Valiente E, Padrós F, Lamas J, Llorens A, Amaro C
Department of Microbiology and Ecology, University of Valencia, Dr. Moliner, 50., 46100 Burjassot, Valencia, Spain.
Microb Pathog. 2008 Nov-Dec;45(5-6):386-93. doi: 10.1016/j.micpath.2008.09.001. Epub 2008 Sep 27.
Vibrio vulnificus biotype 2 serovar E (Bt2-serE) is a zoonotic pathogen that causes a haemorrhagic septicaemia in eels, called warm water vibriosis. The main objective of the present work was to study the onset of the eel vibriosis from the microbiological and histopathological viewpoint, as well as to ascertain the role of the protease Vvp as a lesional factor by comparing the histopathological lesions caused by the wild strain and its vvp deficient derivative. The wild-type strain was observed to attach to the gills, where it multiplied following saturation dynamics, subsequently invading the blood stream and reaching the internal organs. Here it reached population sizes that are notably lower than those associated with other fish septicaemia. Parallel to bacterial growth, there was a notable decrease in haematocrit values and haemoglobin concentration in blood as well as extensive haemorrhages in all the analysed organs. The main histopathological lesions were detected in the head kidney in the form of extensive necrosis affecting the haematopoietic tissue. Very few bacteria were visualized in the different organs, most of which were close to blood cells and capillary vessels, which is compatible with the results obtained in the microbiological study. The same lesions were produced when extracellular products (ECPs) were injected instead of bacteria or when the vvp-defective mutant or its ECPs were injected. The overall results suggest that the pathology caused by V. vulnificus in the eel is not caused by massive bacterial growth in the blood and internal organs but, rather, by the effect of potent toxic factors other than the metalloprotease, which have yet to be determined.
创伤弧菌生物型2血清型E(Bt2-serE)是一种人畜共患病原体,可导致鳗鱼患出血性败血症,称为温水弧菌病。本研究的主要目的是从微生物学和组织病理学角度研究鳗鱼弧菌病的发病情况,并通过比较野生菌株及其vvp缺陷衍生物所引起的组织病理学损伤,确定蛋白酶Vvp作为致病因素的作用。观察到野生型菌株附着在鳃上,在那里它按照饱和动力学进行繁殖,随后侵入血流并到达内部器官。在这里,它达到的种群数量明显低于与其他鱼类败血症相关的数量。与细菌生长同时,血液中的血细胞比容值和血红蛋白浓度显著下降,并且所有分析器官都出现广泛出血。主要的组织病理学损伤在头肾中被检测到,表现为影响造血组织的广泛坏死。在不同器官中很少能看到细菌,其中大多数靠近血细胞和毛细血管,这与微生物学研究结果相符。当注射细胞外产物(ECPs)而非细菌时,或者当注射vvp缺陷突变体或其ECPs时,会产生相同的损伤。总体结果表明,创伤弧菌在鳗鱼中引起的病理变化不是由血液和内部器官中的大量细菌生长导致的,而是由尚未确定的除金属蛋白酶之外的强效毒性因子的作用引起的。