Home
  >  
Section 25
  >  
Chapter 24,903

Investigations on the pathogenesis of tetanus I. The permeability of the C-N-S barrier to tetanal toxin. Passive immunity against toxin introduced by various routes

Friedemann, Ulrich; Zuger, Bernard; Hollander, A.

Jour Immunol 36(5): 473-484

1939


Accession: 024902990

Download citation:  
Text
  |  
BibTeX
  |  
RIS

Abel has explained the pathogenesis of generalized tetanus by the vascular transport of the toxin to the C-N-S. As a logical conclusion from this theory, it should be expected that the neutralization of intramuscularly, intracut., or intraven. injected toxin would require the same amt. of circulating antitoxin. The authors, however, found that 5-80 times more circulating antitoxin is necessary to protect the animals from death after the intramusc. or intracut. than after the intraven. injn. of toxin. In addition, by the identification of free antitoxin in the blood animals dying after the intramusc. injn. of toxin the vascular system actually has been excluded as the pathway of the toxin to the C-N-S. These findings also support the contention of Friedemann and Elkeles, that negatively charged toxins cannot pass the C-N-S barrier.

PDF emailed within 1 workday: $29.90