Human Genetics and Human Sepsis: Is the Tail Wagging the Dog

  • D. Burgner
  • M. Levin
Conference paper

Abstract

In almost every area of clinical practice, individuals respond very differently to the same infectious pathogen. Although humans are repeatedly exposed to potentially life-threatening pathogens, only a minority will succumb to clinical infection and fewer still will die from sepsis. Infectious complications often seen in intensive care, such as septic shock following intestinal perforation or ventilator-associated pneumonia (YAP) occur only in a minority of those potentially at risk [1]. Outside the hospital setting, the inter-individual differences in susceptibility and outcome when confronted with a potentially lethal infection are more dramatic still. This is especially true in children, who globally bear most of the infectious disease burden. For example, an estimated two thirds of the world’s population is infected with Mycobacterium tuberculosis, but the lifetime risk of succumbing to clinically apparent disease is thought to be about one in ten. Of the estimated 500-million falciparum malaria infections per year, only about 20% are symptomatic and the overall mortality is probably only 1–2%. Approximately 10% of people carry Neisseria meningitidis in their nasopharynx, yet only 1 in 40 000 develop invasive meningococcal disease. What factors determine why one individual develops a life-threatening infection, while another carries the same organism as a harmless commensal, or limits the infection to a clinically trivial episode?

Keywords

Human Leukocyte Antigen Cerebral Malaria Human Leukocyte Antigen Class Meningococcal Disease Mannose Binding Lectin 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 2003

Authors and Affiliations

  • D. Burgner
  • M. Levin

There are no affiliations available

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