My sophomore year at Loyola University Chicago, I took an Evolution of Human Disease course with paleopathologist Anne Grauer, PhD. Her class served as an in depth introduction into the evolution of the Mycobacterium family, and why m. Tuberculosis (Mtb) is such a fascinating yet complex bacterium to study. For some initial context, Mtb is a bacteria that can cause the tuberculosis (Tb). It is transmitted when a healthy individual inhales a cough droplet from an infected Tb individual. The bacteria typically lodges itself within the lungs, causing numerous respiratory symptoms that left untreated are fatal. It is a major global health concern because it can become resistant to life saving antibiotics.
From an evolutionary perspective, Mtb evolved to persist in a wide spectrum of environmental conditions. It can lay low in healthy individuals for years, and if a person eventually becomes immunocompromised, it can trigger rapid growth causing Tb. This is due to its incredibly slow growth rate. On the other hand, Mtb can adapt to its current conditions by mutating against antibiotics necessary to treat it. Mtb should not be able to do the latter given its slow growth rate. This is why some consider it “an extraordinary bacteria”. It has successfully co-evolved with humans pointing to its remarkable adaptability in any given environment.
This insight was why I jumped at the opportunity to apply to the Institute for Public Health Summer Research Program – Public & Global Health Track and, despite having minimal microbiology knowledge, I am pleased to work in the mycobacterium lab of Professor Christina Stalling, PhD.
My initial goal was to connect my evolutionary based understanding of Mtb to microbiology. I have always been fond of connecting details together to to create a bigger picture. Those details being Mtb evolution and microbiology lab work and the bigger picture being tuberculosis as a major global health concern. I wanted to understand at a molecular level why Mtb was exceptional at evading antibiotics. To put it another way, as Dr. Grauer had said on numerous occasions “why is it such a smart bacteria?” I wish I had an answer.
What I’m finding is that there are a lot of theories but much of the work revolves around figuring out how the bacteria works. What I mean is that there are many systems in Mtb that either promote growth of the bacteria, or virulence (referring to its ability to infect). Often times, microbiologists know what systems and genes are involved but they are unaware of how that system works or what a gene is acting on. This has made meeting my primary goal difficult, and to be honest I am more confused finishing this program than when I arrived. But I do not view this as a negative because working in the Stallings Lab at Washington University in St. Louis has shown me how complex and fascinating Mtb is.
I have made one major connection: Given Dr. Grauer’s evolutionary perspective on Mtb, it has historically adapted very well to many environments. Therefore, it is not shocking to me that microbiologists are having an incredibly difficult time finding a universal answer to solving the tuberculosis pandemic.
Visit: https://infectious-diseases-conferences.pencis.com/
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