| Summary: | © 2016 Dr Daniel Wright Parasite outbreaks and their control are substantial bottlenecks to mariculture production. In sea-cage culture of Atlantic salmon (Salmo salar), the most farmed marine fish on the globe, parasite control has traditionally relied heavily on lethal chemical or freshwater treatments following infections. The focus on post-infection control measures has allowed parasites to proliferate between treatments, driven treatment resistance evolution in parasite populations, and negatively affected the marine environment (through chemical release and parasitism levels in wild organisms) and production costs. I explored the potential for more preventive chemical-free methods of persistently manipulating the depth and freshwater exposure of sea-caged salmon to control co-occurring outbreaks of sea lice (specifically, Lepeophtheirus salmonis) and the amoebic gill disease (AGD) agent (Neoparamoeba perurans). In field investigations I found that the depth distribution of free-living N. perurans amoebae varied with environmental conditions in commercial salmon sea-cages of SE Tasmania during AGD outbreaks. These amoebae were concentrated in shallow waters in the absence of stratification, deeper during halocline establishment, or ubiquitous throughout the water column. Continuously monitored swimming depth behaviour of salmon in these cages revealed that this too fluctuated dynamically based on light, temperature and potentially hunger levels. During low levels of fish crowding and low numbers of amoebae, no clear link existed between the depth distribution of amoebae and the swimming depths of salmon in cages. This work suggested N. perurans contact is unavoidable at all sea cage depths, though may be reduced by avoiding intense fish crowding in narrow depth bands in cages during AGD outbreaks. I conducted laboratory experiments to test the effects of freshwater on both L. salmonis and N. perurans at a fine temporal resolution. In vivo, I assessed freshwater survival times for each attached stage of L. salmonis, finding the first stage (copepodid) is freshwater sensitive (dying in 1–3 h) compared to later more tolerant stages (some surviving > 8 days). Under in vitro conditions, I found N. perurans attachment to a non-host substrate is immediately compromised in freshwater (entire populations detaching at ≥ 2 min), well before cell death (at ≥ 1 h). These studies indicated exposing sea-caged salmon briefly to freshwater at frequent intervals could suppress both parasites. Finally, I examined the performance of snorkel cages against both parasites at a commercial scale. These cages use a net roof to prevent fish contacting surface layers where L. salmonis infective larvae concentrate, and a roof-to-surface lined tube which can be freshwater-filled and is entered regularly by salmon which jump to refill their open swim bladders with air. Without freshwater-filling, snorkel cages reduced L. salmonis infestations but increased AGD levels (following halocline establishment). However, permanently freshwater-filled snorkels reduced AGD infections, potentially by detaching rather than killing N. perurans. These findings suggest that manipulations of fish behaviour or environmental conditions can successfully prevent infections by co-occurring parasites in salmon culture. Moreover, given the diversity of culture species and their parasites in mariculture across the globe, a shift in focus to prevention from control may yield widespread benefits for the industry.
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