肠炎沙门菌hcp基因缺失株的体内致病性研究  

Pathogenicity of the hcpgene in-frame deletion mutants from Salmonella enteritidis

作　　者：姚丰华[1] 张钰[1] 朱国强[1] 

机构地区：[1]扬州大学兽医学院/江苏省动物重要疫病与人兽共患病防控协同创新中心,江苏扬州225009

出　　处：《扬州大学学报（农业与生命科学版）》2014年第2期1-5,共5页Journal of Yangzhou University：Agricultural and Life Science Edition

基　　金：国家自然科学基金资助项目(30571374;30771603;31072136;31270171);江苏高校优势学科建设工程项目(2010-11-05)

摘　　要：将肠炎沙门菌SPI-19编码的hcp基因缺失株CMCC(B)50336Δhcp和SD-2Δhcp分别皮下接种6周龄BALB/c小鼠和1日龄清远麻鸡,通过半数致死量(LD50)测定比较它们与野生株50336、SD-2以及相应回补株50336Δhcp/phcp和SD-2Δhcp/phcp的致病性差异。结果表明:缺失hcp基因后,肠炎沙门菌50336Δhcp和SD-2Δhcp对小鼠的LD50分别为79.43和125.89cfu,对雏鸡的LD50分别为89.13×107和158.49×107 cfu;回补hcp基因后,50336Δhcp/phcp和SD-2Δhcp/phcp对小鼠的LD50分别为50.12和19.95cfu,对雏鸡的LD50分别为56.23×107和39.81×107 cfu;而亲本株50336和SD-2对BALB/c小鼠的LD50分别为19.95和7.94cfu,对雏鸡的LD50分别为25.12×107和14.13×107 cfu。试验证明相应回补株在BALB/c小鼠和1日龄清远麻鸡的致病力及体重影响指标上与亲本株基本接近,肠炎沙门菌SPI-19编码的hcp基因对肠炎沙门菌的致病性具有增强作用。To investigate the pathogenicity of the hcp gene encoded by SPI-19 in Salmonella enteritidis, the pathogenicity of hcp gene in-frame deletion mutants 50336 △hcp and SD-2△hcp was tested when compared with the two parent strains CMCC（B）50336 and SD-2 and complemented strains 50336 △hcp/phcp and SD-2 △hcp/phcp in 6-week-old BALB/c mice and 1 day-old Qingyuan chickens infected via subcutaneous inoculation, respectively. The animal infection results showed that the LD50 for the two mutants were 79.43 and 125.89 cfu in the mice, and 89.13×10^7 and 158.49×10^7 cfu in the chickens, the LDso for the two complemented were 50.12 and 19.95 cfu in the mice, and 56.23 × 10^7 and 39.81 ×10^7 cfu in the chickens, and the LD50 for the two parents were 19.95 and 7.94 cfu in the mice, and 25.12×10^7 and 14.13 ×10^7 cfu in the chickens. These suggested that the virulence of S. enteritidis decreased sharply when knocked out the hcp gene.

关 键 词：肠炎沙门菌 SPI-19 hcp基因 半数致死量 

分 类 号：S852.612[农业科学—基础兽医学]