Dietary
thiaminase I is a cause of
thiamine deficiency in animals. The physiological significance of
thiaminase in the organisms containing this
enzyme is not known, nor are the factors causing variation in their
thiaminase activity. Tests were performed to evaluate the effect a pathogen might have on
thiaminase activity in fish, when analyzed both with a cosubstrate added (CATA tests) and no cosubstrate added (NCATA tests).
Pyridine is known as a cosubstrate specific for
thiaminase I activity that does not accelerate
thiaminase II activity. Crucian carp Carassius carassius known to harbor
thiaminase I activity were injected intramuscularly with live Aeromonas salmonicida, a pathogenic bacterium of fish. For comparison, other groups were injected with
formalin-killed bacteria and
phosphate-buffered saline, respectively; an untreated group of fish was kept as a control. The bacteria did not contain any
thiaminase activity. Significantly higher
thiaminase activities (CATA and NCATA) were measured in all tissues (whole blood, injected muscle, uninjected muscle, and whole fish homogenates) of fish injected with live bacteria than in the saline-injected and the uninjected groups. The
thiaminase activity of blood and that in the injected, inflamed muscle tissue followed different allocation patterns in fish injected with live A. salmonicida. The amount of
thiaminase I enzyme appeared to be elevated in the whole blood of injected fish in the absence of natural cosubstrate(s). The
thiaminase activity of the injected, inflamed muscle suggested that both the amount of
thiaminase enzyme and some yet-unidentified natural cosubstrate(s) were elevated. This suggests that in addition to the
enzyme, some cosubstrate(s) of fish or pathogen origin play a regulatory role in the so-farunknown physiological significance of
thiaminase I activity in vivo. It is suggested that the health of fish should be considered when searching for factor(s) affecting its
thiaminase activity.