, where I employed evolutionary theory, molecular genetics, and systems biology methods and theory to study differential susceptibility to complex systemic disease affecting the eye.
Agar plate showing a culture of the human pathogen Acinetobacter baumannii ATCC 17978 with fluorescently tagged plasmid pB10::gfp. We use fluorescence as a proxy to detect the presence of multidrug-resistance plasmids. Acinetobacter is a remarkable medical concern as it is responsible for an increasingly high number of multi-drug resistant infections worldwide.
I am currently a Postdoctoral Research Scientist at the University of Idaho, Department of Biological Sciences and Institute for Bioinformatics and Evolutionary Studies, where I am fortunate to work with Dr. Eva Top on a project funded by the Department of Defense. The main goal of this project is to characterize the evolutionary pathways involved in the coevolution of broad-host-range (BHR) multi-drug resistance (MDR) plasmids and some of their human pathogenic bacterial host species. More specifically, we are interested in assessing if and how MDR plasmids can improve their persistence in biofilms formed by various Gram-negative bacteria, and compare their persistence patterns to those characterizing liquid bacterial cultures. It is in fact the spatially structured biofilm environment that characterizes bacterial infections in (war) wounds, and we postulate may promote the maintenance of MDR plasmids, and thus the persistence of drug resistance genes. This project involves both experimental bacterial evolution as well as genomics analyses of coevolved host-plasmid pairs, and is ongoing.
For more information about Silvia’s work, you can contact her at silvia dot anthro at gmail dot com.
