bed, not having a nurse. Case 70 died on the tenth day after convalescence from pneumonia. There were no evidences of typhoid reinfection. Case 64, a negro, alcoholic, died on the twelfth day from asthenia. Death in case 118 resulted from osteomyelitis after a month's duration. Case 120, an ambulatory type, before coming under treatment, had hemorrhage, which determined a fatal issue. Case 124, the wife of this man, being depressed with grief, died a month later, complicated with pneumonia. Of the 144 whites there occurred five deaths, or 3.4%.

Conclusions:

(1) The food factor in the treatment of typhoid fever is the most important practical question to be solved.

(2) Toxemia is more marked in cases having gastrointestinal disturbances.

(3) Clinical evidences do not warrant liberal feeding in but few cases.

(4) The chief source of development of the bacillus typhosus is found in the intestinal canal and lymphopoietic system.

(5) The aim should be to nourish the patient without increasing saprophytosis, and the battle-ground of treatment lies in the gastro-intestines.

(6) A greater danger exists from a toxic paralysis of nutritive activity of the cell than from inanition.

(7) Any vital organs containing pathognomonic lesions of an infectious disease demand absolute rest.

(8) The excessive nitrogenous waste in typhoid fever was not due to the endotoxins of the typhoid bacilli, but probably mixed infections, and the specific typhoid toxin was not necessarily accompanied by high temperatum e.

(9) Emaciation occurs independently of the amount of food taken, and results more rapidly from toxemia than any lack of nourishment.

(10) The patient's life does depend on attempting to maintain a normal nitrogen metabolism.

(11) The proper food management will shield a patient from the usual dangers of typhoid fever.

(12) Sthenic cases furnish the more dangerous types of the disease, and these are more amendable to therapeutic fasting.

(13) Ambulatory cases are not less prone to intestinal complications than others.

(14) A greater danger arises from septic conditions set up by a hemorrhage than the mere loss of blood entails.

(15) Symptoms are no guides as to the presence of intestinal lesions; consequently patients require more or less routine feeding.

(16) Abortive cases showed a greater tendency to relapse.

(17) Tympanites furnishes an increased area for absorption, and is provoked by any surplus of food, which increases peristalsis.

(18) The great desideratum is to treat the patient and not the disease.

(19) Scientific data prove that clinical diagnoses may be made with a reasonable degree of accuracy.

(20) Therapeutic fasting allows an uncomplicated typhoid infection to pursue a normally mild course without any mixed infection, by reducing the bacterial content of the intestines, and was applied only to the severe cases.

(21) Fasting will enhance the effect of hydrotherapy, and frequently renders the use of antipyretic measures

unnecessary.

(22) Gelatin is valuable food, in that it lessens the nitrogenous waste and prevents hemorrhage.

(23) The low mortality in this series of cases was greatly due to the elimination of relapses and complica

tions among the mild or abortive cases by restricted feeding and lessening the dangers in sthenic patients by fasting.

(24) In this report forty-five consecutive cases occurred without a death. Of the 144 whites, five, or 3.4%, died, and the low mortality, 4.7%, of all cases, was ascribed to the dietetic management, and many of the cases had very inefficient nursing.

DIAGNOSIS AND TREATMENT OF BRIGHT'S

DISEASE.

BY H. F. HARRIS, M.D., ATLANTA.

Every intelligent physician will agree that there are few things in medicine of more practical importance than the diagnosis and treatment of those conditions which are collectively spoken of as "Bright's disease." Notwithstanding this there can be no question that mistakes are often made in the recognition of the disease, and it is undoubtedly true that in no inconsiderable proportion of cases nothing or next to nothing is done toward the amelioration of the patient's condition. My attention has often been directed to the fact that physicians frequently make a diagnosis of Bright's on a clinical examination of the urine alone, and it can, therefore, be no matter of wonder that serious errors frequently result. I have seen patients with albuminuria from a simple cystitis who had been informed that they were suffering from an incurable disease of the kidneys, and only a short time ago I saw a young man who had orthostatic albuminuria who had been told by two prominent physicians of Atlanta that he had Bright's, and that the only hope for him would be in decapsulating his kidneys. Under such circumstances the amount of mental worry, and the physical disability that will surely result from a patient being told that he has such a serious malady, give a most serious aspect to mistakes of this kind. And how often is it the case that patients are seen in the latter stages of genuine Bright's for whom nothing has been done-they being in many in

stances not even aware of the real nature of their trouble ? I feel, then, that any effort to correct this state of affairs. is neither time nor energy thrown away.

From a considerable pathological and clinical expe::ence I am convinced that our conception of what should Le regarded as Bright's disease is, for ractical purposes, misleading. To begin with, instances of acute nephritis are not so rare as is generally supposed; on the contrary, a slight inflammation of the kidneys is frequently a com--lication of infectious diseases, and in many instances the kidne conditions do not subside for days, and even weeks, after complete recovery from the original maladv. During such a period albumin and casts may be found in the urine, and an erroneous diagnosis of chronic Bright's might be made. A still more fruitful source of mistake lies in the universally accepted idea that a nephritis necessarily entails the symptoms that occur in Bright's, while as a matter of fact this is anything but the rule. I consider this a most important matter and one which curiously noone seems to have heretofore considered from this standpoint. For a considerable period of my life I was entirely engaged in pathological work, and the fact strongly impressed me that an overwhelming percentage of those cases coming to necropsy showed more or less evidence of nephritis. This was particularly true, of course, of those persons dying after middle life. In a service extending over a number of years as pathologist to the Philadelphia Hospital I do not recall having seen but one or two instances where normal kidneys were observed postmortem. Now, while it is highly probable that a careful examination of the urine of these patients would have resulted in the detection of tube-casts, and, in some instances, a traceof albumin, neither the state of the urine nor the patient's general condition could be looked upon in the vast majority of cases as giving a characteristic picture of Bright's..