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Quantifying Interhospital Patient Sharing as a Mechanism for Infectious Disease Spread
- Susan S. Huang, Taliser R. Avery, Yeohan Song, Kristen R. Elkins, Christopher C. Nguyen, Sandra K. Nutter, Alaka A. Nafday, Curtis J. Condon, Michael T. Chang, David Chrest, John Boos, Georgiy Bobashev, William Wheaton, Steven A. Frank, Richard Piatt, Marc Lipsitch, Robin M. Bush, Stephen Eubank, Donald S. Burke, Bruce Y. Lee
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- Journal:
- Infection Control & Hospital Epidemiology / Volume 31 / Issue 11 / November 2010
- Published online by Cambridge University Press:
- 02 January 2015, pp. 1160-1169
- Print publication:
- November 2010
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- Article
- Export citation
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Background.
Assessments of infectious disease spread in hospitals seldom account for interfacility patient sharing. This is particularly important for pathogens with prolonged incubation periods or carrier states.
Methods.We quantified patient sharing among all 32 hospitals in Orange County (OC), California, using hospital discharge data. Same-day transfers between hospitals were considered “direct” transfers, and events in which patients were shared between hospitals after an intervening stay at home or elsewhere were considered “indirect” patient-sharing events. We assessed the frequency of readmissions to another OC hospital within various time points from discharge and examined interhospital sharing of patients with Clostridium difficile infection.
Results.In 2005, OC hospitals had 319,918 admissions. Twenty-nine percent of patients were admitted at least twice, with a median interval between discharge and readmission of 53 days. Of the patients with 2 or more admissions, 75% were admitted to more than 1 hospital. Ninety-four percent of interhospital patient sharing occurred indirectly. When we used 10 shared patients as a measure of potential interhospital exposure, 6 (19%) of 32 hospitals “exposed” more than 50% of all OC hospitals within 6 months, and 17 (53%) exposed more than 50% within 12 months. Hospitals shared 1 or more patient with a median of 28 other hospitals. When we evaluated patients with C. difficile infection, 25% were readmitted within 12 weeks; 41% were readmitted to different hospitals, and less than 30% of these readmissions were direct transfers.
Conclusions.In a large metropolitan county, interhospital patient sharing was a potential avenue for transmission of infectious agents. Indirect sharing with an intervening stay at home or elsewhere composed the bulk of potential exposures and occurred unbeknownst to hospitals.
7 - Influenza Evolution
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- By Robin M. Bush, Department of Ecology and Evolutionary Biology, University of California, Irvine, Irvine, CA 92697, Nancy J. Cox, Influenza Branch, Centers for Disease Control & Prevention, Atlanta, GA 30333
- Edited by Krishna R. Dronamraju, Foundation for Genetic Research, Houston, Texas
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- Book:
- Infectious Disease and Host-Pathogen Evolution
- Published online:
- 10 August 2009
- Print publication:
- 05 April 2004, pp 175-197
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- Chapter
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Summary
THE VIRUS
The influenza viruses are classified in three genera of the family Orthomyxoviridae. The genera are referred to as “types” A, B, and C. The genome, about 14 KB in size, has eight single-stranded RNA segments of negative sense (seven segments in influenza C viruses). The influenza A genome encodes three polymerase proteins (PB1, PB2, and PA); two major surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA); three structural proteins (NP, M1, and M2); and two non-structural proteins involved in nuclear export (NS1 and NS2) (Lamb, 1989). An eleventh open reading frame recently discovered within PB1 appears to code for a protein involved in host cell apoptosis (Chen et al., 2001).
Two surface glycoproteins have been the object of most evolutionary studies of influenza. Hemagglutinin (HA) is involved in binding to host cell surface receptors. Neuraminidase (NA) is necessary for release of daughter virions from host cells. These proteins protrude from the viral envelope and are exposed to host immune defenses. While the HA is the primary target for neutralizing antibodies, antibodies against NA also may reduce occurrence and severity of illness, and possibly prevent infection if present at high titer. The hemagglutinin esterase (HE) in influenza C assumes the functions of both HA and NA. Broad reviews of influenza biology can be found in Murphy and Webster (1996) and Glezen and Couch (1997).
SUBTYPES
Considerable genetic diversity exists among avian influenza A viruses (Webster et al., 1992).