Abstract
Conclusion
Inflammatory fixation is promptly induced in acute local streptococcus inflammation in the presence of streptococcus antiserum, in contrast with the marked delay in fixation in the presence of normal serum.
The experiment presented above has been repeated on several occasions. Five different strains of Streptococcus hemolyticus, and 4 different commercial brands of polyvalent so-called antitoxic-antibacterial streptococcus antisera have been used with essentially identical results.
The data given above suggest that the factor produced by Streptococcus hemolyticus which is responsible for the active suppression of the formation of the local inflammatory barrier is antigenic and is readily neutralized by streptococcus antiserum. A possible alternative explanation is that the inflammatory fixation is part of an Arthus phenomenon due to the introduction of a mixture of antigen and antibody into the skin. However, in view of the ability of the “inhibitory factor” to suppress fixation in other types of inflammatory response, this explanation would seem to be improbable, and attempts to test the hypothesis experimentally have given negative results.
Ward and Lyons 4 , 5 have shown that the virulence of hemolytic streptococci is ultimately dependent upon the resistance of the organism to phagocytosis. However, invasiveness (i. e., the ability of the organism to disseminate from the portal of entry) is a vitally important corollary of virulence. We have found that avirulent strains of streptococci may rapidly reach the blood stream following injection into the skin, but are quickly disposed of by the cellular defenses of the body; on the other hand the speed with which organisms which are resistant to phagocytosis kill the host may be determined by the ease with which they reach the blood stream. Menkin 6 has recently demonstrated that the early establishment of a nonspecific inflammatory barrier at the site of injection into the skin may protect rabbits against otherwise lethal doses of pneumococci known to be highly resistant to phagocytosis.
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