treatment. I have often remarked on this subject, that you show me a physician whose cases are all typhoid, and they all recover in from two to five weeks (unless some complications arise), and I will show you cases in which Widal's reaction will bear negative results, and malarial parasites will be found in the blood.

It has never been my bad fortune to see the two infections in combination, nor one infection following closely on the track of the other, though I do not deny such possibilities. On this line, Marchiafava and Bignami, in the Twentieth Century Practice, state, "Typhoid fever has been regarded by many as a frequent complication of malaria, but we have never seen a case of the coëxistence of the two infections." Nor have Baccelli and many others seen any, either before or since the discovery of the malarial parasite, while Osler has published the cases of Thayer and Barker, where both diseases were present. Hence we must admit the possibility, but this coëxistence is by no means common.

So closely do typhoid fever and Baccelli's subcontinuous fever simulate each other, that only a microscopical examination could be taken as final; even the administration of quinin fails to settle the diagnosis. In my observations, where Widal's reaction was affirmative, the renal complications were much more infrequent than when the infection was from the estivo-autumnal parasite, the percentage being as 1 to 15 in typhoid, while in my series of one hundred and twenty-six cases of malarial fever, 42 per cent. showed kidney complications.

Dr. W. Britt Burns, of Memphis, Tenn., states that it is his experience in nephritis following malaria, that the urine clears up under large doses of quinin. This has not been my experience. He also reported a necropsy in which the gross pathology showed a large and a small white kidney, with marked hepatic and splenic changes. In my experience the large white kidney is the more common, and congested, granular, pigmented glomeruli are found, and glandular degeneration is noted along the tracts of the tubuli uriniferi, and especially about the loop of Henle, eight-tenths of all the granular, epithelial and blood casts having come from the ascending limb.

Moore, of Galveston, states that after a few days (seven or eight) of single tertian infection there are liable to be manifestations of renal changes; that doubtful tertian infection will produce a nephritis in a large portion of cases even though it runs only a short time. The more chronic the case becomes the more probable will be the kidney complication. He claims a percentage of 68.7 of nephritis in estivo-autumnal fevers. This, though, seems to me to be rather high, and it occurs to me that local conditions and preëxisting lesions may have raised the percentage. He claims that the age of the patient, the height of the temperature and the specific gravity of the urine showed no relation to the presence of albumin and casts.

This is in line with my observations; however I have noticed a relation between the number of parasites and the amount of pigment found in the blood and the rapidity with which the kidney disturbances appear; also there is a relation between the hepatic congestion and the disturbing of the urinary equilibrium.

Rosenstein recognizes an acute nephritis as a result of malarial infection, and finds the support for his opinion in the albuminuria which occurs during the febrile attacks. There is no doubt whatever but that an acute nephritis (diminished urine, blood, albumin, casts, edema and mucus) may develop during the course of an intermittent quotidian fever, whatever the original type may have been.

Bignami claims that this condition is generally relieved by quinin, but in my experience, in cases where the free pigment was excessive, I have had blackwater fever follow the administration of quinin in three instances, with death in two, hence I am of the opinion and follow the rule of using quinin with extreme caution in cases of over five or six days standing, where the infection is virulent, but rather follow the treatment used by the practitioners in the Yazoo and Red river valleys in cases of pernicious malaria, namely, the use of hyposulphite of soda in ten to twelve grain doses.

Dr. John B. Elliot, sr., of New Orleans, recommended this treatment, and it certainly is efficient. However, where there is a profuse medication displayed, and blackwater fever develops, quinin may not be held entirely responsible, for Dr. C.

W. Schlayer reports a case of blackwater fever complicating malaria in a patient who had recently returned to Germany from Africa, in which country he was free from malaria, owing to quinin prophylaxis. The blackwater complication followed the administration of a .75 gm. dose of phenacetine. I have had a case with blackwater fever complication following the administration of a five grain dose of phenacetine.

Reinhold Ruge* reports a case where the blackwater fever followed the administration of a .3 gm. dose of quinin, and concludes, from a broad experience, that quinin prophylaxis is not, in all cases, to be relied upon; however, he thinks that the method recommended by Kleine of the use of quinin enemata during the attack is of benefit. He urges the microscopical examination of the urine, and claims that the blackwater complication can be detected twenty-four hours previous to the appearance of the clinical symptoms, as polychromatophilic degeneration may be observed, together with numerous macrocytes, microcytes and blood shadows.

According to Rosenstein, even chronic parenchymatous nephritis may be the result of malaria, and is developed either during the attack (especially if the sweating stage be absent) or at varying periods after the fever has subsided, even when the patient is sufficiently recovered to think himself able to return to work.

From Bartel's observations on patients in Kiel, who came from the plains of Schleswig Holstein, he draws the conclusion that malarial fever is one of the most active causes of chronic parenchymatous nephritis.

Senator gives malaria as a factor in nephritis, but thinks that there are generally other remote or predisposing causes.

Thayer and Hewetson place the percentage of albuminuria observed in malaria in two hundred and eighty-four cases at 50 per cent. Thayer asserts that he can trace the origin of chronic nephritis to malarial infection. The author in Case III can assign no other cause for the chronic parenchymatous nephritis than the attack of tertian fever.

Rempicci, of the Roman Medical Clinic, made a study of three hundred and fifty cases of malarial infection, and takes * Deutsche Medicinische Wochenschrift, July 10th, 1902.

into account all forms of kidney complications from simple transitory albuminuria to true nephritis, and he estimates that out of three hundred and fifty cases, those showing kidney complications having only malarial origin, were eighty, or about 23 per cent. In his studies at the hospital of Santa Spirito, he finds that acute or chronic nephritis may be developed under the influence of malaria. His cases in which the renal disease was seen from the beginning leave no doubt as to the etiology.

Kelsch and Keiner, who have made a special study of the kidneys in malaria, accredit about 20 per cent. of the albuminuria to malarial infection.

In regard to the cause of this thoroughly recognized complication, there is some doubt. The Twentieth Century Practice states, that as to the pathogenesis of renal lesions in malarial infections, we are at present able only to form theories. We do not as yet know the pathogenic agent of nephritis developing after scarlatina, nor, in malaria has the knowledge of the malarial parasite so far thrown any light upon the pathogenesis of the nephritis. In pernicious infections very few parasites are found in the kidneys (I have found many invaded red corpuscles in the blood casts in the urine), while the retrogressive changes in the epithelium may be so grave as to lead to necrosis. Bignami and Rempicci accredit this to the presence in the blood of a toxin of unknown origin. This I believe, in a great measure, to be true, though the question has been raised, Why are the kidney complications 80 rare? I believe that in a mild attack of malaria, the excreted toxins are readily handled by the excreting organs, but it has been my observation that the nephritic disturbances are principally in the glomeruli and along the central portion of the tubuli uriniferi, where the capillaries are the narrowest and most tortuous. They are first due to a blocking of the circulation by red corpuscles, parasites and pigment, and a migration of parasites into the surrounding tissue, thus causing an acute congestion (transitory albuminuria). Second, where the infection is virulent and matured parasites are found in abundance, the toxin excreted by the parasite is sufficient, and is the causative agent of the severe and often fatal nephritis.

That these toxins are the excreta of matured parasites and are of acid reaction and irritant therapeutic action I firmly believe, although at present I am unable absolutely to demonstrate its truth. However, I will record a few of my most typical cases, and my readers can judge them according to their merits. I will say that my autopsies are obtained with difficulty

and are few.

Case I. Female, aged 9. Saw her first October 11, 1899. Diagnosed autumnal fever. Fever ran an irregular course for ten days, ranging from 98° to 1023°F., pulse running at from 100 to 112. Skin was very dry, tongue dry and coated a heavy brown coat, bowels constipated. On about the tenth day the temperature took a rise to 1031°F., and the pulse attained 120. (I have noticed this rapid pulse in all cases with renal complications.) I found the liver enlarged and tender; the spleen palpable, and the abdomen somewhat distended. (No tenderness in right iliac fossa, no eruption.) Respiration was 24 per minute. Made a chemical examination of the urine and found specific gravity 1015. No albumin, no sugar, excess of chlorates and 1 per cent. excess of uric acid. I was at a loss to account for the rise in temperature, which continued, even attaining 1041°F., and never falling below 100°F. On the third day after elevation of temperature or the fourteenth day of the attack, the urine showed a specific gravity of 1012, and blood and albumin were found. On the twenty-first day the albumin had attained 1 per cent., and there was some edema. The temperature dropped to 102°F., and by the twentyeighth day there was marked improvement. The urine was watched for seven weeks, when the albumin entirely disappeared; the patient completely recovered, and had no subsequent illness.

Case II. Female, aged 28. Saw her first August, 1900; married, two children, had no nephritis. Developed an attack of tertian fever, which ran a rather erratic course for twentyone days, and from which, apparently, she recovered. In about fourteen days she complained of her feet and hands swelling, and on examination of the urine, blood and granular casts were found, and 1 per cent. of albumin. This percentage continued to increase even under treatment, until it attained 43 per cent., when it began to decrease. There has been almost a constant presence of albumin from then till now, and as fall approaches the edema and dyspnea become troublesome. The only possible cause to which I can ascribe this chronic parenchymatous nephritis is malaria.