Coaster brook trout are a migratory form of brook trout Salvelinus fontinalis that spend part of their lives in the Great Lakes. Over the last century the abundance of coaster brook trout in Lake Superior has declined dramatically, and only remnant stocks remain. Recently, the rehabilitation of coaster brook trout in Lake Superior has become a goal of fish management agencies. The specific goal agreed upon by all of the agencies involved is to maintain widely distributed, self‐sustaining populations in as many of the historical habitats as practical. We discuss realistic expectations for rehabilitation and emphasize the need for management agencies, academia, and angling organizations to work cooperatively. We first present a brief history of coaster brook trout in Lake Superior, then discuss habitat requirements and protection, the regulations required for rehabilitation, stocking, species interactions, and the role that human dimensions play in rehabilitation. The management issues that must be addressed are implementation of a basinwide survey to identify remnant stocks and critical habitat, restrictive harvest regulations, watershed rehabilitation, critical biological review, and the formulation of expectations before experimental stocking programs are initiated, along with coordinated, basinwide information sharing and cooperative management among agencies similar to that undertaken during the rehabilitation of lake trout Salvelinus namaycush in Lake Superior. Future research needs include basic coaster biology and life history, habitat use in streams and the lake, interaction with other species in the Lake Superior fish community, and interaction between stream‐resident and coaster brook trout. Successful rehabilitation will require a shift from a harvest fishery to one with minimal or no harvest of coaster brook trout in the Lake Superior basin. Coaster brook trout rehabilitation will take time and will proceed at different rates at different locations, depending on the presence of remnant stocks, quality of habitat, angling pressure, and political will.

During June and July 2012, Buffalo Pound Lake and Blackstrap Lake in Saskatchewan, Canada were visited biweekly and surveyed for sick and dying fish. During this investigation, 2 fish kills were identified. Buffalo Pound experienced a large die-off of yellow perch (Perca flavascens) in June, while Blackstrap experienced a die-off of lake whitefish (Coregonus clupeaformis) in July. In excess of 50 fish were examined for gross lesions at each lake, and dead and moribund fish consistently had 1 or more of the following lesions: multifocal petechial cutaneous hemorrhage, skin ulceration, or branchial necrosis. Of these, 17 fish were collected for necropsy, and major tissues were submitted for histology. Aerobic bacterial culture was performed on 16 out of 17 fish. In 7 out of 8 (88%) yellow perch, the body wall had multiple areas of pale discoloration that corresponded to erosion and ulceration of the skin. Seven out of 8 (88%) whitefish had severe necrotizing branchiitis, and 8 out of 8 (100%) had severe epicardial parasitism, consistent with Ichthyocotylurus erraticus. Wet mounts of skin and gill lesions demonstrated filamentous bacteria with gliding motility, which often formed haystack-like arrangements. Flavobacterium columnare and Aeromonas hydrophila were cultured from skin and gill lesions of all fish. Based on the characteristic appearance and distribution of lesions, mortality was attributed to columnaris disease with secondary infection with A. hydrophila. The current study demonstrates that columnaris disease is an important contributor to fish kills in southern Saskatchewan lakes. However, further research is needed to determine what role environmental factors play in outbreaks of columnaris disease in prairie lakes.

We report two cases of lipoblastoma with chromosome 8-related aberrations, ie, a 92,XXYY,t(7;8Xp22;q11.2)x2 [8]/46,XY[16] in Case 1 and a 46,XY,-8,-13,add(16) (q22),+mar, +r [cp13]/46,XY[7] in Case 2. Using spectral karyotyping and fluorescence in situ hybridization techniques, the karyotype of Case 2 was redesignated as 46,XY, r(8), del(13)(q12), der(16)ins(16;8)(q22; q24q11.2)[cp13]/46,XY[7]. This report delineates a new chromosome rearrangement, ie, der(16)ins(16;8)(q22; q24q11.2) in lipoblastoma, and also confirms the t(7; 8)(p22;q11.2), reported only once previously, as a recurrent translocation involved in such a tumor. These findings provide valuable information for clinical molecular cytogenetic diagnosis of lipoblastoma. Furthermore, this report highlights the value of cytogenetic and molecular cytogenetic analysis in differential diagnosis of childhood adipose tissue tumors and adds to the number of lipoblastomas reported with chromosomal abnormalities at 8q11.2.

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