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Int J Infect Dis. 2008 Nov;12(6):660-70. doi: 10.1016/j.ijid.2008.03.009. Epub 2008 Jun 2.

The role of the innate immune response in hospital- versus community-acquired infection in febrile medical patients.

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Department of Intensive Care, Institute for Cardiovascular Research, Vrije Universiteit Medical Centre, De Boelelaan 1117, 1081 HV Amsterdam, the Netherlands.



To study the role of the innate immune response in the higher mortality of hospital- than of community-acquired infections, in febrile medical patients.


We studied presumably immunocompetent patients with new-onset fever and a clinically presumed focus of infection (N=212) at a university department of internal medicine. Clinical and microbiological data were collected for 2 days from inclusion, and circulating complement activation product C3a, secretory phospholipase A(2), interleukin (IL)-6, procalcitonin, and elastase-alpha(1)-antitrypsin were measured. Patients were followed for septic shock and outcome, up to a maximum of 7 and 28 days after inclusion, respectively. Infection was considered hospital-acquired if it developed at least 72h after admission.


Fifty-four patients had hospital-acquired infections and 158 had community-acquired infections, with septic shock and mortality rates of 15% and 24%, and 4% and 6% (p=0.001), respectively. Bloodstream infection predisposed to septic shock and the latter predisposed to death. Bloodstream infection was relatively more common in septic shock originating from community-acquired infection and was associated with an innate immune response in both hospital- and community-acquired infection, as judged from circulating immune variables. In contrast, circulating C3a, IL-6, and procalcitonin were more elevated when septic shock developed following hospital- than community-acquired infection, independent of infectious focus. The levels of C3a, secretory phospholipase A(2), IL-6, and elastase-alpha(1)-antitrypsin were more elevated in ultimate non-survivors than in survivors in both infection groups.


The data suggest that rates of septic shock and mortality from hospital- vs. community-acquired infections in febrile medical patients are not increased by impaired innate immunity. In contrast, proinflammatory factors may be particularly useful to predict a downhill course in hospital-acquired infections.

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