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Acute Febrile Cerebrovasculitis: A Syndrome of Unknown, Perhaps Rickettsial, Cause

RICHARD P. WENZEL, M.D.; FREDERICK G. HAYDEN, M.D.; DIETER H. M. GRÖSCHEL, M.D.; ROBERT A. SALATA, M.D.; W. SCOTT YOUNG, M.D., Ph.D.; JOHN E. GREENLEE, M.D.; STEVEN NEWMAN, M.D.; PATTI J. MILLER, M.S.; KARIM E. HECHEMY, Ph.D.; WILLY BURGDORFER, Ph.D.; MARIUS G. PEACOCK, M.S.; and LUCIEN J. RUBINSTEIN, M.D.
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▸Requests for reprints should be addressed to Richard P. Wenzel, M.D.; Box 473, University of Virginia Medical Center; Charlottesville, VA 22908.


Charlottesville, Virginia; Albany, New York; and Hamilton, Montana


© 1986 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1986;104(5):606-615. doi:10.7326/0003-4819-104-5-606
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In late 1983, five patients living near Charlottesville, Virginia, were treated for an unusual syndrome of fever, headache, altered mentation, multifocal neurologic signs, and cerebrospinal fluid pleocytosis. Clinical signs of brainstem disease developed in four patients. All five had had recent exposure to forests or wood and contact with flea-infested dogs. Two patients died; one survivor has had recurrent seizures. Brain biopsy samples in two patients and autopsy findings in another showed cerebral vasculitis and perivasculitis involving mostly venules and capillaries. In the autopsy, the severest vascular lesions involved the brainstem and thalami, where they were accompanied by acute fibrinoid necrosis, but discrete vascular lesions of lesser intensity were randomly distributed in the white matter and cortex. Serologic studies on paired specimens in four patients showed significant cross-reacting antibody responses to rickettsial (typhus-group) antigens in the indirect hemagglutination, latex agglutination, and IgM microimmunofluorescence tests, but no agent was visualized or isolated. The cause of this serious inflammatory disorder is unknown.

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