subcutaneous lesions vfhich eventually perforate the epithelium. The 

 ulcers so formed have ragged and irregular margins and are deep red in 

 color, OTivlng to the large accumulation of blood and liquefied tissue 

 (Fish 1935). 



A characteristic of ulcer disease is that the edges of the jaws 

 and the roof of the mouth are very often attacked (Wolf 1938, Davis 194.6), 

 All the soft tissue over a large area of the roof of the mouth may be 

 eaten away and ulcers at the edges of the jaws often progress very 

 rapidly, especially en the lower javf where the bones may be eaten 

 through (Vfolf ].938). 



Small ulcers frequently.' develop on the fins in ulcer disease and 

 these attack the fin rays as vrell as the soft tissue. Often a group 

 of rays is punctured midway, or even closer to the base of the fin 

 (Wolf 1938). Fish (1934) was unable to culture any bacteria from the 

 blood or internal organs of fish v/ith ulcer disease, which is not the 

 case vath furunculosis, as is well-knovm. 



The occurrence of fungus on lesions of ulcer disease is rarer 

 than vri. th furunculosis. Fish (1934-) stated that the lesions of ulcer 

 disease are seldom, if ever, attacked ty fungus during the life of the 

 host, whereas those of furunculosis usually support a luxuriant grcrth 

 of Saprolegnia . \Yolf (1938), however, did obtain several fish at 

 various times from hatcheries Trhich had considerable fungus. 



Fish (1934) believes that the etiological agent is capable of 

 producing a toxin which may be absorbed from lesions and may in part 

 account for the hea-'/y mortality accompanying the disease. This tentative 

 conclusion is based upon the large ajnount of microscopical necrosis 

 surrounding a relatively small accumulation of bacteria. Microscopic 

 areas of necrosis have even been found in the liver and kidney of 

 heavily infected hosts sacrificed at the point of death. These areas 

 showed no evidence of bacterial invasion or cellular infiltration. As 

 already pointed out there has been no suggestion of a toxin with 

 furunculosis (Furunculosis Comm.itt.ee 1935). 



It seems quite probable that the primarj^ site of infection in 

 ulcer disease is at a point of injury to the normal epitheliiun (Fish 

 1934). Yvhether or not the causative agent is capable of independent 

 penetration of the epitheliujn is not Icncvm. The first protective 

 response to the infection is a marked thickening of the epithelium, 

 which is responsible for the appearance of the epithelial tufts and the 

 white line of fin lesions. At this time, the bacteria may be found in a 

 localized area between the base of the epithelium and the subepithelial 

 connective tissue. A slight infiltration of pol3.TnorphonuGlear leucocytes 

 is noticeable at this stage. A progressive necrosis extends in all 

 directions from this picture which results in complete disintegration 

 and sloughing of the scales and subepithelial connective tissue. A 



57 



