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Wed September 4, 2013
Dr. Dana Hawley, Virginia Tech – Why Diseases Evolve Increased Virulence
In today’s Academic Minute, Dr. Dana Hawley of Virginia Polytechnic Institute and State University explains why diseases evolve more virulent strains that pose a greater threat to the host.
Dana Hawley is an associate professor of biological sciences at Virginia Tech. Her research explores the ecological and evolutionary mechanisms that underlie pathogen susceptibility within and across ecological scales. Her current project seeks to link host ecology and behavior with changes in pathogen virulence. She earned her Ph.D. at Cornell University.
Dr. Dana Hawley, Virginia Tech – Why Disease Evolve Increased Virulence
Most of us have experienced a cold or flu so severe that we literally couldn't get out of bed. This is a key paradox for contagious pathogens: why make the very host you rely on for spread too sick to leave the house? It turns out that pathogens walk a fine balance: in order to spread, they must reproduce rapidly, generating enough self-copies to maximize the chances that at least a few of those copies end up on a nearby host.
But this rapid growth, while critical for spread, also causes the very symptoms that make hosts feel so sick that they are less likely to interact with others. Grow too slowly and you won't have the numbers; grow too rapidly, and your host may not leave the house or, in some cases, may even die, taking you with them.
We've been studying this balance in a common bacterial pathogen of songbirds called Mycoplasma gallisepticum, or MG for short. Using isolates of the pathogen that were frozen in time and space, we found that MG rapidly fine-tunes the outcome of this balance depending on how readily it can spread from finch to finch. Where there are high densities of finches, the pathogen can afford to grow rapidly and cause severe illness while still having a good chance of spreading. When finch densities are low, the pathogen causes only mild infection, presumably to ensure that its finch host feels sufficiently healthy to interact and spread the bug. We don't yet know how MG manages to alter its virulence so rapidly- in this case, over only about a decade. Although MG can't infect humans, it serves as a useful model for understanding why some pathogens cause more harm than others.