David Riesman

ENTERICOID FEVER—FEBRIS ENTERICOIDES

During the last few years I have seen a number of cases of continued fever that resembled typhoid fever but did not give the usual laboratory tests nor did they present all of the characteristic clinical features of that disease. In their symptomatology they did not, however, depart from the text-book description more than many well authenticated cases of typhoid fever. I am sure that every physician in active practice sees cases of fever that impress him in the beginning as typhoid, and if he commits himself to this diagnosis he is often much embarrassed to find that the duration is too short for it to be typhoid fever or that the case does not give the laboratory reactions of that disease. I am, of course, not referring to certain widely different infections that may assume a typhoid type, such as ulcerative endocarditis, miliary and cascous tuberculosis, meningitis, etc. One of these typhoid-like infections has already been established as a clinical entity, namely

MITRALSIS OF TRAUMATRAUMATIC ORIGIN

History. —N. H., an able-bodied married man of thiryt-five, a musician by profession, was returning from a playing engagement one morning at 4 oclock in the month of August, 1910. Suddenly, when about three squares from home he was set on by foot-pads. Terror-stricken, he ran as fast as his legs would carry him, grasping tightly in one hand his violin and in the other a heavy box containing his music. He arrived at his home utterly spent and exhausted, and with an intense feeling of choking and suffocation. For half an hour he had to stand up and struggle for breath. Gradually the sense of suffocation lessened, its place being taken by a distressing palpitation. There was no real pain. Later in the day the patient consulted a physician, who told him there was nothing serious the matter with him, and that he would soon be well again. By

TREATMENT OF TYPHOID BY CONTINUOUS SALINE INSTILLATION

I wish to preface what I have to say about the Murphy treatment in typhoid fever by a few remarks on the pathogenesis of the disease. We are accustomed to attribute the symptoms of typhoid fever to the typhoid bacillus and to such lesions, produced by ulceration of the blood-vessels, by perforation, etc., as are the indirect result of its action. The general symptomatology of the disease—the fever, the cerebral symptoms, the altered metabolism, and the acute degenerations in the parenchyma of organs—are ascribed to a typhoid toxemia brought about by the entrance into the blood of the poison of the typhoid bacillus. Unlike the toxin of tetanus, this poison is not a secretory product of the microorganism, but is an endqtoxin laked out of the bodies of dead bacteria. As this view of the pathogenesis of the typhoid toxemia is the one almost universally accepted, it may

ACUTE ARTICULAR RHEUMATISM—ITS ETIOLOGY AND PATHOLOGY.

With the exception of a small and gradually lessening number, modern writers consider acute articular rheumatism an infectious disease. The nervous origin of rheumatic arthritis, proclaimed by the elder J. K. Mitchell 1 in 1831, and defended by Charcot, and more recently by Friedlander 2 , who places the primary lesion in the medulla oblongata, has been abandoned. More tenacious is the lactic acid theory of Prout, Todd, Fuller, Richardson, and others, according to which rheumatism is dependent on an excess of lactic acid in the blood. I need not bring forth any arguments against this theory. As Maclagan 3 says, the advocates of the lactic acid theory have taken one of the phenomena of the disease and raised it from its normal and subordinate position as a symptom to the rank and dignity of an exciting cause. Edwards, 4 Eisemann, and lately Haig, 5 have modified the acid theory, and replaced

Rheumatoid arthritis, with report of two cases

Despite the increasing literature on the subject of rheumatoid arthritis, the ultimate nature of the disease is far from clearly established, and even at this date we do not positively know just what affections of the joints should be grouped under the name. Nothing so clarifies the nosographic atmosphere as the discovery of causes—only through causal knowledge are we able to separate diseases that are similar and to assign to them a definite place in our systems. How easy it has become for us to define typhoid fever, diphtheria, and malaria, since their etiology has been determined. As we are still unable to point out the true cause of rheumatoid arthritis, it would, I believe, be better, following the example of Virchow, Garrod, and others, to use the phrasearthritis deformans, as that expresses the most prominent symptom and is non-committal on the score of pathogenesis. Morbid anatomy. —The lesions