This is a MUST READ for anyone suffering from a CHRONIC staph infection. (vancomycin-resistant!) 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. info from: http://emedicine.medscape.com/article/971358-overview

1. Staphylococcus Aureus Infection
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Author: Elizabeth P Baorto, MD, MPH; Chief Editor: Russell W Steele, MD more...
Updated: Jan 31, 2014
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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:
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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

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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
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Diagnosis based on clinical appearance
Aspiration or incision and culture of purulent material from the lesion occasionally
diagnostic
Osteomyelitis
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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

3. Septic arthritis
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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
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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
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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
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Obtain a blood culture through the intravenous line and a peripheral blood culture
See Workup for more detail.
Management
Antibiotic regimens include the following:
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Empiric therapy with penicillins or cephalosporins may be inadequate because of
community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA)[10]

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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:
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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):
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Eradication of the focal infection to end toxin production
Large doses of intravenous antistaphylococcal agents such as oxacillin or a firstgeneration cephalosporin such as cefazolin, combined with clindamycin
Osteomyelitis:
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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:
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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:

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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:
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Surgical exploration and drainage of all potential foci of infection
Thrombophlebitis:
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Removal of the infected intravenous line in patients who are immunocompromised or
severely ill or when infection cannot be eradicated medically
Bacteremia :
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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

6. 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 pulsedfield 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

7. 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 catheterrelated 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

8. 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

9. 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

10. 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.

11. 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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