Project description:Salmonid Rickettsial Syndrome (SRS), caused by Piscirickettsia salmonis, is the most important disease in the Chilean aquaculture industry since it induces the highest mortality rates among infectious diseases. P. salmonis is a facultative intracellular bacterium comprising two genetically distinct groups (LF-89 and EM-90) in Chile. Previous data suggest that their cohabitation triggers the expression of virulence effectors, which could be related to a higher pathogenicity in salmon during a co-infection. Therefore, we evaluated whether the physical contact between two isolates from LF-89 and EM-90 was needed to activate this effect. Through a spatially separated in vivo co-culture inside Atlantic salmon followed by RNA-seq analysis, we compared the differential expressed genes (DEGs) with our previous results from an in vivo mixed co-culture. Data showed that LF-89 presented a similar virulence factor profile compared to the mixed co-culture. In contrast, EM-90 had more downregulated DEGs and the flagellar-related genes observed during mixed co-culture were absent. Hence, the synergistic effect related to increased pathogenicity to the host may be driven by the physical co-localization of both LF-89 and EM-90 P. salmonis isolates.
Project description:Piscirickettsia salmonis, the biological agent of SRS (Salmon Rickettsial Syndrome), is a facultative intracellular bacterium that can be divided into two genogroups (LF-89 and EM-90) with different virulence levels and patterns. There are studies that have found co-infection of these genogroups in salmonid farms in Chile, but it is essential to assess whether this competitive interaction within the host is related to virulence and changes in pathogen dynamics. In this work, we studied one isolate from each genogroup, EM-90 and LF-89 . The aim was to evaluate how co-cultures could affect their growth performance and virulence factors expression at in vivo cultures in Atlantic salmon. During in vivo co-cultures, transcriptomic analysis revealed an upregulation of transposases, flagellum-related genes (fliI and flgK), transporters and permeases that could unveil novel virulence effectors used in the early infection process of P. salmonis. Thus, our work has shown that the cohabitation of the genogroups of P. salmonis can modulate their behavior and virulence effectors expression. These data can contribute to new strategies and approaches to improve current health treatments against this salmonid bacterium.
Project description:Fuentealb2016 - Genome-scale metabolic
reconstruction (iPF215) of Piscirickettsia salmonis LF-89
This model is described in the article:
Genome-scale metabolic
reconstruction for the insidious bacterium in aquaculture
Piscirickettsia salmonis.
Fuentealba P, Aros C, Latorre Y,
Martínez I, Marshall S, Ferrer P, Albiol J, Altamirano
C.
Bioresour. Technol. 2017 Jan; 223:
105-114
Abstract:
Piscirickettsia salmonis is a fish bacterium that causes the
disease piscirickettsiosis in salmonids. This pathology is
partially controlled by vaccines. The lack of knowledge has
hindered its culture on laboratory and industrial scale. The
study describes the metabolic phenotype of P. salmonis in
culture. This study presents the first genome-scale model
(iPF215) of the LF-89 strain of P. salmonis, describing the
central metabolic pathway, biosynthesis and molecule
degradation and transport mechanisms. The model was adjusted
with experiment data, allowing the identification of the
capacities that were not predicted by the automatic annotation
of the genome sequences. The iPF215 model is comprised of 417
metabolites, 445 reactions and 215 genes, was used to reproduce
the growth of P. salmonis (?max 0.052±0.005h(-1)). The
metabolic reconstruction of the P. salmonis LF-89 strain
obtained in this research provides a baseline that describes
the metabolic capacities of the bacterium and is the basis for
developing improvements to its cultivation for vaccine
formulation.
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