No abstract

Gastric emptying time in Scophthalmus maximus, when fed friable artificial pellets based on fishmeal. is composed of two phases: (a) a delay time ( I d ) during which the meal forms a bolus and which shortens with temperature, and (b) an emptying phase (duration tend) which varies with meal size (8, body weight ( W ) and temperature (0 according to: log, tcnd=4.66+0.448 log, S-0.2664 log, W-0.051 7 (where tend is in h, S is in g, W is in g and Tis C). During the emptying phase, stomach contents decrease curvilinearly according to: S,O.448 = S00.448 -0.448 K (where S, & So is in g and I is in h) in which the instantaneous digestion rate, K , varies with fish weight and temperature as: ~= 0 . 0 2 1 ~0 . 2 6 6 4 p 5 1 iFood pellets were prepared which remained separate and did not form a bolus in the stomach; K increased if a given meal size was subdivided to increase surface area. If meal size was increased by ingestion of identical pellets, K decreased. After a satiation meal, appetite in young turbot returns in direct relation to the degree of stomach emptiness. When food is regularly available, young turbot feed steadily at a rate which maintains their stomachs at c. 85% maximum fullness.When trained to use demand feeders, the fish interact a s a group to feed rhythmically. but feeding rate falls 33% to only two-thirds of the previous rate since stomach fullness, and hence digestion rate (g h-I). i s maintained at a lower level. Reduction in dietary energy density below I kCal g -' increases gastric emptying rate and the turbot demonstrate partial compensation by increasing food intake. On energy-rich diets, protein nitrogen and energy assimilation efficiencies remain high (97.5% and 91 YO respectively) irrespective of feeding rate and frequency.

The seasonality of proliferative kidney disease (PKD) in rainbow trout, Salmo gairdneri Richardson. at the American River Hatchery, California was found to be primarily dependent on the presence or absence of the infectious stage in the water supply. This was determined by introducing sentinel trout into the hatchery water supply on a monthly basis, followed by their transfer to the laboratory for subsequent holding in 18" C, pathogen-free water for one month prior to examination. These exposures demonstrated that infections were obtained from April through October at ambient temperatures 12-20" C. Trout which had recovered from clinical infections were found to be resistant to reinfection. Resistance was induced by active infection and not just previous exposure to the infectious stage. Trout surviving PKD were also found to harbour later sporogonic stages of the parasite for at least one year following initial infection, but fully formed spores, as judged by well-developed valves, were not observed.

The parasite Ceratomyxa shasta has been implicated as a significant source of salmonid mortality in the lower Klamath River, California (i.e., below Iron Gate dam). A study of the prevalence of C. shasta and its geographic and temporal distribution throughout the Klamath River basin was conducted to determine when and where juvenile salmonids encounter lethal parasite doses. Susceptible rainbow trout Oncorhynchus mykiss were exposed to C. shasta 3–4 d at seven locations in the Klamath River between Beaver Creek and Keno Reservoir in April, June, July, September, and November 2003. Individuals from a Klamath River strain of fall Chinook salmon O. tshawytscha were held in three locations in the upper Klamath River in April, June, and July. In June 2004, rainbow trout were exposed to the parasite for 4 d at 18 locations from Klamath Lake to the mouth of the Klamath River, including several major spawning tributaries; one exposure occurred in the lower Klamath River. Rainbow trout mortality due to infection for groups exposed in the upper Klamath River was lower (<8.0%) and delayed (mean time to death, 40–110 d) in comparison with that in groups exposed in the lower Klamath River (>98%; mean time to death, 33–36 d). Experimental fall Chinook salmon did not become infected in the upper Klamath River, but infection was detected in Chinook salmon exposed in the lower Klamath River, nearly 50% of these succumbing to infection. These dramatic differences in mortality between the upper and lower Klamath River could not be explained by differences in water temperatures during exposure and are probably a result of differences in infectious dose. Lack of infection in groups exposed in tributaries supports the hypothesis that the parasite life cycle and the invertebrate host are largely confined to the main‐stem Klamath River.

Animal populations are frequently infected by pathogens, but it is not always easy to determine the importance of pathogens to overall population dynamics. It is especially difficult to detect the effects of disease in population time series data because the effects are often local while overall population dynamics are also affected by larger-scale environmental factors. We overcame this difficulty by applying multivariate time series analysis to extract local effects from spawning abundance data and by comparing the survival rate of juvenile fall-run Chinook salmon Oncorhynchus tshawytscha from two locations in the Klamath River basin of California, one of which is affected by a high concentration of the myxozoan parasite Ceratomyxa shasta. To assess the effect of the disease (ceratomyxosis) caused by C. shasta on the population dynamics, we analyzed spatially structured abundance data for naturally spawning salmon and survival data for hatchery-released salmon for associations with exposure to C. shasta and stream discharge, another important factor with respect to ceratomyxosis in juvenile salmon. The results suggest that ceratomyxosis reduces the survival of the Chinook salmon that migrate through the location where parasite densities are highest and that this effect is also detectable in spawning abundance estimates.