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Staphylococcal Infections

  • Author: Thomas E Herchline, MD; Chief Editor: Mark R Wallace, MD, FACP, FIDSA  more...
 
Updated: Apr 25, 2016
 

Practice Essentials

Staphylococcal infections are usually caused by Staphylococcus aureus. However, the incidence of infections due to Staphylococcus epidermidis and other coagulase-negative staphylococci has also been steadily rising.

The image below depicts embolic lesions in patient with Staphylococcus aureus endocarditis.

Embolic lesions in patient with Staphylococcus aur Embolic lesions in patient with Staphylococcus aureus endocarditis.

Signs and symptoms

Manifestations of staphylococcal infections usually depend on the type of infection the organism causes. Common types of infections include the following:

  • Skin infections (eg, folliculitis, furuncles, impetigo, wound infections, scalded skin syndrome)
  • Soft-tissue infections (eg, pyomyositis, septic bursitis, septic arthritis)
  • Toxic shock syndrome
  • Purpura fulminans
  • Endocarditis
  • Osteomyelitis
  • Pneumonia
  • Food poisoning
  • Infections related to prosthetic devices (eg, prosthetic joints and heart valves; vascular shunts, grafts, catheters): Commonly associated with coagulase-negative staphylococci
  • Urinary tract infection

See Clinical Presentation for more detail.

Diagnosis

Examination in patients with staphylococcal infections may include the following findings:

  • Skin and soft-tissue infections: Erythema, warmth, draining sinus tracts, superficial abscesses, bullous impetigo
  • Toxic shock syndrome: Fever higher than 38.9°C (102.02°F), diffuse erythroderma, hypotension, desquamation
  • Endocarditis: Regurgitant murmur, petechiae/cutaneous lesions, fever

Laboratory testing

  • Complete blood count: Usually shows leukocytosis with a left shift (bands); may reveal thrombocytosis with chronic staphylococcal infection
  • Erythrocyte sedimentation rate and C-reactive protein level: May be helpful in patients with subacute or chronic infections (eg, osteomyelitis)
  • Teichoic acid antibody titers: No longer routinely performed; may indicate a deep-seated (not IV line) infectious focus (eg, endocarditis, abscess, osteomyelitis)
  • Blood cultures with susceptibilities, as appropriate for site of infection
  • Peptide nucleic acid fluorescence in situ hybridization (PNA FISH): High sensitivity for S aureus (99.5%) and coagulase-negative staphylococci from positive blood cultures
  • Screening tests for methicillin-resistant S aureus (MRSA)

Imaging studies

  • Transthoracic echocardiography (TTE): Should be considered in all patients with S aureus or Staphylococcus lugdunensis bacteremia; patients with suspected endocarditis should undergo immediate transesophageal echocardiography (TEE), when possible
  • Transesophageal echocardiography (TEE): For all patients with catheter-related S aureus bacteremia (and no contraindications); for all patients with suspected S aureus endocarditis

See Workup for more detail.

Management

Promptly start antimicrobial therapy when S aureus infection is documented or strongly suspected. Appropriate choices depend on local susceptibility patterns.[1]

Temporary intravascular devices should be promptly removed if infection is suspected.[2] Long-term intravascular devices should be removed if infection with S aureus is documented.

Multiple decolonization regimens have been used in patients with recurrent staphylococcal infection. In one study, treatment with topical mupirocin, chlorhexidine gluconate washes, and oral rifampin plus doxycycline for 7 days eradicated MRSA colonization in hospitalized patients.[3]

Pharmacotherapy

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.

The following antibiotics may be used in the management of staphylococcal infections (listed alphabetically, not necessarily in order of preference):

  • Cefazolin
  • Ceftaroline
  • Cefuroxime
  • Clindamycin
  • Dalbavancin
  • Daptomycin
  • Dicloxacillin
  • Doxycycline
  • Linezolid
  • Minocycline
  • Nafcillin
  • Oritavancin
  • Quinupristin/dalfopristin
  • Tedizolid
  • Telavancin
  • Tigecycline
  • Trimethoprim-sulfamethoxazole
  • Vancomycin

Surgery

Abscesses must be drained and/or debrided. Infections involving a prosthetic joint usually require removal of the prosthesis. Other infections involving a prosthetic device (eg, prosthetic heart valve or implanted intravascular device) may or may not require removal of the device.

See Treatment and Medication for more detail.

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Background

Staphylococcal infections are usually caused by the organism Staphylococcus aureus. However, the incidence of infections due to Staphylococcus epidermidis and other coagulase-negative staphylococci has been steadily increasing in recent years. This article focuses on S aureus but also discusses infections caused by coagulase-negative staphylococci when important differences exist.

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Pathophysiology

S aureus is a gram-positive coccus that is both catalase- and coagulase-positive. Colonies are golden and strongly hemolytic on blood agar. They produce a range of toxins, including alpha-toxin, beta-toxin, gamma-toxin, delta-toxin, exfoliatin, enterotoxins, Panton-Valentine leukocidin (PVL), and toxic shock syndrome toxin–1 (TSST-1). The enterotoxins and TSST-1 are associated with toxic shock syndrome. PVL is associated with necrotic skin[4] and lung infections and has been shown to be a major virulence factor for pneumonia[5] and osteomyelitis.[6] Coagulase-negative staphylococci, particularly S epidermidis, produce an exopolysaccharide (slime) that promotes foreign-body adherence and resistance to phagocytosis.

Nienaber et al have demonstrated that methicillin-susceptible S aureus isolates causing endocarditis are more likely to be from a specific clonal cluster (CC30) and to possess specific virulence genes as compared to MSSA isolates from the same regions causing soft tissue infection. Isolates from patients with endocarditis were more likely to possess genes for 3 different adhesins and 5 different enterotoxins. The gene for PVL was found in the minority of both groups.[7]

In a study of 42 S lugdunensis isolates, most isolates were able to form at least a weak biofilm, but the amount of biofilm formed by isolates was heterogeneous with poor correlation between clinical severity of disease and degree of biofilm formation.[8]

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Frequency

United States

Up to 80% of people are eventually colonized with S aureus. Most are colonized only intermittently; 20-30% are persistently colonized. Colonization rates in health care workers, persons with diabetes, and patients on dialysis are higher than in the general population. The anterior nares are the predominant site of colonization in adults; carriage here has been associated with the development of bacteremia.[9] Other potential sites of colonization include the throat,[10] axilla, rectum, and perineum.

International

S aureus infection occurs worldwide. Pyomyositis due to S aureus is more prevalent in the tropics.

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Mortality/Morbidity

Mortality due to staphylococcal infections varies widely. Untreated S aureus bacteremia carries a mortality rate that exceeds 80%. The mortality rate of staphylococcal toxic shock syndrome is 3-5%. Infections due to coagulase-negative staphylococci usually carry a very low mortality rate. Because these infections are commonly associated with prosthetic devices, the most serious complication is the need to remove the involved prosthesis, although prosthetic valve endocarditis may lead to death.

Risk factors associated with increased mortality among patients with S aureus bacteremia include thrombocytopenia, an elevated score on the Charlson Comorbidity Index, MRSA infection, admission to an intensive care unit, and prior exposure to antibiotics.[11, 12]

Race

Staphylococcal infections have no reported racial predilection.

Sex

The vaginal carriage rate of staphylococcal species is approximately 10% in premenopausal women. The rate is even higher during menses.

Age

Staphylococcal species colonize many neonates on the skin, perineum, umbilical stump, and GI tract. The staphylococcal colonization rate in adults is approximately 40% at any given time.

The mortality rate of S aureus bacteremia in elderly persons is markedly increased.[13]

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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 Ohio, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Clinical Professor of Medicine, University of Central Florida College of Medicine

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, Florida Infectious Diseases Society

Disclosure: Nothing to disclose.

Additional Contributors

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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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Embolic lesions in patient with Staphylococcus aureus endocarditis.
Close-up view of embolic lesions in patient with Staphylococcus aureus endocarditis.
Fifty-six-year-old man with erythema, edema, and drainage from below his right eye.
Gram stain in a 70-year-old woman with rheumatoid arthritis.
 
 
 
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