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disease has developed, and I cannot but wonder if some cases of so-called septicæmia may not really be due to the absorption of an enormous dose of typhoid fever poison, which, by its effect upon the nervous system, causes death before the pathognomonic symptoms of the disease have had time to assert themselves."

I have quoted this passage, not in any sense as an evidence of prescience, but to show that the ideas therein expressed have been present in my mind during the last eight years, and to have formed the basis of the work which this paper purposes to illustrate. The discovery of paratyphoid fever is an argument in the truth towards the disintegration of the idea of typhoid fever as a single clinical entity.

Paratyphoid fever is due to the paratyphoid bacillus. The paratyphoid bacilli (for there are two races) are organisms intermediate in their characters between the true typhoid bacillus and the colon-bacillus, and are placed in the socalled “Gartner” group. The name “paratyphoid ” bacillus appears first to have been used by Archard and Bensaude in 1896, and was re-introduced by Schottmuller in 1901, and would seem to be the preferable designation for those microorganisms that produce typhoidal symptoms. typhoid bacilli, as a rule, resemble the typhoid bacillus in morphology, that is to say, they are multi-flagellate (6-8-12) actively motile bacilli, which do not stain by Gram's method, and do not form spores. Their growths on agar and gelatine also resemble those of the typhoid bacillus, but on other media present striking differences. As regards the agglutination (Widal) reaction, the blood of the paratyphoid fever patient either does not agglutinate the typhoid bacillus (i.e., " Widal reaction is negative"), or agglutinates it only in low dilution, e.g., 1 in 30 or 40; while it agglutinates the paratyphoid bacilli in far higher dilution, e.g., 1 in 100 or 200, or even higher.

These observations are extracted from a paper by Dr. Hewlett in the Practitioner of January, 1904, and are based upon a collection of about 100 cases. Symptomatically, paratyphoid fever simulates typhoid in every detail, but pathologically it differs somewhat, inasmuch as in none of the fatal

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cases have ulcers of the intestines been found, nor has endothelial proliferation in the lymphoid tissue of the intestines, in the mesenteric glands, or in the spleen, been discovered.

It is possible that typhoid and paratyphoid fevers may occur simultaneously in the same individual, and perhaps th case I will now describe was of such a nature. The diagnosis of paratyphoid disease in this case was only made after repeated examinations for typhoid bacillus had proved negative. No doubt had been entertained that the patient was suffering from typhoid, the presumption of the existence of this disease being strengthened by the fact that the patient became ill at the same time as two other women, who had undoubted typhoid, at the same time and in the same ward. All three of these cases showed how greatly the disease typhoid may vary, as one of them proved to be of a severe type, with alarming hæmorrhage occurring from time to time, which seriously endangered the patient's life. The third case was of an exceedingly mild type, but bacteriological proof of its typhoidal origin was present throughout.

M. D., a girl of twenty, was admitted into Ward 13 at the General Hospital on March 24 last year, suffering from pain in the stomach after food, and other symptoms suggestive of ulcer of the stomach ; on more than one occasion she had had hæmatemesis. For a fortnight after admission she did very well, and was getting up, but had to take to bed the third week of her stay in hospital on account of general malaise, associated with a temperature which rose in a manner pathognomonic of typhoid. She had no cough, epistaxis, or hæmorrhage of any kind; no rash, no sordes, but the spleen could be felt below the margin of the ribs; the abdomen was moderately distended, and a persistent diarrhæa was present; the stools were like those of an ordinary case of enteric, but were not foul. She remaind in a febrile condition for about three weeks, at the end of which time the temperature gradually went down, until in the fourth week it became normal. Two Widal tests were negative, but a third examination, made in the seventh week of her stay in hospital, showed paratyphoid reaction in five minutes, and the typhoid and bacillus coli communis reaction in three-quarters of an hour.

In the cases, of which this was one, all occurring at the same time in patients who had been in the hospital for a fortnight suffering from quite ordinary diseases, it is certain that the disease was contracted during their stay in hospital. They are interesting on this account of interest especially from the fact that, presenting almost identical symptoms of very varying intensity, one of them was due, not to typhoid, but to paratyphoid infection. It seems highly probable that further investigations will show that not only paratyphoid, but other bacilli, may be responsible for varieties of cases of what clinically seem all to be typhoid fever.

The discovery of paratyphoid fever, differing as it does but little from an ordinary case of typhoid fever-except in the mildness of the symptoms and the far less liability to a fatal issue—is obviously a decided step in the disintegration of the idea of all cases of what is clinically typhoid being due to a single cause. It is possiblemeven probable--that we shall progress still further in this work of disintegration, but meanwhile it is certain that we must abandon the idea of typhoid fever being a purely intestinal disease, and must regard it as toxæmia, or a modified form of septicæmia, in which the organism which is the actual cause of the disease passes from the local and primary seat of infection into the blood, and produces there the toxins which give rise to the various symptoms. These symptoms will depend (1) upon the intensity of the poison, (2) upon the special conditions of the invaded organism, (3) upon the particular part of the body upon which the disease chiefly spends itself. A certain number of our patients die within a few days from the onset of the disease, from an extreme dose of poison, just as occurs occasionally in every zymotic disease, often before local manifestations of the malady have had time to manifest themselves. Of such a nature was the case of John M., aged thirty, who came under my care on February 9 of last year, and died on the 23rd. It was noted on admission, though he had been ill for only a very few days, that he was very ill ; he lay on his back in a restless, asthenic manner, with flushed face, respirations about 36, and a running dicrotic pulse of

about 130; his tongue was dry, furred, and cracked; the abdomen was distended, but moved a little, and was not rigid; some diarrhea was present, but was not excessive. He gradually sank into a profoundly asthenic state, was very restless, listless, and feeble ; both lungs became congested, but no pneumonia or other complication occurred; the spleen could not be felt, and there were no spots to be seen.

No improvement of any kind occurred, and he died, as stated, fourteen days after admission. It was quite clear that in this case no local mischief was responsible for the patient's death. One felt that never from the first moment he was seen could any hope be entertained of his recovery, and though he was watched and treated with the utmost solicitude, and freely stimulated by brandy and subcutaneous injections of strychnine, no improvement took place. He died from the huge dose of poison. According to Curschmann, this case represents a well-marked type of the disease, and one in which the prognosis is always hopeless. Death occurs even in such cases before the specific intestinal lesions are marked, and may take place as early as at the end of the first week, while it is rarely postponed longer than the end of the second.

In marked contrast with a case of this description is that of a girl, Annie E., aged twenty, who was admitted on the 31st of August, and left cured on the 10th of October. There was no doubt about the nature of the disease. The Widal reaction was positive, and she manifested in the slightest possible manner all the classical symptoms of the disease, with the exception only of the non-presence of spots. Her temperature never exceeded 100.6, and the pulse, though rising to 110, was always regular and good in quality. She never gave us the slightest anxiety, but, with the possibility of perforation always in view, was treated with the same care as though she had been gravely ill. The contrast between these two cases—the one so gravely ill that one felt sure at first sight that there could be no hope of recovery, and the other so slightly ill as never to be the source of anxiety-was most marked, and affords a strong proof, if proof were needed, that it is not the poison, but its amount, which is the danger to our patients.

Variations in the type of the disease are further afforded by those cases in which particular systems, such as the respiratory or nervous systems, are affected. The affections of the respiratory organs may occur in any portion of the respiratory tract, and may be distinguished into those which are due to typhoid infection, and those which are complications of the disease. Epistaxis occurs usually early in the disease, and is of no special moment; but if it occurs at a later period of the febrile stage, may be a source of danger.

Affections of the larynx and trachea are of much greater moment, and, when occurring by themselves or in association with bronchitis, often very seriously endanger the life of the patient. They sometimes occur as complications of the disease, and at others as direct evidence of the influence of the typhoid bacilli which have been found to exist in the laryngeal lymph follicles (by Schultz). Such a case was that of Jessie P., a woman of thirty-seven, who was admitted into the hospital suffering from typhoid on November 8, 1902, and did not leave the hospital until twenty-two weeks later, when, though the typhoid fever had long been cured, she still remained the victim of bronchial catarrh and difficulties of breathing, associated with the laryngeal changes. She was suffering markedly from bronchitis at the time of admission, with some tendency to asthenia. The ordinary typhoid symptoms improved rapidly, and caused no anxiety until at the end of the fourth week she was said to be greatly improved, and, as far as the ordinary typhoid condition was concerned, convalescent; but in the fifth week her condition got worse ; her chief symptoms now were dyspnoea and stridulous breathing ; her lungs were resonant throughout, but were blocked with ronchi; respirations were hurried; her pulse was 142; the temperature never exceeded 100. During the next week her general condition improved, but her cough remained about the same, with the expectoration of a good deal of frothy mucus. In the seventh and eighth weeks her condition remained much the same. The typhoid symptoms had disappeared, but there was a good deal of dyspnoea from the bronchitis, and stridor from the laryngeal inflammation.

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