Host Response of Atlantic Salmon (Salmo salar) Re-Inoculated with Paramoeba perurans

Abstract

In aquaculture, recurrence rates of amoebic gill disease (AGD) caused by the ectoparasite Paramoeba perurans are high and no prophylactic strategies exist for disease prevention. In this study, Atlantic salmon (Salmo salar) were initially inoculated with P. perurans and following the development of amoebic gill disease were treated with freshwater immersion on day 21 and day 35 post inoculation. Fish were re-inoculated following a negative qPCR analysis for the presence of P. perurans. The gill host immune response was investigated at 7, 14, and 18 days post re-inoculation. Differential proteome expression of immune related proteins was assessed by comparison of each time point against naïve controls. In the gill, some proteins of the innate immune system were expressed in response to gill re-colonization by P. perurans, while no features of adaptive immunity were found to be differentially expressed. Many of the proteins identified are novel in the context of AGD and their expression profiles suggest that their roles in the response to disease development and progression in single or multiple infections warrant further investigation.

Integration of host-pathogen functional genomics data into the chromosome-level genome assembly of turbot (Scophthalmus maximus)

“…Furthermore, this gene has been reported to be involved in resistance to bacterial infection (Rodrigues et al, 2006) and used for treatment against bacterial infections and iron disorders (Barroso et al, 2021) in Dicentrarchus labrax. Plg is a key activator of the inflammatory response, which facilitates leukocyte recruitment in the site of infection, as well as coagulation, and has been reported in response against Paramoeba perurans in Atlantic salmon (McCormack et al, 2021). Plg was differentially expressed in head kidney during ES severe infection (up-regulated) and VHSV (downregulated) and in spleen by AS (mostly down-regulated) and PD (upregulated early to mid-infection), pointing to distinct expression profiles for candidate genes across pathogens.…”