R. K. Stroud 

 A. V. Nebeker 



A Study of the | 



Pathogenesis 



of Gas Bubble 



Disease in Steelhead Trout 



(Salmo gairdneri) 



ABSTRACT 



Steelhead trout were exposed to supersaturated water and 

 randomly removed for necropsy at predetermined intervals 

 Lesions included emphysema of fins and opercular, gas emboli, 

 exophthalmia, and hemorrhaging. The hypothesis that death 

 from gas bubble disease is due to hemostasis due to blockage of 

 blood flow by emboli was supported by the necropsy results. A 

 "cascading bubble effect" is described to explain bubble 

 formation. 



Although gas bubble disease (GBD) in salmonid 

 fish has been studied extensively in connection with 

 supersaturation of the Columbia River by hydro- 

 electric projects, few studies of the pathogenesis of 

 GBD have been reported. Observations of lesions 

 such as emphysema of the fins and body, exoph- 

 thalmia, gas emboli within the circulatory system, 

 gill hemorrhage, and others have been made on 

 fish exposed to supersaturated water in hatcheries, 

 under experimental conditions, and in natural situ- 

 ations (Bouck et al., 1970; Ebel, 1969; Harvey and 

 Smith, 1961; Marsh and Gorham, 1905; Rucker and 

 Hodgeboom, 1953; Rucker, 1972; Shirahata, 1966; 

 Wyatt and Beiningen, 1971). Observations in these 

 studies were primarily made on fish that had died 

 or were near death. 



This study attempts to document the events 

 leading to the death of fish and describe the 

 sequence of development and incidence of certain 

 gross lesions in juvenile steelhead trout (Salmo 

 gairdneri) continuously exposed to three levels of 

 supersaturated water in shallow tanks. 



MATERIALS AND METHODS 



Steelhead trout obtained as eyed-eggs from 

 the Alsea Hatchery of the Oregon Wildlife Commis- 

 sion were raised for experimental purposes at the 

 Western Fish Toxicology Station, Corvallis, Oregon. 

 These fish ranged from 17 to 24 cm fork length, with 

 the majority of fish in the 18 to 20 cm range at the 

 time of use. 



The experimental apparatus consisted of four 

 12-ft (3.75 m) diameter circular tanks containing 

 well water supersaturated to various levels by con- 

 trolled air injection. Water in the tanks was main- 

 tained at a depth of 24 in. (60 cm) and 10°C. A more 

 detailed description of the experimental tanks and 

 method of supersaturation has been reported else- 

 where (Nebeker and Stevens, 1975). Supersaturation 

 levels were monitored daily with a Weiss saturom- 

 eter. Supersaturation levels were maintained within 

 ±1% of 120%, 115% and 110% which were the three 

 exposure levels used in this experiment. A 100% 

 saturated tank was used as a control. 



A four-compartment submersible cage was 

 placed in the center of each of the four tanks. Thirty- 

 eight randomly selected fish were divided into four 

 lots and placed in the four compartments of the 

 cage in the 120% supersaturated water. Twenty- 

 nine fish were similarly caged in 115% water, 29 in 

 110% and 12 in 100%. Although caging fish in this 

 manner prevented access to peripheral areas of the 

 tank where the water current was greatest, it did 

 facilitate sampling of fish. 



Random samples consisting of five fish were 

 taken from each tank at predetermined intervals to 

 check the development of lesions associated with 

 GBD. The fish were immediately placed in a high 

 concentration of MS222. Complete anesthesia was 

 achieved in less than 2 min. The water used as a 

 vehicle for the MS222 was dipped from the same 

 tanks from which the fish were taken. This proce- 

 dure kept the fish continually exposed to the same 

 level of supersaturation until they were necropsied. 

 Sampling intervals varied according to previously 



Stroud: Department of Veterinary Medicine, Oregon State 

 University, Corvallis, Oregon; and Nebeker: United States 

 Environmental Protection Agency, Western Fish Toxicology 

 Laboratory, Corvallis, Oregon 



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