Pathogenesis 485 



Klebs-Loffler bacillus is not apparent. It occurred gener- 

 ally, but not always, in the gravest cases, or those known as 

 'septic' cases. It is probable that it may be due to a 

 diminished resistance to the tissue-cells, or of the germicidal 

 power of the blood. In this series of fatal cases the number 

 of infections with the streptococcus and with the Klebs- 

 Iy6ffler bacillus was about even, though slightly in favor of 

 the streptococcus." 



The mixed infections add to the clinical diphtheria the 

 pathogenic effects of the associated bacteria. The diphtheria 

 bacillus probably begins the process, growing upon the 

 mucous membrane, devitalizing it by its toxin, and pro- 

 ducing coagulation-necrosis. Whatever pyogenic germs 

 happen to be present are thus afforded an opportunity to 

 enter the tissues and add suppuration, gangrene, and re- 

 mote metastatic lesions to the already existing ulceration. 



Diphtheritic inflammations of the throat are not always 

 accompanied by the formation of the pseudo-membrane, 

 but in some cases a rapid inflammatory edema in the larynx, 

 without a fibrinous surface coating, may cause fatal suffoca- 

 tion, only a bacteriologic examination revealing the true 

 nature of the disease. 



Lesions. The pseudo-membrane characterizing diph- 

 theria consists of a combined necrosis of the tissues acted 

 upon by the toxin and coagulation of an inflammatory 

 exudate. When examined histologically it is found that 

 the surface of the mucous membrane is chiefly affected. 

 The superficial layers of cells being embedded in coagulated 

 exudate fibrin and show a peculiar hyaline degeneration. 

 Sometimes the membrane seems to consist exclusively of 

 hyaline cells ; sometimes the fibrin formation is secondary to 

 or subsequent to the hyaline degeneration. Leukocytes 

 caught in the fibrin also become hyaline. From the super- 

 ficial layer the process may descend to the deepest layers, 

 all of the cells being included in the coagulated fibrin and 

 showing more or less hyaline degeneration. The walls of the 

 neighboring capillaries also become hyaline, and the necrotic 

 mass forms the diphtheritic membrane. The laminated 

 appearance of the membrane probably depends upon the 

 varying depths affected at different periods, or upon differ- 

 ences in the process by which it has been formed. The 

 pseudo-membrane is continuous with the subjacent tissues 

 by a fibrinous reticulum, and is in consequence removed 



