Tracking a Killer: Disease Behavior and Epidemiology’s Detective Tools

Betsy Foxman

Hunein F. and Hilda Maassab Professor of Epidemiology, Director of the Center for Molecular and Clinical Epidemiology of Infectious Diseases

June 17, 2019

The unfolding of the AIDS epidemic in the early 1980s coincided with the start of my doctoral program. I first heard about Patient Zero during a seminar given by a CDC officer. We didn’t know then that AIDS was caused by HIV. We didn’t know if it was infectious at all. But by using basic epidemiologic methods, a CDC officer found strong evidence that this new condition—at the time called Gay Related Immunodeficiency Syndrome or even “gay cancer,” because it often led to Kaposi sarcoma—was sexually transmitted.

 The ability to use these methods to detect how something was transmitted—even before we knew what the organism was—really demonstrated to me the power of epidemiology.  Immediately following the presentation, several faculty began discussing the need for a longitudinal study to understand this condition better. That was essentially the beginning of the MACS cohort, which is still going today, 35 years later.

In this one seminar, my fellow graduate students and I experienced grassroots public health, where good science detects causal pathways and rapidly moves toward viable solutions because of human relationships imbued with a collaborative spirit.

You don't have to know an organism to track it or to identify risk factors.

This is one of the fundamental insights of epidemiology: Even if you don’t know what causes a disease, you can still track it and identify associated risk factors. With AIDS, for example, doctors had identified the syndrome; by using basic epidemiologic methods, epidemiologists were able to identify who was most likely to get AIDS and the types of behaviors that put people at highest risk.

 A classic example of this insight is the seminal work of John Snow, the father of modern epidemiology. In the mid-1800s, Dr. Snow conducted very detailed studies of cholera in London before anybody could detect the cholera-causing microbe. His evidence that cholera was caused by something related to sewer contamination in water was so strong that he was able to narrow down the cause of one outbreak to a single water source—the Broad Street pump—in one London neighborhood.

Public health professionals often have to make decisions based on imperfect information.

Even though there was much controversy at the time about whether germs caused disease, Dr. Snow eventually convinced officials to remove the handle on the Broad Street pump to prevent further cases of cholera. Similarly, before we had ever isolated HIV, we knew that engaging in sexual activity was strongly associated with getting AIDS. We knew how to start addressing the problem.

Something my department chair said at the Patient Zero seminar has stuck with me: “If we don't act now—when we are relatively sure that health education, condom distribution, and so on will help us—then, like any other sexually transmitted disease this syndrome is going to become a problem of the poor and other vulnerable populations.”

 He called out the whole confluence of sex and sexually transmitted disease, social stigma, and policy. The epidemic nature of HIV in Africa shows us that this disease’s success is not solely contingent on men having sex with men. It is about any kind of sex—and condom use can reduce transmission. We had an opportunity to save millions of lives, yet social stigma hindered the translation of scientific evidence to good public health policy.

Technology has advanced, but has human nature?

The recent Zika virus outbreak highlights some of the technological changes since the 1980s that have rapidly accelerated disease identification. Like AIDS, we first identified a syndrome, in this case microcephaly. But unlike AIDS, the microcephaly outbreak had followed the recent introduction of Zika virus to Brazil, suggesting Zika was the cause. It took less than a week to sequence the Zika virus, and shortly thereafter the epidemic was tracked in real time using nanopore sequencing technology—a relatively new, low-cost genotyping method that can be performed in the field. By contrast, AIDS was first reported in the US in 1981, HIV was identified in 1983, and a commercial test to screen the blood supply was licensed in 1985. The first full-genome sequence of HIV was produced in 1999.

It is truly a whole new ballgame and a very exciting time to be an epidemiologist. Our sequencing capabilities are so great that we can answer disease questions—recognition and association—at a speed we could only fantasize about at the start of the AIDS epidemic and unimaginable to John Snow in 1854. But as wonderful as these tools are, they provide a complement to rather than a replacement for the types of evidence uncovered by the basic epidemiologic investigations conducted by Dr. Snow and of Patient Zero. And as during the time of Dr. Snow, the decisions about when and how to act on these associations are often politically, rather than scientifically, driven.

There are several reasons for this, but I will highlight two. First, public health actions have unintended consequences. For example, recalling a food implicated in a foodborne outbreak hurts business. And if we are wrong, we risk losing public trust and support for public health activities. Second, public health actions can interfere with individual choices. In extreme cases, you can be confined to your house (quarantined!), because with infectious diseases, what seems like a personal choice has implications for everyone else. Mandatory measles vaccination of school children was an essential part of the successful elimination of measles from the Americas in 2011. And the increasing number of people challenging this mandate is why, as of May 2019, there have been more cases of measles in the US than in the previous four years combined.

I am excited about the implementation of new technologies into public health practice and research. The benefits are real. But they do not replace basic epidemiologic methods nor change the challenges faced when designing and implementing public health policy.

• Read about Betsy Foxman’s path to public health.
• Learn more about UM’s Integrated Training in Microbial Systems program.
• Support research at Michigan Public Health.

ABOUT THE AUTHOR

Dr. Betsy Foxman is the Hunein F. and Hilda Maassab Professor of Epidemiology, Director of the Center for Molecular and Clinical Epidemiology of Infectious Diseases (MAC-EPID), and Director of the Interdisciplinary Training Program in Infectious Diseases. She is also a faculty fellow in the Integrated Training in Microbial Systems (ITiMS) program at the University of Michigan. Foxman received her Bachelor of Science in Conservation of Natural Resources from the University of California, Berkeley, and MSPH and PhD in Epidemiology from the UCLA School of Public Health. Foxman studies the transmission, pathogenesis, ecology, and evolution of infectious agents with an emphasis on transmission. Current research projects include the role of oral and vaginal microbiota in pre-term birth, transmission of antibiotic resistance among E. coli and Group B Streptococcus, biofilm growth on medical devices, and the effectiveness of cranberries in preventing urinary tract infections.