280 OBJECTIONS TO THE OPSONIN THEORY 



index may be due to a failure of the serum or leucocytes to gain 

 access to the lesions which are densely surrounded by inflam- 

 matory material. We have adduced a similar reason to explain 

 the non-success of certain bactericidal sera. But it is otherwise 

 when we find that a patient improves when there is a low index, 

 for here we must admit that even this deficient amount of opsonin 

 is sufficient ; and, further, it is impossible to explain the formation 

 of new lesions (e.g., staphylococcic) in patients in whom the 

 opsonic index is high often very high on any such grounds. 

 Again, a great rise in the opsonic index not infrequently occurs 

 just before death, as in the chart of the index in a fatal case of 

 erysipelas already figured. The more carefully the opsonic index 

 is considered, the more certain will it appear that a high index is 

 not an indication of immunity ; it neither proves that the lesion 

 is undergoing cure nor that a fresh infection will not occur. It 

 may, of course, occur concurrently with other properties in the 

 blood or tissues on which immunity does depend indeed, since it 

 is commonly due to the presence of a natural or artificial vaccine, 

 it usually does so but the parallelism between a rise in the 

 amount of opsonins and an increase in the grade of immunity is 

 not absolute. Nor is a low index any proof of lack of immunity, 

 since patients may improve remarkably during a prolonged 

 negative phase. One of the most striking cases of amelioration 

 of a severe case of tubercle which I have ever seen occurred 

 during a negative phase lasting over three weeks. Allen has 

 noted a similar occurrence in gonorrhceal infections, from which, 

 however, he draws the assumption that the clinical signs are 

 a totally unreliable guide to the appropriate time for a fresh 

 injection a deduction which is logical only if we regard the 

 raising of the opsonic index, and not the cure of the patient, as 

 the object of treatment. 



It seems probable, from a consideration of the phenomena of 

 phagocytosis in vitro, that a very small amount of opsonin even 

 less than that which is present in a serum in which the index is 

 very low is quite sufficient to sensitize any bacteria that are 

 likely to gain access to the tissues or blood. In our laboratory 

 experiments the conditions are certainly much less favourable 

 than they are in the living body ; the leucocytes are certainly not 

 in the same state of functional activity as they are in the body, 

 and there is a limited supply of serum instead of a constant stream 

 thereof. In spite of this, an enormous number of bacteria are 



