Following phagocytosis of certain streptococci human neutrophils undergo a rapid disintegration: the leukotoxic reaction. Monocytes and eosinophils are similarly injured, as are polymorphonuclear cells of rabbit and guinea pig blood.

The leukotoxic injury is not produced by culture filtrates of leukotoxic cocci nor does it follow phagocytosis of heat-killed cocci. The leukotoxic effect does not appear to be due to action of any presently known streptococcal product.

The distribution of leukotoxicity among streptococci is not random, for it was found in all strains tested of certain types of group A (6, 12), and was absent from almost all strains of other types (5, 14, 30). Still other types (3, 4) had both leukotoxic and non-leukotoxic representatives. The injury was also produced by some group C and G strains.

Often the streptococci that cause leukocyte death remain alive and proliferate in the cellular debris, but sometimes they are injured by the phagocyte before the latter disintegrates and are unable to proliferate on the slides. The capacity of a strain of streptococcus to injure leukocytes does not necessarily confer virulence on it. This is thought to be because a chain of streptococci, having survived its sojourn in a leukocyte it has killed, is still susceptible to phagocytosis by a fresh leukocyte, and serial phagocytoses may continue until the chain has been exposed sufficiently to the unfavorable intracellular environment to be, itself, killed.

Whether leukotoxicity plays a role in naturally occurring streptococcal disease is unknown. The high incidence of leukotoxicity in Type 12 strains suggested that it might be involved in acute hemorrhagic nephritis, but if so there must be other factors since leukotoxic strains are present in types and groups not now known to be associated with nephritis.

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