Assistant Professor, Epidemiology
Dr. Mathema studies infectious disease epidemiology by considering multiple dimensions of transmission. He has led the design, analysis, and management of molecular epidemiologic studies in New York, China, and at various sites in South Africa, and teaches master’s students to appreciate the broadest possible context—scientific, economic, cultural—for understanding infectious diseases.
We talk about epidemiology as the core science of public health. Why is that the case?
Epidemiology affords the possibility to take disparate fields and view them with a common lens. That’s why I didn’t pursue molecular biology or immunology, which are fascinating areas of study. Epidemiology observes the interface of evolution, biology, society, and more, to get at the underpinnings of disease. Of course, scientists in every field care deeply about making the population healthier. But epidemiology can take drug discoveries and evolutionary biology and more, and fuse them together to understand the determinants of good health.
You teach a course on tuberculosis. How can there be anything left to know about a disease that’s been around for more than a century?
TB is embedded in the DNA of modern science and social politics and art. In our course, “Tuberculosis Epidemiology and Control,” we consider all aspects of TB, from the molecular genetics to the clinical, from its history to patient advocacy to new research. The study of TB can be instructive to understanding public health. First of all, its discovery gave birth to germ theory—the idea that we can isolate a pathogen, introduce it to a healthy host, produce the same illness, and monitor the disease trajectory. Dating to 1882—March 24, as a matter of fact, World TB Day—TB gave us the first proof scientists ever had that A causes B. Before that, TB was considered the result of miasma theory or poor moral character. You can imagine the implications from that discovery, still rippling through public health today.
TB taught us something about advocacy as well. To explain, I’ll be a historian again. In the 19th century, everyone who was anyone had TB—from Chopin to Chekhov to Modigliani to Camus. The creative fervor thought to sustain artistic genius made it a sought-after condition. Think of Mimi in “La Bohème” or Keats in Rome, scribbling feverishly until the end. Today we seldom have the kind of patient population that drives public, political, and scientific interest, although with HIV we have come close. You start to see it in a lot of HIV/AIDS literature, and with that other Mimi, in “Rent.” Humanity runs cyclically, doesn’t it?
So what’s left to be known about TB? What are you looking at in your research?
There’s a global disconnect with TB. We have an effective cure, yet two million people die each year. If you think about who those two million people are, you begin to see part of the answer.
Remember, the pathogen, M. tuberculosis is necessary but not sufficient for the disease. What factors lead to illness? At Mailman, people study chronic disease in such innovative ways. They look at the cultural, the spatial, the political, the historical dimensions of a disease, all of which are vital to understanding. In a way, infectious disease, which has focused for so long on disease etiology, missed this memo. Finally that kind of thinking—modern epidemiology, mind you—is entering the study of infectious disease and it’s mindboggling. Now I interact with mathematical modelers, demographers, and a crew of immunologists, molecular biologists, and population geneticists to study how a mix of attributes of pathogen, host, and risk factors coalesce to drive TB epidemics. We need to understand the full measure of that complexity to be able to address them.