Studies on the Mechanism of Recovery in Pneumococcal Pneumonia

Wood, William B.; McLeod, Charlotte; Irons, Edwin N.

doi:10.1084/jem.84.4.377

Cited by 18 publications

(3 citation statements)

References 21 publications

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“…The results also indicate that in the case of non-encapsulated (rough) pneumococci surface phagocytosis is of little significance (9,25). In systematic histologic studies of the pre-antibody phase of experimental pneumococcal pneumonia (9,20,26,27), appreciable phagocytosis of pneumococci has been shown to occur only in those portions of the lesion where the leucocytic exudate has become relatively concentrated (see Figs. 1 and 2).…”

Section: A Quantitative Measurement Of Surface Phagocytosis--mentioning

confidence: 99%

Surface Phagocytosis

Smith

Wood

1958

The Journal of Experimental Medicine

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Experiments recently reported (18) have been interpreted to indicate that surface phagocytosis plays no significant part in natural antipneumococcal defense. A repetition of these experiments has revealed: (a) that the cellular content of the leucocytic suspensions used in the phagocytic tests was of a different order of magnitude from that of the exudates which usually exist in infected tissues, (b) that the suspensions were too dilute to allow surface phagocytosis of pneumococci to occur, and (c) that the ratio of bacteria to leucocytes. was such that, when a sufficiently concentrated exudate was employed, the pneumococci injured the leucocytes and thus prevented phagocytosis from taking place. When conditions of the tests were suitably controlled, and conventional quantitative methods were employed to measure the end results of the phagocytic reaction, the essential observations relating to surface phagocytosis were fully confirmed. The significance of this non-antibody mechanism of defense in pneumococcal infections was thus further substantiated.

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Section: A Quantitative Measurement Of Surface Phagocytosis--mentioning

confidence: 99%

Surface Phagocytosis

Smith

Wood

1958

The Journal of Experimental Medicine

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“…The experimental approach was based upon the following facts established during previous studies on pneumococcal pneumonia (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16).…”

Section: Pla~s 21 and 22mentioning

confidence: 99%

An Experimental Analysis of the Curative Action of Penicillin in Acute Bacterial Infections

Wood

Smith

1956

The Journal of Experimental Medicine

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Three strains of pneumococcus (types I and III), equally sensitive to penicillin, have been shown to be killed by the antibiotic in vitro when grown either in enriched beef infusion broth or in a thin serous exudate. Killing of the bacteria resulted promptly when the penicillin was added during the logarithmic phase of growth but failed to occur if addition of the antibiotic was delayed until the later "stationary" growth phase. In analogous experiments with thick purulent exudates from established subcutaneous abscesses, the pneumococci failed to grow rapidly, and added penicillin exerted only a relatively slow bactericidal effect. The relevance of these in vitro observations to the curative action of penicillin was demonstrated in a systematic histologic study of the antimicrobial effect of the drug in experimental (type I) pneumococcal pneumonia. Evidence was obtained that at least two distinct processes are involved. The first, the direct bactericidal effect of the penicillin itself, was shown to operate in the outer edema zone of the spreading pneumonic lesion where the micro-organisms multiply rapidly in the thin serous exudate. The second, which predominates in the older more central portions of the lesion, was demonstrated to depend upon destruction of the pneumococci by phagocytosis. Here the bacteria, having presumably reached a relatively stationary phase of growth in the alveolar exudate, are resistant to the bactericidal action of the penicillin but are readily destroyed by the phagocytes.

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“…The antibody that promotes phagocytosis is identical with the antibody that promotes precipitation and killing of bacteria (3). In surface phagocytosis, a virulent capsulated pathogen can be phagocyteozed in the absence of antibodies by trapping the pathogen against a solid surface such as the alveolar wall, or between two polymorphonuclear leukocytes (4–8). An excess of antigen may combine and thus neutralize the osmotic effect of the antibody.…”

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confidence: 99%