scholarly journals DIFFERENTIATION BETWEEN SOME TOXIC SUBSTANCES IN ANAEROBICALLY PRODUCED AUTOLYSATES OF PNEUMOCOCCI (TYPES I AND II)

1929 ◽  
Vol 49 (4) ◽  
pp. 695-700 ◽  
Author(s):  
Julia T. Parker

The necrotizing and lung-toxic principles present in certain anaerobically prepared autolysates of Pneumococcus Types I and II are similar in respect to extreme sensitiveness to heat and to oxidation, and to their ability to be neutralized by the same anti-autolysate serums. These two poisons differ, however, in their ability to be adsorbed or inactivated by red cells; the lung-toxic principle being adsorbed or inactivated by such procedure while the necrotizing principle is not. Since pneumococcus hemotoxin is present in the anaerobic autolysates and is also adsorbed by red cells, it seemed possible that it was this substance in the autolysates which caused the diffuse lung lesions and death of guinea pigs. However, it was found that the intratracheal injection of pneumococcus hemotoxin prepared by the method of Avery and Neill only occasionally produced the characteristic reaction caused by the intratracheal injection of the anaerobic autolysates.

1912 ◽  
Vol 16 (5) ◽  
pp. 644-664 ◽  
Author(s):  
Rufus Cole

1. The filtered blood serum of rabbits infected with pneumococci is not toxic. 2. Extracts of pneumococci prepared by keeping emulsions of the bacteria in salt solution at 37° C. for varying periods of time may be toxic, and when injected intravenously into guinea pigs, may produce a train of symptoms followed by acute death resembling that seen in acute anaphylaxis. Such extracts, however, are not uniformly toxic and it has been impossible to discover the exact conditions under which such extracts become toxic. 3. When the centrifugalized peritoneal washings of guinea pigs infected with pneumococci are injected into the circulation of normal guinea pigs, these animals very frequently exhibit symptoms like those seen in acute anaphylaxis, and a considerable proportion of the animals die acutely. 4. When pneumococci are dissolved in dilute solutions of bile salts and the solution resulting is injected intravenously into rabbits and guinea pigs, these animals show with great constancy the same symptoms that are seen in acute anaphylaxis. The solution of pneumococci in bile may occur in ten minutes at 37° C. or in half an hour on ice. This is considered evidence that the toxicity of the solution does not result from digestion of the bacterial protein, but is due to substances preformed in the bacterial cells and set free on their solution. The toxicity of the solution is diminished or destroyed by heating to 55° C. or over.


1982 ◽  
Vol 16 (3) ◽  
pp. 290-296 ◽  
Author(s):  
Margaret Baskerville ◽  
A. Baskerville ◽  
Margery Wood

Three types of lesion were present in the lungs of guinea pigs with chronic pneumonia - pulmonary interstitial fibrosis, perivascular lymphoid hyperplasia and foreign body granulomas. Bordetella bronchiseptica was present in the nasopharynx, trachea and lungs of a high proportion of animals from 4 weeks old, and antibodies to this organism were also found. Animals removed at 4 days old and reared in isolation from the main colony and free from B. bronchiseptica developed similar lung lesions, so that B. bronchiseptica appeared to have no causative role in these forms of chronic pneumonia.


Toxicology ◽  
1986 ◽  
Vol 38 (2) ◽  
pp. 197-202 ◽  
Author(s):  
Sanjay Gupta ◽  
Shri Dhar Pandey ◽  
Virendra Misra ◽  
P.N. Viswanathan

2019 ◽  
Vol 61 (10) ◽  
pp. 1062-1063
Author(s):  
Hiroyuki Yoshizawa ◽  
Keiji Nogami ◽  
Hiroaki Yaoi ◽  
Midori Shima

2005 ◽  
Vol 26 (3) ◽  
pp. 605-612 ◽  
Author(s):  
Emerich S. Fiala ◽  
Ock Soon Sohn ◽  
Chung-Xiou Wang ◽  
Eleanore Seibert ◽  
Junji Tsurutani ◽  
...  

1948 ◽  
Vol 88 (3) ◽  
pp. 343-353 ◽  
Author(s):  
William F. Friedewald ◽  
Edward W. Hook

A study of influenza virus infection in the hamster has yielded the following results: 1. Two influenza A strains (Ga. 47 and PR8) multiplied readily in the hamster lung, although no lung lesions were produced during six serial passages. On further passage both viruses abruptly acquired the capacity to produce pulmonary consolidation and death of the animals. 2. Extracts of the lungs during the early passages contained complement-fixing antigen and infectious virus, as revealed by titration in mice and embryonated eggs. Agglutinins for chicken, human, and guinea pig red cells, however, were not demonstrable at this time. With further passage a close correlation was observed between the capacity of the virus to produce lung lesions in the hamster and to agglutinate mammalian types of red cells. In addition, quantitative changes in the virus population were demonstrated in the lung extracts by complement fixation tests and titrations in mice and eggs. 3. Incubation at 37°C. was effective in bringing out agglutinins in high titer for chicken red cells in lung extracts, which originally failed to agglutinate chicken cells but agglutinated mammalian red cells. This method did not increase the titers of mammalian cell agglutinins. 4. The body temperature of the hamster was found to decrease within 1 to 4 days after inoculation of influenza virus. In the early passages the temperature returned to normal within 24 hours, but with the development of the pathogenic strain of virus the temperature remained at subnormal levels until death. 5. The Lee strain of influenza B virus produced pulmonary lesions in the hamster on the first passage and no increase in pathogenicity of the virus occurred during eleven serial passages. Virus was demonstrable in extracts of the lungs by all the methods used and no difference was observed in its capacity to agglutinate fowl and mammalian types of red cells. The implications of these findings are considered briefly in the discussion.


2004 ◽  
Vol 72 (2) ◽  
pp. 1147-1149 ◽  
Author(s):  
Todd M. Lasco ◽  
Oliver C. Turner ◽  
Lynne Cassone ◽  
Isamu Sugawara ◽  
Hiroyuki Yamada ◽  
...  

ABSTRACT Guinea pig eosinophils were positively identified in bronchoalveolar lavage populations and in the lung granulomas of Mycobacterium tuberculosis-infected guinea pigs. It is possible that the rapid influx of these cells, and their subsequent degranulation during acute pulmonary tuberculosis, may play a key role in the susceptibility of this animal model.


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