冷水鱼致病性细菌的毒力因子

Alicia E. Toranzo, Juan L. Barja
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引用次数: 107

摘要

细胞表面相关特性和细胞外产物(ECP)作为毒力因子的重要性在本综述中考虑的鱼类病原体中有所不同。在弧菌属的成员中,沙门氏菌弧菌和奥达里弧菌不分泌蛋白酶、溶血素或细胞毒素,而鳗弧菌、创伤弧菌和豆瓣弧菌则是强外毒素的产生者。在沙门氏菌中,疏水表面抗原VS-P1 (40 Kd)的存在被认为可能是保护细菌免受宿主血清作用的毒力决定因素。尽管在鳗鲡中,与粘附性和侵袭性相关的表面特性以及不同的外酶(即溶血素、细胞毒素和皮肤毒素)可促进感染的发展,但金属蛋白酶和未确定的低MW物质是导致其ECP致死的主要毒素。尽管创伤弧菌对鳗鱼和小鼠的毒力机制似乎不同,其胶囊的存在仅与对哺乳动物的致病性有关,但所有豆sela弧菌菌株对变温和等温宿主具有相似的毒力决定因素,分泌一种具有溶血和细胞毒活性的强效致死磷脂酶毒素。虽然与A层相关的细胞表面特征可以在沙门氏菌气单胞菌产生的疾病中发挥作用,但体内疖形成的发病机制是由于两种酶的共同作用,一种是70 Kd的丝氨酸蛋白酶,另一种是25 Kd的磷脂酶。鳗毒假单胞菌、嗜branchophilum黄杆菌和滑翔细菌(Flexibacter-Cytophage spp)都是蛋白水解酶的生产者,但ECP参与鱼外部组织的第一次攻击仅在黄杆菌中得到证实。然而,在P. anguilliseptica中,K抗原的存在与毒力之间的关系已得到明确证实。拉克氏耶尔森氏菌缺乏其他致病性耶尔森氏菌的大多数细胞表面毒力特性,蛋白酶和/或溶血素是造成ECP致死效应的主要毒素。相比之下,来自沙门氏菌大肠杆菌的ECP缺乏蛋白水解、溶血和细胞毒活性,对鱼类不致命。沙门氏菌的毒力与细胞包膜的性质密切相关,如疏水性、自聚集性、血凝性和57 Kd抗原蛋白的存在。虽然在这些细菌中,铁获取系统可以在它们的致病性中发挥作用,但只有在V. anguillarum中,才最终证明了对鱼的毒力与拥有两种分别由质粒和染色体基因编码的铁载体介导的铁转运机制之间存在直接关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Virulence factors of bacteria pathogenic for coldwater fish

The importance of cell surface associated properties and extracellular products (ECP) as virulence factors varies among the fish pathogens considered in this review. Among members of the genus Vibrio, V. salmonicida, and V. ordalii do not secrete proteases, hemolysins, or cytotoxins, while V. anguillarum, V. vulnificus, and V. damsela are strong exotoxin producers. In V. salmonicida, the presence of a hydrophobic surface antigen, VS-P1 (40 Kd), has been described as a possible virulence determinant protecting the bacterium against the action of host serum. Although in V. anguillarum surface properties related to adherence and invasiveness, as well as different exoenzymes (i.e. hemolysins, cytotoxins, and dermatotoxins) can contribute to the development of infections, metallo-proteases, and undetermined low MW substances are the main toxins responsible for the lethality of their ECP. Whereas V. vulnificus seems to have a different mechanism of virulence for eels and mice, with the presence of a capsule being associated only with its pathogenicity for mammals, all V. damsela strains possess similar virulence determinants for poikilotherm and homoiothermic hosts secreting a potent lethal phospholipase toxin with hemolytic and cytotoxic activities. Although cell surface characteristics linked to the A layer can play a role in disease produced by Aeromonas salmonicida, the pathogenesis of furuncle formation in vivo is due to a combined effect of two enzymes, a 70 Kd serine protease and a 25 Kd phospholipase. Pseudomonas anguilliseptica, Flavobacterium branchiophilum, and the gliding bacteria (Flexibacter-Cytophage spp) are producers of proteolytic enzymes, but the involvement of ECP in the first attack of external fish tissues has only been demonstrated in Flavobacterium. In P. anguilliseptica, however, a relationship between the presence of K antigens and virulence has been clearly confirmed. Yersinia ruckeri lacks most of the cell-surface virulence properties present in other pathogenic Yersinia spp., with proteases and/or hemolysins being the main toxins responsible of the lethal effects of the ECP. In contrast, ECP from Renibacterium salmoninarum are devoid of proteolytic, hemolytic, and cytotoxic activities, and are not lethal for fish. The virulence of R. salmoninarum is strongly correlated with the nature and properties of the cell envelope such as hydrophobicity, autoaggregation, hemagglutination, and the presence of a 57 Kd antigenic protein.

Although in some of these bacteria, the iron-acquisition systems can play a role in their pathogenicity, only in V. anguillarum has it been conclusively demonstrated that a direct relationship exists between virulence for fish and the possesion of two siderophore-mediated iron transport mechanisms coded, respectively, by plasmidic and chromosomal genes.

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