Tissue culture cells of human origin (HeLa, Lich, and AV3) were inoculated with the AL complex. By immunofluorescent staining, AL complex antigen was detectable in the cytoplasm of infected cells as punctate fluorescent granules during the early stage and as homogeneous fluorescence during the late stage of infection. By combining fluorescence and phase-contrast microscopy, many infected cells with cytoplasmic AL complex antigen were shown to have a normal nuclear morphology indistinguishable from uninfected cells. Initiation of AL complex infection was interpreted as occurring by transfer of transmissible factor(s) from cell to cell by contact and mutiplication of such factor(s) therein.
Chick embryos were susceptible to AL complex infection following allantoic or amniotic inoculations. Antigen and infectious AL complex were demonstrable in the liver, brain, intestines, lungs, and embryonic membranes. Further investigations on AL complex and its relation to human disease are suggested.
Summary
The pathogenesis of R. tsutsugamushi in infected suckling and weanling mice was studied by the use of fluorescein-labeled antibodies. Although the areas of involvement differed with the route of inoculation, rickettsial antigen was observed primarily in connective tissues of mesenchymal origin. X-irradiation increased the mortality, shortened the incubation period and intensified the antigenic involvement. Rickettsiae could be found by infectivity titrations but not by fluorescent antibody staining in mice infected up to a year before. Attempts to cause a recrudescence by the use of various stresses were unsuccessful.
Summary
The pathogenesis of an attenuated and an unattenuated strain of Venezuelan equine encephalomyelitis virus infection in suckling mice as studied by infectivity titrations and direct fluorescent antibody-staining technique was described. Both strains of VEE virus caused a pantropic infection in suckling mice regardless of the concentration of inoculum used or the route of inoculation given. Viral antigen was detected in many tissues, notably in the central nervous system and in the pancreas. However the intensity of antigenic fluorescence was rather weak, making it difficult to discern sequential development of the viral antigen in infected tissues.
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