The concept of passive immunization began in the 17th century when Lower and King
conducted transfusion experiments, described by Pepys as “… mending of bad blood by
borrowing from a better body.”
101
In 1889 von Behring and Kitasato
97
demonstrated that the blood of tetanus immune rabbits could eliminate the toxic property
of tetanus poison and that it had a protective effect when transferred to nonimmune
rabbits. At the Pasteur Institute in 1889, Roux and Yersin demonstrated that diphtheria
antitoxin could provide passive immunization in children. In the same year Marmerek
published studies on passive immunization against scarlet fever; however, the efficacy
of the scarlet fever antitoxin was controversial for many years.
98
Within a few years, the study of passive immunization was extended to snake venom,
69
diphtheria,
- Phisalix C.
- Bertrand G.
Sur la presence de glandes venimeuses chez les couleuvres et la toxicite du sang de
ces animaux: sur la propriete antitoxique du sang des animaux vaccines contre le venin
de vipere: reponse a M. Calmette: sur les effets de l'ablation des glandes a venin
chez la vipere.
Comptes rendus de la Societe de Biologie. 1894; 46: 747-749
31
and botulinum antitoxin.
34
In 1895 von Behring founded an institution for the production of diphtheria antitoxin
and conducted further studies of the other uses of passive immunization.
34
In 1903 the American Medical Association initiated successful studies on the prophylactic
use of tetanus antitoxin after injuries from Fourth of July fireworks.
34
In 1907 Cenci
22
used sera from patients recovering from measles in the prevention of this highly
contagious disease. Nicolle and Conseil at the Pasteur Institute confirmed the effectiveness
of this procedure in 1917. Subsequently, pooled sera from normal subjects was used
with better results and less severe reactions. By 1933, human gamma globulin was extracted
from placental tissue by using ammonium sulfate precipitation and demonstrated to
be effective in prevention of measles.
62
At the beginning of the World War II, Cohn and colleagues
23
,
24
from Harvard University developed a method to separate plasma proteins into stable
fractions. The concept of Cohn's fractionation was lowering ionic strength to 0.14,
reducing the pH to 7.2, and lowering the temperature to −3°C in the presence of low
concentrations of ethanol. One of these fractions, fraction II, was an antibody rich
fraction. This fraction could be administered in small amounts intramuscularly and
had a protective effect against measles and hepatitis A.
91
,
92
Cohn's fraction II could be given intravenously to normal persons but children with
severe infections and who were later recognized to have congenital immune deficiencies
developed immediate severe anaphylaxis or anaphylactoid reactions.
7
,
8
,
45
In 1952 when Bruton
described the first case of agammaglobulinemia, replacement of immunoglobulin was
shown to be effective in the treatment of these patients. The replacement, however,
could be done only intramuscularly; administration intravascularly caused serious
side effects. In the early 1960s Barandun and colleagues
7
with the cooperation of the Swiss Red Cross Laboratories developed the methods to
adapt the Cohn fraction II immunoglobulin for intravenous use. A number of intravenous
preparations were used in Europe in the 1960s and 1970s.
77
In 1981 the first commercial intravenous immunoglobulin was available in the United
States.To read this article in full you will need to make a payment
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Footnotes
Address reprint requests to Mark Ballow, MD Division of Allergy and Clinical Immunology and Pediatric Rheumatology Children's Hospital of Buffalo 219 Bryant Street Buffalo, NY 14222
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Copyright
© 2001 W. B. Saunders Company. Published by Elsevier Inc. All rights reserved.
