The correlation of biochemical virulence factors and enterotoxin production with LD50 of Salmonella typhimurium in mice.

Microbiologica Pub Date : 1991-04-01
S Khurana, N K Ganguly, D Panigrahi, M Khullar, B N Walia
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Abstract

Five strains of Salmonella typhimurium were examined to determine the parameters of virulence. The virulent species significantly resisted the macrophage bactericidal activity (p less than 0.05). The chemiluminescent (CL) response was studied to determine the level of Oxygen-free radicals (OFR) generated and the antioxidant enzymes superoxidase dismutase (SOD), catalase and glutathione peroxidase were assayed to determine the antioxidant mechanism of S. typhimurium to subvert these microbicidal pathways. The levels of the various enzymes were correlated with the virulence (as determined by LD50) and the ability of the microorganisms to induce diarrhoea. Oxygen free radical (OFR) generation elicited by macrophages, in the presence of virulent and avirulent salmonellae was not statistically significant (p greater than 0.05). No correlation was found between the levels of the antioxidant enzymes and the LD50 values. Thus the oxygen-dependent pathways do not appear to play a role in the pathogenesis of salmonellosis, and do not specify the virulence of the microorganism. Immunological and biological assays revealed the virulent strain to be more toxigenic than the avirulent strain. Therefore, the basis of differing virulence in S. typhimurium may be the ability to make and release more toxin in vivo.

鼠伤寒沙门菌生化毒力因子及肠毒素产生与小鼠LD50的关系。
对5株鼠伤寒沙门菌进行了毒力测定。毒株对巨噬细胞的杀菌活性有显著抑制(p < 0.05)。通过化学发光(CL)反应测定鼠伤寒沙门氏菌产生的氧自由基(OFR)水平,并测定抗氧化酶超氧化酶歧化酶(SOD)、过氧化氢酶和谷胱甘肽过氧化物酶的活性,探讨鼠伤寒沙门氏菌破坏这些杀微生物途径的抗氧化机制。各种酶的水平与毒力(由LD50确定)和微生物诱导腹泻的能力相关。巨噬细胞诱导的氧自由基(OFR)生成,在有毒和无毒沙门氏菌存在时无统计学意义(p > 0.05)。抗氧化酶水平与LD50值无相关性。因此,氧依赖途径似乎在沙门氏菌病的发病机制中没有发挥作用,也没有指定微生物的毒力。免疫学和生物学试验表明,毒毒株比无毒毒株具有更强的毒性。因此,鼠伤寒沙门氏菌不同毒力的基础可能是在体内制造和释放更多毒素的能力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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