Adult mortality and low egg hatch rate were observed among American alligators Alligator mississippiensis in Lake Griffin, Florida, between 1998 and 2003. Previous studies show that the alligator mortality is due to neurological impairment associated with
thiamine (
vitamin Bt) deficiency. This study determined the rate of
thiaminase activity in gizzard shad Dorosoma cepedianum, a fish often eaten by alligators, and examined the
thiamine status of captive adult alligators fed only gizzard shad. We found that the
thiaminase activity of gizzard shad in Lake Griffin is 16,409 +/- 2,121 pmol/g/min (mean +/- 2SEs). This high rate of
thiaminase activity was present in most months and across a wide range of shad sizes. Seven alligators were captured in the wild from Lake Griffin and Lake Woodruff, held in captivity, and fed gizzard shad. We monitored blood and muscle
thiamine levels throughout the experiment and liver
thiamine at the end. Over a period of 6-12 months, all of the alligators maintained weight but blood and muscle
thiamine levels decreased to 25-50% of the original (healthy) values. Three animals with the greatest reduction in
thiamine died, demonstrating mobility impairment and neural histopathology similar to those seen in wild alligators in Lake Griffin. Two alligators were fed shad for 10 months but then treated with
thiamine. These animals showed a reduction in
thiamine while eating shad, but treatment restored their
thiamine levels to the initial values, which were comparable to those of normal wild Lake Griffin alligators. We demonstrated that
thiamine deficiency can be induced by a diet of gizzard shad and cause neurological signs and death in alligators in captivity. We conclude that the
thiaminase activity in gizzard shad is high enough to cause
thiamine deficiency in wild alligators when shad are a major part of their diet.