C3H/HeNMTV mice were immunised intraperitoneally (i.p.) with lipopolysaccharide (LPS) or detoxified LPS (D-LPS) derived from Salmonella typhimurium strain SR-11. In both cases, effective protection was achieved against a challenge dose of greater than 2 x lo2 LD50 of the same organism given by i.p. injection. However, by comparison with LPS, approximately 6-to 10-fold more of D-LPS by weight was needed to protect mice to an equivalent degree. Histopathological studies showed that the initial lesions in infected mice protected with either LPS or D-LPS were composed of self-limiting abscesses which transformed into granulomas as the animals recovered. It is suggested that D-LPS may be modified to become a highly effective, non-toxic salmonella vaccine.
Swiss-Webster mice were vaccinated with heat-killed salmonellae and then were infected with virulent Salmonella typhimurium. Only 1 of the 18 vaccinated mice died from a challenge of 104 x the 50% lethal dose, and about 70% of them survived a challenge of 105 x the 50% lethal dose. Histopathological examinations of the lesions developed in these vaccinated mice showed that they followed the characteristic features of a primary lesion in murine salmonellosis. There was an early necrosis with infiltration of polymorphonuclear leukocytes and abscess formation within the first 6 to 7 days after infection. However, these abscesses remained small and discrete. By days 7 to 10, the lesions began to transform into granulomas, first with the appearance of peripheral mononuclear cells and then by the replacement of polymorphs. By the third week of the infection, minute and discrete granulomas were seen scattered in the spleen, liver, and lymph nodes. Beyond this stage, healing and tissue regeneration followed. Thus, the characteristics of infectious lesions developed in mice vaccinated with heat-killed salmonellae are distinctly different from those developed in mice protected by the avirulent vaccine.
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.
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