Staphylococcal Infections Medication

  • Author: Thomas E Herchline, MD; Chief Editor: Burke A Cunha, MD   more...
 
Updated: May 18, 2012
 

Medication Summary

Historically, isolates resistant to oxacillin (commonly referred to as methicillin-resistant S aureus [MRSA]) were resistant to most agents other than vancomycin, but these isolates were limited to nosocomial infections. More recently, many reports have described community-acquired MRSA infections that have been susceptible to various non–beta-lactam antibiotics. As such, patients with serious staphylococcal infections should be initially started on agents active against MRSA until susceptibility results are available. Many coagulase-negative staphylococci are oxacillin-resistant. The duration of treatment and the use of synergistic combinations depend on the type of infection encountered. Endocarditis due to S aureus may require a prolonged course of antibiotics.

Although many strains of MRSA that cause community-acquired infection are susceptible to trimethoprim-sulfamethoxazole, treatment with trimethoprim-sulfamethoxazole has been associated with clinical failure, especially in the presence of significant tissue damage.[22]

Vancomycin-resistant isolates have been reported; isolates with an increased minimum inhibitory concentration (MIC) to vancomycin are becoming more common and include both MRSA and methicillin-susceptible S aureus (MSSA).[23] Consensus guidelines recommend dosing vancomycin to avoid a trough of less than 10 mcg/mL; trough levels of 15-20 mcg/mL are recommended to treat complicated infections.[24]

In a study of 296 consecutive MRSA bacteremia episodes, several factors were predictive of high vancomycin MIC, including age older than 50 years, prior vancomycin exposure, history of MRSA bacteremia, history of chronic liver disease, and presence of a nontunneled catheter.[25]

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Antibiotics

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

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Nafcillin (Nafcil, Unipen, Nallpen)

 

Preferred therapy for methicillin-susceptible S aureus (MSSA) staphylococci infections. Use parenteral therapy initially in severe infections. Oxacillin may be substituted for nafcillin based on hospital formulary. Change to oral therapy as condition warrants.

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Vancomycin (Vancocin, Vancoled)

 

Indicated for patients who cannot receive penicillins and cephalosporins or have infections with resistant staphylococci. To lessen the risk for toxicity, assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use CrCl to adjust dose in patients diagnosed with renal impairment.

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Telavancin (Vibativ)

 

Lipoglycopeptide antibiotic that is a synthetic derivative of vancomycin. Inhibits bacterial cell wall synthesis by interfering with polymerization and cross-linking of peptidoglycan. Unlike vancomycin, telavancin also depolarizes the bacterial cell membrane and disrupts its functional integrity. Indicated for complicated skin and skin structure infections caused by susceptible gram-positive bacteria, including Staphylococcus aureus (both methicillin-resistant and methicillin-susceptible strains), Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus anginosus group, and Enterococcus faecalis (vancomycin-susceptible isolates only).

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Cefazolin (Ancef, Kefzol)

 

First-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth. Primarily active against skin flora, including S aureus (MSSA). Typically used alone for skin and skin-structure coverage. IV and IM dosing regimens are similar.

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Clindamycin (Cleocin)

 

Lincosamide for treatment of serious skin and soft tissue staphylococci infections. Also effective against aerobic and anaerobic streptococci (except enterococcal) (MSSA). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

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Dicloxacillin (Dycill, Dynapen)

 

Binds to one or more penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. For treatment of infections caused by penicillinase-producing staphylococci susceptible to methicillin (MSSA). Also active against most nonenterococcal streptococci. May use to initiate therapy when staphylococcal infection is suggested.

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Trimethoprim-sulfamethoxazole (Bactrim, Bactrim DS, Septra, Septra DS)

 

Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Active against most staphylococci (MSSA), including some strains resistant to methicillin (MRSA).

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Minocycline (Minocin)

 

Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. Active against MSSA/MRSA. Less active against coagulase-negative staphylococci. Doxycycline (Vibramycin) may be used in place of minocycline

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Linezolid (Zyvox)

 

Prevents formation of functional 70S initiation complex, which is essential for bacterial translation process. Bacteriostatic against staphylococci (MSSA/MRSA).

The FDA warns against the concurrent use of linezolid with serotonergic psychiatric drugs, unless indicated for life-threatening or urgent conditions. Linezolid may increase serotonin CNS levels as a result of MAO-A inhibition, increasing the risk of serotonin syndrome.[26]

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Quinupristin/dalfopristin (Synercid)

 

Belongs to the streptogramin group of antibiotics. Mechanism of action is similar to macrolides/lincosamides. Inhibits protein synthesis and is usually bacteriostatic. Also an option for methicillin-resistant S aureus (MRSA) infections.

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Daptomycin (Cubicin)

 

Indicated to treat complicated skin and skin structure infections caused by S aureus (including MRSA strains), Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus dysgalactiae, and Enterococcus faecalis. Also indicated for right-sided endocarditis due to S aureus. First of new antibiotic class called cyclic lipopeptides. Binds to bacterial membranes and causes rapid membrane potential depolarization, thereby inhibiting protein, DNA, and RNA synthesis and ultimately causing cell death.

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Tigecycline (Tygacil)

 

A glycylcycline antibiotic that is structurally similar to tetracycline antibiotics. Inhibits bacterial protein translation by binding to 30S ribosomal subunit, and blocks entry of amino-acyl tRNA molecules in ribosome A site. Indicated for complicated skin and skin structure infections and complicated intra-abdominal infections. Active against S aureus (including MRSA), as well as most streptococci, enterococci (including VRE), and gram-negative organisms (including anaerobes).

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Contributor Information and Disclosures
Author

Thomas E Herchline, MD  Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of America, and Infectious Diseases Society of Ohio

Disclosure: Nothing to disclose.

Specialty Editor Board

Klaus-Dieter Lessnau, MD, FCCP  Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

John L Brusch, MD, FACP  Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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