Departamento de Microbiología y Parasitología, Instituto de Acuicultura y Facultad de Biología-CIBUS, Universidade de Santiago de Compostela, Santiago de Compostela, Spain.
Centro de Investigacións Científicas Avanzadas (CICA) e Departamento de Química, Facultad de Ciencias, Universidade da Coruña, A Coruña, Spain.
Front Cell Infect Microbiol. 2021 Oct 25;11:750567. doi: 10.3389/fcimb.2021.750567. eCollection 2021.
is an inhabitant of mollusc microbiota and an opportunistic pathogen causing disease outbreaks in marine bivalve mollusc species including oysters and clams. Virulence of mollusc pathogenic vibrios is mainly associated with the production of extracellular products. However, siderophore production is a common feature in pathogenic marine bacteria but its role in fitness and virulence of mollusc pathogens remains unknown. We previously found that produces amphibactin, one of the most abundant siderophores in marine microbes. In this work, synthesis of the siderophore piscibactin was identified as the second siderophore produced by . Single and double mutants in biosynthetic genes of each siderophore system, piscibactin and amphibactin, were constructed in and their role in growth ability and virulence was characterized. Although the High Pathogenicity Island encoding piscibactin is a major virulence factor in vibrios pathogenic for fish, the wild type did not cause mortality in turbot. The results showed that amphibactin contributes more than piscibactin to bacterial fitness . However, infection challenges showed that each siderophore system contributes equally to virulence for molluscs. The strain unable to produce any siderophore was severely impaired to cause vibriosis in clams. Although the inactivation of one of the two siderophore systems (either amphibactin or piscibactin) significantly reduced virulence compared to the wild type strain, the ability to produce both siderophores simultaneously maximised the degree of virulence. Evaluation of the gene expression pattern of each siderophore system showed that they are simultaneously expressed when is cultivated under low iron availability and . Finally, the analysis of the distribution of siderophore systems in genomes of spp. pathogenic for molluscs showed that the gene clusters encoding amphibactin and piscibactin are widespread in the Coralliilyticus clade. Thus, siderophore production would constitute a key virulence factor for bivalve molluscs pathogenic vibrios.
是软体动物微生物群的居民，也是一种机会性病原体，可导致包括牡蛎和蛤在内的海洋双壳贝类软体动物发病。软体动物致病性弧菌的毒力主要与细胞外产物的产生有关。然而，铁载体的产生是海洋致病性细菌的共同特征，但它在软体动物病原体适应性和毒力中的作用尚不清楚。我们之前发现产生 amphibactin，这是海洋微生物中最丰富的铁载体之一。在这项工作中，鉴定出合成铁载体 piscibactin 是 产生的第二种铁载体。在 和 中构建了每个铁载体系统（piscibactin 和 amphibactin）生物合成基因的单突变体和双突变体，并对其生长能力和毒力进行了表征。尽管编码 piscibactin 的高致病性岛是鱼类致病性弧菌的主要毒力因子，但 野生型不会引起大菱鲆死亡。结果表明，amphibactin 对细菌适应性的贡献大于 piscibactin。然而，感染挑战表明，每个铁载体系统对软体动物的毒力贡献相等。不能产生任何铁载体的 菌株严重受损，无法在蛤中引起弧菌病。尽管与野生型菌株相比，两种铁载体系统之一（amphibactin 或 piscibactin）的失活显着降低了毒力，但同时产生两种铁载体的能力最大限度地提高了毒力程度。对每个铁载体系统的基因表达模式进行评估表明，当 在低铁可用性 和 下培养时，它们会同时表达。最后，分析了软体动物致病性 spp.基因组中铁载体系统的分布，结果表明编码 amphibactin 和 piscibactin 的基因簇在 Coralliilyticus 进化枝中广泛存在。因此，铁载体的产生将成为贝类软体动物致病性弧菌的关键毒力因子。
