Escara nos sítios de fixação do carrapato Amblyomma ovale: morfologia das lesões infectadas e não infectadas por Rickettsia parkeri

• Ano de defesa: 2020
• Autor(a) principal: Rodrigues, Alessandra Castro
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Uberlândia; Brasil; Programa de Pós-graduação em Imunologia e Parasitologia Aplicadas
• Palavras-chave em Português: Rickettsia; Escara; Parkeri; Rickettsia parkeri; Eschar; Brazil; Lesions; Amblyomma ovale; CNPQ::CIENCIAS BIOLOGICAS; Imunologia; Carrapatos como transmissores de doenças
• Link de acesso: https://repositorio.ufu.br/handle/123456789/32437; http://doi.org/10.14393/ufu.di.2020.426

Two well characterized tick-borne rickettsiosis occur in Brazil. Rickettsia rickettsii caused spotted-fever is a severe disease with a high case-fatality rate in the southeastern region of the country whereas Rickettsia parkeri strain Atlantic rainforest (ARF) infections transmitted by adult Amblyomma ovale ticks cause a milder non-lethal febrile disease with eschar (necrosis) at tick-bite site. In Brazil, such eschar is considered the main clinical feature of mild R. parkeri infection and used to differentiate it from severe R. rickettsii infection. However, knowledge on the pathogenesis of eschar and its clear relationship with R. parkeri ARF is lacking. We herein evaluated gross and histopathology of skin lesions of guinea pigs caused by R. parkeri ARF infected or uninfected A. ovale parasitism sites as well as skin lesions of needle inoculated Rickettsia. Lesions were also evaluated in guinea pigs undergoing first tick infestation (tick-bite naïve) and on those sensitized by previous infestations or R. parkeri infections (immunized). Gross examination revealed that after detachment of infected and uninfected ticks and Rickettsia needle inoculation all animals developed skin hyperemia and induration. Necrosis, however, was lacking from needle inoculated animals and was much larger at skin sites where ticks detached after a second or third tick infestation. This observation shows that an immune response to ticks is at the basis of necrosis pathogenesis. Histopathology revealed that vasculitis and slight intravascular fibrin aggregates were an inconspicuous feature of both infected or uninfected tick attachment sites and absent at Rickettsia needle inoculation sites. Nevertheless, Rickettsia infection enhanced and extended over time focal necrosis at tick attachment sites as well as increased focal inflammatory infiltrate at the dermis-hypodermis interface. These results indicate that eschar in guinea pigs exposed to infected A. ovale ticks are caused rather by tick-bite of previously tick-bite sensitized animals and that concomitant Rickettsia infection may increases such lesion under microscopic evaluation at least. Nonetheless eschar may be used as a tick-bite sign and eventually Rickettsia inoculation site. Therefore, febrile diseases with eschars still need laboratory confirmation of Rickettsia infection. Additional studies are needed to reveal eschar physiopathology and related morphology in other hosts and Rickettsia species and strains.