IDSA 2011: Infectious Disease Epidemiology and Chronic Disease, Part II


Julie Parsonnet, MD, discussed well-established links between infectious disease and chronic disease and microorganisms disappearing from the human microbiome.

BOSTON, MA—In the first part of her lecture to the annual meeting of the Infectious Diseases Society of America, Julie Parsonnet, MD, professor of medicine at the Stanford University School of Medicine, argued that the relationship between infectious disease and chronic disease is far broader than generally recognized, but urged skepticism in the face of claims of specific links between the two. (To read our article on the first part of her speech, click here.)

Continuing with her speech, Parsonnet explained that Helicobacter pylori provides an example of a microorganism with well-established relationships to various chronic conditions. A pair of Australian scientists, Robin Warren and Barry Marshall, first posited that H. pylori caused peptic ulcers in the early 1980s, though their hypothesis was slow in winning acceptance. (Marshall went so far as to drink a culture of the organisms, after which he promptly developed gastritis; the pair won the Nobel in 2005.) Today, H. pylori has been shown to be related to four different diseases and has been linked to many other conditions, and not only in a negative sense. It is thought to cause iron-deficiency anemia, pancreatic cancer, atherosclerosis, and a number of other conditions, but to protect against esophageal adenoca, asthma, and GERD.

As H. pylori is just one among thousands of microorganisms that live in or on our bodies, Parsonnet asked the audience to consider how many other associations we might find once we look for them. Among the long list of types of associations being investigated between infection and chronic disease are: pressure on natural selection in host; infections causing direct damage to cells; localized inflammatory effects; systemic inflammatory effects; hit-and-run effects (e.g., cysticercosis can hit once and cause life-long epilepsy); endocrine effects; autoimmune phenomenon; immune switching or priming caused by infection; influence on metabolytes; and inheritance of a viral gene.

At the same time that we have been uncovering the relationship between microorganisms and chronic disease, many of these microorganisms have been disappearing from our bodies. H. pylori has almost entirely disappeared over the last century, as have tuberculosis, ear infections, rotavirus, Epstein-Barr virus, rheumatic fever, dysentery, and hepatitis A, B, and C. Though these all sound like positive steps, Parsonnet suggested that it was worth asking what happens to the human microbiome when a given microorganism is eliminated.

One area of particular interest is obesity rates, which have skyrocketed over the last 50 years or so, just as infectious disease rates have plummeted. As Parsonnet pointed out, acute infection reduces one’s caloric intake and increases one’s metabolic rate 12% for every degree Celsius increase in body temperature; a single day of measles can set one back 2000 calories. Of course, a more sedentary lifestyle and poor eating habits must play a role, but one of the reasons people were thinner in the past was the toll taken by tuberculosis and other infectious diseases—and one reason so many are overweight today is that we are not exposed to famine and pestilence as we were in the past.

As an epidemiologist, Parsonnet said that she recognizes how complicated it is to establish a causal relationship between infection and a complex phenomenon such as weight or chronic disease. However, as an infectious disease specialist, she said she is convinced that we are going to discover ever more extensive relationships between infectious disease and a range of chronic disease, from cancers to inflammatory conditions.

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