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. 1988 Dec;19(12):1449-54.
doi: 10.1016/s0046-8177(88)80238-7.

Pathogenesis of rickettsial eschars: the tache noire of boutonneuse fever

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Pathogenesis of rickettsial eschars: the tache noire of boutonneuse fever

D H Walker et al. Hum Pathol. 1988 Dec.

Abstract

Prospective investigation of cutaneous lesions of 24 Sicilian patients revealed that 17 were taches noires from patients with a documented diagnosis of boutonneuse fever. Immunofluorescent Rickettsia conorii were demonstrated in 14 of 17 taches noires. The major pathologic lesions observed were a moderate-to-severe lymphohistiocytic vasculitis (17 of 17 cases), generally moderate dermal edema (17 of 17 cases), and cutaneous necrosis (12 of 16 cases). In contrast with previous observations of eschars in Rocky Mountain spotted fever, thrombosis was usually absent (nine of 17 cases) or inconsequential (five of 17 cases). Thus, it appears that the pathogenic mechanism of the ischemic necrosis is not thrombosis, suggesting either compression of the microcirculation by the dermal edema or another mechanism. Review of the biomedical literature related to eschars and cutaneous arthropod bites strongly argues against a pathogenetic contribution of the tick bite itself other than the intradermal inoculation of rickettsiae. The tache noire offers an excellent, accessible model for the study of the human-rickettsia interaction, including the pathogenic mechanisms leading to necrosis and the immune mechanisms resulting in killing the rickettsiae.

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