Abstract

Prior to the advent of potent bacteriostatic and bacteriocidal agents, it was common practice to subdivide cases of bacterial endocarditis into two groups: acvte bacterial endocarditis, i.e. bacterial endocarditis of less than the three or four weeks’ duration, and subacute bacterial endocarditis, which persisted for more than four weeks. The discovery and utilization of present-day antibiotics have changed the entire picture and course of bacterial invasion of the endocardium and made the distinction meaningless. Preferably, in classification emphasis should be placed on the specific organism responsible for the bacterial invasion and, where known, the name of the organism should be made a part of the disease designation. Some bacteria prove relatively resistant to penicillin; others actually produce a specific penicillin-destroying enzyme known as penicillinase. Bacteria which are resistant to penicillin are in some cases susceptible to large doses of the antibiotic. Bacteria which are penicillin-resistant but with individual cells sensitive to the action of the antibiotic form an important group: their sensitivity, as measured in the laboratory, may vary 1,000-fold or more according to the inoculum. Whether or not such organisms will be affected by large doses of penicillin would, therefore, seem to depend more on heaviness of infection than on resistance of the organism as determined by laboratory tests. Although the organism most commonly responsible for bacterial endocarditis in patients with rheumatic valvular disease or congenital lesions of the heart and vessels is Str. viridans, this organism poses little problem in therapy because-along with pneumoccoci, gonococci and group A hemolytic streptococci-strains of Str. viridans all are moderately or highly susceptible to penicillin therapy. Enterococci, which are relatively resistant to penicillin alone, now account for about 15 per cent of cases, contrasted with 4 or 5 per cent in the pre-antibiotic era. Endocarditis due to enterococci or coliform organisms occurs most frequently in patients with infections of the genitourinary or the intestinal tract or after various diagnostic or therapeutic procedures carried out in these areas. Most stubborn, chronic cases of bacterial endocarditis today are caused by staphylococci. Infection with staphylococci produces hypersensitivity toward these organisms: although the patient builds up a fair degree of immunity toward further overwhelming invasions of micrococci, paradoxically he responds with definite lesions to amounts of exotoxin so minute they would pass unnoticed in ordinary persons. Staphylococci have been

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