PNEUMOCOCCUS TYPE III PNEUMONIA. AN ANALYSIS OF 500 CASES

1936 ◽  
Vol 191 (3) ◽  
pp. 305-318 ◽  
Author(s):  
RUSSELL L. CECIL ◽  
NORMAN PLUMMER ◽  
MARSH McCALL
Keyword(s):  
Type Iii ◽  
1948 ◽  
Vol 87 (5) ◽  
pp. 445-455 ◽  
Author(s):  
Walther F. Goebel ◽  
Peter K. Olitsky ◽  
Arturo C. Saenz

The action of periodic acid on two biologically active proteins, crystalline ribonuclease and pneumococcus Type III immune globulin, and on the virus of Western equine encephalomyelitis has been studied. The biological activity of the two proteins and the pathogenic action of the virus were destroyed by the reagent; the specific antigenicity of the immune globulin was retained, however, but that of the equine virus was lost. The bearing of these reactions on the chemical alteration of the respective substances has been discussed.


1923 ◽  
Vol 38 (2) ◽  
pp. 149-161 ◽  
Author(s):  
Russell L. Cecil ◽  
Gustav I. Steffen

1. Three subcutaneous injections of Pneumococcus Type II vaccine confer on monkeys a complete immunity against experimental Pneumococcus Type II pneumonia. A similar protection can be bestowed on monkeys against Pneumonococcus Type IV pneumonia by three subcutaneous injections of a vaccine prepared from the same strain of pneumococcus. 2. The subcutaneous injection of monkeys with three doses of Pneumococcus Type III vaccine confers a complete immunity against this type in only 50 per cent of cases (four out of eight monkeys vaccinated). 3. In spite of the immunity induced in monkeys by three subcutaneous injections of Pneumococcus Types II, III, and IV vaccine, specific protective bodies against the homologous types are not demonstrable in their serums when the vaccine is so administered.


1949 ◽  
Vol 90 (1) ◽  
pp. 85-96 ◽  
Author(s):  
W. Barry Wood ◽  
Mary Ruth Smith

Five strains of type III pneumococcus have been shown to possess wide capsular slime layers during the logarithmic phase of growth in serum broth. The slime layer stains metachromatically with methylene blue and can be visualized under the electron microscope as a fuzzy halo which extends well beyond the surace of the capsule proper and causes centrifugates of the organism to be of extremely large volume. This outer capsular structure is most readily demonstrated in vivo and in nutrient broth containing glucose and serum. It disappears from the surface of the cell with aging of the culture, and is easily removed by dilute alkali, alcohol, and heat. Exposure of slime-covered type III pneumococci to homologous antibody and to type III polysaccharidase reveals that the slime layer contains the same type-specific polysaccharide that is present in the rest of the capsule. From a type III strain producing a prominent slime layer an intermediate mutant has been isolated which forms small non-mucoid colonies on blood agar and possesses a relatively small capsule with a barely discernible slime layer. The wide slime layer protects virulent type III pneumococci from surface phagocytosis. Whenever the type III cells lose their broad slime layer, whether from aging of the culture, from mutation, from exposure to injurious chemicals, or from the action of type III polysaccharidase, they become susceptible to phagocytosis by the surface mechanism. Once phagocyted the type III pneumococci are promptly destroyed, even in the absence of antibodies.


1936 ◽  
Vol 64 (2) ◽  
pp. 307-330 ◽  
Author(s):  
John F. Enders ◽  
Morris F. Shaffer ◽  
Chao-Jen Wu

Among the experimental findings reported in this paper to which we wish to give particular emphasis are the following: 1. The results which follow the intravenous injection into rabbits of two strains of Pneumococcus Type III of different degrees of virulence vary with the state of the capsule. Thus when this structure is completely developed both remain in the blood. A culture of either strain begins to become susceptible to the blood-clearing mechanism contemporaneously with the onset of capsular degeneration and the initiation of other concomitant changes at the surface of the organism (cf Paper II), which occur much earlier with the less virulent strain. 2. When, in either case, removal from the blood stream occurs, this is effected by the phagocytic cells of the body. There is no suggestion that a new or unknown mechanism is involved. The greatest share of the burden is borne by the fixed phagocytic cells of the liver and spleen, and to a less extent by those of the lung and bone marrow. Nevertheless, it has been demonstrated that the polymorphonuclear leucocytes may also participate. 3. Phagocytosis by the leucocytes of the normal animal either in intro or in vivo has been observed only at such a time as the capsule has become impaired. Ingestion of the organisms by the fixed tissue cells appears also to be effective only under the same condition and is accordingly observed with much younger cultures of the less virulent strain. 4. Following their removal from the blood and their accumulation within the fixed phagocytes of the organs, destruction of most of the cocci proceeds within 2 to 4 hours. Both strains are destroyed provided they are in the state favorable to phagocytic attack. 5. Evidence has been presented which indicates that just as in vitro, so in a local area of inflammation within the body, aging with attendant capsular loss and increasing susceptibility to phagocytosis may take place. 6. With organisms from either strain a variable period of lag follows their injection into the blood stream, even when they are introduced in a state of active multiplication and complete encapsulation. 7. Differences in virulence for rabbits of two strains of Pneumococcus Type III do not imply that this animal possesses a defensive mechanism which is absent in other species, since it has been possible to demonstrate similar differences when the organisms are injected intravenously into mice. This fact indicates that the factors determining the degree of virulence of these strains are to be sought in the organisms themselves, rather than in the kind of host.


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