Marques M B, Weller P F, Parsonnet J, Ransil B J, Nicholson-Weller A
Harvard Medical School, Charles A. Dana Research Institute, Harvard-Thorndike Laboratories, Beth Israel Hospital, Boston, Massachusetts.
J Clin Microbiol. 1989 Nov;27(11):2451-4. doi: 10.1128/jcm.27.11.2451-2454.1989.
Phosphatidylinositol-specific phospholipase C (PIPLC), an enzyme that can specifically release phosphatidylinositol-linked proteins from host cells, is one of the extracellular enzymes produced by Staphylococcus aureus. To investigate whether PIPLC might be a virulence factor, we assessed PIPLC production by S. aureus strains that had been isolated from healthy carriers and from infected patients with or without toxic shock syndrome. Although none of five vaginal isolates from healthy women was a PIPLC producer, only 10 of 32 selected pathogenic strains that caused significant infections or toxic shock syndrome elaborated PIPLC enzyme activity. Seven of 24 toxic-shock-associated strains, compared with 3 of 8 non-toxic-shock-associated strains, were positive for PIPLC. The majority of strains that produced PIPLC were negative for toxic shock syndrome toxin 1 (P less than 0.05); this association between PIPLC production and strains negative for toxic shock syndrome toxin 1 was even stronger among strains isolated only from patients with toxic shock syndrome (P less than 0.01). Among all 32 pathogenic isolates, PIPLC-producing S. aureus strains were isolated from four of four patients developing adult respiratory distress syndrome and four of five patients with disseminated intravascular coagulation, suggesting a significant association between PIPLC production and adult respiratory distress syndrome and/or disseminated intravascular coagulation (P less than 0.002). On the basis of these results, we propose that PIPLC is a virulence factor of S. aureus and is implicated in the development of adult respiratory distress syndrome and disseminated intravascular coagulation.
磷脂酰肌醇特异性磷脂酶C(PIPLC)是一种能够从宿主细胞中特异性释放磷脂酰肌醇连接蛋白的酶,是金黄色葡萄球菌产生的细胞外酶之一。为了研究PIPLC是否可能是一种毒力因子,我们评估了从健康携带者以及患有或未患有中毒性休克综合征的感染患者中分离出的金黄色葡萄球菌菌株的PIPLC产生情况。虽然从健康女性中分离出的5株阴道菌株均不产生PIPLC,但在32株导致严重感染或中毒性休克综合征的选定致病菌株中,只有10株具有PIPLC酶活性。与8株非中毒性休克相关菌株中的3株相比,24株中毒性休克相关菌株中有7株PIPLC呈阳性。产生PIPLC的大多数菌株中毒性休克综合征毒素1呈阴性(P<0.05);仅从患有中毒性休克综合征的患者中分离出的菌株中,PIPLC产生与中毒性休克综合征毒素1阴性菌株之间的这种关联更强(P<0.01)。在所有32株致病分离株中,产生PIPLC的金黄色葡萄球菌菌株从4例发生成人呼吸窘迫综合征的患者中的4例以及5例弥散性血管内凝血患者中的4例中分离得到,这表明PIPLC产生与成人呼吸窘迫综合征和/或弥散性血管内凝血之间存在显著关联(P<0.002)。基于这些结果,我们提出PIPLC是金黄色葡萄球菌的一种毒力因子,并与成人呼吸窘迫综合征和弥散性血管内凝血的发生有关。