speak of the absence of any one of these complications as singular; it is the exemption from all. Regarding the commonest one, pneumonia, we may say this, that whether we adopt the view of Klebs, that it is caused by the direct access of the bacillus typhosus through the respiratory tract, or the more probable one that it is a septic inflammation from the hæmic contamination incident to the fever, that any germicide and antiseptic inhibitory of these agencies will as easily arrest the pneumonia as it will abate the fever. So if glandular infiltration is interrupted, and ulceration is prevented, there will be no intestinal hemorrhage, no perforation, no peritonitis.

What of auxiliary treatment? Such treatment is very rarely required. In not more than one case in twenty has the question whether it were not well to give stimulants ever occurred to me. There is a general appearance of well-being and well-doing to the patient that is sufficiently reassuring to the physician without the need of extra precautions. Almost equally seldom will the question of giving quinine arise. A tonic seems as unnecessary as an alco. holic stimulant, while as an antipyretic quinine might certainly be left out of the question.

It would seem that laxatives, and especially cathartics, might be almost wholly dispensed with, unless it should appear that prolonged constipation had preceded the onset of the fever. Even then the laxative could be selected without any reference to antiseptic effects, so that the choice need not of necessity fall upon calomel. Its antiseptic effect would not add appreciably to that already attained by the salicylate.

Opium will find a useful place oftener than any other adjuvant; but as already intimated, it will be needed less than under former modes of treatment, while on the other hand, a safeguard is guaranteed for a much freer use, since the constant maintenance of free elimination is not now of such vital consequence.

To raise the question of the mode by which ammonium salicylate interrupts the course of typhoid and remittent fevers would, at the present time, be to open up a field of boundless conjecture. This will have to be determined by future investigations, and by those qualified by experience in such researches. Still, I cannot forego expressing the belief that when this and similar questions are cleared up the conclusion will be in harmony with the views advanced by Professor Semmola before the Ninth International Medical Congress.

"The true part played by bacteria in pathology" he says, "is the production by them of certain noxious and decomposed elements of the blood, which substances, and not the bacteria, are the potent factors in the causation of disease.

Not forgetting the cause of this cause, it is still probable that all the striking phenomena of these fevers proceed directly from this condition of the blood, this ptomainemia, if we may use such a word, and it is at least presumable that phenomena may be interrupted or averted by chemically changing those ptomaines, or undetermined noxious substances, so as to render them innocuous, and that without necessarily destroying the vitality of the bacteria causing them. The very unstable nature of these substances already known would invite such a mode of attack, and would justify the use of the feebler germicides, capable, nevertheless, of decomposing these substances.

While believing that the ammonium salicylate reaches the first cause of these fevers by a destructive or inhibitory action upon their specific germs, I believe also that this is likely to prove the lesser of its two leading effects, being led to this view by the clinical fact, reported two years ago, of the recrudescence of the fever when the salicylate is prematurely dropped out of the treatment, as at any time before the end of the first week. This, occurring after a day or more of normal temperature, would argue a re-intoxication by the products of the vital activity of bacteria still living; which is equivalent to saying that the bacilli may be present without fever so long as their immediate effects are neutralized, just as they may be present without fever when their vitality is seriously compromised.

Do the foregoing facts justify the conclusion that ammonium salicylate is a specific remedy for typhoid and remittent fevers? I think they do. The advocates of the iodine treatment of typhoid advance the unchallenged claim that it is a specific, while Liebermeister has shown that it is attended by a mortality of more than 14 per cent. Ziemssen admits the same claim for calomel, while denying that it is able to shorten the disease: but the mortality following this treatment is nearly 12 per cent. The mortality for the cold water treatment, as reported by Erand, of Stettin, out of a total of more than 8,000 collected cases is 7.4 per cent. Under all modes of treatment, as determined by Jaccoud from more than 80,000 cases, the fatality

is, 19.25 per cent. Up to the present the mortality percentage for the ammonium salicylate is somewhat less than 3.

It will undoubtedly be objected that cases ending in resolution during the first week, or before pathognomonic symptoms of the fever have time to develop, cannot be fairly classified as typhoid. This is a rational objection, but it holds equally against all statistics of specific treatment; for no medication with a view to aborting the disease many days later than this period will be availing. If then we are to await the occurrence of the distinctive anatomical lesions before being permitted to announce a diagnosis, it is clear that no remedy, now or hereafter can successfully claim to be abortive or specific. It ought to be a basis for a diagnosis having all the elements of probable correctness, that a given case has occurred during the prevalence of typhoid, especially in the same family; that the usual prodromata have been present, and that high fever, characterized by the usual thermometric curve has existed for two or three days.

While it is possible that my diagnosis has not always been subject to these limitations, it is certain that the exceptions have been very few. It must be admitted that the number of cases has been too small to have great statistical value, but they cover a period of four years, and so represent the average severity of the disease, whereas the same number occurring in the course of an epidemic might repre sent only a benign form of the malady, where the fatality would be light under any treatment, or without any.

If the consideration of the treatment of these two fevers in a single paper needs an explanation or apology it is this:

Save in unimportant particulars the treatment is identical. Both are arrested by the ammonium salicylate; such arrest being limited to the pre-inflammatory stage of typhoid, while it is doubtless practicable in any stage of remittent fever. This is so probable that it may serve in the differential diagnosis of cases hard to make out— cases which occur with sufficent frequency to the most careful and observing clinician. It may be fairly assumed that in a case of supposed typhoid seen after the occurrence of striking abdominal symptoms, and shortly aborted, a revision of diagnosis is warranted if not demanded. At the same time it is practically unimportant to make the distinction, since the revision, when made, involves no corresponding change of treatment.

ARTICLE VIII.

CLINICAL STUDY OF EXOPHTHALMIC GOITRE.

BY IRVING D. WILTROUT, M. D., OF HUDSON.

Many names have been applied to the peculiar condition of disease characterized by rapid action of the heart, protrusion of the eyeballs, and enlargement of the thyroid gland. Most of them are open to the objection of not indicating definitely either the principal symptoms, or the essential character of the affection. I think it is on this account, that we should much prefer the name, "Exophthalmic Goitre," to either that of Graves' disease, or Basedow's disease, by one or the other of which it is most commonly described.

Exophthalmic Goitre is not a distinct and specific disease, in the sense that typhoid fever and acute, croupous pneumonia are; but still it has a perfectly well-established claim to its place in our nosology. It is true that in well marked cases there are certain features which are dependent on the anemia which is so frequently present, and others which are due to the general neurasthenia that is usually attendant. But apart from these, there is the clearly defined group. of symptoms first mentioned, which are so peculiar, and so constantly associated in this disease, as to clearly establish its separate identity, and to show that it is connected with some special morbid condition. A good idea of the cause of this disease in its aggravated form, may be gathered from the following history.

CASE 1. Jennie S., a tall, spare woman of nervous temperament, when about 27 years of age, suffered a severe disappointment in a love affair. Soon afterwards, she began to present symptoms of impaired nutrition, loss of color, emaciation, debility, etc. She became nervous and excitable. At the same time, the action of the heart became more rapid and excited, and the thyroid gland enlarged. There was marked irregularity in menstruation. There was a marked anæmic, bellows murmur, over base of the heart. The carotid arteries pulsated violently, aad were the seat of a strong thrill, and

aneurismal bruit. There were also, pulsations of the thyroid gland, with thrill and murmur. Under the use of iron, digitalis, and tonics, she improved so much, that she discontinued treatment. Before long, she suffered from a return of the same symptoms in an aggravated form, and in addition, there was prominence of the eye-balls. Again she found relief; but during the next five years she had several similar relapses, and each time, the symptoms were more advanced. The degree of enlargement of the thyroid, varied consider ably, being extremely marked at times. Both lobes were equally affected. The prominence of the eye-balls, also varied much from time to time; during several of the attacks being so extreme that the eyelids would not close over them. On one occasion, there was slight conjunctivitis. The attacks were always marked by a great increase in her debility and nervous excitability. The heart's action never regained its normal state, but continued rapid and easily excited by slight causes. At times, the pulse was exceedingly rapid, 130 to 150 in the minute. After several such attacks her health became permanently impaired. The bellows murmur became harsher in character. The area of cardiac dullness increased and the sounds of the heart became sharp and weak, indicating the development of dilatation, with slight mitral insufficiency. (Edema of the feet and other evidences of impaired circulation, now appeared. In the following spring, she again came under my observation, and in a far worse condition. She had suffered greatly, and had used stimulants freely. The heart's action was very rapid and feeble, and there was violent pulsation in the cervical vessels. The thyroid gland had diminished somewhat in size, but was hard and inelastic. The eyes still protruded greatly; there was no relief. Edema and ascites supervened, and a few days later jaundice appeared, soon followed by death.

At the post-mortem examination, the heart was found to be much enlarged, and its cavities, especially the right ventricle, extremely dilated; both the mitral and the tricuspid leaflets presented thickened edges and were insufficient. The thyroid gland was still enlarged; its tissue was dense and very hard, evidently from interstitial, fibroid change. It was infiltrated with serum, but there was no cystic degeneration. The cervical ganglia of the sympathetic were not dissected for.

It will be observed, in the first place, that in the above case, the