Bioelectronic monitoring of parasite‐induced stress in brown trout and roach

Abstract

A non‐contact bioelectronic monitoring system was used to record changes in heart rate, ventilation rate and swimming activity in brown trout Salmo trutta and roach Rutilus rutilus, following exposure to two species of cercariae of digenean trematodes: Diplostomum pseudospathaceum which is a common parasite in the lens of fishes and xiphidiocercariae of Plagiorchis elegans, a parasite of anatid birds, both of which have the snail Lymnaea stagnalis as their first intermediate host. Swimming activity increased significantly in roach exposed to Diplostomum cercariae at densities as low as 3.8l−1 and remained elevated for 24–36 h post exposure. Brown trout showed no response when exposed to low densities of Diplostomum (2.9 and 5.7 cercariae 1−1) but there was a significant response at higher cercarial exposure densities (>501−1). Total activity of brown trout increased immediately, peaking after 2 h and returning to pre‐exposure levels within 5–6 h. There was a simultaneous increase in heart and ventilation rates which both declined following the reduction in activity of the fish. Heart rate then increased for a second time to a maximum level at 14–16 h and thereafter declined to reach a steady state at 3 days post‐exposure. During this period there was no significant change in total activity. The qualitative nature of the heart response was identical in five infected brown trout although the magnitude of the response varied widely among fish. Exposure to cercariae of P. elegans elicited no response in either fish species. (c) 1996 The Fisheries Society of the British Isles

Shoaling with infected conspecifics does not improve resistance to trematode infection

“…This may vary not only with the ratio of donors to receivers but also with exposure doses experienced by the donors and the resulting infection intensities. For example, in some fish species, physiological responses associated with exposure to D. pseudospathaceum have been observed only at high exposure doses (Laitinen et al, 1996). Although exposure doses and the resulting parasite loads in the present study were in the range of those expected (dose) or observed (load) under natural conditions (e.g.…”

“…Then, they move towards its eye lenses, causing damage to body tissues and blood vessels during migration (Erasmus, 1959;Ratanara-Brockelman, 1974). Fish hosts have been shown to suffer from pathogenic stress caused directly by the acute invasion of the parasite, as heart rates can increase for several days following exposure (Laitinen, Siddall, & Valtonen, 1996), and activity decreases (Gopko, Mikheev, & Taskinen, 2015). In the host's eye lens, the parasites develop to metacercariae (the bird-infecting stage) within 4-8 weeks that induce eye cataracts (Chappell et al, 1994;Karvonen, 2012).…”

Grouping facilitates avoidance of parasites by fish

“…In addition, higher motility can increase ventilation volume which, in turn, may facilitate transportation of D. pseudospathaceum cercariae to fish [34]. Increased and conspicuous motility of fish injured by penetrating cercariae [13] and/or release of alarm substances [14] could be efficient signals. The most explorative fish would take a higher risk of infection while acquiring information about predators, food and surroundings.…”

“…This makes detection and avoidance of trematode cercariae difficult. Individual fish may only become aware of the parasite’s presence when irritated by penetrating cercariae [13,14]. Juvenile rainbow trout, Oncorhynchus mykiss , experimentally exposed to cercariae of the trematode Diplostomum spathaceum , fled from the site of high parasite concentration shortly after penetration of the first few cercariae [8].…”

A brain‐infecting parasite impacts host metabolism both during exposure and after infection is established

“…Similar to the 'ecology of fear' described for predator-prey relationships (reviewed by Buck et al, 2018;Raffel et al, 2008), after detection of infectious stages, hosts may minimize infection risk by modifying activity, changing social behaviour or physically dislodging attacking parasites (James et al, 2008;Stumbo et al, 2012), all of which can increase metabolic rate (Speakman & Selman, 2003). Hosts can also exhibit physiological signs of stress following exposure to infectious parasite stages, including changes in ventilation, respiration and heart rates (Laitinen et al, 1996;Luong et al, 2017;Voutilainen et al, 2008). Such behavioural and physiological responses may also be learned or developed following initial parasite exposures, which could result in amplified host responses to subsequent encounter with the same parasite.…”