Wigley Paul, Jones Michael A, Barrow Paul A
Institute for Animal Health, Compton Laboratory, Compton, Newbury RG20 7NN, UK.
Avian Pathol. 2002 Oct;31(5):501-6. doi: 10.1080/0307945021000005879.
Functional mutations were made in the type III secretion systems encoded by Salmonella pathogenicity island 1 (SPI 1) and Salmonella pathogenicity island 2 (SPI 2) of Salmonella enterica serovar Pullorum, the cause of pullorum disease in poultry. Their role in cell invasion in vitro, and in virulence in vivo was determined. The SPI 1 mutant showed decreased invasiveness for chicken cells but was capable of causing disease in orally infected 1-day-old chicks, although it showed some reduction in virulence. The SPI 2 mutant showed no reduction in invasiveness, but was fully attenuated for virulence in 1-day-old chicks, and was not detected following oral infection in 1-week-old chickens. Following intravenous infection, the SPI 2 mutant was also attenuated and cleared more rapidly than the parent strain. This indicates that S. Pullorum requires SPI 2 for virulence and persistence but SPI 1 appears to contribute to, but is not essential for, the virulence of S. Pullorum.
鸡白痢沙门氏菌是家禽中鸡白痢病的病原体，对其编码于沙门氏菌致病岛1（SPI 1）和沙门氏菌致病岛2（SPI 2）的III型分泌系统进行了功能突变。确定了它们在体外细胞侵袭和体内毒力中的作用。SPI 1突变体对鸡细胞的侵袭性降低，但尽管其毒力有所降低，但仍能够在经口感染的1日龄雏鸡中引起疾病。SPI 2突变体的侵袭性没有降低，但在1日龄雏鸡中的毒力完全减弱，并且在1周龄鸡经口感染后未检测到。静脉感染后，SPI 2突变体也比亲本菌株毒力减弱且清除更快。这表明鸡白痢沙门氏菌的毒力和持续性需要SPI 2，但SPI 1似乎对鸡白痢沙门氏菌的毒力有贡献，但不是必需的。
