Diet-Induced Thiamine Deficiency in Captive Marine Mammals
IAAAM 1968
Joseph R. Geraci, BSc, DVM, PhD
Montreal Aquarium, Montreal, Canada

Chastek paralysis a dietary disease of foxes, is caused by incorporating certain species of raw fishes into the diet.6 It is an acute paralytic and often fatal condition which may be prevented or cured by supplemented thiamine.7 The factor causing this disease is a beat labile substance,14 which, when ingested renders dietary thiamine(Vitamin B1) unavailable to the fox. Because of its enzymic nature, this factor, which splits thiamine into its pyrimidine and thiazole components10 is called thiaminaise.18

Fish-thiaminase was first discovered in high concentrations in the viscera of carp,16 and subsequently has been isolated from a number of freshwater and marine species.2,4,9,12,19 Among them, herring (Clupea harengus and smelt Osmerus mordax, make up a substantial portion of the diet of most captive marine mammals in North America.

Since the discovery of Chastek paralysis in foxes, the utilization of a thiaminase-containing diet has become an efficient method of producing selective B1 avitaminosis in fishes,1,8 chicks,16 pigeons rats, and cats.15

The possibility of naturally occurring B1 deficiency in captive marine mammals was first suggested in an early work on the behavior of a captive Grey seal maintained on smelts.11 During the same period inadequate diet was believed to result in the death of two sea lions "Otaria californiana", maintained exclusively on whiting. It was concluded that the post-mortem findings were consistent with those of known thiamine deficiency in other mammals.13

The latter work is of particular interest, in that the fish involved, most likely the Atlantic whiting, Merluccius bilinearis, has been shown to be free of thiaminase in vitro.4,19 There is substantial evidence, however, that this species is biologically active in destroying thiamine when added to a fox diet6 (Figure 1).


There is additional evidence for the occurrence of thiamine deficiency in pinnipeds, but from which a specific diagnosis cannot be made in the absence of known measurable parameters for these animals. Presently, the criteria are based on non-specific histological findings, coupled with a history of ingesting thiaminase-containing fishes and variable clinical signs related to central nervous system disturbance Reference I-as been made only to pinnipeds because of the obvious problem of recognizing clinical signs in cetacea, and due to the paucity of available post-mortem findings referable to thiamine deficiency in this Order.

A partial list of the fishes, now known the contain thiaminase is presented on Figures 2 and 3.

Among these species, one fish likely to be employed in marine mammal diets are smelts Osmerus mordax. Based on its known enzyme activity,3 the theoretical quantities of thiamine required to overcome a "smelt-induced" insufficiency in a 300 lb. dolphin are shown on Figure 4. The number of various commercially available supplements which would then be required to meet the thiamine demand are shown on Figure 5.



Figure 4

Theoretical Quantities of Thiamine Required to Overcome Insufficiency
Due to Diet of Raw Whole Smelt

44 micrograms of B 1 are destroyed by 1 gram smelts3
44 x 450 = 11,800 micrograms destroyed/lb of smelts

300 lb. dolphin eats a minimum of 15 lbs. of fish daily
15 lbs x 110, 800 µg=177, 000 /c(rT (177. 0 mg)

177 mg of B1 is required to overcome the
thiamine destroying activity of pure smelt diet.


The correlation between in vitro and in vivo thiaminase activity must be demonstrated in order to verify the theoretical thiamine demands. Meanwhile, greatest testimony to the potency of the enzyme, as well as a resolution to some of the disparity in the literature regarding its presence, # may be gleaned from the clever study by Stout and his coworkers.22 The investigators showed that the thiaminase-free Pacific hake Merlucius products which contain anchovies Engraulis mordax as ingesta are biologically active in producing B1 deficiency in mink. Removing the stomach contents of the hake prior to feeding cured or prevented the condition. The anchovies had constituted only about 7% of the total diet, but this level was sufficient to destroy the dietary thiamine.

These data, collectively, offer evidence that thiaminase-containing food-fishes may dangerously reduce the availability of dietary thiamine in marine mammals.

(Particularly notable is the question of enzyme, activity in the Atlantic whiting wit, reference to Sea Lion mortality.)


  1. Alexander, I., Green, R.G., Evans, C.A. and Wolf, L.E.; Alcoholic Encephalopathy in Man and Fish - Diet Disease in Foxes and Fishes. Trans. Am. Nerol. Assoc. 67, 1941: 119-122.
  2. Deolalkar, S.T. and Sohonie, K.: Thiaminase from Freshwater, Brackish-Water, and Salt-water Fish. Nature, 173, (4402) March, 13, 1954: 489-490.
  3. Deutsch, H.F., Ott, G.L. : Mechanism of Vitamin B1,.Destruction by a Factor in Raw Smelt, Proc. Soc. Exp. Biol.& Med., 51, 1942 : 119-122.
  4. Deutsch, H.F. and Hasler, A.D.: Distribution of a Vitamin B1 Destructive Enzyme in Fish. Proc. Soc. Exp, Biol. & Med., 53, 1943 : 63-65.
  5. Geraci, J.R.,: unpublished data
  6. Green, R.G., Carlson, W.E. and Evans, C.A.: A Deficiency Disease of Poxes Produced by Feeding Fish. J. Nut. 21, Jan-June, 1941: 243-256.
  7. Green, R.G. Carlson, W.F., and Evans, C.A.: The Inactivation of Vitamin B1 in Diets Containing Whole Fish. J. Nut. 23, Jan-June, 1942:165-174.
  8. Harrington, R.W.: Contrasting susceptibilities to Two Fish Species to a Diet Destructive to Vitamin B1. J.Fish. Res. Rd. Can. 11 (5) 1954: 529-534.
  9. Hilker, D.M. and Peter, G.F.: Anti-Thiarnine Activity in Hawaii Fish. J. Hut. 89(4) Aug. 1966 - 419-421.
  10. Krampitz, L.O. and Woolley, D.W.: The Manner of Inactivation of Thiamine by Fish Tissue. T. Biol. Chem. 152, 1944: 9-17.
  11. Myers, R.J.: The rearing of a Grey Seal in captivity Can. Field Naturalist 69, (4): Oct.-Dec. 1955.
  12. Neilands, J.B.: Thiaminase in Aquatic Animals of Nova-Scotia J. Fish. Res. Bd. Can., 7 (2) 1947: 94-99
  13. Rigdon, R.H. and Drager G.A.: Thiamine Deficiency in Sea Lions (Otaria californiana) Fed only Frozen Fish. J. Am. Vet. Med. Assoc., 127, (944), Nov. 1955: 453-455.
  14. Sealock, R.R., Livermore, A.H., and Evans, C.A.: Thiamine Inactivation by the Fresh-fish or Chastek Paralysis Factor. J. Am. Chem. Soc. 65, 1943: 935.
  15. Smith, D.C. and Proutt, L.M.: Development of Thiamine Deficiency in the on a Diet of Raw Fish. Proc. Soc. Exp. Biol. & Med. 56, 1944
  16. Spitzer, F. H. Coombes, A.I., Elvehyem C.A. & Wisnicky, W.: Inactivation of Vitamin B 1 by Raw Fish. Proc. Soc. Exp. Biol. & Med. 48, 1941: 376-379.
  17. Stout, F.M., Oldfield, J.E. & Adair, J. A secondary induced thiamine deficiency inMink. Nature, 197 (4869): Feb. 23, 1963 810-811.
  18. Sumner, J.R. and Somers, G.F.: Chemistry and Methods of Enzymes. Academic Dress, New York, 1947: 314.
  19. Yudkin, W.H.: Occurrence of Thiaminase in Marine Teleosts. Proc. Exp. Biol. & MPH., 60 , 1945 - 268-269.
  20. Yudkin, W.H.: Thiaminase, the Chastek Paralysis Factor. Physiol. Rev. 29, 1949: 389-401.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Joseph R. Geraci, BSc, DVM, PhD

MAIN : All : Thiamine Deficiency
Powered By VIN