CHAPTER III.

ON THE AGENCIES WHICH GOVERN IMMUNITY AGAINST INFECTIONS AND INTOXICATIONS—THE ORIGIN OF FEVER.

FROM the moment of our birth we are constantly exposed to the incessant attacks of innumerable bacteria and to the effects of a large amount of poisonous material formed within our body or introduced from without, and if we survive this ceaseless battle it is due to the powerful weapon we possess in the internal secretion of the ductless glands, especially of the thyroid gland. That this gland possesses very energetic antitoxic properties can be shown by the fact that when it is extirpated animals or persons very readily acquire infectious diseases of all sorts. Thus, the late Professor Charrin,[44] of Paris, showed several years ago how readily dogs that have lost their thyroid succumb to all possible infections. Professor W. S. Greenfield,[45] of Edinburgh, has found that persons suffering from myxœdema (athyroidia) very often die from tuberculosis, and Professor Pel,[46] of Amsterdam, found a great frequency of tuberculosis in the families of myxœdematous persons. This coincides with the conclusions of Prof. G. R. Murray,[47] Professor Lanz, and ourself, that the properties of the thyroid can be inherited. Sajous has shown, moreover, that the pituitary, the adrenals and the thyroid constituted the autoprotective mechanism of the body against disease, a fact not only sustained by the above evidence, but also by a vast number of additional facts.

Footnote 44:

Charrin: “Les Defenses naturelles de l’organisme,” Paris, 1898 (Masson).

Footnote 45:

Greenfield: Quoted after Ewald, “Die Erkrankungen der Schilddrüse,” Nothnagel’s Handbuch, Wien. p. 159, 1896.

Footnote 46:

Pel: “Myxœdema,” Volkmann’s Sammlung klin. Vorträge, 1895, No. 123.

Footnote 47:

Murray: “Diseases of the Thyroid Gland,” Part i, London, 1901.

As we showed at the last Congress of Tuberculosis in Paris, 1905, tuberculosis is especially frequent as a sequel to any process deleterious to the thyroid gland, as after the puerperium, especially with prolongated lactation; after sexual excesses, as there is a relation between the sexual glands and the thyroid; after various infectious diseases; after rapid growth in puberty, due to hyperactivity of the thyroid which influences the growth of the body; after severe diabetes due to exhaustion of the thyroid; and after previous hyperactivity in chronic alcoholism due to the action of alcohol upon the thyroid. On the other hand, all those agencies which excite thyroid activity may be a preventive against tuberculosis, such as raw meat and milk. It has been shown that milk contains the internal secretion of the thyroid.

The thyroid protects us against poisons of different origin, such as the products of decomposition of protein food. This fact is shown by the experiments of Dr. Leo Breisacher, of Detroit,[48] formerly assistant of the late Professor Munk, of Berlin, and from those of Dr. Blum,[49] of Frankfort. The experimental results of Dr. Chalmers Watson,[50] showing alteration of the thyroid in certain animals after an exclusive diet of raw meat, and those of Dr. D. Forsyth[51] concerning the pituitary body in some animals, may be correlated with this fact. As is well known, the thyroid and pituitary body stand in very close relationship. Galeotti and Lindemann,[52] in 1897, have also shown that the products of decomposition of meat produce an increase of the colloid substance of the thyroid.

Footnote 48:

Breisacher: “Untersuchung über die Gland Thyroidea,” Archiv für Anatomie und Physiologie, Suppl., Bd., p. 509, 1889.

Footnote 49:

Blum: Pflüger’s Archiv, vol. xc., p. 285, 1902; Archiv für die Gesammte Physiologie, p. 617, 1902.

Footnote 50:

Chalmers Watson: The Lancet, p. 347, Feb. 11, 1905.

Footnote 51:

Forsyth: The Lancet, p. 154, Jan. 19, 1907.

Footnote 52:

Lindemann: Virchow’s Archiv, p. 202, 1897.

The antitoxic properties of the thyroid against different products is also shown by the observations of Lanz[53] and Walter Edmunds,[54] who have found that animals without thyroid resist narcosis badly; and, as we have shown in a communication to the Paris Biological Society,[55] chloroform, like alcohol, produces a condition of hyperactivity in the thyroid gland, which results also in an excited mental condition. The observation that cases of Graves’s disease and of severe diabetes cannot stand narcosis may be related to this fact.

Footnote 53:

Lanz: Zur Schilddrüsenfrage, Leipzig, 1894.

Footnote 54:

W. Edmunds: The Lancet, May 11th, p. 1317; 18th, p. 1381; 25th, p. 1449, 1901.

Footnote 55:

Lorand: C. R. de la Société de biologie, 1906.

It has been shown recently by Hunt[56] that the thyroid protects us against poisons like acetonitril, and that iodine acts through the thyroid. Garnier,[57] of Paris, has found that certain chemical products, such as iodine, produce great alterations in the thyroid. As is well known, cases of Graves’s disease (hyperthyroidia) have been observed after iodine treatment. That the thyroid fulfils a protective rôle against infectious diseases may already be considered proved by the fact that, as Roger and Garnier,[58] Crispin,[59] Torre,[60] Bayon,[61] of Würzburg; de Quervain, and others have found, the thyroid is, as a rule, altered in infectious diseases. As Roger and Garnier have shown by a series of investigations confirmed by the above-named authors, the thyroid shows in acute infectious diseases with fever an increased activity with enlargement of the follicles, which are filled with a large quantity of colloid substance which may even enter into the adjacent lymphatic spaces. However, this hyperactivity of the thyroid gland may be followed by its exhaustion, and thus after a certain duration of high fever there may be no colloid substance at all in the folliculi.

Footnote 56:

Hunt: International Congress of Physiology, Heidelberg, 1907.

Footnote 57:

Garnier: “La Thyroide dans les maladies infectieuses,” Thèse de Paris, 1899.

Footnote 58:

Roger et Garnier: Presse médicale, April 19, 1899.

Footnote 59:

Crespin: Giornale dell’ Associazione Napolitano di Medici, xii, 3.

Footnote 60:

Torre: “La Tiroide nei Morbi Infettivi,” Il Policlinico, No. 6, p. 145; No. 8, p. 226; No. 10, p. 280.

Footnote 61:

Bayon: Würzburger Abhandlungen, 1904.

It is only logical to suppose that with anatomo-pathological alterations of the thyroid, indicating a condition of hyperactivity, there must be corresponding clinical symptoms and that these must necessarily be similar to those found in another condition of hyperactivity of the thyroid gland—i.e., in Graves’s disease, the condition of hyperthyroidia. And, indeed, such must be the case, for, as we shall try to show, fever and Graves’s disease have similar clinical symptoms. Thus their most typical symptom is the same: tachycardia or increased frequency of the pulse, without which no case of Graves’s disease should be diagnosed. There is a sensation of heat in most of the cases of Graves’s disease, and the temperature sometimes reaches a dangerous degree in fully developed cases of this disorder. Thirst, frequent in fever, is also a frequent symptom in Graves’s disease (polydipsia in 14 out of 59 cases recorded by Albert Kocher[62]), and can also be produced by thyroid feeding (Lanz,[63] Georgiewski,[64] and others). After a certain duration of fever further symptoms of an increased activity of the thyroid appear, such as abundant perspiration—a typical feature of Graves’s disease. Vaso-dilatation and excessive perspiration can also be produced by thyroid feeding. The latter symptom of fever is a device by which nature tries to eliminate toxic products, and accordingly there generally follows upon it a fall in the temperature and an amelioration of the symptoms of fever. The diarrhœa which we find in some infectious diseases, like that of typhoid fever, trypanosomiasis, etc., is also a typical symptom in Graves’s disease. When the fever subsides there appears another typical symptom of this condition: polyuria. To complete this analogy we may mention toxic decomposition of proteins, diminution in the body weight, great muscular weakness, and increased elimination of urea and uric acid as typical symptoms of both conditions. As in Graves’s disease, there is also in fever an augmentation of the processes of oxidation. Glycosuria is frequent in both conditions, and acetonuria may occur in fever and also in Graves’s disease. Glycosuria and diabetes in consequence of infectious diseases are, as we have shown in a paper read before the London Pathological Society,[65] probably due to the increased activity of the thyroid, and their disappearance, occasionally after a high fever, may be ascribed to the exhaustion of the thyroid after a previous hyperactivity. We know that a condition of Graves’s disease may be followed by a myxœdematous condition in which, as we have shown previously, glycosuria is very rare. In the few hitherto published cases there was no complete myxœdema.

Footnote 62:

A. Kocher: “Mittheilungen aus den Grenzgebeiten,” etc., 1901.

Footnote 63:

Lanz: Quoted after Buschau, Wein, 1895.

Footnote 64:

Georgiewski: Zeitschrift für klin. Medicin, Bd., xxxiii, f. 1-2, p. 153, 1897.

Footnote 65:

Lorand: Transactions of the Pathological Society of London, vol. lvii,