Abstract
Menkin 1 recently demonstrated that various materials are fixed in situ when injected into an acutely inflamed area, and that the mechanism of fixation of such substances as bacteria and trypan blue is primarily mechanical obstruction in the form of a fibrinous net-work and thrombosed lymphatics at the site of inflammation. Obviously the speed with which an inflammatory irritant causes the region to be blocked off is a significant factor in determining its ability to disseminate into the contiguous tissues or blood stream. Menkin 1 observed that Staphylococcus aureus caused the formation of thrombi in the lymphatics and fixation of trypan blue within about one hour after their introduction into the skin of rabbits, while the more invasive Streptococcus hemolyticus produced fixation only about 45 hours later. Menkin believed that the delayed fixation in the latter case was due to the “relatively mild local effects” of the streptococcus.
Using Menkin's 1 method, we have fully confirmed his observations of the behavior of Strep. hemolyticus and Staph, aureus in vivo, but our additional data show that the delayed inflammatory fixation of streptococci is due to the production by these organisms of a substance or substances, active both in vivo and in vitro, which when present in sufficient concentration is capable of inhibiting inflammatory fixation for many hours, thus enabling the organisms to disseminate relatively freely through the lymphatics.
Our in vivo observations have been carried out on more than 150 rabbits. The organisms studied were the Dochez and Griffith scarlatinal strains and Birkhaug's E1 erysipelas strain of Strep. hemolyticus, a virulent strain of Strep, viridans, and 2 strains of Staph, aurevis. The “fixation time” for each strain was: Dochez 48–56 hr.; Griffith 48 hr.; E1 48 hr.; Strep, viridans 36 hr.; Staph. aureus 1–2 hr. The staphylococcus strains used always produced fixation of the dye in less than 2 hours.
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