PHAGOCYTOSIS 285 



different in the two cases. We have already shown that incre- 

 ments in the amounts of opsonin cause smaller and smaller 

 rises in the opsonic index as we proceed. There is, however, 

 a much closer parallelism between the bacteriolytic power and 

 the amount of thermostable opsonin present as shown by the 

 degree of dilution. This is well shown (in the case of typhoid 

 fever) by the chart given by Klien and inserted previously 



(Fig. 58). 



To sum up : Amboceptor appears to have the power of 

 sensitizing bacteria for phagocytosis, and this power appears to 

 be increased by the concurrent action of complement. Further, 

 there appears to be no sufficient evidence for the existence of 

 a thermostable opsonin apart from amboceptor, as has been 

 maintained by Neufeld and Hime. 



(There is an additional possibility that the part of a thermo- 

 stable opsonin may be enacted by agglutinin. 



I believe that in the case of the haemopsonins of normal 

 human serum the substance is a thermostable agglutinin with a 

 second thermolabile zymotoxic group. Natural haemopsonic sera 

 are, as far as I have seen, always powerful agglutinators of the 

 red corpuscles which they opsonize, and when they are heated to 

 60 C. the opsonic power is destroyed, but the agglutinative 

 faculty is unaltered.) 



These facts may serve to explain the discordant results as to 

 the presence of thermostable opsonins in the sera of tuberculous 

 patients. It has been shown by Bruck that antibodies to the 

 tubercle bacillus are not always or usually present in the blood of 

 infected persons, and it is only when they are present that we 

 should find a thermostable opsonin. 



If thermostable opsonins resemble amboceptor in their pro- 

 perties, there is an equally close resemblance between thermo- 

 labile opsonin and complement. Each occurs in normal serum, 

 and is destroyed by a short heating to 55 to 60 C. Are they the 

 same ? 



The main fact against the theory of their identity is the 

 specificity, partial though it may be, of the opsonins ; for there is 

 no reason to think that different bacteria are attacked by different 

 complements, even if we accept the theory of the multiplicity of 

 these bodies to the fullest degree. But we have already seen 

 that the specificity of the opsonins is not complete, and that the 



