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PROCEDURE Forty-two boys, aged from 5 to 14 years, with scarlet fever were selected at the Willard Parker Hospital for these observations. (Girls were not included because of the difficulty of obtaining uncontaminated specimens of urine.) Twenty-two were treated with injections of moccasin venom (1:3,000) subcutaneously, and twenty others were used as controls, the division being arbitrary on admission of the patients. Patients who had received scarlet fever antitoxin were excluded.The administration of moccasin venom was begun on admission, usually on the second or third day of illness; the plan of treatment was to give courses of eight, twelve or sixteen injections. The dose for the first injection was 0.5 cc.; if there was no untoward reaction, 1 cc. was given daily thereafter until half the course was completed; the remainder was administered in doses of 1 cc. every other day. In most of the cases there was a

In a series of cases of acute nephritis in children studied on the Children's Medical Division at Bellevue Hospital in the past seven years, we have had the opportunity to observe the manifestations of this disease and to note its progress. Though we speak of it as a disease entity involving one organ, the kidney, it must be remembered that at least two distinct types of acute renal involvement may be present, depending on whether glomeruli or tubules are predominantly involved. The classification of acute nephritis on a purely clinical basis affords no great difficulty if one remains aware that no system of classification is absolute. A pure acute glomerular nephritis without tubular damage may be postulated, but it probably exists rarely, if at all. Capon1 said:It is a truism to state that when a child's kidneys become inflamed it is rare to find on histological examination that

It seems fair to say that the increasing difficulty in the diagnosis of cases with cerebral, or rather central nervous system, manifestations has not been lessened by the increased data concerning epidemic encephalitis and its bizarre symptomatology. One cannot help but feel that the recognition of this feature of encephalitis has led in great measure to a certain laxness in following puzzling cases to a definite conclusion.Discussion as to the ultimate diagnosis in one fatal case gave rise to the question whether an apparently noninflammatory condition of the central nervous system could produce a spinal fluid like that in epidemic encephalitis or in other inflammatory conditions. Is increased protein (albumin and globulin) in the cerebrospinal fluid always a sign of inflammation? Could chronic nephritis with uremia, a supposedly noninflammatory condition in relation to the central nervous system, account for a similar picture?Baar1 studied the diagnostic value of increased

Kottmann1 first described his test for thyroid activity in 1920. He had previously studied the serum in pregnancy, and from this work assumed that certain physicochemical differences must be present in the serums of patients suffering from thyroid dysfunction. Petersen, who first investigated the test in this country, thus describes the process:Because of the peculiar relation of iodin to the glandular metabolism, he (Kottmann) began his experiments with colloidal iodin preparations, using silver iodid for this purpose because of its well known photosensitivity. In the test as developed by him, certain phenomena commonly observed in photography play a rôle. Thus, when silver nitrate is added to potassium iodid, silver iodid is formed. In the presence of a protective colloid, the growth of the particles is retarded, depending on the protective property of the colloid used. In the photographic plate, a gelatin preparation is used for this purpose, and

The sera of 310 patients have been studied for precipitins against 2 protein fractions of S hemolyticus, the nucleoprotein of S. viridansand the group specific carbohydrate of S. hemolyticus.The S. hemolyticusfractions were freshly prepared. The S. viridansprotein first used∗was 5 years old. Later tests with a sample newly isolated from the same strain gave identical results. A description of the precipitin test and the antigens used has been presented in a previous communication.1Sera from the following groups of cases have been studied:1. A control group of 39 healthy nurses during the fall season.†2. A control group of 16 healthy medical students and nurses during the spring season.3. A control disease group .of 17 cases with temperatures of 102° or over. These patients were not affected with hemolytic streptococcus disease. All these sera were obtained during the spring season.4. A control disease group of 100 cases during the spring season. None of these patients was known to have rheumatic fever, rheumatoid arthritis, sub-acute S. viridansendocarditis, proven hemolytic streptococcus disease, glomerular nephritis or peptic ulcer.5. Twenty-three cases of proven sub-acute S. viridansendocarditis.16. Thirty-six cases of rheumatoid arthritis.‡7. Sixteen cases of proven hemolytic streptococcus disease.8. Fourteen cases of acute glomerular nephritis.9. Sixteen cases of sub-acute glomerular nephritis.10. Seven cases of healed glomerular nephritis.11. Five cases of healed glomerular nephritis during hemolytic streptococcus infection.12. Twenty-one cases of peptic ulcer with symptoms.

DIFFERENTIAL DIAGNOSIS Differential diagnosis between the various forms of meningeal or central nervous system disease has not become simpler as our knowledge of the pathology and chemistry of these conditions has increased. While it is relatively easy to diagnose clinically the acute inflammatory or purulent types of disease from those of a less acutely inflammatory nature, the differentiation between the diseases comprising each group is still clinically and chemically confused. The clinical picture of epidemic, pneumococcal, influenzal or streptococci meningitis is, as a rule, distinct from that of epidemic encephalitis, anterior poliomyelitis, polioencephalitis or tuberculous meningitis.Bacteriologically, the distinction in the former group is clearly enough defined. Chemically, the evidence is less definite in both groups. Differentiation between meningitis and meningismus, tetany and certain types of birth injuries at times may be very difficult. The determination of the primary lesion in instances of combined cardiorenal and meningeal conditions is often

This article constitutes an outline of a clinicopathologic study of ureteral obstruction in infancy and childhood, a detailed report of which, with follow-up histories, will be presented later. The conclusions in this work were drawn from observation in seventy-four cases of ureteral lesions discovered by autopsy, by urologic examination and, in some instances, by both.In infants, as in adults, urinary stasis predisposes to and perpetuates infection of the urinary tract. Stasis is predominantly the result of obstruction, and in infants the majority of urinary obstructions are found along the course of the ureter. A recent autopsy study of 2,420 pediatric cases at Bellevue Hospital revealed gross evidence of ureteral blockage in forty-seven cases, an incidence of nearly 2 per cent. Infection was demonstrated in four fifths of these by urinalysis or autopsy, allowing one to deduce that approximately one in fifty of all children has some form of ureteral

A previous paper1 has shown that the reported hospital medical admission rate for acute glomerulonephritis is similar in four latitude regions of the United States and southern Canada. In contrast, there is a diminished case frequency for scarlet fever and rheumatic fever in the South as compared with the North. Since clinical and laboratory evidence favors the hypothesis that acute glomerulonephritis is chiefly related to a preceding hemolytic streptococcus infection, it appeared peculiar that the diminution in incidence of the hemolytic streptococcus diseases scarlet fever and rheumatic fever in the southern latitudes did not also occur in the group of patients with acute nephritis. Osman,2 who studied the data on deaths from acute and chronic nephritis compiled from tables in the League of Nations International Year Book for 1928, found it impossible to correlate the figures with climatic or racial factors.In order to gain more accurate information

Todd1has demonstrated that the serums of animals immunized with S. hemolyticusdevelop a significant amount of an antibody which inhibits the activity of the streptococcal hemolysin. The serums of animals immunized to a number of other bacteria (pneu-mococcus, hemolytic staphylococcus, non-hemolytic streptococcus, and B. diphtheriae) do not contain appreciable quantities of this antihemolysin.In subsequent studies Todd2working in conjunction with Coburn and Pauli3showed that there was a consistent increase in the anti-streptohemolysin titre (termed antistreptolysin by Todd) in human serums afterhemolytic streptococcus infections. This antibody did not appear in significant amounts in the serums of patients convalescing from such other infections as lobar pneumonia, hemolytic staphylococcus osteomyelitis, joint tuberculosis and measles. The presence of high antistreptolysin titres in the serums of patients with rheumatic fever was additional immunological evidence leading to Coburn and Pauli's hypothesis that S. hemolyticusinitiates the rheumatic process.Todd found that at least 0.01 cc. of the serum of a normal individual without a recent hemolytic streptococcus infection was required to neutralize the hemolysin unit he utilized. He observed that as little as 0.0008 cc. of the serum of patients convalescing from hemolytic streptococcus disease contained the same neutralizing dose of antistreptolysin. Todd has described the antihemolysin titres of serums by recording the reciprocals of the fractions of the neutralizing doses of the serums as units. Thus a neutralizing dose (N.D.) of 0.01 cc. is equivalent to 100 units of antistreptolysin. He considers this value the upper limit of normal in the serums of healthy individuals without a preceding hemolytic streptococcus infection.The accompanying table shows the degree of the antistreptolysin titre∗ of the serum 6-57 days after the onset of acute glomerular nephritis in 22 unselected cases. A throat or upper respiratory infection preceded the onset of acute nephritis in 21 of these patients. Fifteen of these infections were associated with the presence of the hemolytic streptococcus in the pharynx.Twenty of the 22 serums from this group of cases contain a sufficiently high antistreptolysin titre to be indicative of a recent hemolytic streptococcus infection. The remaining 2 serums contain 100 units each of the antibody. These data offer strong additional evidence to the concept that acute glomerular nephritis in New York City is chiefly related to a preceding hemolytic streptococcus infection.