@article{fdi:010046347,
  title = {{P}rediction of rickettsial skin eschars in humans using an experimental guinea pig model},
  author = {{L}a {S}cola, {B}. and {B}echah, {Y}. and {L}epidi, {H}. and {R}aoult, {D}idier},
  editor = {},
  language = {{ENG}},
  abstract = {{U}ntil now, when a new {R}ickettsia 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. {G}uinea pigs are injected intradermally with 25 different {R}ickettsia species or subspecies: 16 induced an eschar, 5 induced inflammatory lesions and 4 have no effect. {W}e 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). {T}he most common histological finding was mononuclear cell infiltration. {P}olymorphonuclear cell infiltration was observed for {R}ickettsia australis, {R}ickettsia japonica, and, as in humans, {R}ickettsia africae. {T}he treatment of guinea pigs with corticosteroids prevents the apparition of eschar following {R}ickettsia bellii inoculation. {V}irulent, but not avirulent, {R}ickettsia prowazekii induced transient inflammatory lesions that were associated with dermal vasculitis, as is {R}ickettsia typhi. {T}herefore, the intradermal injection of {R}ickettsia in guinea pigs appears to be a relevant model for the prediction of the development of escharotic lesions following {R}ickettsia infection in humans. {W}e speculate that skin eschar is the reflect of a local control avoiding extreme virulence.},
  keywords = {{R}ickettsia ; {E}merging rickettsiosis ; {E}schar},
  booktitle = {},
  journal = {{M}icrobial {P}athogenesis},
  volume = {47},
  numero = {3},
  pages = {128--133},
  ISSN = {0882-4010},
  year = {2009},
  DOI = {10.1016/j.micpath.2009.06.004},
  URL = {https://www.documentation.ird.fr/hor/fdi:010046347},
}