Antibiotic prophylaxis

نویسنده

  • THOMAS J. PALLASCH
چکیده

The age of antibiotic prophylaxis began shortly after World War II with the introduction of penicillin to the general population and received significant impetus from the introduction of the first American Heart Association (AHA) recommendations for the prevention of bacterial endocarditis (BE) in 1955. Since that time, considerable effort has been expended to prove its efficacy, develop the appropriate drugs and dosages and determine its clinical indications. It was not until the mid-1980s that any attention was directed towards its potential adverse effects, particularly regarding penicillin allergy. Currently, one of the major concerns with antibiotic prophylaxis is its use in large populations and how this might contribute to the global problems with microbial resistance to antibiotics. The potential value of antibiotic prophylaxis is based upon an assumption that if antibiotics aid host defenses to eliminate infections and restore homeostasis, then they must prevent infections. That these are very different microbiological processes has essentially gone unappreciated. On the one hand, antibiotics kill or prevent the growth of microbes that will be eliminated eventually by the patient’s immune system, while on the other, the antibiotic is expected to prevent the colonization of any or all microbes of varied virulence, adhesion factors, nutritional requirements and antibiotic sensitivity in any or all organ systems. One ends microbial virulence, while the other anticipates it. Antibiotic prophylaxis as a public health measure has a serious fault. In most public health prevention measures (sanitation, fluoridation, immunization), it is required that the benefits greatly outweigh the risks. Generally, the risk must be minimal and the benefit great as millions will receive the proposed preventive measure. With antibiotic prophylaxis, just the opposite occurs: virtually, no one will benefit except for a few. This also assumes that prophylaxis is effective, although there are limited experimental and clinical data to support this assumption. Great care should be taken to document the efficacy of a procedure that will be applied to many in the hope that a few will benefit. Antibiotics have also been termed ‘societal drugs’ (1) in that they not only affect the microbial flora of those to whom they are administered, but also those close to them (the transfer of antibiotic resistance genes among family members) and society as a whole (2). The world epidemic of antibiotic-resistant Streptococcus pneumoniae, Enterococcus, Staphylococcus aureus and S. epidermidis, Pseudomonas aeruginosa, Klebsiella pneumoniae and the oral pathogens, viridans group streptococci (VGS) and Prevotella and Porphyromonas, did not happen by chance, but by the massive application of antibiotics in health care and agriculture. Each dentist or physician on any given day likely feels that only they are prescribing the antibiotic, when in reality, millions of their colleagues are doing the very same thing. After only a short time, the millions become billions and the microbes decide to rebel against those trying to extinguish them as a life form. Microorganisms will always be with us and ahead of us (2). In a best case scenario, antibiotic prophylaxis may prevent 10% of all cases of BE (3). Studies in the Netherlands indicate that antibiotic prophylaxis may prevent 5.7% of all native valve endocarditis and 3.8% of all prosthetic valve endocarditis which, if it is assumed that the prophylaxis were 49% effective, would prevent five endocarditis cases annually in a population of 14.5million (4, 5). In the United States, it has been estimated that optimal antibiotic prophylaxis could prevent 240–280 of the annual 11 200 cases of infective endocarditis (IE) (6). If VGS accounts for 25% of all endocarditis cases in the United States and dental procedures are responsible for 1% of these cases (28 episodes), then it is important that proper risk– and cost–benefit appraisals be made. It should also be appreciated that VGS-induced BE is less than 10% fatal

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تاریخ انتشار 2003