ON THE NATURE OF BACTEREMIA IN EXPERIMENTAL PNEUMOCOCCAL PNEUMONIA IN THE DOG

Abstract

With the purpose of ascertaining the influence exerted by the pneumococcidal activity of the blood on the course of bacteremia occurring in experimental canine pneumococcal pneumonia, a study was made of the rates at which intravenously injected pneumococci disappeared from the circulation and the shed blood of diseased dogs. Preliminary studies on normal animals showed that blood containing hundreds of thousands of pneumococci per cc. immediately after injection usually became sterile or nearly so within an hour's time. Simultaneous observations carried out on the blood in vitro showed an analogous rapid disappearance of the microorganisms, although the effect was not quite as marked. Similar tests on non-bacteremic dogs with pneumonia revealed essentially the same ability of the body to dispose of large numbers of circulating pneumococci. The shed blood likewise exhibited marked bactericidal power. The occurrence of bacteremia during pneumonia did not retard greatly the rate at which injected pneumococci disappeared from the circulation, as compared with the non-bacteremic state. After several hours the numbers of circulating microorganisms were approximately the same as prior to the intravenous injection. Blood in vitro often cleared as fully as it did in vivo over the same length of time. Studies on the role played by humoral immune substances in the bactericidal action of the blood showed that while their presence was necessary for maximum killing power, and that bacteremic blood lacking humoral immune properties was rarely capable of self-sterilization in vitro, nevertheless such blood often retained considerable bactericidal potency as shown by its ability to reduce materially the numbers of pneumococci added to it. This phenomenon is discussed. The marked pneumococcidal capacity of the blood exhibited by dogs with experimental pneumococcal pneumonia and its persistence during bacteremia suggest that this constitutes the principal mechanism for limiting the degree of blood invasion. The similarity of the findings in canine and human pneumococcal lobar pneumonia is pointed out.