J. p. SIMONDS 781 



From the foregoing review, the experimental evidence of the relation between 

 bacterial toxic products and nephritis may be summarized as follows: (i) soluble 

 poisons like diphtheria toxin produce their effects upon the glomerular capillaries 

 because of their concentration as a result of the loss of water from the blood at this 

 place; (2) bacteria of the colon-typhoid group may give rise to toxic products which 

 will damage the kidneys as a result of bacteriolysis to which this group of bacteria are 

 particularly susceptible; (3) the mechanism by which toxic substances injurious to 

 the kidneys are derived from streptococci is not clear because they are not readily 

 dissolved by bacteriolysis; (4) incontestable evidence of the successful production of 

 chronic nephritis by bacterial toxic products is very scanty if not wholly lacking. 



The etiology of nephritis occurring spontaneously in man has been repeatedly 

 sought in the possible absorption of toxic products from areas of focal infection, such 

 as chronically diseased tonsils, abscessed teeth, etc. The mere coexistence of ne- 

 phritis and focal infection does not prove an etiological relation. Newburgh' insists 

 that in order to establish a relation between focal infection and the causation of ne- 

 phritis by toxic products absorbed from such a focus, it must be shown that patients 

 are generally cured or at least greatly benefited by the removal of the focus. In his 

 extensive experience, "The eradication of foci of infection in patients coming to the 

 University Hospital has thus far not resulted in a single cure." 



SPECIFIC EFFECTS 



The problem of the specific effects of bacterial toxins is complex. Many of the 

 effects that appear to be specific are not the result of any special affinity of the toxin 

 for a given tissue. For example, the immediate cause of death in pneumonia is fre- 

 quently failure of the heart. This is not due to any specific action of any product of 

 the pneumococcus upon the heart itself, but to the fact that the myocardium is the 

 site of a parenchymatous degeneration similar to that which occurs simultaneously 

 in other parenchymatous organs, such as the liver and kidneys. 



Diphtheria toxin, however, does have a special affinity for nerve tissue and, in 

 the guinea pig at least, for the adrenals. Courmont and Rochaix-^ have suggested 

 that lipoids, especially those which contain phosphorus, may be concerned in the 

 fixation of this toxin in these locations. 



The toxins of B. tetanus and of B. botulinus have a specific affinity for the central 

 nervous system. They become fixed in brain tissue both in vitro and in vivo. But the 

 mode of action of the poison is different in the two cases. Tetanus toxin causes con- 

 vulsions, probably by increasing the activity of the synapses and by upsetting the 

 co-ordinating mechanism of antagonistic muscles. The poison of botulism causes 

 mydriasis and paralysis of the muscles concerned with swallowing and with speech. 



The truly specific effects of bacterial toxins are based upon a chemical affinity of 

 these poisons for special tissues as a consequence of which they become concentrated 

 in some particular location. Other organs and tissues are thus protected against their 

 action while the particular organ receives the whole force of their destructive action. 



' Newburgh, L. H.: Medicine, 2, 77. 1923. ^ Courmont, J., and Rochaix, A.: loc. cit. 



