Summary. Inbred female C3H mice were given 2 x lo7 cfu virulent SulrnondiQ typhimzrriurn by intraperitoneal injection. Peritoneal washings were harvested between 3 h and 72 h after infection and examined by electronmicroscopy. There was evidence of intracelIuIar killing by polymorphs and macrophages. The degeneration of intracellular salmonellae was seen initially as enlarging central electron-lucent areas in the cytoplasm and peripheral condensation of cytoplasmic granules, followed by disruption of the bacterial envelope and disintegration of cellular structure. Alternatively, the initial injury appeared as an irregular and discontinuous bacterial envelope with compression of the bacterium and diffuse condensation of cytoplasmic granules. It was also evident that virulent salmonellae multiplied extracellularly in the peritoneal cavity of the infected mice.
The highly susceptible inbred C3H/HeNMTV mice were vaccinated with fragments derived from sonicated Salmonella typhimurium and then infected with the pathogen. All of the vaccinated mice survived an otherwise rapidly fatal challenge of 10(5) organisms, i.e., greater than 10(3) x mean lethal dose (LD50). The vaccine also protected two-thirds of the mice infected with 10(6) bacteria and extended the survival time of the remainder in their fatal disease. Histopathological findings showed that, like the control mice, the vaccinated and infected mice developed abscesses with infiltration of polymorphonuclear leukocytes in the organs of the reticuloendothelial system during the early stage of the infection. However, unlike the primary lesions in the control mice, the lesions of the vaccinated mice tended to be discrete and self-limiting. They began to transform into granulomas after the first week of infection. Recovery and regeneration of tissues were evident 3 weeks after the infection.
Summary. Inbred female C3H mice were given, by intraperitoneal injection, 4 x lo7 virulent Salmonella typhimurium organisms opsonised with specific antiserum. Peritoneal washings were obtained between 1.5 and 24h after injection and examined by electronmicroscopy. Opsonised salmonellae were ingested rapidly by peritoneal exudate cells and were digested rapidly. The presence of antibody facilitated the phagocytic efficiency of the host cells. Destruction of ingested bacteria appeared to be an innate capacity of the host phagocytes independent of the presence of antibody.
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