Ben Haj Khalifa Anis, Moissenet Didier, Vu Thien Hoang, Khedher Mohamed
Service de microbiologie, Hôpital Tahar Sfar, Mahdia, Tunisie.
Ann Biol Clin (Paris). 2011 Jul-Aug;69(4):393-403. doi: 10.1684/abc.2011.0589.
Pseudomonas aeruginosa is a bacterium responsible for severe nosocomial infections, life-threatening infections in immunocompromised persons, and chronic infections in cystic fibrosis patients. The bacterium's virulence depends on a large number of cell-associated and extracellular factors. The virulence factors play an important pathological role in the colonization, the survival of the bacteria and the invasion of tissues. There are two types of virulence factors: (1) factors involved in the acute infection: these factors are either on the surface of P. aeruginosa, either secreted. The pili allow adherence to the epithelium. The exoenzyme S and other adhesins reinforce the adherence to epithelial cells. The exotoxin A is responsible of tissue necrosis. Phospholipase C is a thermolabile haemolysin. The pathogenic role of exoenzyme S is attributable to the disruption of normal cytoskeletal organization, the destruction of immunoglobulin G and A, leads to depolymerization of actin filaments and contributes to the resistance to macrophages. P. aeruginosa produces at least four proteases causing bleeding and tissue necrosis; (2) factors involved in the chronic infection: siderophores (pyoverdin and pyochelin), allow the bacteria to multiply in the absence of ferrous ions. The strains isolated from patients with cystic fibrosis have a pseudocapsule of alginate that protects the bacterium from phagocytosis, dehydration and antibiotics. Moreover, it improves adherence to epithelial cells forming a biofilm. Two different types of regulation systems control the expression of the majority of these virulence factors: the two-component transcriptional regulatory system and the quorum sensing system. These two mechanisms are necessary to the survival and the proliferation of this microorganism in the host.
铜绿假单胞菌是一种可导致严重医院感染、免疫功能低下者危及生命的感染以及囊性纤维化患者慢性感染的细菌。该细菌的毒力取决于大量与细胞相关和细胞外的因子。这些毒力因子在细菌的定植、存活及组织侵袭过程中发挥着重要的病理作用。毒力因子有两种类型：（1）参与急性感染的因子：这些因子要么位于铜绿假单胞菌表面，要么是分泌型的。菌毛可使其黏附于上皮细胞。外毒素S和其他黏附素可增强对上皮细胞的黏附。外毒素A可导致组织坏死。磷脂酶C是一种不耐热的溶血素。外毒素S的致病作用归因于其破坏正常的细胞骨架组织、破坏免疫球蛋白G和A、导致肌动蛋白丝解聚以及有助于抵抗巨噬细胞。铜绿假单胞菌至少产生四种导致出血和组织坏死的蛋白酶；（2）参与慢性感染的因子：铁载体（绿脓菌素和焦磷酸铁）可使细菌在没有亚铁离子的情况下繁殖。从囊性纤维化患者分离出的菌株有一层藻酸盐假荚膜，可保护细菌免受吞噬作用、脱水作用及抗生素的影响。此外，它还可改善对上皮细胞的黏附，形成生物膜。两种不同类型的调节系统控制着这些毒力因子中大多数的表达：双组分转录调节系统和群体感应系统。这两种机制对于该微生物在宿主体内的存活和增殖是必需的。
