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Abstract: Pathogenic rickettsiae of the spotted fever group (SFG) induce skin lesions called “eschars” at the sites of arthropod bites. We recently described a guinea pig model based on eschar formation to predict the eventual pathogenicity of new Rickettsia species, and in this study, we used the model to study cross-protection among SFG Rickettsia species and subspecies. We showed that the intradermal inoculation of guinea pigs with Rickettsia conorii subsp. conorii significantly reduced, but not completely prevented, the number of eschars after sub-challenges with the same pathogen (P =0.0004). The same effect was also observed for other subspecies of the R. conorii complex. Additionally, the bacterial load in the eschars was significantly lower in immunized animals than in naïve animals. No protection was observed when sub-challenges were performed with other Rickettsia species, such as R. africae, R. sibirica subsp. mongolitimonae, R. aeschlimannii and R. massiliae. Our data suggest that patients may experience several episodes of infection with related or with the same species of Rickettsia. Moreover, the absence of cross-protection between Rickettsia species may explain the co-existence of two or more tick-borne rickettsioses in the same geographic areas. [Copyright &y& Elsevier]

To determine the usefulness of noninvasive cutaneous swab specimens for detecting rickettsiae, we tested skin eschars from 6 guinea pigs and from 9 humans. Specimens from eschars in guinea pigs were positive for rickettsiae as long as lesions were present. Optimal storage temperature for specimens was 4°C for 3 days. [ABSTRACT FROM AUTHOR]

Abstract: Until now, when a new Rickettsia species was isolated in a tick, it was not possible to predict whether it was a human pathogen or if it would cause a skin eschar at the infection site. Guinea pigs are injected intradermally with 25 different Rickettsia species or subspecies: 16 induced an eschar, 5 induced inflammatory lesions and 4 have no effect. We observed that the occurrence of skin eschars in this model was significantly correlated (P <0.05) with observations of skin eschars in humans (14/16). The most common histological finding was mononuclear cell infiltration. Polymorphonuclear cell infiltration was observed for Rickettsia australis, Rickettsia japonica, and, as in humans, Rickettsia africae. The treatment of guinea pigs with corticosteroids prevents the apparition of eschar following Rickettsia bellii inoculation. Virulent, but not avirulent, Rickettsia prowazekii induced transient inflammatory lesions that were associated with dermal vasculitis, as is Rickettsia typhi. Therefore, the intradermal injection of Rickettsia in guinea pigs appears to be a relevant model for the prediction of the development of escharotic lesions following Rickettsia infection in humans. We speculate that skin eschar is the reflect of a local control avoiding extreme virulence. [Copyright &y& Elsevier]