Staphylococcus Aureus Infection

Author: Elizabeth P Baorto, MD, MPH; Chief Editor: Russell W Steele, MD more...

Updated: Jan 31, 2014

Practice Essentials

Background

Pathophysiology

Frequency

Mortality/Morbidity

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Multimedia Library

References

Practice Essentials

Both community-associated and hospital-acquired infections with Staphylococcus aureus have

increased in the past 20 years, and the rise in incidence has been accompanied by a rise in

antibiotic-resistant strains—in particular, methicillin-resistant S aureus (MRSA) and, more

recently, vancomycin-resistant strains.

Essential update: Adult vancomycin dosing nomograms inadequate for older

pediatric patients

In a validation study, Gillon et al found that 2 nomograms designed to predict appropriate dosing

of vancomycin (often used to treat MRSA) in adults could not accurately predict dosing levels

for pediatric patients aged 10 years or older.[1, 2] Both nomograms predicted mean daily doses of

vancomycin that significantly differed from the actual average daily dose prescribed to achieve

therapeutic trough concentrations.

Signs and symptoms

Types and presentation of S aureus infection include the following:

Skin and soft tissue (impetigo): A small area of erythema that progresses into bullae

(filled with cloudy fluid) that rupture and heal with the formation of a honey-colored

crust

Scalded skin syndrome (Ritter disease): A relatively rare, toxin-mediated disorder with

superficial fragile blisters that burst, leaving a tender base; often accompanied by fever

and occasionally by mucopurulent eye discharge

Folliculitis: A tender pustule that involves the hair follicle

Furuncle: Small abscesses characterized by exuding purulent material from a single

opening; involves both the skin and the subcutaneous tissues in areas with hair follicles

Carbuncle: An aggregate of connected furuncles, with several pustular openings

Bone infections (osteomyelitis): In children, sudden onset of fever and bony tenderness

or a limp; pain may be throbbing and severe; however, presentation in neonates can be

subtle

Septic arthritis: Decreased range of motion, warmth, erythema, and tenderness of the

joint with constitutional symptoms and fever; however, these signs may be absent in

infants (in whom the hip is the most commonly involved joint)

Endocarditis: Initially presents as fever and malaise; peripheral emboli may be present;

may involve healthy valves

Toxic shock syndrome: Fever, diffuse macular erythema, and hypotension, with

involvement of 3 or more organ systems; can be rapidly progressive in previously healthy

individuals

Pneumonia: Most common in infants, young children, and debilitated patients; a short

prodrome of fever followed by rapid onset of respiratory distress; prominent GI

symptoms may also occur

Thrombophlebitis: Fever, pain, and occasionally erythema at the insertion site of an

intravenous catheter; usually affects hospitalized patients

Deep tissue abscess and infection: Muscles[3, 4, 5, 6] and organs can become infected,

including the parotid gland, eyes, liver, spleen, kidneys, and central nervous system[7] ;

deep abscesses also may occur[8] ; fever with or without localizing pain is typical

See Clinical Presentation for more detail.

Diagnosis

Folliculitis, furuncle, and carbuncle

Diagnosis based on clinical appearance

Aspiration or incision and culture of purulent material from the lesion occasionally

diagnostic

Osteomyelitis

Cultures of bone aspirate

Blood culture results positive in only 30-50% of pediatric patients

C-reactive protein levels and erythrocyte sedimentation rate are generally elevated in

acute disease

Bone scan with increased technetium-99m–labeled diphosphonate uptake supports the

clinical diagnosis; however, this modality is not as useful in neonates or after trauma or

surgery

MRI is the best imaging modality for defining purulent collections and for planning

surgery

On plain film radiographs, destructive bone changes are usually observed 2 weeks after

infection

Septic arthritis

Gram stain and culture of joint fluid is the primary means of diagnosis

Direct inoculation of synovial fluid into culture bottles may improve culture yield

Median white blood cell count in joint fluid is 60.5 × 109, with neutrophil predominance

>75%

Synovial fluid glucose levels are often low

Plain radiographs show capsular swelling

MRI or CT scanning is the imaging method of choice for pyogenic sacroiliitis

Endocarditis

Blood culture is the most important diagnostic procedure

Inject the blood sample into hypertonic media if the patient has been exposed to

antibiotics

Obtain 3-5 sets of large-volume blood cultures within the first 24 hours

Echocardiography is a valuable adjunct

Pneumonia

Blood cultures are more likely to be positive in secondary than primary disease (90% vs

20%)

An adequate respiratory tract specimen should be obtained prior to initiating therapy;

specimens may include endotracheal sampling, pleural fluid, or lung tap

Sputum specimens are inadequate because upper respiratory tract colonization is common

No radiologic features are highly specific

Typical radiographic features are unilateral consolidation in primary staphylococcal

pneumonia and bilateral infiltrates in secondary cases

Early in the disease course, the chest radiograph may reveal minimal infiltrates, but

within hours, infiltrates progress rapidly

Pleural effusion, pneumatoceles, and pneumothorax are also common

In oncology patients, S aureus may cause pulmonary nodules[9] Current reference

Thrombophlebitis

Obtain a blood culture through the intravenous line and a peripheral blood culture

See Workup for more detail.

Management

Antibiotic regimens include the following:

Empiric therapy with penicillins or cephalosporins may be inadequate because of

community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA)[10]

Combination therapy with a penicillinase-resistant penicillin or cephalosporin (in case the

organism is methicillin-sensitive S aureus [MSSA])[11] and clindamycin or a quinolone

Clindamycin, trimethoprim-sulfamethoxazole (TMP-SMX), rifampin, doxycycline, or a

quinolone

TMP-SMX and rifampin in combination, rather than singly

Clindamycin (rather than TMP-SMX) may become the preferred outpatient antibiotic

therapy in regions with a relatively low incidence of clindamycin resistance[12]

The Infectious Diseases Society of America has published treatment guidelines for

MRSA infection[13]

Treatment of specific infections

Impetigo, folliculitis, furuncle, carbuncle:

Superficial or localized skin infections: A topical agent such as mupirocin or retapamulin;

however, most CA-MRSA strains are (or readily become) resistant to mupirocin

More extensive or serious skin disease and bullous impetigo: Oral antistaphylococcal

agents[14]

Drainage of pus collections is of paramount importance[15]

Scalded skin syndrome (Ritter disease):

Eradication of the focal infection to end toxin production

Large doses of intravenous antistaphylococcal agents such as oxacillin or a first-

generation cephalosporin such as cefazolin, combined with clindamycin

Osteomyelitis:

Empiric semisynthetic penicillin and clindamycin

In patients with allergy to penicillin, a first-generation cephalosporin and clindamycin

Vancomycin or linezolid when the other drugs mentioned are absolutely not tolerated or

when resistance or the clinical course dictates

Minimum effective treatment time is 4-6 weeks; therapy can be completed orally[16]

Surgery to drain purulent material from the subperiosteal space or remove infected

foreign material

Septic arthritis:

A parenteral antistaphylococcal drug (eg, oxacillin, which is penicillinase resistant;

clindamycin; cefazolin)

Therapy usually continues for at least 4 weeks; duration of parenteral therapy is debated

Joint fluid that reaccumulates should be removed and a sample should be cultured

Hip or shoulder infections in infants require prompt drainage to prevent bony destruction

Surgical drainage is indicated if needle drainage is inadequate

Endocarditis:

The combination of a beta-lactam and an aminoglycoside (eg, nafcillin and gentamicin)

In patients with MRSA, combinations of vancomycin with aminoglycosides

Rifampin can be added to combination therapy, especially for prosthetic valve

endocarditis

Duration of therapy is at least 4 weeks

Bacteremia, fever, and leukocytosis for at least a week after therapy is initiated

Toxic shock syndrome:

Surgical exploration and drainage of all potential foci of infection

Thrombophlebitis:

Removal of the infected intravenous line in patients who are immunocompromised or

severely ill or when infection cannot be eradicated medically

Bacteremia :

Daptomycin, with or without beta-lactams, controls S aureus bacteremia without

worsening renal dysfunction. In a cohort of patients with mild or moderate renal

insufficiency, more than 80% responded to treatment, with no detrimental effect on their

kidneys. Currently, the combination of daptomycin with beta-lactams is recommended

only as salvage therapy for refractory MRSA bacteremia.[17]

See Treatment and Medication for more detail.

Image library

See the image below.

Posteroanterior chest radiograph of a 15-year-old with

staphylococcal endocarditis and multiple septic emboli, revealing borderline cardiomegaly,

multiple nodular infiltrates, and bilateral pleural effusions.

Next Section: Background

Background

Bacteria of the genus Staphylococcus are gram-positive cocci that are microscopically observed

as individual organisms, in pairs, and in irregular, grapelike clusters. The term Staphylococcus is

derived from the Greek term staphyle, meaning "a bunch of grapes." Staphylococci are

nonmotile, non–spore-forming, and catalase-positive bacteria. The cell wall contains

peptidoglycan and teichoic acid. The organisms are resistant to temperatures as high as 50°C, to

high salt concentrations, and to drying. Colonies are usually large (6-8 mm in diameter), smooth,

and translucent. The colonies of most strains are pigmented, ranging from cream-yellow to

orange.

The ability to clot plasma continues to be the most widely used and generally accepted criterion

for the identification of Staphylococcus aureus. One such factor, bound coagulase, also known as

clumping factor, reacts with fibrinogen to cause organisms to aggregate. Another factor,

extracellular staphylocoagulase, reacts with prothrombin to form staphylothrombin, which can

convert fibrinogen to fibrin. Approximately 97% of human S aureus isolates possess both of

these forms of coagulase.

S aureus is ubiquitous and may be a part of human flora found in the axillae, the inguinal and

perineal areas, and the anterior nares. von Eiff et al described 3 patterns of carriage: those who

always carry a strain, those who carry the organism intermittently with changing strains, and a

minority of people who never carry S aureus.[18] Persistent carriage is more common in children

than in adults. Nasal carriers may be divided into persistent carriers with high risk of infection

and intermittent or noncarriers with low risk of infection.[19]

Wenzel and Perl found that, among healthy adults, carrier rates of 11-32% were detected in the

general population, and a prevalence of 25% was detected in hospital personnel.[20] Using pulsed-

field gel electrophoresis (PFGE) for molecular typing, von Eiff et al found that, in most patients

with S aureus bacteremia, the isolate from the patient's blood is identical to that found in the

anterior nares.[18] Persistent nasal carriage depends on host genetic determinants.[21]

Curiously, community-associated methicillin-resistant S aureus (CA-MRSA) is less often found

in the anterior nares than are methicillin-sensitive S aureus (MSSA) and hospital-acquired

methicillin-resistant S aureus (HA-MRSA)[22, 23, 24, 25] ; rather, it colonizes the skin, particularly in

the perineal area[26] and the rectum.[27] It also colonizes the pharynx,[28] gut,[29] and vagina.[30, 31]

Another interesting finding is the protective effect of consumption of hot coffee or tea for nasal

carriage of MRSA.[32] In contrast, hormonal contraceptive use is a significant risk factor for nasal

carriage of S aureus.[33]

Previous

Next Section: Background

Pathophysiology

The organism may cause disease through tissue invasion and toxin production.[34] The toxins

liberated by the organism may have effects at sites distant from the focus of infection or

colonization.

Tissue invasion

The postulated sequence of events that leads to infection is initiated with carriage of the

organism. The organism is then disseminated via hand carriage to body sites where infection

may occur (either through overt breaks in dermal surfaces, such as vascular catheterization or

operative incisions, or through less evident breakdown in barrier function, such as eczema or

shaving-associated microtrauma).

The hallmark of staphylococcal infection is the abscess, which consists of a fibrin wall

surrounded by inflamed tissues enclosing a central core of pus containing organisms and

leukocytes. From this focus of infection, the organisms may be disseminated hematogenously,

even from the smallest abscess. The ability to elaborate proteolytic enzymes facilitates the

process. This may result in pneumonia, bone and joint infection, and infection of the heart

valves. In immunocompromised hosts (eg, patients with cancer who are neutropenic and have a

central venous line), 20-30% develop serious complications or fatal sepsis following catheter-

related S aureus bacteremia.

Persistent deep-seated infections have now been linked to small-colony variants of the

organism.[35] This population is more resistant to antibiotics and grows slowly. These organisms

have been described in patients with cystic fibrosis and may contribute to the persistence of S

aureus in these patients.

Toxin-mediated disease

The organism also elaborates toxins that can cause specific diseases or syndromes and likely

participate in the pathogenesis of staphylococcal infection.[36] Enterotoxin-producing strains of S

aureus cause one of the most common food-borne illnesses. The most common presentation is

acute onset of vomiting and watery diarrhea 2-6 hours after ingestion. The symptoms are usually

self-limited. The cause is the proliferation of toxin-producing organisms in uncooked or partially

cooked food that an individual carrying the staphylococci has contaminated.

A rare but well-described disorder in neonates and young children is staphylococcal scalded skin

syndrome (Ritter disease). The organism produces an exfoliative toxin produced by strains

belonging to phage group II. Initial features include fever, erythema, and blisters, which

eventually rupture and leave a red base. Gentle shearing forces on intact skin cause the upper

epidermis to slip at a plane of cleavage in the skin, which is known as the Nikolsky sign. How

the exfoliative toxins produce epidermal splitting has not been fully elucidated.[37]

The most feared manifestation of S aureus toxin production is toxic shock syndrome (TSS).

Although first described in children, it was most frequently associated with women using

tampons during menstruation. Since the early 1990s, at least half of the cases have not been

associated with menstruation. The syndrome is associated with strains that produce the exotoxin

TSST-1, but strains that produce enterotoxins B and C may cause 50% of cases of nonmenstrual

TSS. These toxins are superantigens, T-cell mitogens that bind directly to invariant regions of

major histocompatibility complex class II molecules, causing an expansion of clonal T cells,

followed by a massive release of cytokines. This cytokine release mediates the TSS; the resultant

pathophysiology mimics that of endotoxic shock.

CA-MRSA

In a worldwide trend,[38] the proportion of infections caused by CA-MRSA has increased.[39]

Initially noted in tertiary care centers, these infections are now increasingly common in the

community.[40, 41] Resistance to methicillin confers resistance to all penicillinase-resistant

penicillins and cephalosporins. This high level of resistance requires the mec gene that encodes

penicillin-binding protein 2a. This protein has decreased binding affinity for most penicillins and

cephalosporins. Methicillin resistance has a wide variety of phenotypic expression.

Heterogeneous resistance, recognized in the first clinical isolates described, is the typical

phenotype. In this case, all cells carry the genetic markers of resistance but only a small fraction

of them express the phenotype. Homogenous resistance is less frequent, with a single population

of cells that are inhibited only through high concentrations of antibiotics.

Methicillin-resistant S aureus (MRSA) was initially described in hospitalized populations.[42]

University affiliation and greater number of beds were institutional risk factors. In pediatric

centers, number of beds, region, and metropolitan population correlated with increased risk.

Since 1996, more patients with CA-MRSA have been described. The strains isolated from these

patients are different from typical nosocomial organisms in their susceptibility patterns and in

their PFGE characteristics. A clonal population, designated USA-300, has become the

predominant circulating organism in most communities.[43, 44] Many of these strains produce the

Panton-Valentine leukocidin, which is associated with a tendency to produce abscesses,

invasiveness, thrombogenesis, and morbidity and mortality.[45, 46, 47, 48] A 2012 report corroborates

earlier reports which describe an increased prevalence of USA300 strains causing invasive

infections.[49] High levels of antibody to the leukocidin are not protective,[50] however, so the role

of this and other virulence factors and immunomodulatory bacterial products

remainsunderinvestigation.[51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67]

A dose-dependent increase in risk of infection due to CA-MRSA with exposure to antibiotics has

been reported.[68]

More recently, S aureus that is intermediately resistant to vancomycin has been reported in 2

hospitalized patients, which suggests that full resistance to vancomycin may eventually

emerge,[69] although that has not yet occurred in the pediatric population.[70] Although the

possibility of interspecies transfer of vancomycin-resistance genes from vancomycin-resistant

Enterococcus was originally considered as the cause of this phenomenon, none of the species

isolated have carried vanA, vanB, vanC1, vanC2, or vanC3 genes. Of note, the clinical isolates

with intermediate resistance to vancomycin were from patients who had undergone prolonged

vancomycin therapy for MRSA. Morphologically, these isolates were found to have increased

extracellular material associated with the cell wall that may have been selected for during a

prolonged antibiotic course. Some virulence genes appear to be linked to decreased susceptibility

to vancomycin.[71, 72]

Most recently, the emergence of newly described mec genes and chromosomal cassettes from

bovine sources has been described.[73, 74] Thus, the issue of antimicrobial resistance in S aureus

continues to evolve.[75]

Previous

Next Section: Background

Frequency

United States

Numbers of both community-associated and hospital-acquired infections have increased in the

past 20 years. From 1990-1992, data from the National Nosocomial Infections Surveillance

System for the Centers for Disease Control and Prevention (CDC) revealed that S aureus was the

most common cause of nosocomial pneumonia and operative wound infections and the second

most common cause of nosocomial bloodstream infections.

A recent analysis of laboratory-confirmed MRSA cases in the Active Bacterial Core Surveillance

database (which covers 9 geographic regions and represents some 4.4 million children younger

than 18 years of age) indicates that community-acquired invasive MRSA infection is increasing

among children, particularly among black children and infants younger than 90 days of age. The

incidence of community-acquired MRSA increased from 1.1 case per 100,000 children in 2005

to 1.7 cases per 100,000 in 2010. The yearly increase in incidence, adjusted for race and age, was

10.2%. The adjusted incidence of invasive MRSA among black children was 6.7 cases per

100,000 in 2010, compared with 1.6 cases per 100,000 for children of other races.[76, 77]

An analysis of 148 consecutive patients with acute musculoskeletal S aureus infection (111 with

MSSA and 37 with MRSA) found that the proportion of pediatric MRSA infections increased

from 11.8% to 34.8% between 2001 and 2009, resulting in longer mean hospitalizations (13 vs 8

days).[78] . In addition, children with MRSA infection more often required surgical procedures

(38% vs. 15%), experienced more infection-related complications (24% vs 6%), and were more

often admitted to the intensive care unit (16% vs 3%).

Frequency of antibiotic resistance: In a disturbing trend, antibiotic resistance among these

isolates has increased because of antibiotic pressure. Currently, less than 5% of clinical isolates

remain sensitive to penicillin. Resistance to penicillin was reported as early as 1942 and is

mediated by beta-lactamase, a serine protease that hydrolyzes the lactam ring. In the 1980s,

MRSA emerged as a prominent hospital-based infection; consequently, the use of vancomycin

increased. A CDC survey revealed that the proportion of methicillin-resistant isolates with

sensitivity only to vancomycin increased from 22.8% in 1987 to 56.2% in 1997.[79] Scattered

reports of vancomycin resistance have been noted.[80] Community-onset MRSA infections are

increasingly common,[81, 82] although geographic variations persist.[83] Recent data suggest that the

incidence of MRSA infection may have peaked.[84, 85]

International

The USA300 lineage of community-associated MRSA has become widespread in Latin

America.[86] Incidence of staphylococcal skin and complicated infections among children in the

United Kingdom has increased over the past decade or so as well[87, 88] , although the incidence of

community-associated MRSA blood stream infection in the United Kingdom is less than that

seen in the United States.[89] Other strains of community-associated MRSA have been described

in Canada,[90, 91, 92, 93] Australia, Asia,[94, 95] and elsewhere in Europe.[96, 97, 98, 99, 100, 101, 102, 103, 104]

Previous

Next Section: Background

Mortality/Morbidity

Morbidity and mortality from S aureus infection widely varies depending on the clinical entity.

Although mortality is low in children with scalded skin syndrome, most fatalities are associated

with delay in diagnosis.

Sex

The male-to-female ratio of skeletal infections is 2:1, mostly because boys are more likely to

experience traumatic events.

Previous

Proceed to Clinical Presentation

Contributor Information and Disclosures

Author

Elizabeth P Baorto, MD, MPH Director, Division of Pediatric Infectious Diseases, Atlantic

Health System

Disclosure: Nothing to disclose.

Coauthor(s)

David Baorto, MD, PhD Medical Knowledge Engineer, Department of Medical Informatics,

Columbia University Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

José Rafael Romero, MD Director of Pediatric Infectious Diseases Fellowship Program,

Associate Professor, Department of Pediatrics, Combined Division of Pediatric Infectious

Diseases, Creighton University/University of Nebraska Medical Center

José Rafael Romero, MD is a member of the following medical societies: American Academy of

Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, New

York Academy of Sciences, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center

College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Larry I Lutwick, MD Professor of Medicine, State University of New York Downstate

Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care

System, Brooklyn Campus

Larry I Lutwick, MD is a member of the following medical societies: American College of

Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Daniel Rauch, MD, FAAP Director, Pediatric Hospitalist Program, Associate Professor,

Department of Pediatrics, New York University School of Medicine

Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric

Association, American Academy of Pediatrics, and Society of Hospital Medicine

Disclosure: Baxter Honoraria Consulting

Chief Editor

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's

Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of

Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of

Pediatrics, American Association of Immunologists, American Pediatric Society, American

Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical

Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern

Medical Association

Disclosure: Nothing to disclose.

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