Activation of a Toxic Component of Clostridium botulinum Types C and D by Trypsin

Abstract

When the Stockholm and 468C strains of type C and the 1873 strain of type D Clostridium botulinum are “cured” of their prophages, they simultaneously discontinue the production of their dominant toxins (C 1 and D), but they continue to produce a second antigenically monospecific toxin (C 2 ). These “cured” strains of types C and D therefore become indistinguishable with respect to the toxin produced. Fifteen type C cultures received from other laboratories discontinued to produce the dominant toxin when subcultured in broth. The C 2 toxin, however, was produced by eight of these cultures. The C 2 toxin is produced by these cultures as a protoxin that requires treatment with trypsin before its toxicity can be demonstrated. Of the 21 type C cultures that produce the C 1 toxin, 20 were shown to produce the C 2 toxin. The filtrates of 14 of these cultures required trypsin treatment before the C 2 toxicity could be demonstrated. Low levels of toxicity could be demonstrated in the six remaining culture fluids without trypsin; toxicity, however, was increased with trypsin.