Tropism and Pathogenicity of Rickettsiae

Abstract

Rickettsiae are obligate intracellular parasitic bacteria that cause febrile exanthematous illnesses such as Rocky Mountain spotted fever, Mediterranean spotted fever, epidemic, and murine typhus, etc. Although the vector ranges of each Rickettsia species are rather restricted; i.e., ticks belonging to Arachnida and lice and fleas belonging to Insecta usually act as vectors for spotted fever group (SFG) and typhus group (TG) rickettsiae, respectively, it would be interesting to elucidate the mechanisms controlling the vector tropism of rickettsiae. This review discusses the factors determining the vector tropism of rickettsiae. In brief, the vector tropism of rickettsiae species is basically consistent with their tropism toward cultured tick and insect cells. The mechanisms responsible for rickettsiae pathogenicity are also described. Recently, genomic analyses of rickettsiae have revealed that they possess several genes that are homologous to those affecting the pathogenicity of other bacteria. Analyses comparing the genomes of pathogenic and non-pathogenic strains of rickettsiae have detected many factors that are related to rickettsial pathogenicity. It is also known that a reduction in the rickettsial genome has occurred during the course of its evolution. Interestingly, Rickettsia species with small genomes, such as Rickettsia prowazekii, are more pathogenic to humans than those with larger genomes. This review also examines the growth kinetics of pathogenic and non-pathogenic species of SFG rickettsiae (SFGR) in mammalian cells. The growth of non-pathogenic species is restricted in these cells, which is mediated, at least in part, by autophagy. The superinfection of non-pathogenic rickettsiae-infected cells with pathogenic rickettsiae results in an elevated yield of the non-pathogenic rickettsiae and the growth of the pathogenic rickettsiae. Autophagy is restricted in these cells. These results are discussed in this review.

“Rickettsia amblyommii” Induces Cross Protection Against Lethal Rocky Mountain Spotted Fever in a Guinea Pig Model

“…Agents belonging to the SFG are closely related phylogenetically but vary tremendously in regard to pathogenicity in humans. The endothelial tropism of the more pathogenic rickettsiae causes a cascade of events that can lead to vascular hyperpermeability, edema, intravascular volume depletion, hypoperfusion, resultant end organ damage (e.g., pneumonitis, encephalitis, acute kidney injury), and death (Uchiyama 2012). Rickettsia rickettsii is the agent responsible for Rocky Mountain spotted fever (RMSF), the most severe of the rickettsioses.…”

Proteínas transmembranales de organismos tipo rickettsia (OTR) en animales acuáticos: Factores de adherencia, invasión e infección

“…El mecanismo de infección de OTR hacia la célula huésped es usualmente conservado entre huéspedes pertenecientes a distintos grupos taxonómicos (Uchiyama 2012). El proceso de invasión inicia con la adhesión entre el receptor Ku70 de la célula huésped con el receptor bacteriano llamado antígeno de superficie celular 5 (Sca5), también conocido como OmpB (Chan et al 2009); posteriormente ocurre la adhesión de antígenos de superficie celular como Sca0 conocido también como OmpA, que participa en la adhesión e invasión celular y Sca1 que participa solamente en la adherencia de la célula huésped (Riley et al 2010).…”

“…La bacteria ya libre en el citosol, utiliza la proteína RicA y Sca2 para reclutar a la proteína Arp2/3 y polimerizar actina, con el fin de obtener motilidad dentro del citosol, logrando con ello poder trasladarse e invadir el núcleo celular o alguna célula vecina, donde podrá llevar a cabo su replicación por fisión binaria (tanto en la célula vecina, el citosol o el núcleo celular), para después lisar la membrana de la célula huésped gracias a la citotoxicidad producida por la bacteria con la ayuda de algunos efectores (Sec7, LepA, LepB y patatinas). La forma en que ocurre la lisis celular no se encuentra completamente dilucidada, por lo que es necesario realizar un mayor número de investigaciones (Uchiyama 2012).…”

Rickettsiosis transmitidas por garrapatas en las Américas: avances clínicos y epidemiológicos, y retos en el diagnóstico

“…En cuanto a la fisiopatología, las células endoteliales son el blanco donde invaden y proliferan estos microorganismos, a excepción de R. akari (tropismo por los macrófagos), causando daño endotelial directo asociado a liberación de citocinas proinflamatorias y estrés por oxidación, lo que lleva a un proceso de vasculitis de pequeños y medianos vasos, acompañado de extravasación de líquidos (2,38).…”