JUI.Y 3, 1903.] 



SCIENCE. 



Vi 



bumens are converted iuto uou-coajrulable 

 proteitl, and certain by-products, among 

 them leiiein and tyrosin, make their ap- 

 pearance. 



Differences are noticeable in the readi- 

 ness with which autolysis of organs takes 

 place under different pathological condi- 

 tions. Jacoby found that liver autolysis 

 was much accelerated in animals poisoned 

 with phosphonis; and I have made .some 

 tentative experiments upon the rapidity 

 with which organs from infected and non- 

 infected human beings undergo this change. 



Many of you will have been impressed 

 with the remarkable softness presented by 

 the liver, spleen, kidneys and other organs 

 in per.sons who have succumbed to typhoid 

 fever, peritonitis, septicemia, etc. This 

 softness has nothing to do with putrefac- 

 tion, and I think it reasonably certain that 

 it is the result of autolytic proees.ses which 

 may have begun to operate even before 

 death. The changes through which the 

 acutely swollen spleen, such as is met with 

 in typhoid fever, goes illustrate very well 

 the manner of action of these ferments. 

 The dififliient quality of the spleen in this 

 disease quickly develops outside the body; 

 and it can be shown to be independent 

 of the post-mortem growth either of the 

 typhoid bacilli or putrefactive bacilli. 

 Every pathologist has seen a moderately 

 firm spleen outside the body become soft 

 and semifluid in a few hours; and I find 

 that, reduced to pulp and placed under 

 toluol-water, the same change takes place. 



In view of the resemblance of the hepatic 

 lesions of advanced phosphorous poisoning 

 to those of the liver in acute yellow atro- 

 phy, and the frequency with which the lat- 

 ter obscure disease supervenes upon acute 

 infections, and, further, in view of the 

 close agreement of the chemical products 

 of degeneration of liver tis.sue in yellow 

 atrophy with those of autolysis of the liver. 



the question arises whether the hepatic 

 lesions in acute atrophy may not be the 

 result of active autolytic processes set up 

 by some agent that is as yet unknown. 



The alterations in structure and consist- 

 ence of muscle occurring in certain acute 

 diseases (such as the so-called Zenker's de- 

 generation which appears in typhoid fever) 

 have features in common with changes 

 noted in autolysis. The softening and 

 preparation for absorption of infarcted 

 areas in the brain, kidneys, spleen and 

 other organs are also attributable to the 

 action of intracellular ferments; and a 

 similar form of softening occurs, if im- 

 perfectly, in malignant tumors, notably 

 carcinoma, and in .syphilis, where ferment 

 action is possibly accelerated through the 

 use of drugs, of which potassium iodide is 

 the most efficient in use. 



On the other hand, not all dead tissues 

 are subject to this digestive liquefaction 

 and absorption. Tuberculous foci, though 

 degenerated, are remarkably persistent; 

 and, as Prudden has shown, undergo soft- 

 ening probably only when certain bacteria 

 invade secondarily the necrotic areas. It 

 is of importance, in this connection, to re- 

 call that streptococci, which in themselves 

 are not energetic tissue dissolvers, bring 

 about softening and cavity formation in 

 tuberculous foci; and the question as to 

 whether their action is a direct one through 

 products of their growth, or an indirect 

 one by causing an inerea.se in autolytic 

 ferments, is pertinent but not as yet to be 

 answered. 



Fresh pus obtained, let us say, from an 

 empyema, or fresh sputum, kept under 

 toluol at the body temperature, becomes 

 fluid, and a creamy layer collects upon the 

 surface. The cells and nuclei disappear, 

 and there appears in the fluid, as Xaunyn 

 first ascertained in 1865, various distin- 

 tegration products, among which are leu- 



