The energetic costs of fasting and Ichthyophonus infection were measured in juvenile Pacific herring (Clupea pallasii) in a lab setting at three temperatures. Infected herring incurred significant energetic costs, the magnitude of which depended on fish condition at the time of infection (fat versus lean). Herring that were fed continually and were in relatively good condition at the time of infection (fat) never stored lipid despite ad libitum feeding. In feeding herring, the energetic cost of infection was a 30% reduction in total energy content relative to controls 52 days post infection. Following food deprivation (lean condition), infection caused an initial delay in the compensatory response of herring. Thirty-one days after re-feeding, the energetic cost of infection in previously-fasted fish was a 32% reduction in total energy content relative to controls. Body composition of infected herring subsequently recovered to some degree, though infected herring never attained the same energy content as their continuously fed counterparts. Fifty-two days after re-feeding, the energetic cost of infection in previously-fasted fish was a 6% reduction in total energy content relative to controls. The greatest impacts of infection occurred in colder temperatures, suggesting Ichthyophonus-induced reductions in body condition may have greater consequences in the northern extent of herring's range, where juveniles use most of their energy reserves to survive their first winter. 1. Introduction Ichthyophonus is a commonly occurring Mesomycetozoean parasite that has been reported in more than 100 species of fish [1–3]. Ichthyophonus is highly pathogenic to Pacific herring (Clupea pallasii) [4] and occurs in high prevalence and intensity in herring populations throughout the northeast Pacific Ocean [5–7]. Epizootics of the parasite are known to structure herring populations and populations of other fish species [1, 2, 8, 9]. Infection by Ichthyophonus is not 100% fatal (see Gregg et al. this issue). Infection elicits systemic inflammation and tissue destruction resulting in vital organ failure [10]. In survivors, quantification of reduced fitness or identification of chronic problems associated with the parasite is limited to a study which found decreased swimming performance in salmon (Oncorhynchus) as a result of tissue damage. Authors surmised that poor swimming ability may lead to fatigue and elevated depletion of lipid reserves that would ultimately interfere with migrations [11]. Differences in swimming stamina between Ichthyophonus-infected and uninfected
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