Ohman D E, Burns R P, Iglewski B H
J Infect Dis. 1980 Oct;142(4):547-55. doi: 10.1093/infdis/142.4.547.
The data presented indicate that in experimental infections of the mouse cornea, toxin A of Pseudomonas aeruginosa contributes to the organism's pathogenicity, whereas active elastase may not be required. After traumatization, corneas were infected with wild-type parental toxin A-producing strains, two toxin A-deficient mutants (Tox-), or an elastase mutant. The infections produced by both Tox- mutants were less severe than infections produced by their parental strains. Furthermore, the Tox- mutants were not able to persist in the eyes as long as their parental strains. Addition of subdamaging doses of exogenous toxin A to eyes infected with the Tox- mutant PA103-29 significantly increased is virulence. The course of infection and the resulting corneal damage produced by the elastase mutant were indistinguishable from those of its parental strain.
所呈现的数据表明，在小鼠角膜的实验性感染中，铜绿假单胞菌的毒素A有助于该生物体的致病性，而活性弹性蛋白酶可能并非必需。角膜创伤后，用野生型亲本产毒素A菌株、两种毒素A缺陷突变体（Tox-）或一种弹性蛋白酶突变体进行感染。两种Tox-突变体产生的感染都不如其亲本菌株产生的感染严重。此外，Tox-突变体在眼中持续存在的时间不如其亲本菌株长。向感染了Tox-突变体PA103 - 29的眼睛中添加亚损伤剂量的外源性毒素A可显著增加其毒力。弹性蛋白酶突变体产生的感染过程和由此导致的角膜损伤与其亲本菌株无法区分。
