Morton Hamburger

Expulsion of group a hemolytic streptococci in droplets and droplet nuclei by sneezing, coughing and talking

Abstract 1.1. The numbers of beta and alpha streptococci discharged into the air of an experimental room-during sneezing, coughing and talking were determined in a series of forty-eight carriers of group A streptococci. By simultaneous employment of exposed blood agar plates placed upon the floor, and broth bubbler samplers whose intake was 3 feet from the floor, streptococci expelled in large, rapidly falling droplets could be differentiated from those discharged as droplet nuclei which remained in the air for at least several minutes. 2.2. The material dispersed into the air during a sneeze is chiefly saliva. 3.3. Four dispersion patterns of beta hemolytic streptococci by sneezing were evident. In the most common, moderate numbers were expelled in large droplets which fell rapidly to the floor 1.5 feet from the sneezer, but very few or none in droplet nuclei. In one of two less common patterns, small numbers of beta streptococci were sneezed as droplet nuclei but none in large droplets; in the other, no beta streptococci were recovered from the air. In the rarest, of which only one example was found, large numbers of beta (and alpha) streptococci were expelled both as droplet nuclei and in large droplets; many were collected as far as 9.5 feet from the sneezer. The saliva of this carrier contained huge numbers of beta streptococci. 4.4. Thirty-five per cent of twenty carriers sneezed out large numbers of alpha (salivary) streptococci as droplet nuclei. Eighty per cent discharged moderate or large numbers in heavy droplets which fell rapidly to the floor. 5.5. About one-half the streptococci expelled into the air as droplet nuclei by sneezing were still present as long as twenty minutes after the first sneeze. 6.6. The material expelled during coughing apparently originates in the back of the throat or below the epiglottis and contains little if any saliva. 7.7. Only one of twenty carriers coughed large numbers of beta streptococci into the air as droplet nuclei or in large droplets; he expelled no alpha streptococci. Ninety-five per cent of the carriers coughed few or no streptococci collected by either type of air culture. 8.8. Practically no streptococci were recovered from the air of rooms while carriers counted out loud for five minutes.

Aortic valve perforation

Abstract This paper describes fifteen patients with aortic valve perforation, in fourteen of whom this complication developed during the course of bacterial endocarditis. Aortic cusp perforation should be suspected whenever moderately severe or severe aortic insufficiency appears during bacterial endocarditis. The murmur of aortic insufficiency caused by cusp perforation is of the common decrescendo blowing quality, and is only occasionally of musical quality. In patients with aortic cusp perforation and attendant severe aortic insufficiency, congestive heart failure often develops within a few days or weeks. In our series heart failure appeared within one week to four and a half months in eleven of the fifteen patients. Eight of these patients, who had not been treated by aortic valve surgery, died within one day to six months after the appearance of heart failure. Three of our patients with acute bacterial endocarditis apparently died of a cardiac arrhythmia resulting from infection of the atrioventricular node or bundle of His. In seven of our patients the aortic insufficiency was treated surgically. In two patients the perforation was small enough to be closed by direct suturing; in five the aortic valve was excised and replaced by a Starr-Edwards prosthesis. Five of these seven patients survived to be discharged from the hospital, but one of the five died suddenly three months postoperatively, and another died of Candida endocarditis four and a half months after insertion of the prosthesis.

Susceptibility to sulfadiazine of hemolytic streptococci recovered in army camps

Abstract 1.1. The administration of 1 Gm. of sulfadiazine a day to forty-five carriers of Group A hemolytic streptococci was not followed by the appearance of sulfonamide-resistant variants. The duration of treatment varied from four to fifty days. 2.2. Eighty-six per cent of 107 strains recovered from seventy-six untreated carriers of Types 1, 3, 6, 11, 12, 14, 17, 19, 24, 44 and untypeable Group A streptococci were susceptible to sulfadiazine in vitro. Thirteen per cent, all of these Type 17 except for one Type 19, were highly resistant. 3.3. The importance of local factors in influencing the bacteriostatic effect of sulfonamides in vivo was emphasized by the observation that the action of sulfadiazine upon sulfonamide-sensitive streptococci in the nose was more marked than upon sulfonamide-sensitive strains of the same serological type in the throat.

Transfer of beta hemolytic streptococci by shaking hands

Abstract Quantitative cultures of the hands of nasal carriers of hemolytic streptococci and of individuals who shook hands with these carriers showed that several hundred to as many as 49,900 of these pathogens could be transferred by ordinary handshakes. The greatest numbers were transferred by carriers who had just blown their noses into sterile handkerchiefs.

Tuberculous pericarditis; its treatment with streptomycin and some observations on the natural history of the disease.

Abstract 1.1. Three patients with clinically primary tuberculous pericarditis have been treated with streptomycin for ninety, ninety and 112 days each, respectively. The duration of fever following admission to the hospital was thirteen weeks, as compared with twenty-one weeks in four patients whose pericarditis healed spontaneously without the aid of streptomycin. In the treated cases streptomycin was not given until the patients had been in the hospital two weeks or longer. The three treated patients are entirely well and leading normal lives at an average of twenty-eight months after the cessation of fever. 2.2. Of nine patients with clinically primary tuberculous pericarditis not treated with streptomycin five died within a few months of miliary spread of the tuberculosis or of cardiac failure. Spontaneous healing of the pericarditis occurred in the other four, but after an average asymptomatic period of 16.5 months tuberculosis appears elsewhere in the body.

THE REPLACEMENT OF STREPTOMYCIN-RESISTANT COLIFORM BACTERIA IN THE STOOLS BY STREPTOMYCIN-SENSITIVE VARIANTS DURING AND FOLLOWING THE CESSATION OF STREPTOMYCIN THERAPY

Thouglh the appearanice of streptomycini-resistant bacteria during the course of streptomycin therapy has been abundantly demonstrated (1), less attention has been paid to the ultimate fate of these resistant formiis. Our attention was drawn to this problem during an investigation of the development of streptomycin-resistant variants among the normally commllensal but potentially pathogenic flora of the body. Though streptomycin-resistant coliformii bacilli are almost uniformly absent from the stools of human beings who have not receive(d streptomycin. they frequently appear during the intramiuscular administration of streptomycin for certain types of tuberculosis (2) and during its oral a(Idmiinistration for various purposes. Our investigationis lhave shown that in mnany cases the normally senisitive coliformiis were replace(d during treatmenit by resistant strains of the same species. However, when streptomycin was discontinued, and in special instances, even before the (Irug was (lisconitinued, sensitive coliforms began to reappear an(d finally crow(le(l out the resistant variants altogetlher. It is the purpose of this paper to presenit the dlata dealing with this replacemiient of resistant by sensitive strains.

Canicola fever with meningitis: Report of a case in a human treated with penicillin

Abstract A case of severe canicola fever, apparently contracted from a sick dog, is described. The chief clinical features were those of Weils disease, namely, chills, fever, headache, muscle pains, delirium, ecchymoses, jaundice, anuria and meningitis. Striking improvement was manifest within twenty-four hours of the administration of penicillin. Muscle biopsy revealed lesions previously described in Weils disease. Liver biopsy showed focal hepatitis although liver function tests were within normal limits.

SULFAPYRIDINE IN EXPERIMENTAL PNEUMOCOCCIC PNEUMONIA IN THE DOG

Previously reported studies of the action of sulfapyridine in experimental pneumococcic infection have been carried out in the mouse, rabbit, and rat-species which, unlike man, are highly susceptible to the pneumococcus. Whitby ( 1 ) found that mice infected with Type I pneumococci and treated with sulfapyridine possessed after recovery considerable immunity to the same organism. A similar observation was made by Schmidt and Hilles (2). Whether acquired immunity plays an essential role in the mechanism of recovery in treated mice is not known, but there is some indirect evidence to suggest that it may do so. Especially significant is MacLeods (3) observation on mice infected with pneumococci Types I, II and III, respectively, that the survival rate for each type was closely similar in actively immunized and in sulfapyridinetreated groups. Furthermore, there is clearly demonstrable a synergistic antipneumococcic action in tivo between artificially induced immunity and sulfapyridine, as shown by the work of Powell and Jamieson (4), MacLean, Rogers, and Fleming (5, 6), and Kepl and Gunn (7). From these considerations it would seem that natural antipneumococcic resistance of a relatively high order, such as that possessed by human beings as a group (8), may enhance the effectiveness of sulfapyridine. The dog resembles man in ability to localize pneumococci in the tissues and in degree of natural humoral immunity. 0. H. Robertson and coworkers (9, 10), have shown that lobar pneumonia, which in all essential respects is comparable to the human disease, can be produced in the dog. They have demonstrated further that mortality in the experimental disease can be regulated, within certain limits, by varying the infect-

Some effects of injecting sterile solutions of streptokinase-streptodornase into the subarachnoid space of normal rhesus monkeys.

Streptokinase (SK) and streptodornase (SD) solutions have been injected into the subarachnoid space of patients with meningitis, in order to promote the resolution of the inflammatory exudate (1-6). Because side reactions have been reported in certain cases (2, 3), it seemed desirable to ascertain the effect of injecting the enzymes into the uninfected subarachnoid space. Such a study was carried out in 31 rhesus monkeys,3 along with six others in which sterile saline was substituted for the enzyme. It is the purpose of this paper to report the results of the study.