What is the clinical impact of macrolide resistance?

被引:19
作者
Lonks J.R. [1 ]
机构
[1] Miriam Hospital, Providence, RI 02906
关键词
Azithromycin; Macrolide; Acute Otitis Medium; Antimicrob Agent; Pneumococcal Pneumonia;
D O I
10.1007/s11908-004-0018-1
中图分类号
学科分类号
摘要
Respiratory tract infections are treated empirically. Treatment is based on the likely pathogens and their antibiotic susceptibility. The most common respiratory tract pathogen is Streptococcus pneumoniae. In the United States, approximately 25% to 30% of S. pneumoniae are resistant to erythromycin and other macrolides. There are two mechanisms of resistance: ribosomal methylation that causes high-level resistance, and an efflux pump that causes low-level resistance. Macrolides are ineffective in animal models that use pneumococcal isolates with the methylase- or efflux-mediated resistance mechanisms. There are many case reports that describe clinical failure and isolation of a macrolide-resistant pneumococcus while a patient receives macrolide treatment. Two recent studies that included macrolide-susceptible and macrolide-resistant pneumococci showed that breakthrough bacteremia in patients receiving macrolide treatment occurred only with macrolide-resistant isolates. Study of bacteremic disease ensures the pathogenic role of the pneumococcus; however, it underestimates the true clinical impact of macrolide resistance. Copyright © 2004 by Current Science Inc.
引用
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页码:7 / 12
页数:5
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  • [1] Cherry D.K., Burt C.W., Woodwell D.A., National Ambulatory Medical Care Survey: 2001 summary, Adv. Data, 337, pp. 1-44, (2003)
  • [2] Hall M.J., DeFrances C.J., 2001 National Hospital Discharge Survey, Adv. Data, 332, pp. 1-18, (2003)
  • [3] Fang G.D., Fine M., Orloff J., Et al., New and emerging etiologies for community-acquired pneumonia with implications for therapy. A prospective multicenter study of 35 9 cases, Medicine, 69, pp. 307-316, (1990)
  • [4] Ostergaard L., Andersen P.L., Etiology of community-acquired pneumonia. Evaluation by transtracheal aspiration, blood culture, or serology, Chest, 104, pp. 1400-1407, (1993)
  • [5] Niederman M.S., Mandell L.A., Anzueto A., Et al., Guidelines for the management of adults with community-acquired pneumonia. Diagnosis, assessment of severity, antimicrobial therapy, and prevention, Am. J. Respir. Crit. Care Med., 163, pp. 1730-1754, (2001)
  • [6] Bartlett J.G., Dowell S.F., Mandell L.A., Et al., Practice guidelines for the management of community-acquired pneumonia in adults. Infectious Diseases Society of America, Clin. Infect. Dis., 31, pp. 347-382, (2000)
  • [7] Jacobs M.R., Felmingham D., Appelbaum P.C., Gruneberg R.N., The Alexander Project 1998-2000: Susceptibility of pathogens isolated from community-acquired respiratory tract infection to commonly used antimicrobial agents, J. Antimicrob. Chemother., 52, pp. 229-246, (2003)
  • [8] LeClercq R., Courvalin P., Bacterial resistance to macrolide, lincosamide, and streptogramin antibiotics by target modification, Antimicrob. Agents Chemother., 35, pp. 1267-1272, (1991)
  • [9] Sutcliffe J., Tait-Kamradt A., Wondrack L., Streptococcus pneumoniae and Streptococcus pyogenes resistant to macrolides but sensitive to clindamycin: A common resistance pattern mediated by an efflux system, Antimicrob. Agents Chemother., 40, pp. 1817-1824, (1996)
  • [10] Farrell D.J., Douthwaite S., Morrissey I., Et al., Macrolide resistance by ribosomal mutation in clinical isolates of Streptococcus pneumoniae from the PROTEKT 1999-2000 study, Antimicrob. Agents Chemother., 47, pp. 1777-1783, (2003)