Figure 8

Summary of salmon responses to lice in skin and spleen. The present study dealt with responses until 15 dpi as shown in the left side of the figure. Host responses to mature lice stages from literature are shown by a dotted line (right side). The figure illustrates the bi-phasic responses to L. salmonis with abrupt changes in gene expression profiles taking place between 5 and 10 dpi, when lice molts from copepodids to chalimus. Ig genes show an initial decrease followed by gradual increase. MHC and related genes are down regulated. A: early sensing was witnessed both in skin and spleen. At point B, PGE₂ and other secreted components start to increase [31, 34] and this may lead to immune modulation, and can partly explain the pronounced shift in immune responses. Resistant salmonids (e.g. coho salmon) reject lice at point C, 7-14 dpi [10, 11] and the number of lice per fish (LiceR) starts to decrease (see the hypothetical curve on the right side). In susceptible species including Atlantic salmon, the lice number (LiceS) remains relatively stable until they reach the pre-adult/adult stages where lice falls off the fish possibly due to aging, competition, and other factors. In spleen, secretory proteases show dramatic fluctuation. Increased MMPs in all tissues suggest inflammation. When the louse enters the pre-adult stage (i. e, ~ after day 20), the effects on host increase and can cause high mortality. The risk of secondary infections increase, and cortisol levels rise significantly (point D), which indicates severe stress [9, 26, 34]. At this point, it is difficult to differentiate the direct and stress mediated effects of lice [26]. The figure summarizes responses observed after single pulse infection. However, under natural conditions, salmon can carry parasites at different developmental stages and responses can be modified with diverse environmental factors.