Tuberculin in diagnosis and treatment : a text-book of the specific diagnosis and therapy of tuberculosis for practitioners and students / By Dr. Bandelier ... and Dr. Roepke.

  • Bandelier, B. (Bruno), 1871-1924.
Date:
1913
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Licence: Public Domain Mark

Credit: Tuberculin in diagnosis and treatment : a text-book of the specific diagnosis and therapy of tuberculosis for practitioners and students / By Dr. Bandelier ... and Dr. Roepke. Source: Wellcome Collection.

Provider: This material has been provided by the Augustus C. Long Health Sciences Library at Columbia University and Columbia University Libraries/Information Services, through the Medical Heritage Library. The original may be consulted at the the Augustus C. Long Health Sciences Library at Columbia University and Columbia University.

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    in relatively large doses. The same was found in animal experi- ment : 0.5 c.c. old tuberculin kills a tubercular guinea-pig, while a healthy animal tolerates this dose without reaction. Thus Koch saw in tuberculin a true toxin, which by injection in slowly increasing doses is capable of producing immunity. When the doctrines of immunity were subsequently revised and extended, he changed his ideas, inasmuch as he considered tuberculin treatment an active immunizing process. Almost greater attention was paid at the Hertwig. time of its description to Hertwig's toxin theory, which, influenced by Metchnikoff's phagocyte teaching, explained the tuberculin reaction as a primary focal reaction pro- duced by a chemotactic influence of the leucocytes. Hertwig [15] based his theory on Stahl and Pfeffer's laws of chemotaxis; he considered that the leucocytes of a tubercular organism, by virtue of the continual production of toxin in the foci, became tolerant of the tuberculin, and that after an injection of tuberculin a positive chemotactic irritation is exerted on the leucocytes pre- viously at rest owing to the increased concentration of the tuber- culin. This influx of leucocytes causes the focal reaction, on which the febrile and general reaction is dependent. Ehrlich [16] localized the reaction in the middle of the three cell layers which en- circle the tubercular focus like the layers of an onion. While the central caseated and the adjoining normal tissues were un- damaged by tuberculin and insensitive to the toxin, the inter- mediate zone, damaged by the toxins of the bacilli, was specially capable of reaction. The production of specific antibodies took place in these toxin-sensitive cells; and the production of anti- bodies was the essential part of the mechanism of the reaction. Of late the standpoint has been increasingly Tuberculin a taken up that tuberculin is a primary toxin Primary Toxin for for the tubercular organism, chiefly because the Tubercular there is no proof of the presence of an Organism. anaphylactic reactionary body, either by a serum reaction or by transference of hypersusceptibility (R. Kraus, Lowenstein, Volk, and others). It is now generally considered that there circulates in the tubercu- lar organism a hypothetical antibody—Wassermann calls it anti- tuberculin, Wolff-Eisner an albuminolytic, Sahli a bacteriolytic amboceptor, Citron a sessile receptor—which changes the tuber- culin, inert in itself, into a highly toxic substance. On this basis the tuberculin reaction is explained by assuming that the tuber- culin set free in the focus first causes hyperemia—focal reaction— 2