Parasitism perturbs the mucosal microbiome of Atlantic Salmon.

Interactions between parasite, host and host-associated microbiota are increasingly understood as important determinants of disease progression and morbidity. Salmon lice, including the parasitic copepod Lepeophtheirus salmonis and related species, are perhaps the most important problem facing Atlantic Salmon aquaculture after feed sustainability. Salmon lice parasitize the surface of the fish, feeding off mucus, scales and underlying tissue. Secondary bacterial infections are a major source of associated morbidity. In this study we tracked the diversity and composition of Salmo salar skin surface microbiota throughout a complete L. salmonis infection cycle among 800 post-smolts as compared to healthy controls. Among infected fish we observed a significant reduction in microbial richness (Chao1, P = 0.0136), raised diversity (Shannon, P < 7.86e-06) as well as highly significant destabilisation of microbial community composition (Pairwise Unifrac, beta-diversity, P < 1.86e-05; P = 0.0132) by comparison to controls. While undetectable on an individual level, network analysis of microbial taxa on infected fish revealed the association of multiple pathogenic genera (Vibrio, Flavobacterium, Tenacibaculum, Pseudomonas) with high louse burdens. We discuss our findings in the context of ecological theory and colonisation resistance, in addition to the role microbiota in driving primary and secondary pathology in the host.

Transcriptional response of Atlantic salmon (Salmo salar) after primary versus secondary exposure to infectious salmon anemia virus (ISAV).

Following an infection with a specific pathogen, the acquired immune system of many teleostean fish, including salmonids, is known to retain a specific memory of the infectious agent, which protects the host against subsequent infections. For example, Atlantic salmon (Salmo salar) that have survived an infection with a low-virulence infectious salmon anemia virus (ISAV) isolate are less susceptible to subsequent ISAV infections. A greater understanding of the mechanisms and immunological components involved in this acquired protection against ISAV is fundamental for the development of efficacious vaccines and treatments against this pathogen. To better understand the immunity components involved in this observed resistance, we have used an Atlantic salmon DNA microarray to study the global gene expression responses of preexposed Atlantic salmon (fish having survived an infection with a low-virulence ISAV isolate) during the course of a secondary infection, 18 months later, with a high-virulence ISAV isolate. We present global gene expression patterns in both preexposed and naïve fish, following exposure by either cohabitation with infected fish or by direct intra-peritoneal injection of a high-virulence ISAV isolate. Our results show a clear reduction of ISAV viral loads in head-kidney of secondary infected fish compared to primary infected fish. Further, we note a lower-expression of many antiviral innate immunity genes in the secondary infected fish, such as the interferon induced GTP-binding protein Mx, CC-chemokine 19 and signal transducer and activator of transcription 1 (STAT 1), as well as MHC class I antigen presentation involved genes. Potential acquired immunity genes such as GILT, leukocyte antigen transcript CD37 and Ig mu chain C region membrane-bound form were observed to be over-expressed in secondary infected fish. The observed differential gene expression profile in secondary and primary infected fish head-kidney provides great insight into immunity components involved during primary and secondary ISAV infection.