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MORTIMER RAPHAEL, M.D.; AUGUSTUS E. ANDERSON, M.D.

AMA Arch Intern Med. 1953;91(2):278-280.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

SINCE the discovery of Pasteurella tularensis by McCoy¹ in 1910 and the demonstration that it produces disease in man, as reported by Francis² in 1922, tularemia has been found masquerading in many forms. These have been classified as ulceroglandular, oculoglandular, glandular, and typhoidal; occasionally are added pleuropulmonary and oral-abdominal forms.

Initial pathologic changes occur at the site of inoculation of the organism, and a bacteremia soon follows. The organism then appears to have a predilection for lodging in the lungs, liver, spleen, and lymph nodes. Following the septicemia, neurological symptoms and signs may appear, the most frequent being nonspecific phenomena; i. e., delirium, stupor and restlessness. These have been attributed to the severe septic or toxic state induced by the organism. The next most frequent neurological complication is lymphocytic meningitis.³ Finally, there have been two reported cases of encephalitis.⁴ The case of tularemia reported here is unusual in that the . . . [Full Text PDF of this Article]

Author Affiliations
NEW ORLEANS

From the Medical Service, Veterans Administration Hospital, and the Department of Medicine, The Tulane University of Louisiana School of Medicine.

Footnotes
Reviewed in the Veterans Administration and published with the approval of the Chief Medical Director. The statements and conclusions published by the authors are the result of their own study and do not necessarily reflect the opinion or policy of the Veterans Administration.

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