Chapter 129. Staphylococcal Infections (Part 13)

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Antimicrobial Therapy for Selected Settings For uncomplicated skin and soft tissue infections, the use of oral antistaphylococcal agents is usually successful. For other infections, parenteral therapy is indicated. S. aureus endocarditis is usually an acute, life-threatening infection. Thus prompt collection of blood for cultures must be followed immediately by empirical antimicrobial therapy. For S. aureus native-valve endocarditis, a combination of antimicrobial agents is often used. In a large prospective study, an SPRP combined with an aminoglycoside did not alter clinical outcome but did reduce the duration of S. aureus bacteremia. As a result, many clinicians begin therapy for life-threatening infections with...

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Chapter 129. Staphylococcal Infections (Part 13) Antimicrobial Therapy for Selected Settings For uncomplicated skin and soft tissue infections, the use of oral antistaphylococcal agents is usually successful. For other infections, parenteral therapy is indicated. S. aureus endocarditis is usually an acute, life-threatening infection. Thus prompt collection of blood for cultures must be followed immediately by empirical antimicrobial therapy. For S. aureus native-valve endocarditis, a combination of antimicrobial agents is often used. In a large prospective study, an SPRP combined with an aminoglycoside did not alter clinical outcome but did reduce the duration of S. aureus bacteremia. As a result, many clinicians begin therapy for life-threatening infections with a 3- to 5-day course of a β-lactam and an aminoglycoside (gentamicin, 1 mg/kg IV every 8 h). If a MRSA strain is
isolated, vancomycin (30 mg/kg every 24 h, given in two equal doses up to a total of 2 g) is recommended. Patients are generally treated for 6 weeks. In prosthetic-valve endocarditis, surgery in addition to antibiotic therapy is often necessary. The combination of a β-lactam agent—or, if the isolate is β- lactam-resistant, vancomycin (30 mg/kg every 24 h, given in two equal doses up to a total of 2 g)—with an aminoglycoside (gentamicin, 1 mg/kg IV every 8 h) and rifampin (300 mg orally or IV every 8 h) is recommended. This combination is used to avoid the possible emergence of rifampin resistance during therapy if only two drugs are used. For hematogenous osteomyelitis or septic arthritis in children, a 4-week course of therapy is usually adequate. In adults, treatment is often more prolonged. For chronic forms of osteomyelitis, surgical debridement is necessary in combination with antimicrobial therapy. For joint infections, a critical component of therapy is the repeated aspiration or arthroscopy of the affected joint to prevent damage from leukocytes. The combination of rifampin with ciprofloxacin has been used successfully to treat prosthetic-joint infections, especially when the device cannot be removed. The efficacy of this combination may reflect enhanced activity against staphylococci in biofilms as well as the attainment of effective intracellular concentrations.
The choice of empirical therapy for staphylococcal infections depends in part on susceptibility data for the local geographic area. Increasingly, vancomycin (in combination with an aminoglycoside or rifampin for serious infections) is the drug of choice for both community- and hospital-acquired infections. The increase in community-based MRSA skin and soft tissue infections has drawn attention to the need for initiation of appropriate empirical therapy. Oral agents that have been effective against these isolates include clindamycin, TMP- SMX, doxycycline, and linezolid. The antimicrobial susceptibility of isolates in different geographic regions has varied. Therapy for Toxic Shock Syndrome Supportive therapy with reversal of hypotension is the mainstay of therapy for TSS. Both fluids and pressors may be necessary. Tampons or other packing material should be promptly removed. The role of antibiotics is less clear. Some investigators recommend a combination of clindamycin and a semisynthetic penicillin. Clindamycin is advocated because, as a protein synthesis inhibitor, it reduces toxin synthesis in vitro. A semisynthetic penicillin is suggested to eliminate any potential focus of infection as well as to eradicate persistent carriage that might increase the likelihood of recurrent illness. Anecdotal reports document the successful use of IV immunoglobulin to treat TSS. The role of glucocorticoids in the treatment of this disease is uncertain at present.
Therapy for Other Toxin-Mediated Diseases Therapy for staphylococcal food poisoning is entirely supportive. For SSSS, antistaphylococcal therapy targets the primary site of infection. Figure 129-4 Evidence of staphylococcal scalded-skin syndrome in a 6-year-old boy. Nikolsky's sign, with separation of the superficial layer of the outer epidermal layer, is visible. (Reprinted with permission from LA Schenfeld et al: Images in clinical medicine. Staphylococcal scalded skin syndrome. N Engl J Med
342:1178, 2000. © 2000 Massachusetts Medical Society. All rights reserved.) Further Readings Diep BA et al: Complete genome sequence of USA300, an epidemic clone of community-acquired meticillin-resistant Staphylococcus aureus. Lancet 367:731, 2006 [PMID: 16517273] Fowler VG Jr et al: Staphylococcus aureus endocarditis: A consequence of medical progress. JAMA 293:3012, 2005 [PMID: 15972563] ——— et al: Role of echocardiography in evaluation of patients with Staphylococcus aureus bacteremia: Experience in 103 patients. J Am Coll Cardiol 30:1072, 1997 Fridkin SK et al: Methicillin-resistant Staphylococcus aureus disease in three communities. N Engl J Med 352:1436, 2005 [PMID: 15814879] Grundmann H et al: Emergence and resurgence of meticillin-resistant Staphylococcus aureus as a public-health threat. Lancet 368:874, 2006 [PMID: 16950365]
Lowy FD: Antimicrobial resistance: The example of Staphylococcus aureus. J Clin Invest 111:1265, 2003 [PMID: 12727914] McCormick JK et al: Toxic shock syndrome and bacterial superantigens: An update. Annu Rev Microbiol 55:77, 2001 [PMID: 11544350] Moran GJ et al: Methicillin-resistant S. aureus infections among patients in the emergency department. N Engl J Med 355:666, 2006 [PMID: 16914702] Mylotte JM, Tayara A: Staphylococcus aureus bacteremia: Predictors of 30-day mortality in a large cohort. Clin Infect Dis 31:1170, 2000 [PMID: 11073748] Seybold U et al: Emergence of community-associated methicillin-resistant Staphylococcus aureus USA300 genotype as a major cause of health care– associated blood stream infections. Clin Infect Dis 42:647, 2006 [PMID: 16447110] Bibliography Lowy FD: Staphylococcus aureus infections. N Engl J Med 339:520, 1998
[PMID: 9709046] Hiramatsu K et al: The emergence and evolution of methicillin-resistant Staphylococcus aureus. Trends Microbiol 9:486, 2001 [PMID: 11597450] Ing MB et al: Bacteremia and infective endocarditis: Pathogenesis, diagnosis, and complications, in The Staphylococci in Human Disease, KB Crossley, GL Archer (eds). New York, Churchill Livingstone, 1997, pp 331–354 von Eiff C et al: Pathogenesis of infections due to coagulase-negative staphylococci. Lancet Infect Dis 2:677, 2002