

50 BACTERIAL POISONS 



the body of the organisms and are only liberated when these undergo 

 disintegration, while the true toxins are actively secreted by the 

 living cells. This is one of the essential points of difference also 

 which distinguish the exotoxins, or toxins in short, as they are usually 

 designated from the ptomains. The ptomains are products of 

 bacterial action upon certain foodstuffs, and their formation is, hence, 

 possible only when such foodstuffs are directly available, while toxin 

 production is within certain limitations independent of the food 

 supply, and represents, a specific function on the part of the micro- 

 organisms in question.' The toxin is in a certain sense a product of 

 j ^ the anabolic activity of the organism, while the ptomain is merely 

 i_a katabolic product. The production of a given ptomain, moreover, 

 ~uti i is not confined to a given type of organism, while true toxin produc- 

 tion is specific. Only one organism is known to form diphtheria 

 toxin, only one is known to produce tetanuatoxin, and only one 

 is the source of botulismus toxin. That these* toxins are actually 

 responsible for the clinical picture of the corresponding diseases is 

 now a recognized fact, and just as the toxins in question are specific 

 products of the bacteria, so also are the symptoms to which they 

 give rise in a large measure specific of the homologous infections. 



The tetanus toxin when injected by itself into suitable animals thus 

 causes tonic spasms of the muscles in the neighborhood of the point 

 infection, increased reflex irritability, dyspnea, increased heart 

 action, and hematolysis exactly as if the animal had been inoculated 

 with the living bacteria instead. The diphtheria toxin produces 

 edema, infiltration, and necrosis at the point of injection, increase 

 of temperature followed by a drop, and in non-fatal doses paralysis 

 and marked emaciation. Botulismus toxin, no matter how intro- 

 duced, gives rise to external and internal ophthalmoplegia, dys- 

 phagia, aphonia, retention of urine and feces, and to respiratory 

 and circulatory disturbances, with absence of fever and of cerebral 

 symptoms, etc. 



We may accordingly assume that the toxins in question have a 

 special selective affinity for certain tissues and produce their symp- 

 toms in consequence of such affinity. This is seen especially well 

 in the case of the tetanus toxin, which produces its clinical effect 

 through its action upon the central nervous system to which it 

 becomes anchored, as is shown in the following experiment: If 

 1 gram of guinea-pig brain is triturated with 10 c.c. of normal salt 



of 

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