**ABSTRACT NOT
FOR CITATION WITHOUT AUTHOR PERMISSION. The title, authors, and abstract
for this completion report are provided below.
For a copy of the full completion report, please contact the author via e-mail
at mpurcell@usgs.gov. Questions? Contact the GLFC via email at frp@glfc.org or via telephone at 734-662-3209.**
IMPACT OF STRESSORS
ON TRANSMISSION POTENTIAL OF RENIBACTERIUM
SALMONINARUM IN CHINOOK SALMON
May 2014
ABSTRACT:
Renibacterium salmoninarum is the causative agent of bacterial
kidney disease (BKD) affecting several species of Pacific salmon. The severity of BKD can range from a chronic
infection to overt disease with high mortality as in the case of large losses
of adult Chinook salmon (Oncorhynchus tshawytscha)
in the Great Lakes during late 1980s. The goal of this study was to empirically
evaluate how environmental stressors relevant to the Great Lakes impact R. salmoninarum disease
progression and bacterial shedding, the latter parameter being a proxy of
horizontal transmission. In the first study (Aim 1), we focused on how
endogenous host thiamine levels and dietary fatty acids impacted resistance of
Chinook salmon to R. salmoninarum.
Juvenile fish were fed one of four experimental diets, including a (1)
thiamine replete diet formulated with fish oil, (2) thiamine deplete diet
formulated with fish oil, (3) thiamine replete diet formulated with soybean
oil, and (4) thiamine deplete diet formulated with soybean oil, before being
challenged with buffer or R. salmoninarum. We observed significantly higher
mortality in the R. salmoninarum
infected groups relative to the corresponding mock controls in only the
thiamine replete diet groups. We also observed a significant effect of time and
diet on kidney bacterial load and bacterial shedding, with a significant trend
towards higher shedding and bacterial load in the fish oil – thiamine replete
diet group. However, during the course of the
study, unexpected mortality occurred in all groups attributed to the myxozoan parasite Ceratomyxa shasta.
Since the fish were dually-infected with C.
shasta, we evaluated parasite DNA levels
(parasitic load) in the kidney of sampled fish. We found that parasite load
varied across time points but there was no significant effect of diet. However,
parasite load did differ significantly between the mock and R. salmoninarum
challenge groups with a trend towards longer persistence of C. shasta DNA
in fish dually-infected with R. salmoninarum. Overall, results in Aim 1 indicated: 1)
that the experimental diets impacted bacterial but not parasitic infection
patterns, 2) that low thiamine levels may reduce the severity of R. salmoninarum
infection, and 3) that fish infected with R.
salmoninarum may be less able to clear a
secondary infection with a parasite. The second study (Aim 2) focused on the
role that temperature plays in the progression of BKD from the asymptomatic
infected state to a diseased state. Lake Michigan Chinook salmon were infected
with R. salmoninarum
at a common intermediate water temperature and, at 2 weeks post-infection,
were split into three temperature groups (cool, intermediate and warm). Fish
held at the cool temperature (8°C) had significantly greater mortality
following challenge, significantly higher levels of bacteria in the kidney, and
shed significantly greater amounts of bacteria into the water relative to fish
held at the intermediate (12°C) and warm (15°C) temperatures. Thus, our results
support the hypothesis that, for BKD, warm temperature stress does not
contribute to greater disease progression and increased bacterial shedding. Our
laboratory results are consistent with field epidemiological observations that
BKD mortality in the Great Lakes is commonly associated with declining water
temperatures in the fall or when water temperatures begin to increase but are
still cool after over-wintering.