feeding gradually ceased and many emaciated 

 fish or "pin heads" with a characteristic severe 

 concave or "pinched" abdomen occurred. Some 

 loss of ability to control the dorsal and pectoral 

 fins was noted in moribund specimens. Loco- 

 motion consisted of a slow, rolling action and 

 a general loss of equilibrium . The coloration 

 of affected fish changed from a dark hue at the 

 onset of the clinical manifestations of the de- 

 ficiency to a more transparent condition when 

 moribund or dead. 



The pyridoxine deficiency syndrome 

 manifested itself by loss of equilibrium and by 

 rapid flashing and erratically skipping action 

 along the surface of the water just prior to death . 

 Upon death, these fish assumed a lateral cres- 

 cent shape and were light in color. The char- 

 acteristic blue color previously described in 

 Chinook salmon (Halver 1957a) was not noted. 

 During the early stages of the malady, the ap- 

 petite was fair but changed to a complete lack 

 of feeding during the late stages of the experi- 

 ment. Severely affected fish exhibited indiffer- 

 ence to strong lig^t in contrast to the controls' 

 definite negative phototropism . 



The folic acid group exhibited no clinic- 

 al syndrome and periodic blood counts did not 

 indicate any gross anemia. However, when this 

 group was divided, the section receiving the 

 complete diet indicated a definite benefit from 

 the addition of folic acid by a rapid growth 

 response and a significant increase in weight 

 over the deficient lot. 



The biotin deficiency syndrome was 

 characterized by loss of appetite, emaciated 

 bodies and the caudal fins were contracted to 

 form a triangular point. Although the feeding 

 habits of the deficient fish were retarded, the 

 individuals seemed fairly active throughout the 

 experiment. The recovery group regained 

 normal appetite and weight quickly, and within 

 2 weeks these fish appeared normal. Mortalities, 

 fairly consistent in other groups, were virtually 

 non-existent in the biotin recovery gfroup after 

 replacement of the missing vitamin in the diet. 



Pantothenic acid depleted fish had the 

 characteristic clubbed gills previously noted by 

 many investigators. As the syndrome started 

 to appear, these fish gradually lost their appetite 



until they ceased feeding entirely near the end 

 of the experiment. The recovery group exhibited 

 a rapid positive response in appetite and growth 

 as soon as the gill damage was repaired, and 

 near the end of the experiment, was gaining 

 rapidly . 



The appetite and growth of the inositol 

 deficient group was reduced, although a con- 

 sistent gain in weight was noted. Upon replace- 

 ment of the missing vitamin in the diet the 

 recovery group showed a significant growth 

 response and a corresponding reduction in mor- 

 tality from that of the deficient lot. 



The choline deficient fish fed actively 

 throughout the experiment but failed to gain 

 weight, resulting in emaciated fish in the entire 

 population. When one -half the group was fed the 

 complete diet, they immediately started to gain 

 whereas the group continued on the choline de- 

 ficiency continued to lose weight . The growth 

 curve of the choUne deficient group was not 

 graphed because a general straight line relation 

 existed from the start to the end of the experi- 

 ment, and the mortality rate was consistently 

 low throughout. 



Disease decimated the niacin deficient 

 group before any specific syndromes became ap- 

 parent. This group was split at the end of 12 

 weeks but at the 16-week period there were no 

 significant differences between the deficient and 

 recovery groups. Since these fish were held in- 

 doors, the common "sunburn" symptom described 

 by DeLong, Yasutake and Halver (1958) in Chin- 

 ook salmon and rainbow trout did not appear . 

 Exposure of these fish to ultraviolet light in- a 

 more carefully controlled environment might have 

 resulted in the appearance of a specific deficiency 

 syndrome. 



Similarly, the riboflavin deficient group 

 did not exhibit any gross clinical symptoms. 

 Growth continued parallel to the controlled lot 

 throughout the course of the experiment but a 

 slight clouding of the lenses of the eyes appeared 

 in some of the moribund fish late in the experi- 

 ment. Some food was probably introduced through 

 the screens in the creek water supply and may 

 have been sufficient to partially supplement the 

 diet to an extent preventing severe clinical man- 

 ifestations of riboflavin deficiency. 



