440 Diphtheria 



is probable that it may be due to a diminished resistance of 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-Loffler bacillus was about even, though slightly in 

 favor of the streptococcus." 



The mixed infections add to the clinical diphtheria the patho- 

 genic effects of the associated . bacteria. The diphtheria bacillus 

 probably begins the process, growing upon the mucous membrane, 

 devitalizing it by its toxin, and producing coagulation-necrosis. 

 Whatever pyogenic germs happen to be present are thus afforded 

 an opportunity to enter the tissues and add suppuration, gangrene, 

 and remote metastatic lesions to the already existing ulceration. 



Diphtheritic inflammations of the throat are not always accom- 

 panied 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 suffocation, only a bacteriologic 

 examination revealing the true nature of the disease. 



Lesions. — ^The pseudo-membrane characterizing diphtheria con- 

 sists 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 are embedded 

 in coagulated exudate — ^fibrin — and show a peculiar hyaline degen- 

 eration. 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 superficiallayer the proc- 

 ess may descend to the deepest layers, all of the cells being included 

 in the coagulated fibrin and showing more or less hyaline degenera- 

 tion. 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 differences 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 with diflaculty, leaving an abraded 

 surface. When the membrane is divulsed during the course of the 

 disease, it immediately forms anew by the coagulation of the in- 

 flammatory exudate. 



The coagulation-necrosis seems to depend upon the local effect 

 of the toxin. Morax and Elmassian* found that when strong 

 diphtheria toxin is applied to the conjunctiva of rabbits every three 

 minutes for eight or ten hours, typical diphtheritic changes are 

 produced. 



Flexnerf has made a study of the minute lesions caused by bac- 



*''Ann. de I'Inst. Pasteur," 1898, p. 210. 

 t "Johns Hopkins Hospital Reports," VI, 259. 



