Staphylococcal Infections

Updated: Apr 18, 2024
  • Author: Thomas E Herchline, MD; Chief Editor: John L Brusch, MD, FACP  more...
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Overview

Practice Essentials

Staphylococcal infections usually are caused by Staphylococcus aureus (S aureus). However, the incidence of infections due to Staphylococcus epidermidis (S epidermidis) and other coagulase-negative staphylococci (CoNS) also has been steadily rising. [1]

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

Embolic lesions in patient with Staphylococcus aurEmbolic 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 [2] :

  • 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 CoNS

  • 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

Background

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

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), [7] and toxic shock syndrome toxin–1 (TSST-1). [8] The enterotoxins and TSST-1 are associated with toxic shock syndrome. PVL is associated with necrotic skin [9] and lung infections and has been shown to be a major virulence factor for pneumonia [10] and osteomyelitis. [11]  CoNS, 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 (MSSA) 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. [12]

S aureus has evolved to develop numerous immune evasion strategies to combat neutrophil-mediated killing, such as neutrophil activation, migration to the site of infection, bacterial opsonization, phagocytosis, and subsequent neutrophil-mediated killing. As many as 40 immune-evasion molecules of S aureus are known, and new functions are being identified for these evasion proteins. [13]

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. [14]

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. [15] Other potential sites of colonization include the throat, [16] axilla, rectum, and perineum. The rate of MRSA hand colonization among health care workers has been shown to exceed 4% (over 8% in North America). [17]

International

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

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 CoNS 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. [18, 19]

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. [20]

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