In Atlantic Canada, Moritella viscosa is often cultured from Atlantic salmon skin ulcers in the summer and autumn months when water temperature is > 10 degrees C. The objectives of our study were to: 1) describe the development of skin ulcers associated with an Atlantic Canadian M. viscosa isolate; and 2) determine if this isolate could be transmitted horizontally between fish via water under laboratory conditions. Atlantic salmon in salt water were bath-immersed with M. viscosa (5.6 x 10(6) cfu ml-1) at 10.9 +/- 0.2 degrees C. After observing skin lesions, water from each bath-challenge tank was diverted to a "delayed-challenge" tank with previously unexposed fish. The initial bath-challenge fish expressed clinical signs of skin ulcers within four days of exposure. Fish that were not sacrificed during our trial fully recovered by 26 days post-challenge. No clinical signs of disease were observed in fish from the delayed-challenge tanks. Our results suggest skin lesions induced by an M. viscosa isolate from Atlantic Canada have similar pathology to winter ulcer disease described in Europe. Most bath-challenged fish were not systemically infected until the development of visible skin ulcerations. None of the delayed-challenge fish were infected with M. viscosa, which suggests horizontal transmission via the water was not sufficient to cause disease in our study.

Skin ulcers in Atlantic salmon Salmo salar in the Canadian east coast salmon aquaculture industry lead to high mortality rates. This condition is clinically similar to winter ulcer disease in Norway with the exception that it occurs at temperatures above 10°C. Moritella viscosa is thought to be the causative agent for winter ulcer disease in Norway, and it is occasionally also isolated from skin ulcer cases in Atlantic Canada. This bacterium is known to produce cytotoxins. The objective of this study was to determine if extracellular products (ECP) from an Atlantic Canadian strain of M. viscosa could induce a tissue response similar to what is observed with M. viscosa infections in Atlantic salmon in eastern Canada. We injected fish subcutaneously with ECP and monitored the development of skin lesions. We sampled fish with early skin lesions and ulcers to describe the pathology associated with the condition. Samples were taken for histopathology, bacterial culture, and quantitative PCR (qPCR). All experimental fish expressed early skin lesions, with 5 fish (8.3%) developing deep skin ulcers after 12 d post-exposure. Our results suggest the ECP of M. viscosa from the east coast of Canada induces a similar tissue response to what is described in ulcer disease in Atlantic salmon. These extracelluar products may partially explain the pathology associated with M. viscosa.

Skin ulcers have been increasing in occurrence on Atlantic salmon (Salmo salar) farms in Atlantic Canada during summer and autumn months when water temperatures are elevated above 10 degrees C. The clinical presentation in Atlantic Canada resembles lesions associated with winter ulcer disease in Europe caused by Moritella viscosa, but this bacterium is not always identified from skin lesions in North American cases. The objectives of our study were to: 1) describe the onset, duration, magnitude, and temporal and spatial distributions of Atlantic Canadian skin ulcer cases at the cage and farm levels; 2) develop hypotheses regarding potential sources and transmission routes for infection based on the patterns of disease occurrence; and 3) identify potential risk factors associated with total percent mortality during skin ulcer outbreaks. We summarized weekly cage-level data from 29 salmon farms in Atlantic Canada, from April 2014 to January 2016. Cage and farm-level prevalence, onset, duration, and total percent mortality associated with skin ulcer outbreaks were determined. The association of potential risk factors for skin ulcers with total percent mortality during skin ulcer outbreaks was assessed using a mixed-effects linear regression model with random farm effects. The overall farm-level prevalence of skin ulcers on Atlantic Canadian farms included in our study was 41%. The descriptive epidemiology of skin ulcers suggests cages are likely exposed to the causative agent(s) only at certain times of the year and exposure is not uniform across farms based on the patterns of disease occurrence. The onset of skin ulcer outbreaks in our study occurred from late-summer to mid-autumn. The pattern of disease is also suggestive of point source exposures to the causative agent across farms. In our final regression model, year of outbreak onset, and the interaction between the diagnosis of skin ulcers at the cage level and antibiotic treatment during the outbreaks were significantly associated with the log of total percent mortality during the outbreaks (P < .001). Our results did not identify any management factors that could reduce the severity of skin ulcer outbreaks on affected farms.