**ABSTRACT NOT FOR CITATION WITHOUT AUTHOR PERMISSION.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

Maureen K. Purcell1 and James R. Winton1

 

 

1Western Fisheries Research Center, US Geological Survey, 6505 NE 65th St., Seattle, WA 98115

 

 

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 (8C) 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 (12C) and warm (15C) 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.