384 RIBOFLAVIN 



2. Dogs and Foxes 



SebrelP^' ^^ was probably the first to critically evaluate the pathological 

 state in dogs now known to be due to a deficiency of riboflavin. Among the 

 signs noted was the characteristic "yellow liver" due to fatty infiltration. 

 Later, during studies of canine blacktongue, it was shown that riboflavin 

 often prevents death in animals on blacktongue-producing diets. ^^"^^ With 

 inadequate riboflavin, collapse, coma, and death occurred in less than 102 

 days. The onset was sudden and characterized by ataxia, weakness, and 

 loss of deep reflexes, so that the dog was unable to stand. The animal ap- 

 peared fully conscious and without pain prior to final collapse, as though 

 death were due to a cellular asphyxia brought on by a failing chemical 

 mechanism.^^ This collapse syndrome was also noted by Street and CowgilP^ 

 in dogs on diets which contained not more than traces of riboflavin. 



Street et al.,^^ while investigating neurological manifestations of ribo- 

 flavin deficiency, were not able to confirm the finding of fatty degeneration 

 of the liver in their dogs. They noted myelin degeneration in peripheral 

 nerves and in the posterior columns of the spinal cord, becoming more ex- 

 tensive with the length of the period on the deficient diet. Opacities of the 

 cornea were also noted. The suggestion of these authors that inanition was 

 the cause of previously published reports of fatty liver cannot be reconciled 

 with the observations of Potter et al.,^^ who noted no fatty liver in their 

 inanition-control dogs, whereas their riboflavin-deficient, choHne-supple- 

 mented diets produced typical friable, fatty, yellow livers. Also noted was a 

 dry, flaky dermatitis, usually accompanied by a marked erythema on the 

 hind legs, chest, and abdomen, and a purulent discharge from the eye, 

 which was associated with a conjunctivitis. This was followed in a few 

 days by vascularization of the cornea, which in several dogs went on to 

 corneal opacification. 



Anemias have been noted in riboflavin-deficient dogs,^^' ^^' "" but it 

 remains a question whether this is a specific part of the deficiency syndrome. 



The deficiency symptoms which develop in the fox closely resemble those 



63 W. H. Sebrell, Public Health Repls. {U.S.) 44, 2697 (1929). 

 6« W. H. Sebrell, Natl. Insts. Health Bull. 162, Part 3, 23 (1933). 



65 W. H. Sebrell, D. J. Hunt, and R. H. Onstott, Public Health Repts. {U.S.) 52, 

 235 (1937). 



66 W. H. Sebrell, R. H. Onstott, and D. J. Hunt, Public Health Repts. {U.S.) 52, 427 

 (1937). 



6' W. H. Sebrell and R. H. Onstott, Public Health Repts. {U.S.) 53, 83 (1938). 

 68 H. R. Street and G. R. Cowgill, Am. J. Physiol. 125, 323 (1939). 

 «9 R. L. Potter, A. E. Axelrod, and C. A. Elvehjem, J. Nutrition 24, 449 (1942). 

 ^0 H. Spector, A. R. Maass, L. Michaud, C. A. Elvehjem, and E. B. Hart, /. Biol. 

 Chem.im, 75 (1943). 



