Abstract
Aoi 1 found that 88% of all Staphylococcus strains isolated from “pusturating foci” are capable of dissolving Congo-red-fibrin. Applying their routine plasma-clot technic, however, Tillett and Garner 2 found only an “occasional” strain that was thrombolytic. Moreover, these few strains were of very low fibrinolytic titer, requiring approximately 24 hours to cause demonstrable softening of the plasma-clot.
We have tried to harmonize the 2 sets of data by titrating 145 local strains of S. aureus or albus † for fibrinolysin, using the more delicate isolated-fibrin technic. 2 Data thus obtained are summarized in Table I.
The table shows that 77% of all local strains of Staphylococcus isolated from superficial human lesions (acne, boils, nasal sinus, etc.) are without demonstrable fibrinolytic function, even when tested by the 10-fold enzyme-concentration method. In contrast, 90% of all local strains isolated from internal human lesions (septicemia, osteomyelitis, empyemia, cellulitis, etc.) are fibrinolytic, 37% of them yielding as many as 5 to 10 lytic units per cc. of broth culture.
None of the 24 local veterinary strains (horse, cow, dog, swine) is capable of liquifying human fibrin.
The fibrinolytic factor formed or secreted by the Staphylococcus is not of the same immunologic specificity as the streptofibrinolysin. Streptococcus antiserum‡ containing as many as 1000 antifibrinolytic units per cc. does not neutralize the staphylofibrinolysin.
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