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May 2010  |  Return to issue home

Sepsis and Public Health: A New Perspective

By Jerry Kim, Institute for Public Health Genetics

Jerry Kim

Jerry Kim

As a candidate in the master of public health program of the Institute for Public Health Genetics, I am studying a problem that does not evoke the image of the prototypical public health disease: sepsis. However, sepsis is not only important in its impact on national health; it is also related to more familiar issues of public health, including the control of transmittable infections within communities.

Sepsis is a medical condition involving a whole-body response to a severe infection. A common type of initiating infection is bacterial pneumonia, but the infection can be caused by other organisms and start in any part of the body. If the infection is not cleared immediately, it may spread to the bloodstream or other organs and cause the generalized inflammatory reaction known as sepsis. Sepsis is the tenth leading cause of death among all Americans and third among hospitalized patients, and as many as half of severe cases of sepsis, which involve organ failure, are fatal. Despite these startling statistics, many in the public are not aware of this important medical problem.

With the exception of resistant strains of bacteria (another distinct problem), the bacterium itself does not kill people in cases of sepsis. Rather, the culprit is the body’s inflammatory reaction to the bacteria: a release of chemicals that can alter blood and oxygen delivery to organs. Thus far, attempts to block these chemicals in clinical trials have not been successful. It is not well known why some patients progress from infection to sepsis to organ failure while others in apparently the same circumstances recover without difficulty, but research in the last decade has shown that a patient’s innate immune system and inflammatory system play key roles in this process. And ultimately, the genes that code for the proteins and receptors involved in these systems influence the body’s ability to recognize and react to infection.

My research is focused on two related areas. First, I am seeking to identify genes that are associated with the development of sepsis in infants and children. To do so, gene variants from both parents and children with sepsis are tested to see which ones are associated and which are not. The results from this study will allow a better understanding of the involvement of immune system genes and help identify those children at greatest risk of death.

Second, I want to evaluate the effectiveness of the current process of enrolling families in similar genetic research studies. There are some important questions underlying this issue: what are parents’ motivations for involving their children in genetic research? Does the current process of informing and gaining consent from parents truly help them understand the research being conducted?

I hope my research will help us to understand the genes influencing sepsis, a major cause of death in the U.S., and to improve the conduct of genetic research for the benefit of both participants and medical science.

May 2010  |  Return to issue home

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