PATHOGENICITY AND TOXIN PRODUCTION 593 



relatively thermostable. It is not inactivated in one hour at 70° C, but is completely 

 inactivated at 85° C. for a similar period. 



Several observers (JuUanelle and Reimann 1926, Reimann and Julianelle 1926, Mair 

 1928, Pittman and Falk 1930, Goodner 1931) have noted purpuric lesions following the 

 injection of pneumococcal extracts and autolysates. The active agent would appear to 

 be an " endotoxin," i.e. some constituent of the bacterial cell, rather than a soluble toxin. 

 It may be noted that Avery and Goebel (1933) report that mice may develop purpura after 

 injections of the acetylated form of the Type I pneumococcal polysaccharide, while this 

 effect is not produced by the deacetylated form. 



Pneumococci produce hyaluronidase in varying amount, but there appears to be no 

 relation between their activity in this respect and their virulence (Humphrey 1944). 

 Whether they form a fibrinolysin against human fibrin is not certainly known. The 

 formation of the characteristic fibrin network in the alveoli in lobar pneumonia in man 

 would seem to make it unlikely that the pneumococci concerned act vigorously on human 

 fibrin ; but it would appear that they are able to attack rabbit fibrin or fibrinogen. 

 Goodner (1931, 1933) has recorded that the oedema fluid, withdrawn from the spread- 

 ing oedematous lesions caused by the injection of virulent pneumococci into the rabbit's 

 skin, not only fails to clot, but retards the coagulation of normal rabbit's blood, and 

 that a similar anticoagulant property is possessed by pneumococcal extracts and auto- 

 lysates. The active substance is relatively thermostable, since it withstands heating to 

 70° C. for 15 minutes. Such autolysates, when injected into the skin together with a 

 slightly virulent strain of pneumococcus, greatly extend the area of the lesion produced. 



None of the other groups, species, or types of streptococci that we have described 

 above have been studied, in regard to their pathogenicity for laboratory animals, 

 in the same detail as Str. pyogenes and Str. fneumonice. A few brief notes will 

 give most of the information that we possess. 



Streptococci of Group D. — The organisms of this group are far less pathogenic than 

 Str. pyogenes or Str. pneutnonice. They have, however, occasionally been isolated from 

 the blood stream in man, usually in cases of subacute endocarditis (see Chapter 68), rarely 

 in other conditions. They are normal inhabitants of the intestinal tract, and are not 

 infrequently present in suppurative abdominal lesions, though their pathogenic role is 

 often doubtful. They are also not uncommonly present in infections of the urinary 

 tract. Their virulence for laboratory animals is usually low. Dible (1921) tested 83 faecal 

 strains by injection into mice, and 6 of these showed some degree of pathogenicity. It 

 is very probable that such pathogenicity as this group possesses is confined to particular 

 species, or strains ; and that many strains, such for example as most of those isolated 

 from mUk or cheese, are altogether non-pathogenic. It may, perhaps, be noted that 

 the hsemolytic strains belonging to this group do not produce a fibrinolysin active against 

 human fibrin. 



Streptococci of the Viridans Group, — The position of this group, in regard to patho- 

 genicity, is very similar to that of Group D. Streptococci of the viridans type are of 

 low virulence, both for man and for animals. In man they are frequently isolated from 

 locaUzed septic lesions in cormection with the teeth and gums, and they are the most 

 frequent cause of subacute bacterial endocarditis. Here again, it is probable that different 

 species or types within the group vary considerably in their pathogenicity for different 

 animal species. Many of them are probably quite avirulent. In none of them is the 

 virulence high. 



Very brief notes must suffice for the remaining labelled groups of hsemolytic 

 streptococci, since our knowledge of their pathogenic potentialities is as yet in 

 its earliest infancy. The data available are contained in the recent papers by 

 Lancefield, Hare, and others, to which frequent reference has already been made. 



