BIOLOGICAL PROPERTIES OF CELL WALL MUCOPEPTIDE OF HEMOLYTIC STREPTOCOCCI

Several of the toxic properties of streptococcal mucopeptide have been studied in detail. Intravenous injection of as little as 1 µg of mucopeptide, solubilized by ultrasonic treatment, elicits a reproducible febrile response. Rabbits which are made tolerant to Escherichia coli endotoxin are only partially tolerant to the subsequent injection of streptococcal mucopeptide. Soluble mucopeptide was successfully employed to prepare and provoke the localized Shwartzman reaction. Intravenous injection of 80 µg of solubilized mucopeptide leads to diffuse cellular infiltration as well as focal areas of myocardial necrosis, surrounded by inflammatory cells.

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STUDIES ON THE PATHOGENESIS OF FEVER

Journal of Experimental Medicine ◽

10.1084/jem.106.6.787 ◽

1957 ◽

Vol 106 (6) ◽

pp. 787-809 ◽

Cited By ~ 23

Author(s):

Robert G. Petersdorf ◽

Willis R. Keene ◽

Ivan L. Bennett

Keyword(s):

Intravenous Injection ◽

Bacterial Endotoxin ◽

Endogenous Pyrogen ◽

Febrile Response ◽

Single Intravenous Injection ◽

Shwartzman Reaction ◽

Endogenous Serum Pyrogen ◽

Indirect Action ◽

Local Shwartzman Reaction ◽

Bacterial Products

The "endogenous serum pyrogen" that appears in the circulating blood after a single intravenous injection of endotoxin does not produce leukopenia in normal animals, fails to provoke the local Shwartzman reaction, and elicits no "tolerance" when injected daily. Suppression of the febrile response to endotoxin by prednisone does not prevent the appearance of pyrogen in the blood. Animals given large amounts of endotoxin daily continue to respond with high fevers despite failure of endogenous serum pyrogen to appear in detectable amounts after the first two or three injections. Analysis of the response to daily injections shows clearly that the fever during the first 2 hours after administration of endotoxin is unrelated to levels of endogenous serum pyrogen; in contrast, the magnitude of the fever after the 2nd hour correlates well with endogenous pyrogen in some instances. The leukopenic response to endotoxin could not be correlated with the appearance of endogenous serum pyrogen. The differences between endotoxin and endogenous pyrogen and the similarities between leukocyte extracts (sterile exudates) and endogenous pyrogen are summarized and discussed. Dissociation of the febrile response to bacterial endotoxin and levels of endogenous serum pyrogen are discussed and it is concluded that a mechanism involving both direct and indirect action of endotoxins offers the best explanation for the pyrogenic action of these bacterial products.

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Death following ceftazidime-induced Kounis syndrome

Medico-Legal Journal ◽

10.1177/0025817217695904 ◽

2017 ◽

Vol 85 (4) ◽

pp. 215-218 ◽

Cited By ~ 2

Author(s):

IDG Kitulwatte ◽

S Gangahawatte ◽

ULMS Perera ◽

PAS Edirisinghe

Keyword(s):

Care Management ◽

Myocardial Injury ◽

Healing Process ◽

Myocardial Necrosis ◽

Inflammatory Cells ◽

Cellular Infiltration ◽

Laryngeal Oedema ◽

Kounis Syndrome ◽

Tryptase Level ◽

Allergic Angina

Kounis syndrome, also known as allergic myocardial infarction or allergic angina syndrome, coincides with chest pain and allergic reactions. It involves the activation of interrelated inflammatory cells following allergic, anaphylactic or anaphylactoid insults. We report a case of Kounis syndrome complicated by an injection of ceftazidime. A 52-year-old man developed shortness of breath and hypotension, leading to immediate unconsciousness, after a ceftazidime injection. Despite intensive care management, he showed no improvement and died approximately 19 h after ceftazidime administration. Autopsy showed massive laryngeal oedema, mucous plugging and collapsed lungs. An ImmunoCAP tryptase assay showed the tryptase level in an autopsy sample to be 118 µg/L (normal < 11.4 µg/L). Microscopy of the myocardium showed cellular infiltration preceding myocardial necrosis. These findings support the pathophysiological theory of Kounis syndrome, with cellular infiltration proposed as the cause of myocardial injury rather than an effect related to the healing process.

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Sites of Adsorption of the Bacteriophages T3 and T5 on the Wall of Escherichia Coli B.

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100060490 ◽

1967 ◽

Vol 25 ◽

pp. 96-97

Author(s):

Manfred E. Bayer

Keyword(s):

Escherichia Coli ◽

Cell Wall ◽

Electron Microscope ◽

Uranyl Acetate ◽

E Coli ◽

Receptor Sites ◽

Rigid Cell Wall ◽

Host Cell Surface ◽

Bacterial Viruses ◽

Escherichia Coli B

Bacterial viruses adsorb specifically to receptors on the host cell surface. Although the chemical composition of some of the cell wall receptors for bacteriophages of the T-series has been described and the number of receptor sites has been estimated to be 150 to 300 per E. coli cell, the localization of the sites on the bacterial wall has been unknown.When logarithmically growing cells of E. coli are transferred into a medium containing 20% sucrose, the cells plasmolize: the protoplast shrinks and becomes separated from the somewhat rigid cell wall. When these cells are fixed in 8% Formaldehyde, post-fixed in OsO4/uranyl acetate, embedded in Vestopal W, then cut in an ultramicrotome and observed with the electron microscope, the separation of protoplast and wall becomes clearly visible, (Fig. 1, 2). At a number of locations however, the protoplasmic membrane adheres to the wall even under the considerable pull of the shrinking protoplast. Thus numerous connecting bridges are maintained between protoplast and cell wall. Estimations of the total number of such wall/membrane associations yield a number of about 300 per cell.

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