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The mechanisms by which patients ill with brucellosis develop their characteristic symptoms of fever, chills, myalgia, asthenia and malaise have not been precisely elucidated. In particular, the contributions of the brucella cell itself to the pathogenesis of these clinical features have not been extensively investigated. An unusual clinical observation (1) suggested that some component of the cell did play a significant role. When patients seriously ill with brucellosis due to Brucella melitensis were treated with chlortetracycline, an unexpected abrupt febrile response often occurred within 8 to 12 hours after the initial dose of the antibiotic. These adverse reactions could be abolished or ameliorated by administering smaller initial doses of the antibiotic. Such effects suggested to the observers that, as a result of the antibrucella activity of the chlortetracycline, brucella cells were killed, thus liberating some cellular component which then produced the febrile response. This component was presumably the endotoxin of the cell.

STUDIES WITH BRUCELLA ENDOTOXIN IN HUMANS: THE SIGNIFICANCE OF SUSCEPTIBILITY TO ENDOTOXIN IN THE PATHOGENESIS OF BRUCELLOSIS