Version January 2024
INTRODUCTION — Staphylococcus aureus is an important pathogen responsible for a broad range of clinical manifestations ranging from relatively benign skin infections to life-threatening conditions such as endocarditis and osteomyelitis. It is also a commensal bacterium colonizing up to two-thirds of the human population, depending upon patient characteristics, technical methods of identifying S. aureus, and body sites [1,2].
Changes in the predominant circulating clones of S. aureus in a population can influence clinical presentations over time [3]. Two major shifts in S. aureus epidemiology have occurred since the 1990s: an epidemic of community-associated skin and soft tissue infections (largely driven by specific methicillin-resistant S. aureus [MRSA] strains), and an increase in the number of health care-associated infections (especially infective endocarditis and prosthetic device infections).
The clinical manifestations of S. aureus infection will be reviewed here. The clinical approach to S. aureus bacteremia is discussed separately. (See "Clinical approach to Staphylococcus aureus bacteremia in adults".)
Issues related to MRSA are also discussed separately. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Epidemiology" and "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of skin and soft tissue infections" and "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of bacteremia".)
CLINICAL MANIFESTATIONS
Skin and soft tissue infection — Skin and soft tissue infections due to S. aureus include:
●Impetigo (infection of the epidermis) (see "Impetigo")
●Folliculitis (infection of the superficial dermis) (see "Infectious folliculitis")
●Furuncles, carbuncles, and abscess (infection of the deep dermis) (see "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis")
●Hidradenitis suppurativa (follicular infection of intertriginous areas) (see "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis")
●Cellulitis, erysipelas, and fasciitis (infection of the subcutaneous tissues) (see "Necrotizing soft tissue infections" and "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis")
●Pyomyositis (infection of skeletal muscle) (see "Primary pyomyositis")
●Mastitis (see "Nonlactational mastitis in adults")
●Surgical site infections (see "Antimicrobial prophylaxis for prevention of surgical site infection in adults")
S. aureus is the most common pathogen isolated from purulent cellulitis, cutaneous abscesses, and surgical site infections [4,5]. Superficial skin and soft tissue infections caused by S. aureus generally present with purulence or abscess; the diagnosis of S. aureus is established by culture of purulent material. Management may consist of local wound care, debridement, and antibiotics (see related topics).
Bacteremia — S. aureus bacteremia is defined as positive blood cultures for S. aureus; frequently, this occurs in association with correlating symptoms such as fever or hypotension. S. aureus is a leading cause of community-acquired and hospital-acquired bacteremia. Bacteremia may develop as a complication of a primary S. aureus infection such as skin and soft tissue infection, bone and joint infection, or pneumonia. Vascular catheters are a common source of bacteremia. Bacteremia may also lead to subsequent S. aureus infection at a previously sterile site, such as endocarditis or prosthetic device infection [6,7].
The clinical approach to evaluation of patients with S. aureus bacteremia is discussed in detail separately. (See "Clinical approach to Staphylococcus aureus bacteremia in adults" and "Staphylococcus aureus bacteremia in children: Management and outcome".)
Infective endocarditis — S. aureus is the most common cause of infective endocarditis (IE) in resource-rich settings [8-10]. The incidence of IE in the setting of S. aureus bacteremia is 10 to 15 percent [11-17]; however, studies examining the frequency of IE among patients with S. aureus bacteremia have been impacted by sampling bias. The likelihood of IE is related to the circumstances of bacteremia; community-acquired bacteremia is likely to be detected later and therefore more likely to be associated with complications than health care-associated bacteremia.
Risk factors for IE in the setting of S. aureus bacteremia include [12,18-21]:
●Prosthetic heart valve
●Cardiac implantable electronic device (CIED), such as permanent pacemaker or implantable cardioverter defibrillator
●Predisposing cardiac abnormalities
●Injection drug use
●Intravascular catheter infection
●Bacteremia of unclear origin
●Persistent bacteremia
IE due to S. aureus can be more severe than IE due to other organisms, including more frequent association with severe sepsis (39 versus 6 percent), major neurological events (18 versus 8 percent), multiorgan failure (29 versus 10 percent), and higher mortality (34 versus 10 percent) [22]. (See "Complications and outcome of infective endocarditis".)
Cardiac device infection — Patients with a CIED who develop S. aureus bacteremia are at increased risk for endocarditis and/or infection involving the device. Among 33 patients with CIEDs who developed S. aureus bacteremia in one series, the rate of device infection was 45 percent [23]; in a later cohort including 152 patients with S. aureus bacteremia at the same institution the rate of device infection was 55 percent [24]. (See "Infections involving cardiac implantable electronic devices: Epidemiology, microbiology, clinical manifestations, and diagnosis".)
Intravascular catheter infection — The presence of an indwelling intravascular catheter is a risk factor for development of S. aureus bacteremia, and onset of S. aureus bacteremia in the setting of an indwelling intravascular catheter should prompt evaluation for catheter-associated infection. (See "Intravascular catheter-related infection: Epidemiology, pathogenesis, and microbiology" and "Intravascular non-hemodialysis catheter-related infection: Clinical manifestations and diagnosis".)
Septic thrombophlebitis can occur in the setting of intravascular catheter infection. Clinical manifestations include venous congestion (eg, venous distension or asymmetric swelling of the extremities). (See "Catheter-related septic thrombophlebitis".)
Sepsis and toxic shock syndrome — Manifestations of staphylococcal toxic shock syndrome include fever, hypotension, and dermatologic manifestations. (See "Staphylococcal toxic shock syndrome".)
Splenic abscess — Splenic abscess is an infrequent complication of staphylococcal bacteremia and/or endocarditis [25-29]. Clinical manifestations include left upper quadrant pain (with or without splenomegaly) and fever (which may be recurrent or persistent despite appropriate antimicrobial therapy) [25]. (See "Splenomegaly and other splenic disorders in adults", section on 'Abscess and infarction'.)
Bone and joint infection — S. aureus is the most common pathogen causing osteomyelitis, septic arthritis, and prosthetic joint infection [4]. Development of back or joint pain should raise the suspicion of an occult site of infection in patients with current or recent S. aureus bacteremia.
Osteomyelitis — Osteomyelitis develops via one of two mechanisms: hematogenously (in the setting of S. aureus bacteremia) or secondary to a contiguous focus of infection. (See "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)
In adults, hematogenous osteomyelitis most commonly presents in the form of vertebral involvement [30]. In one series including 309 patients with hematogenous S. aureus osteomyelitis, vertebral osteomyelitis and/or discitis occurred most frequently among patients >50 years with community-acquired bacteremia and no evident inciting source [30]. Epidural abscess may accompany vertebral osteomyelitis. (See "Vertebral osteomyelitis and discitis in adults" and "Spinal epidural abscess".)
Prosthetic joint infection — The mechanism for development of prosthetic joint infection (PJI) depends on the timeframe for onset of symptoms. Early (<3 months after surgery) and delayed infections (3 to 12 months after surgery) are mostly acquired during implantation, whereas late infections (>12 months after surgery) are primarily due to hematogenous seeding. (See "Prosthetic joint infection: Epidemiology, microbiology, clinical manifestations, and diagnosis".)
In a prospective series of 80 patients with orthopedic devices and S. aureus bacteremia, the rate of hematogenous seeding was 34 percent [31]. One retrospective study including 85 patients (143 arthroplasties) noted that hematogenous infection of at least one prosthetic joint occurred in 41 percent of patients; infection was community acquired in all cases [32]. The risk of PJI was greatest in patients with multiple arthroplasties and in patients who had undergone arthroplasty revision. The risk of PJI was twice as high for knee arthroplasties compared with hip arthroplasties (35 versus 19 percent). Asymptomatic infection was very rare, occurring in only one patient.
Septic arthritis or bursitis — Most cases of septic arthritis arise via hematogenous spread of bacteria to the joint; the joint is particularly susceptible to hematogenous infection because the joint space synovium is a highly vascular tissue without a basement membrane. Other mechanisms include trauma, direct inoculation of bacteria during joint surgery, or extension of bony infection into the joint space. (See "Septic arthritis in adults".)
Septic bursitis arises as a result of direct inoculation via bursa puncture or via contiguous spread from adjacent skin or soft tissue infection. (See "Septic bursitis".)
Pulmonary infection — Pulmonary infection due to S. aureus can occur among individuals with S. aureus colonization of the skin or nares, either in the community or in a hospital setting (particularly in the context of intubation or other respiratory tract instrumentation). S. aureus pneumonia can also occur following viral pneumonia or in the setting of right-sided endocarditis with pulmonary emboli.
S. aureus pneumonia can also occur in the setting of right-sided endocarditis with pulmonary emboli. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults", section on 'S. aureus' and "Overview of pulmonary disease in people who inject drugs" and "Seasonal influenza in adults: Clinical manifestations and diagnosis", section on 'Pneumonia'.)
Meningitis — S. aureus meningitis most commonly occurs in the setting of head trauma or neurosurgery; less commonly, it can also occur as a complication of S. aureus bacteremia [33-35]. (See "Treatment of bacterial meningitis caused by specific pathogens in adults", section on 'Staphylococcus aureus'.)
Bacteriuria — Bacteriuria due to S. aureus can occur via ascending infection in the presence of a urinary catheter or in the setting of S. aureus bacteremia. In the absence of systemic signs of infection, S. aureus bacteriuria associated with the presence of a urinary catheter does not warrant routine investigation for bacteremia; catheter and antibiotic management are discussed in detail separately. (See "Catheter-associated urinary tract infection in adults".)
S. aureus bacteriuria in the absence of a urinary catheter may be an indicator of S. aureus bacteremia [36-40]; blood cultures should be obtained together with clinical evaluation for signs and symptoms of a metastatic or occult staphylococcal infection, particularly if there are other clinical clues of infection such as fever, leukocytosis, or localizing symptoms such as back pain. In one retrospective study including 2054 patients with S. aureus bacteriuria, S. aureus bacteremia was diagnosed within 3 months in 6.9 percent of cases [41].
Other manifestations — Other manifestations of S. aureus infection include:
●Foodborne illness – Toxin elaborated by S. aureus is ingested with the contaminated dish, and disease follows shortly thereafter in the form of nausea and vomiting. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-rich settings", section on 'Vomiting'.)
●Waterhouse-Friderichsen syndrome – Waterhouse-Friderichsen syndrome (characterized by petechial rash, coagulopathy, cardiovascular collapse, and adrenal hemorrhage) is usually associated with fulminant meningococcemia. It has also been described in the setting of sepsis due to Streptococcus pneumoniae, Neisseria gonorrhoeae, Escherichia coli, and Haemophilus influenzae. Reports of a syndrome of fatal severe sepsis in children caused by S. aureus, both methicillin-sensitive S. aureus and community-associated methicillin-resistant S. aureus, suggest that S. aureus may also be an etiologic agent [42-45]. (See "Clinical manifestations of meningococcal infection".)
●Immunoglobulin A vasculitis (IgAV; Henoch-Schönlein purpura [HSP]) – A case report and review of the literature identified 14 cases of IgAV (HSP) associated with S. aureus infection [46]. S. aureus superantigen action on T cells may have caused the autoimmune phenomenon. (See "IgA vasculitis (Henoch-Schönlein purpura): Clinical manifestations and diagnosis".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Management of Staphylococcus aureus infection".)
SUMMARY
●Staphylococcus aureus is a frequent colonizer of the skin and mucosa and can cause a broad range of clinical manifestations. Risk factors for complications of S. aureus infection include community acquisition of bacteremia, presence of a prosthetic device, and underlying medical conditions including immunosuppression. (See 'Introduction' above.)
●Clinical manifestations of S. aureus infection include skin and soft tissue infection, bacteremia, and associated conditions (including infective endocarditis, cardiac device infection, intravascular catheter infection, and toxic shock syndrome). (See 'Clinical manifestations' above.)
●Bacteremia may develop as a complication of a primary S. aureus infection (such as skin and soft tissue infection). Bacteremia may also lead to subsequent S. aureus infection at a previously sterile site (such as vertebral osteomyelitis). (See 'Bacteremia' above.)
●Development of back or joint pain should raise the suspicion of an occult site of infection in patients with current or recent S. aureus bacteremia. In adults, hematogenous osteomyelitis most commonly presents in the form of vertebral involvement. (See 'Bone and joint infection' above.)
●Pulmonary infection due to S. aureus can occur among individuals with S. aureus colonization of the skin or nares, either in the community or in a hospital setting (particularly in the context of intubation or other respiratory tract instrumentation). S. aureus pneumonia can also occur following viral pneumonia or in the setting of right-sided endocarditis with pulmonary emboli. (See 'Pulmonary infection' above.)
●S. aureus bacteriuria in the absence of a urinary catheter may be an indicator of S. aureus bacteremia. (See 'Bacteriuria' above.)
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