Red vent syndrome in wild Atlantic salmon Salmo salar in Scotland is associated with Anisakis simplex sensu stricto (Nematoda: Anisakidae)

Abstract

Simultaneous reports were received between June and July 2007 of wild Atlantic salmon Salmo salar with red, swollen, bloody vents returning to geographically diverse rivers in Scotland. By the end of September the condition, colloquially known as 'red vent syndrome' (RVS), was reported from > 50 rivers across Scotland. Fish were generally in good overall condition but the vent area showed mild to severe lesions. External characteristics of the syndrome included a swollen, raised, haemorrhagic vent and surrounding tissues, with erosion of the skin, scale loss and moderate to severe bleeding in more advanced cases. Predominantly, the fish affected were 1-sea-winter grilse; however, RVS was also recorded in 2-sea-winter salmon and sea trout S. trutta. High numbers of the nematode Anisakis Type I larvae were found infesting the discrete region of the vent, a localisation that is reported as novel for the parasite. The hypothesis that this is a different species than that commonly found in the body cavity and viscera was investigated through molecular studies. These studies failed to show evidence that the parasites infesting the vent were different from those in the body cavity, i.e. all were identified as A. simplex sensu stricto. No other disease agent was found associated with the lesions or was isolated systemically, and no mortality or prevention of spawning was recorded during the 2007 season. Possible causes, including warming environments in the North Atlantic, are hypothesised as playing a role in the development of RVS in Atlantic salmon.

Relationship Between Red Vent Syndrome and Anisakid Larvae Burden in Wild Atlantic Salmon (Salmo Salar)

“…were present in the perianal region of 91% of examined salmon, regardless of the presence or absence of red vent syndrome. This confirms the observation by Noguera et al (2009) that only the presence of Anisakis sp. larvae is not sufficient to explain the macroscopic lesions observed in salmon with red vent syndrome.…”

“…The differences in intensities of inflammation observed microscopically paralleled the macroscopic lesions; salmon with red vent syndrome generally had higher grades of inflammation than control salmon. Although fine-scale evaluation of the histologic sections was limited by changes due to freezing, inflammatory infiltrates were located around nematode larvae, as reported previously (Beck et al, 2008;Noguera et al, 2009). Histologic examination of the perianal region was less sensitive than enzymatic digestion in assessing the presence of Anisakis sp.…”

“…Although variations in the time from death to sampling could have caused a bias, this variable was assumed to be evenly distributed between groups of salmon with or without lesions. Noguera et al (2009) proposed that the cumulative effect of a large number of larvae concentrated in the vent region might be a determining factor in the occurrence of this syndrome. Our study supports this hypothesis by showing that the odds of having red vent syndrome significantly increased with the number of larvae per gram detected in perianal tissue.…”

“…This emerging syndrome of wild Atlantic salmon, which was first identified in Great Britain in 2004 (Beck et al, 2008), is characterized by reddening, swelling, and inflammation of the perianal region with or without cutaneous ulceration, scale loss, and bleeding. The lesions observed in this syndrome are associated with the presence of nonencapsulated nematode larvae of the species Anisakis simplex in the body wall, the lower intestinal wall, and the visceral cavity surrounding the vent region (Beck et al, 2008;Noguera et al, 2009). The adult nematodes are found in the gastric chambers of cetaceans.…”

“…The reasons for the apparent emergence of red vent syndrome in salmon are not fully understood. A high intensity of parasitic larval infection in salmon has been proposed as a determining factor in the development of this syndrome (Noguera et al, 2009).…”