Thromb Haemost 2001; 86(03): 871-879
DOI: 10.1055/s-0037-1616145
Review Articles
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Hemostatic/Fibrinolytic Protein Changes in C3H/HeN Mice Infected with Rickettsia conorii

A Model for Rocky Mountain Spotted Fever
Alvin H. Schmaier
1   Departments of Internal Medicine and Pathology
,
Sujata Srikanth
1   Departments of Internal Medicine and Pathology
,
Tarek M. Elghetany
2   Department of Pathology, The University of Texas Medical Branch, Galvestson, TX, USA
,
Daniel Normolle
3   Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI
,
Sumita Gokhale
2   Department of Pathology, The University of Texas Medical Branch, Galvestson, TX, USA
,
Hui-Min Feng
2   Department of Pathology, The University of Texas Medical Branch, Galvestson, TX, USA
,
David H. Walker
2   Department of Pathology, The University of Texas Medical Branch, Galvestson, TX, USA
› Author Affiliations
Further Information

Publication History

Received 28 December 2000

Accepted after revision 02 April 2001

Publication Date:
14 December 2017 (online)

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Summary

Changes in plasma hemostatic and fibrinolytic proteins were determined during courses of a murine model of fatal and non-fatal Rocky Mountain spotted fever. C3H/HeN mice were infected with Rickettsia conorii and coagulation and histopathologic studies were performed at prescribed periods of time. A significant decrease in plasma factor VIII activity and rise in plasma factor V procoagulant activity correlated with a fatal infection. Factor VII levels were unchanged; factor XI levels dropped early in the course in the lethally infected animals, but returned to normal. Factor XII, high molecular weight kininogen, and prekallikrein levels were unchanged by the sublethal infection. Prekallikrein levels fell during the lethal infection. Antithrombin concentrations were decreased significantly in all animals, but plasma plasminogen levels did not change in either group of animals. Nonocclusive thrombi were microscopically observed rarely and only in animals surviving a sublethal infection. A fall in tissue plasminogen activator activity and a rise in plasminogen activator inhibitor activity highly correlated with a lethal outcome. Lethal infection with R. conorii is associated with primary endothelial cell injury resulting in decreased tissue plasminogen activator and increased plasminogen activator inhibitor.