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

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.