J. p. SIMONDS 777 



and of the staphylococcus produced no temperature changes in guinea pigs, even in 

 relatively large doses. It may be remarked that failure to induce a rise in temperature 

 by injections of extracts of these organisms was the result of the method employed 

 to liberate the bacterial protein. Neither the tubercle bacillus nor the staphylococcus 

 are readily susceptible to lysis by immune serum. The typhoid anaphylatoxin of 

 Moreschi and Golgi in proper dosage did induce a rise in temperature. Dold and 

 Hanau' report somewhat similar results in which they attempt to differentiate be- 

 tween an anaphylatoxin and an endotoxin in the bodies of these bacteria. But Thiele 

 and Embleton^ criticize this work. They contend that in the attempt to disanaphyla- 

 toxinize the bacterial protein Dold and Hanau removed from the solution a great 

 part of the more readily attackable protein, and hence the doses which they used 

 were not proportionally large enough to produce the same effects as the untreated 

 bacterial protein. 



In the causation of fever it is the products of bacteria and not the bacteria them- 

 selves that act as the stimulus. Fever has long been looked upon as a protective 

 mechanism in infections. The manner in which it serves as such is not clear, for the 

 temperature ordinarily reached does not interfere seriously with the growth of bac- 

 teria in the body. Roily and Meltzer^ found that animals kept at relatively high 

 temperatures developed antibodies much more rapidly and in larger amounts than 

 when kept at room temperature. This fact has significant possibilities in immunologi- 

 cal work. 



With the increase in temperature in spontaneous infections and following injec- 

 tions of bacterial toxic products there is also an increase of metabolism. Animals that 

 have been injected with the toxic products of the typhoid bacillus often show a fall 

 in temperature and emaciate and die in a week to ten days. Occasionally they recover 

 after a period of such emaciation. Whether this loss of weight is associated with the 

 effect of the bacterial toxic products upon metabolism is not clear. 



rOCAL OR METASTATIC EFFECTS 



Bacterial toxic products often produce their effects after they have been absorbed 

 from the focus of infection or from the place where they were injected. These effects 

 usually occur at the site of the elimination of the toxic products from the body. 



Flexner and Sweet'' found that the toxin of the Shiga dysentery bacillus was harmless 

 when administered by mouth. But when injected intravenously it induced a severe coHtis, 

 sometimes with the formation of ulcers. They believed that this toxin was excreted in rabbits 

 and probably in man, by the intestine, chiefly the large intestine, which being injured by 

 the act of elimination reacted by the development of inflammation. 



Fahrs observed fatty changes and focal necroses in the visceral organs after infections 

 with the diphtheria baciUus. In guinea pigs, diphtheria toxin affects especially the adrenals 

 causing hyperemia and hemorrhage into these organs, the differences between lethal and 



' Dold, H., and Hanau, A.: ibid., p. 31. 1913. 



^ Thiele, F. H., and Embleton, D.: ibid., p. 666. 1913. 



3 Roily, F., and Meltzer, K. S.: loc. cit. 



4 Flexner, S., and Sweet, J. E.: /. Exper. Med., 8, 514. 1906. 

 s Fahr, T.: Virclww's Arch. f. path. Anal., 221, ^^S>. iot6. 



