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SG 9R 株对鸡伤寒的致病性研究

Pathogenicity of SG 9R, a rough vaccine strain against fowl typhoid.

机构信息

Zoonotic Disease Institute, Seoul National University, Shillim-Dong, Gwanak-Gu, Seoul, Republic of Korea.

出版信息

Vaccine. 2011 Feb 1;29(6):1311-8. doi: 10.1016/j.vaccine.2010.11.067. Epub 2010 Dec 4.

DOI:10.1016/j.vaccine.2010.11.067
PMID:21134445
Abstract

SG 9R, a rough vaccine strain of Salmonella gallinarum, has been used for the prevention of fowl typhoid and paratyphoid in the world despite the presence of residual virulence. SG 9R-like rough strains have been recently isolated from fowl typhoid cases; however, molecular markers to differentiate SG 9R from field strains are not well-characterized and the molecular mechanisms of SG 9R residual virulence are unclear. Therefore, we analyzed LPS biosynthesis (rfa gene cluster) and virulence genes (spv, SPI-2) of both SG 9R and S. gallinarum rough field strains. SG 9R carried a unique nonsense mutation in rfaJ (TCA to TAA) and a shared rfaZ mutation (G-deletion) by rough and smooth S. gallinarum strains. SG 9R also carried intact SPI-2 and spvC, B, A, and R (except deleted spvD). SG 9R-like rough strains (n=10) carried identical mutations in virulence-related genes to SG 9R. SG 9R and SG 9R-like rough strains did not demonstrate significant mortality or liver lesions under normal conditions. However, fowl typhoid was successfully reproduced in the present study by SG 9R inoculation to 1-day-old male brown layer chicks per os following starvation. Therefore, the LPS defect may be one of the major mechanisms of SG 9R attenuation, and the possession of intact SPI-2, spvC, B, A, and R virulence genes may be associated with residual SG 9R virulence.

摘要

SG9R 是鸡白痢沙门氏菌的粗糙疫苗株,尽管存在残余毒力,但已在世界范围内用于预防禽伤寒和禽副伤寒。最近从禽伤寒病例中分离到了与 SG9R 相似的粗糙株,但区分 SG9R 与田间株的分子标记尚未得到很好的描述,SG9R 残余毒力的分子机制也不清楚。因此,我们分析了 SG9R 和鸡白痢沙门氏菌粗糙田间株的 LPS 生物合成(rfa 基因簇)和毒力基因(spv、SPI-2)。SG9R 在 rfaJ 中携带独特的无意义突变(TCA 到 TAA)和粗糙和光滑鸡白痢沙门氏菌菌株共有的 rfaZ 突变(G 缺失)。SG9R 还携带完整的 SPI-2 和 spvC、B、A 和 R(除了缺失的 spvD)。SG9R 样粗糙株(n=10)在与毒力相关的基因中携带与 SG9R 相同的突变。SG9R 和 SG9R 样粗糙株在正常条件下没有表现出明显的死亡率或肝脏病变。然而,本研究通过 SG9R 接种饥饿 1 日龄雄性棕色层小鸡,经口途径成功复制了禽伤寒。因此,LPS 缺陷可能是 SG9R 减毒的主要机制之一,而完整的 SPI-2、spvC、B、A 和 R 毒力基因的存在可能与 SG9R 的残余毒力有关。

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