348 SEQUENCE OF EVENTS IN LOCAL LESIONS 



reasons : (i) There is a mechanical obstacle to the access of 

 leucocytes to the bacteria, which make their way through the 

 slough with some difficulty. In ordinary healthy tissues, permeated 

 by capillaries, the leucocytes have never very far to go to reach a 

 given area; but when death of these tissues has occurred, the 

 leucocytes have to crawl in from the still patent capillaries of the 

 periphery, a distance, maybe, of several millimetres. (2) The 

 bacteria in the centre of the lesion have time to elaborate a 

 powerful toxin, which is not diluted by the blood or lymph, since 

 the vessels are all thrombosed, and can only escape by diffusion. 

 As a result, there is a central zone where the toxin is present in so 

 high a concentration that it may either repel the leucocytes by 

 negative chemotaxis or kill them outright. The latter process 

 certainly takes place, as the large number of dead bacteria present 

 in pus sufficiently proves. (3) There is an insufficient supply of 

 opsonin, and perhaps of other defensive substances also, in the 

 fluids at the centre of the lesion. This is brought about partly by 

 removal of these substances by the bacteria of the region. In the 

 case under consideration the staphylococcus opsonin is absorbed 

 by the cocci which, in the absence of the leucocytes, it is power- 

 less to injure. Another possible factor in the removal of these 

 substances is the action of proteolytic enzymes, the defensive 

 materials being digested and rendered inert before they reach the 

 bacteria. Lastly, there is reason to think that opsonins make 

 their way with difficulty through the inflamed tissues. Thus 

 Bulloch found that the serum or liquor puris which was collected 

 from an abscess immediately after it had been cleansed was almost 

 devoid of opsonic power, and this is the case with the fluid portion 

 of pus in general. In some cases I have been able to demonstrate 

 the existence of an antiopsonin, perhaps consisting of cast-off 

 receptors of the bacteria. (4) There is an increase in the virulence 

 of the bacteria, due to conditions already discussed. 



The absence of opsonin from the fluid at the centre of the 

 lesion suggests several considerations of some importance. We 

 see, for instance, that it is not sufficient in the cure of a local 

 lesion for there to be an abundant supply of opsonin in the blood : 

 two other factors are required a permeable lesion and a region 

 suited for the activity of leucocytes. This is very well seen in the 

 case of tubercle, where the opsonic index may be greatly raised (to 

 i '8 or more), and the lesion show no indication of recovery. There 

 is, as a rule, little or no tendency of the disease to spread or 



