Background— Antibiotic prophylaxis recommendations for the prevention of infective endocarditis are based in part on studies of bacteremia from dental procedures, but toothbrushing may pose a greater threat. The purpose of this study was to compare the incidence, duration, nature, and magnitude of endocarditis-related bacteremia from single-tooth extraction and toothbrushing and to determine the impact of amoxicillin prophylaxis on single-tooth extraction. Methods and Results— In this double-blind, placebo-controlled study, 290 subjects were randomized to (1) toothbrushing, (2) single-tooth extraction with amoxicillin prophylaxis, or (3) single-tooth extraction with identical placebo. Blood was drawn for bacterial culturing and identification at 6 time points before, during, and after these interventions. The focus of our analysis was on bacterial species reported to cause infective endocarditis. We identified 98 bacterial species, 32 of which are reported to cause endocarditis. Cumulative incidence of en...

Bacteremia Associated With Toothbrushing and Dental Extraction

Society of America, the International Society of Chemotherapy for Infection and Cancer, and this guideline has been endorsed by the American Academy of Pediatrics, Infectious Diseases American Dental Association has approved the guideline as it relates to dentistry. In addition, Timothy Gardner, David Goff, David T. Durack and The Council on Scientific Affairs of the Thomas Pallasch, Stanford T. Shulman, Anne H. Rowley, Jane C. Burns, Patricia Ferrieri, Jane W. Newburger, Brian L. Strom, Lloyd Y. Tani, Michael Gerber, Robert O. Bonow, Matthew Levison, Ann Bolger, Christopher H. Cabell, Masato Takahashi, Robert S. Baltimore, Walter Wilson, Kathryn A. Taubert, Michael Gewitz, Peter B. Lockhart, Larry M. Baddour, the Quality of Care and Outcomes Research Interdisciplinary Working Group Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Guideline From the American Heart Association Rheumatic Fever, Endocarditis, and Prevention of Infective Endocarditis: Guidelines From the American Heart Association: A

Prevention of infective endocarditis.

One of the unique features of p-lactam antibiotics and other cell-wall inhibitors like vancomycin and bacitracin is that they can rapidly kill and in many cases lyse susceptible bacteria. Many other types of antibacterial agents (e.g., trimethoprim or chloramphenicol) are primarily bacteriostatic: they inhibit multiplication but do not cause an irreversible inactivation of the cell. In 1970 the characterization of a novel type of pneumococcal mutant was reported in the literature [1]. This mutant grows in normal generation times and is as sensitive to growth inhibition by penicillin as the wild-type parent strain. However, while cultures of the parent

Antibiotic tolerance among clinical isolates of bacteria.

Although enterococci are relatively resistant to penicillin, the mechanism of resistance is largely unknown and enzymatic inactivation does not play a role. In this study, an isolate of Streptococcus faecalis was found to have beta lactamase activity resulting in complete inactivation of penicillin. With a high inoculum, this strain was resistant to greater than 1,000 micrograms/ml of penicillin. Penicillin resistance and beta lactamase activity were transferred by conjugation at a high frequency to an enterococcal laboratory recipient strain together with two plasmids of molecular size 34 X 10(6) and 56 X 10(6), thus demonstrating the emergence of plasmid-mediated penicillin resistance in the genus Streptococcus.

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Transferable beta-lactamase. A new mechanism for in vitro penicillin resistance in Streptococcus faecalis.

When antibiotic combinations are used to provide a broader spectrum of antimicrobial activity or in an attempt to prevent the emergence of resistant organisms, it is rarely necessary or practical to perform tests of drug interactions in vitro. In vitro testing of combinations may be useful when combinations are used in an attempt to attain synergistic interactions. In some cases, screening methods can be used as substitutes for formal synergy testing. This paper examines the mechanisms of antibiotic interaction leading to synergism or antagonism, surveys attempts to correlate in vitro observations with efficacy in animal models, and reviews clinical data providing evidence for or against a useful role of synergistic antibiotic interactions in the treatment of human infections.

Antibiotic combinations: should they be tested?

OPTIMAL management of patients with rheumatic heart disease or a previous bout of acute rheumatic fever includes the administration of prophylactic antibiotics to prevent pharyngeal infection with Group A streptococci.1 , 2 Several studies have shown that oral penicillin prophylaxis is associated with a high prevalence of penicillin-resistant bacteria in the gingival flora.3 4 5 6 7 8 9 An original concern was that continuous low-dose prophylaxis would result in a high incidence of endocarditis due to resistant organisms that would be difficult to cure. Follow-up studies of large numbers of patients taking prophylactic penicillin have found no increase in the incidence of endocarditis,10 and few cases of . . .

Mark H. Mazur

Papers

Endocarditis Due to Resistant Viridans Streptococci during Oral Penicillin Chemoprophylaxis