Stability of the Lake Michigan fishery for chinook salmon Oncorhynchus tshawytscha at high levels became questionable after stocks declined dramatically following spring epizootics in which bacterial kidney disease (BKD) was a major factor. Initially stocked in 1967, favorable survival and growth of chinook salmon through the 1970s led to increases in abundance and in popularity with anglers. Returns of chinook salmon improved annually until the late-1980s, when, with little warning, spring epizootics reduced the abundance of adult salmon by 50% or more. Reduced abundance of alewives (Alosa pseudoharengus), coupled with an increase in chinook salmon density and heavy parasite infection rates were hypothesized to have reduced chinook salmon growth and fitness and to have increased their susceptibility to BKD. Evidence of slower growth exists and low food availability may be the stressor that triggered the epizootics. Chinook salmon were a major component of the economic development and subsequent hardship of the sportfishing industry on Lake Michigan. Sustaining the chinook salmon fishery at previous levels may require managing for high abundance of alewives, which may be inconsistent with overall fish community management goals. The future sustainability and role of chinook salmon needs to be reevaluated in the context of the entire Lake Michigan fish community. * Corresponding author: markholey@mail.fws.gov so abruptly. The crash of the chinook salmon population also resulted in a significant decline in angling effort.The dynamics of BKD within Lake Michigan are poorly understood. Coho salmon Oncorhynchus kisutch, steelhead Oncorhynchus mykiss, and chinook salmon have shown clinical signs of BKD, but chinook salmon was the only Lake Michigan salmonine to experience epizootics and high mortalities. This paper describes the rise and fall of the chinook salmon population and fishery in Lake Michigan. We review available data, much of it previously unpublished, before and after the population crash and discuss the possible factors contributing to the epizootics. How the future management of chinook salmon in Lake Michigan may change because of the species susceptibility to BKD is also discussed.

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To assess the extent that early mortality syndrome (EMS) impacts different Pacific salmonid stocks and the association of EMS with thiamine, we collected eggs of coho salmon Oncorhynchus kisutch from three Lake Michigan tributaries (Platte River, Thompson Creek, and Root River) in 1996-2001. We also obtained eggs of Chinook salmon O. tshawytscha from Lake Michigan (Little Manistee River) and Lake Huron (Swan River) in 1998-2001. Unfertilized eggs from individual females were frozen for thiamine analysis, and the remainder were fertilized and reared until first feeding. We observed a high incidence of EMS in offspring when total egg thiamine levels were less than 1.7 nmol/g in both coho and Chinook salmon. In Lake Michigan strain coho salmon from the Platte River, EMS occurred in more than 70% of monitored families in 1996, 1999, 2000, and 2001, while 1997 and 1998 were years when EMS was low (Ͻ25%). Hinchenbrooke strain coho salmon from Thompson Creek exhibited greater impacts from EMS in the years when EMS was low in the Lake Michigan strain coho salmon from the Platte River. Similar to coho salmon, Lake Michigan Chinook salmon also exhibited EMS (Ͼ70%) in 1999, 2000, and 2001. Chinook salmon from Lake Huron exhibited high (Ͼ70%) EMS in 2001, moderate (40-60%) EMS in 1999, and low (Ͻ25%) EMS in 1998. Our data suggest that the incidence of EMS in salmonids varies by species, location, and year. The data support the general contention that EMS in salmonids is associated with low egg thiamine content.

In the late 1960s, Chinook salmon Oncorhynchus tshawytscha from the Green River, Washington, were successfully introduced into Lake Michigan. During spring from 1988 to 1992, large fish die-offs affecting Chinook salmon occurred in the lake. Multiple ecological factors probably contributed to the severity of the fish kills, but the only disease agent found regularly was Renibacterium salmoninarum, the causative agent of bacterial kidney disease. In this study, survival after challenge by R. salmoninarum was compared between two Chinook salmon stocks: a Lake Michigan stock from Wisconsin (WI) and the progenitor stock from the Green River. We found that the WI stock had significantly greater survival than the Green River stock. Next, the WI and Green River stocks were exposed to the marine pathogen Listonella anguillarum (formerly Vibrio anguillarum), one of the causative agents of vibriosis; survival after this challenge was significantly poorer for the WI stock than for the Green River stock. A close genetic relationship between the Green River and WI stocks was confirmed by analyzing 13 microsatellite loci. These results collectively suggest that disease susceptibility of Lake Michigan Chinook salmon has diverged from that of the source population, possibly in response to pathogen-driven selection.

In 1996 and again in 1999, hatchery personnel noted that some Lake Michigan coho salmon Oncorhynchus kisutch from fall spawning runs on the Platte River weir exhibited abnormal wiggling behavior that was similar to the behavior exhibited by thiamine‐deficient Atlantic salmon Salmo salar, from the Baltic Sea. Samples of eggs or gonads, muscle, and liver from salmon and lake trout Salvelinus namaycush exhibiting abnormal behaviors were collected to determine the extent to which the behaviors were related to a thiamine deficiency. We compared these values with those found in normally behaving fish that produced offspring with high embryonic survival. In all adult fish exhibiting abnormal behavior, tissue residues of thiamine were among the lowest observed in the Great Lakes. Where embryonic survival was assessed, abnormal adult behavior was also associated with very high levels of offspring mortality due to early mortality syndrome. While the overall ecological significance remains to be determined, it appears that adult fish also exhibit neurological dysfunction and mortality associated with thiamine deficiency.