Ultrastructural study of the response of cells infected in vitro with causative agent of spotted fever group rickettsiosis in Japan

Abstract

The response of host cells L929 infected with causative agent of spotted fever group (SFG) rickettsiosis in Japan, the Katayama strain, was studied by electron microscopy. The rickettsiae penetrated the cytoplasm and multiplied here and after prolonged incubation progressed into the dilated cisternae of rough endoplasmic reticulum (rER), the perinuclear space, the deep invaginated nuclear membrane, and then the nucleoplasm of the host cells. The intranuclear rickettsiae showed different states: one type was enclosed by the double membrane of the host cell and the other type was free in the nucleoplasm. In addition to these double membrane‐bound and membrane‐free intranuclear rickettsiae, various membrane structures, including rER‐like structures, were also found in the nucleus. The cells infected with the rickettsiae underwent distinctive morphological alterations which occurred mainly within intracellular membranes of the host cells. These findings indicate the possibility that the intracellular membranes are characteristic cytopathological sites in rickettsia‐host cell interaction, and that these alterations may be related to a possible route of rickettsial penetration into the nucleus: passage through vesicles formed from invaginations in the nuclear membrane.

Organelle targeting during bacterial infection: insights from Listeria

“…This has so far been primarily documented for endosymbionts such as the bacterial inhabitants of Paramecium macroand micronuclei [97] and the intra-mitochondrial bacterial species discovered in ticks, Candidatus Midichloria mitochondrii [3], and intranuclear growth has also been reported for a pathogen, the spotted fever agent Rickettsia rickettsii [98,99].…”

Rickettsial phospholipase A2 as a pathogenic mechanism in a model of cell injury by typhus and spotted fever group rickettsiae.

“…Ultrastructural demonstration of the entry of R. conorii and R. japonica via phagosomal vacuoles and lysis of the vacuolar membrane has been described previously. 17,18 The lack of significant evidence that escape of R. prowazekii or R. conorii from the phagosomal vacuole is reduced by inhibition of a rickettsial phospholipase A 2 suggests that phospholipase A 2 may not be the mechanism of phagosomal escape. However, it is conceivable that the population of rickettsiae that had gained entry into the host cell possessed a larger quantity of uninhibited phospholipase A 2 , enabling not only entry but also lysis of the phagosomal membrane.…”

Rickettsia japonica, the Etiologic Agent of Oriental Spotted Fever

“…Primary chicken embryo fibroblast culture, BHK21/13 and L929 cells allow R. japonica to grow with CPE. Ultrastructural studies of the response of cultured cells with SFG rickettsiae isolated in other laboratories have also been reported (1,32).…”