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Aims To investigate and identify the antibacterial action and mechanism of rose essential oil (REO) against Aeromonas veronii isolated from Northern snakehead for the first time by the phenotypic and metabolic analysis. Methods and results The 2-fold broth microdilution and spread-plate method identified that the minimum inhibitory concentration and minimum bactericidal concentration of REO against A. veronii were 1.25 μl ml−1 and REO impaired the growth in a concentration-dependent manner, indicating that REO possessed a significant bacteriostatic activity. Electron microscopy and live-dead cell staining found that REO caused a severe disruption of cellular morphology and increased the membrane permeability. Additionally, REO treatment induced the leakage of intracellular biomolecules such as proteins and nucleic acids from the bacteria. Metabolomics analysis showed that compared with the control, the REO treatment group exhibited a total of 190 differential metabolites (118 down-regulated and 72 up-regulated), which involved in the main metabolic pathways such as biotin metabolism, arginine biosynthesis, glutathione metabolism, lysine degradation, and histidine metabolism and the TCA cycle. These results verified that REO disturbed the metabolic processes of A. veronii to achieve the bacteriostatic effect. Conclusion The rose essential oil exhibited the effective antibacterial activity against A. veronii via breaking the cellular structure, increasing the membrane permeation and disrupting the metabolic processes. [ABSTRACT FROM AUTHOR]

Edwardsiella piscicida is an important fish pathogen with a broad host that causes substantial economic losses in the aquaculture industry. Ferric uptake regulator (Fur) is a global transcriptional regulator and contains two typical domains, the DNA-binding domain and dimerization domain. In a previous study, we obtained a mutant strain of full-length fur of E. piscicida, TX01Δfur, which displayed increased siderophore production and stress resistance factors and decreased pathogenicity. To further reveal the regulatory mechanism of Fur, the DNA-binding domain (N-terminal) of Fur was knocked out in this study and the mutant was named TX01Δfur2. We found that TX01Δfur2 displayed increased siderophore production and enhanced adversity tolerance, including a low pH, manganese, and high temperature stress, which was consistent with the phenotype of TX01Δfur. Contrary to TX01Δfur, whose virulence was weakened, TX01Δfur2 displayed an ascended invasion of nonphagocytic cells and enhanced destruction of phagocytes via inducing overpowering or uncontrollable pyroptosis, which was confirmed by the fact that TX01Δfur2 induced higher levels of cytotoxicity, IL-1β, and p10 in macrophages than TX01. More importantly, TX01Δfur2 displayed an increased global virulence to the host, which was confirmed by the result that TX01Δfur2 caused higher lethality outcomes for healthy tilapias than TX01. These results demonstrate that the mutation of the Fur N-terminal domain augments the resistance level against the stress and pathogenicity of E. piscicida, which is not dependent on the bacterial number in host cells or host tissues, although the capabilities of biofilm formation and the motility of TX01Δfur2 decline. These interesting findings provide a new insight into the functional analysis of Fur concerning the regulation of virulence in E. piscicida and prompt us to explore the subtle regulation mechanism of Fur in the future. [ABSTRACT FROM AUTHOR]

The B acillus cereus group is composed of Gram-positive spore-forming bacteria of clinical and ecological importance. More than 200 B . cereus group isolates have been sequenced. However, there are few reports of B . cereus group antibiotic resistance genes. This study identified two functional classes of macrolide phosphotransferases ( Mphs) in the B . cereus group. Cluster A Mphs inactivate 14- and 15-membered macrolides while Cluster B Mphs inactivate 14-, 15- and 16-membered compounds. The genomic region surrounding the Cluster B Mph gene is related to various plasmid sequences, suggesting that this gene is an acquired resistance gene. In contrast, the Cluster A Mph gene is located in a chromosomal region conserved among all B . cereus group isolates, and data indicated that it was acquired early in the evolution of the group. Therefore, the Cluster A gene can be considered an intrinsic resistance gene. However, the gene itself is not present in all strains and our comparative genomics analyses showed that it is exchanged among strains of the B . cereus group by the mean of homologous recombination. These results provide an alternative mechanism to intrinsic resistance. [ABSTRACT FROM AUTHOR]

Edwardsiella piscicida is an important fish pathogen with a broad host that causes substantial economic losses in the aquaculture industry. Ferric uptake regulator (Fur) is a global transcriptional regulator and contains two typical domains, the DNA-binding domain and dimerization domain. In a previous study, we obtained a mutant strain of full-length fur of E. piscicida , TX01Δ fur , which displayed increased siderophore production and stress resistance factors and decreased pathogenicity. To further reveal the regulatory mechanism of Fur, the DNA-binding domain (N-terminal) of Fur was knocked out in this study and the mutant was named TX01Δ fur 2. We found that TX01Δ fur 2 displayed increased siderophore production and enhanced adversity tolerance, including a low pH, manganese, and high temperature stress, which was consistent with the phenotype of TX01Δ fur . Contrary to TX01Δ fur , whose virulence was weakened, TX01Δ fur 2 displayed an ascended invasion of nonphagocytic cells and enhanced destruction of phagocytes via inducing overpowering or uncontrollable pyroptosis, which was confirmed by the fact that TX01Δ fur 2 induced higher levels of cytotoxicity, IL-1β, and p10 in macrophages than TX01. More importantly, TX01Δ fur 2 displayed an increased global virulence to the host, which was confirmed by the result that TX01Δ fur 2 caused higher lethality outcomes for healthy tilapias than TX01. These results demonstrate that the mutation of the Fur N-terminal domain augments the resistance level against the stress and pathogenicity of E. piscicida , which is not dependent on the bacterial number in host cells or host tissues, although the capabilities of biofilm formation and the motility of TX01Δ fur 2 decline. These interesting findings provide a new insight into the functional analysis of Fur concerning the regulation of virulence in E. piscicida and prompt us to explore the subtle regulation mechanism of Fur in the future.