Ruth M. Duncan Wayne I. Jensen 1980 <p><span>Most strains of&nbsp;</span><i>Clostridium botulinum</i><span><span>&nbsp;</span>type C, after having lost their capacity to produce their dominant toxin (C</span>₁<span>) as a result of being“cured”of their prophages, continue to produce C</span>₂<span>, a trypsin-activable toxin reported by other investigators. While of relatively low toxicity when administered perorally to the adult mallard duck (</span><i>Anas platyrhynchos</i><span>), it was highly toxic when given parenterally. By the intravenous route, for example, it was more than 1, 000 times as toxic as C</span>₁<span><span>&nbsp;</span>toxin by the same route, when compared on the basis of mouse intraperitoneal toxicity. The cause of death in every instance was massive pulmonary edema and hemorrhage rather than the respiratory paralysis that occurs in C</span>₁<span><span>&nbsp;</span>intoxication.</span><span>抄録</span></p> application/pdf 10.7883/yoken1952.33.81 en National Institute of Health The susceptibility of the mallard duck (Anas platyrhynchos) to Clostridium botulinum C2 toxin article