244 IMMUNO-CATALYSIS 



added to the buffered growth medium. The hydrolysis of hyaluronate 

 by streptococcal hyaluronidase destroys this stimulative effect on these 

 organisms, whereas the action of testicular hyaluronidase does not. 

 Staphylococci and CI. sefticum do not respond to the inclusion of 

 hyaluronate either in the simplified or in the more complex growth 

 media. These organisms require factors present in peptone or digest 

 media for optimal hyaluronidase production. Streptococci and CI. 

 welchii do not require such factors. Rogers (1946) also reported that 

 potassium hyaluronate hydrolyzed by crude or purified testicular 

 hyaluronidase can stimulate hyaluronidase production by streptococ- 

 cus or CI. welchii equally as well as the unhydrolyzed polysaccharide. 

 In contrast, potassium hyaluronate hydrolyzed by streptococcal or CI. 

 welchii enzymes does not stimulate hyaluronidase production by strep- 

 tococcus. The streptococcal hydrolysate does, however, stimulate 

 hyaluronidase production by CI. welchii, whilst the CI. welchii hydrol- 

 ysate has a small but probably significant effect on the latter organ- 

 ism. Hydrolysis of hyaluronate by mild treatment with acids destroys 

 the ability of the polysaccharide to enhance hyaluronidase production 

 by streptococcus. (For a discussion of the relation of the above observed 

 effects to the "adaptive enzyme" concept see elsewhere in this mono- 

 graph and Sevag, 1946). 



b. Relation of Capsular Polysaccharide and Hyaluronidase to the 

 Virulence of Streptococcus and Pneumococcus. In connection with 

 the relation of hyaluronidase to virulence, it is significant that Kass 

 and Seastone (1944) found a noteworthy role for the capsular polysac- 

 charide in the virulence of Group A haemolytic streptococcus. Hyalu- 

 ronidase added to a phagocytic system containing defibrinated human 

 blood, immune or non-immune, greatly increased the rate of phagocy- 

 tosis of Group A streptococci. Under the same conditions phagocytosis 

 of Type I pneumococci was not affected by hyaluronidase. The bacteri- 

 cidal activity of non-immune blood against Group A streptococci was 

 increased by hyaluronidase; the activity of immune blood was, how- 

 ever, somewhat inhibited by the enzyme. Mice could be protected 

 against Group A streptococcus infection by frequent treatment with 

 200 turbidity-reducing units of hyaluronidase. Mice infected with type 

 I pneumococcus and treated with hyaluronidase died somewhat sooner 

 than the untreated controls. The consistent presence of hyaluronic 

 acid in Group A streptococci isolated from human infections indicated 



