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Biophys J. 2017 Nov 7;113(9):2100-2109. doi: 10.1016/j.bpj.2017.09.001.

Structure, Mechanics, and Instability of Fibrin Clot Infected with Staphylococcus epidermidis.

Author information

1
Department of Chemical Engineering, University of Michigan, Ann Arbor, Michigan.
2
Department of Emergency Medicine, Michigan Center for Integrative Research in Critical Care, University of Michigan, Ann Arbor, Michigan; Department of Biomedical Engineering, Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan. Electronic address: mjsolo@umich.edu.
3
Department of Chemical Engineering, University of Michigan, Ann Arbor, Michigan; Department of Biomedical Engineering, Biointerfaces Institute, University of Michigan, Ann Arbor, Michigan. Electronic address: jvane@med.umich.edu.

Abstract

Health care-associated infection, over half of which can be attributed to indwelling medical devices, is a strong risk factor for thromboembolism. Although most experimental models of medical device infection draw upon isolated bacterial biofilms, in fact there is no infection without host protein contribution. Here we study, to our knowledge, a new model for medical device infection-that of an infected fibrin clot-and show that the common blood-borne pathogen Staphylococcus epidermidis influences this in vitro model of a blood clot mechanically and structurally on both microscopic and macroscopic scales. Bacteria present during clot formation produce a visibly disorganized microstructure that increases clot stiffness and triggers mechanical instability over time. Our results provide insight into the observed correlation between medical device infection and thromboembolism; the increase in model clot heterogeneity shows that S. epidermidis can rupture a fibrin clot. The resultant embolization of the infected clot can contribute to the systemic dissemination of the pathogen.

PMID:
29117532
PMCID:
PMC5685636
DOI:
10.1016/j.bpj.2017.09.001
[Indexed for MEDLINE]
Free PMC Article

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