2Q4 EFFECT OF VIRULENCE ON PHAGOCYTOSIS 



a case of general haemic infection by this organism which ran a 

 rapid fatal course in spite of all the organisms (as far as could be 

 seen) being taken up by the leucocytes. In general, however, the 

 law holds good, and where there is abundant leucocytosis the 

 disease tends to recovery ; when there is little or none, to death. 



As far as we know at present, the failure of phagocytosis which 

 occurs with virulent bacteria is due to their deficient opsonization ; 

 but whether this is because they require a large dose of opsonin 

 before they can be ingested, or whether the opsonin cannot com- 

 bine with them, has not yet been determined quite satisfactorily. 

 It is this resistance which very virulent bacteria exert to phago- 

 cytosis which causes the very high indices seen in meningococcic 

 infections. If the index is determined using the very virulent 

 organisms recently isolated from a case of cerebro-spinal fever, 

 very little, if any, opsonization and phagocytosis take place in 

 the specimen in which normal serum is used, whereas a fair 

 number are taken up when the serum from a patient is employed. 

 If, however, the index be determined using an old laboratory 

 culture, much more phagocytosis will be caused by normal serum, 

 and the index will be nearer unity. The relation between viru- 

 lence and lack of phagocytosis is discussed subsequently in the 

 section on immunity to bacteria. 



Lastly, many bacteria form toxins, of one sort or another, which 

 prevent phagocytosis by a direct action on the leucocytes. It has 

 been shown that tetanus spores and bacilli, when washed per- 

 fectly free of toxin, are quite innocuous to all animals, and are 

 readily taken up by the phagocytes ; the presence of toxin, it may 

 be in small amounts, by killing or injuring the leucocytes, allows 

 the bacilli to grow in the tissues and elaborate more toxin. Similar 

 facts probably occur in the case of diphtheria. We have already 

 referred to the production of leucocidin by streptococci, and it is 

 obvious that when this is formed in the tissues in large amount 

 phagocytosis will be reduced or stopped altogether. 



The nature of phagocytosis requires some discussion. We are, 

 perhaps, rather too apt to be influenced by the readily observed 

 phenomena of ingestion of bacteria, diatoms, etc., by amoebae, 

 and to assume that it is in all cases an active process on the part 

 of the leucocytes, which are usually considered to approach their 

 prey by active movements directed by positive chemotaxis, and 

 to seize them by means of their pseudopodia. Chemotaxis does, 

 of course, occur in the tissues, but it is clear that it does not take 



