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Methicillin-resistant Staphylococcus aureus infections in children: Epidemiology and clinical spectrum

Methicillin-resistant Staphylococcus aureus infections in children: Epidemiology and clinical spectrum
Author:
Sheldon L Kaplan, MD
Section Editor:
Morven S Edwards, MD
Deputy Editor:
Diane Blake, MD
Literature review current through: Jan 2024.
This topic last updated: Jan 05, 2023.

INTRODUCTION — The epidemiology and clinical spectrum of Methicillin-resistant Staphylococcus aureus (MRSA) infections in children will be reviewed here. The treatment and prevention of MRSA infections in children is discussed separately.

(See "Skin and soft tissue infections in children >28 days: Evaluation and management".)

(See "Staphylococcus aureus in children: Overview of treatment of invasive infections".)

(See "Methicillin-resistant Staphylococcus aureus (MRSA) in children: Prevention and control".)

MRSA DEFINITION — Methicillin resistance in S. aureus is defined as an oxacillin minimum inhibitory concentration (MIC) ≥4 mcg/mL. Isolates resistant to oxacillin or methicillin also are resistant to all beta-lactam agents, including cephalosporins (with the exception of ceftobiprole and ceftaroline).

Methicillin resistance is mediated by the mecA gene, which encodes for an abnormal low-affinity binding protein, PBP 2a, which permits the organism to grow and divide in the presence of methicillin and other beta-lactam antibiotics. The mecA gene is located on a mobile genetic element called staphylococcal cassette chromosome (SCCmec). A single clone probably accounted for most MRSA isolates recovered during the 1960s; by 2002, five major MRSA clones emerged worldwide [1-3]. Dissemination of resistance was mediated by horizontal transfer of the mecA gene and related regulatory sequences [4]. (See "Methicillin-resistant Staphylococcus aureus (MRSA): Microbiology".)

CLASSIFICATION — MRSA has traditionally been classified into health care-associated (HA-MRSA) and community-associated (CA-MRSA). However, from a molecular standpoint, the HA-MRSA and CA-MRSA classifications are no longer distinct [5-9]. HA-MRSA can spread to community contacts [6,10], and CA-MRSA is an important cause of health care-associated infection [8,11-16]. Thus, some authorities, including the United States Centers for Disease Control and Prevention Active Bacterial Core (CDC ABC) Surveillance System, subdivide HA-MRSA according to the setting of onset (hospital or community) [11,15,17].

Several criteria are used to classify MRSA infections into one of these groups, although the classification scheme has not been standardized [18,19]. The criteria include:

The time of isolation (eg, an infection is considered to have onset in the hospital if the pathogen is isolated after a certain time period (variably defined, but usually 48 hours) [11,18,20])

Host risk factor profile (although the risk factors are not standardized)

Antimicrobial susceptibility pattern (with CA-MRSA usually resistant to two or fewer classes of antibiotics, and HA-MRSA resistant to three or more)

Molecular characteristics of the isolate, including the SCCmec type, pulsed-field gel electrophoresis (PFGE) type, and presence of the genes for Panton-Valentine leukocidin (see 'Microbiologic characteristics' below)

HA-MRSA infections — HA-MRSA is usually defined by MRSA infection in a patient with one of the following risk factors [11,21]:

Presence of an invasive device at the time of onset of infection

History of HA-MRSA infection or colonization

History of surgery, hospitalization, or dialysis

A previous history of CA-MRSA infection is not, by itself, a risk factor for HA-MRSA infection. However, if treatment of the CA-MRSA infection required hospitalization, the patient would be at risk for HA-MRSA as described in the third bullet above.

Hospital-onset — The CDC ABC Surveillance System defines invasive hospital-onset (nosocomial) HA-MRSA as cases with positive culture result from normally sterile site obtained >48 hours after hospital admission [11]. These cases might have one or more of the risk factors for HA-MRSA, described above. (See 'HA-MRSA infections' above.)

Community-onset — The CDC ABC Surveillance System defines invasive community-onset HA-MRSA (CO HA-MRSA, also called non-nosocomial HA-MRSA) as cases with onset in the community and at least one of the health care risk factors described above (see 'HA-MRSA infections' above) [11]. Underlying illness possibly predisposing to frequent hospitalizations or visits to medical facilities is another risk factor for CO HA-MRSA infection in children [14,15,17].

Although the defining risk factors for CO HA-MRSA are similar to those for nosocomial health care-associated infection, the molecular characteristics of MRSA isolated from children in this group more closely resemble those of CA-MRSA strains [14,15]. (See 'Microbiologic characteristics' below.)

CA-MRSA infections — CA-MRSA usually is defined as an MRSA infection with onset in the community in a patient who is without risk factors for HA-MRSA, although the defining risk factors have varied from study to study [21,22].

The term CA-MRSA also has been used to refer to MRSA strains with bacteriologic characteristics (eg, genotype, antimicrobial susceptibility patterns) typical of isolates obtained from patients with CA-MRSA infections [22,23]. (See 'CA-MRSA strains' below.)

MICROBIOLOGIC CHARACTERISTICS — Several microbiologic features, including antimicrobial susceptibility patterns, pulsed-field gel electrophoresis (PFGE) type, staphylococcal cassette chromosome (SCCmec) type, and presence or absence of Panton-Valentine leukocidin (PVL), have traditionally distinguished health care-associated MRSA (HA-MRSA) strains from community-associated MRSA (CA-MRSA) strains [24,25]. However, as CA-MRSA isolates move into the hospital, it has become more difficult, using molecular techniques, to determine whether MRSA isolates associated with an outbreak are related to health care workers, other patients, the hospital environment, or the community [8,11-16]. Rapid whole-genome sequencing may be helpful in this regard, but it is not widely available [26,27].

The observation that CA-MRSA and HA-MRSA strains initially were genetically distinct suggests that CA-MRSA strains did not originate from spread of health care-associated strains into the community [24,28,29]. However, CA-MRSA appears to be related to some clones of community methicillin-susceptible S. aureus (MSSA) [22]. Strains of MSSA with PVL genes and PFGE patterns closely related to MRSA USA300 and USA400 have been isolated from patients with community-associated MSSA (CA-MSSA) infection [30-33]. Between 2001 and 2006, approximately 25 percent of invasive CA-MSSA isolates at a single children's hospital were USA300; the proportion of USA300 increased from 14 percent to 35 percent during the study period [33]. From 2007 to 2014, the proportion of invasive CA-MSSA isolates that were USA300 declined back to 25 percent [34]. Strains of MSSA with PVL genes and/or pulsed-field gel electrophoresis (PFGE) patterns closely related to MRSA USA300 and USA400 may represent ancestors of the MRSA strains or MRSA strains that have lost mecA [22].

HA-MRSA strains — HA-MRSA strains tend to have multidrug resistance and carry SCCmec type II or SCCmec type III [24,35]. HA-MRSA strains are typified by a USA100 or USA200 PFGE pattern [36]. SCCmec type IV, which is most typical of CA-MRSA strains, is also found in some HA-MRSA PFGE types [36].

CA-MRSA strains — Most CA-MRSA strains are susceptible to nonbeta-lactam antibiotics. However, resistance to commonly prescribed antibiotics (eg, clindamycin, fluoroquinolones, tetracyclines, mupirocin, trimethoprim-sulfamethoxazole) appears to be increasing [15,37-40]. Local antimicrobial susceptibility patterns influence treatment of suspected or confirmed S. aureus infections. (See "Skin and soft tissue infections in children >28 days: Evaluation and management", section on 'Management approach' and "Staphylococcus aureus in children: Overview of treatment of invasive infections", section on 'Empiric antimicrobial therapy'.)

Most CA-MRSA strains carry SCCmec type IV or V [9,28]. These types are smaller and theoretically more easily transferable between organisms than SCCmec types I through III [22,41]. CA-MRSA strains are typified by a USA300 or USA400 PFGE pattern [36,42,43].

CA-MRSA strains frequently carry genes for PVL, a cytotoxin that confers enhanced virulence in both MSSA and MRSA [33,44-47]. The presence of PVL is associated with increased morbidity in children with osteomyelitis and increased mortality in patients with S. aureus pneumonia [48-51]. PVL and other virulence determinants for MRSA are discussed separately. (See "Virulence determinants of community-acquired methicillin-resistant Staphylococcus aureus", section on 'Virulence determinants and their regulation'.)

CA-MRSA strains also produce high concentrations of peptides that recruit, activate, and lyse neutrophils, which are the main component of the host's cellular defense against S. aureus [52]. These cytolytic peptides may account, at least in part, for the increased virulence of CA-MRSA compared with HA-MRSA in children.

Community-onset HA-MRSA strains — MRSA strains isolated from children with risk factors for HA-MRSA but with onset of infection in the community share features of HA-MRSA and CA-MRSA [14,15]. Most community-onset HA-MRSA (CO HA-MRSA) strains carry the SCCmec type IV cassette, suggesting that CA-MRSA strains are now endemic in hospital settings [14,15].

In one case series, CO HA-MRSA had greater PFGE molecular diversity, were less likely to contain sequences for PVL, and were more likely to be resistant to ≥3 classes of antibiotics than CA-MRSA [14]. This observation has important implications when choosing empiric therapy for suspected MRSA infection and highlights the importance of differentiating between CO HA-MRSA and CA-MRSA. (See "Skin and soft tissue infections in children >28 days: Evaluation and management", section on 'Management approach' and "Staphylococcus aureus in children: Overview of treatment of invasive infections", section on 'Choice of therapy'.)

Resistance and reduced susceptibility to other antibiotics

LinezolidLinezolid resistance has been observed among MRSA isolates, primarily in strains that are health care-associated.

Ceftaroline – Reduced susceptibility to ceftaroline (minimum inhibitory concentration of ≥2 mcg/mL) has also been reported and is discussed separately. (See "Staphylococcus aureus bacteremia in children: Epidemiology and clinical features", section on 'Reduced susceptibility to ceftaroline'.)

EPIDEMIOLOGY AND RISK FACTORS — MRSA was initially a health care-associated pathogen, with only small numbers of community-acquired cases, but has become an increasingly prevalent community-acquired pathogen [17,53-55].

Health care-associated infection

Epidemiology — The prevalence of health care-associated MRSA (HA-MRSA) among hospitalized patients varies geographically. It is generally high in the United States, Japan, and southern Europe (eg, >30 percent in Spain, France, and Italy) but is very low (<1 percent) in Scandinavia and Switzerland [56-62].

In contrast to reports of declining invasive HA-MRSA in adults, the prevalence of HA-MRSA in children has remained relatively stable since 2005 [63-66]. MRSA isolates account for approximately 40 to 60 percent of S. aureus isolates from hospitalized patients in the United States, depending upon the site of infection [40,62,67].

In the pediatric age group, invasive HA-MRSA infections predominantly occur in children younger than one year of age, and hospital-onset HA-MRSA infections are more common than community-onset HA-MRSA infections (CO HA-MRSA). In the United States in 2020, the incidence of invasive hospital-onset HA-MRSA infections in children younger than 12 months was approximately 12 per 100,000 and the incidence of community-onset HA-MRSA infections in children younger than 12 months was approximately 3 per 100,000 [68].

Invasive HA-MRSA infections are relatively rare in children older than one year of age, but rates of invasive HA-MRSA infections vary among children's hospitals. In the United States in 2020, the incidence of invasive HA-MRSA infections (both hospital-onset and community-onset) was <1 per 100,000 for children age 1 year, 2 to 4 years, and 5 to 17 years [68].

Risk factors

Hospital onset HA-MRSA – Risk factors for hospital-onset HA-MRSA infection are listed below; the first three are the risk factors that traditionally define HA-MRSA [19,22]:

Presence of an invasive device at the time of admission

History of MRSA infection or colonization [69]

History of surgery, hospitalization, or dialysis

Prolonged hospitalization (>14 days)

Surgery or surgical site infection

Admission to intensive care unit or burn unit

Endotracheal/tracheostomy/nasogastric tube

Parenteral nutrition/enteral feedings

Proximity to others with MRSA colonization or infection [70]

Community-onset HA-MRSA – Risk factors for CO HA-MRSA are not standardized; those identified in publications describing this category [14,15,17] or review articles [19] are listed below; the first three traditionally define HA-MRSA:

Presence of an invasive device

History of HA-MRSA infection or colonization

History of surgery, hospitalization, or dialysis

Chronic disease (other than asthma or eczema)

Antibiotic use in the previous six months

Tympanostomy tube for recurrent otitis media

Day-care center attendance

Household contact with identified risk factor

Age younger than two years

CA-MRSA infection — The prevalence of CA-MRSA varies geographically [9,21]. In the early 2000s, surveillance from individual health care facilities demonstrated an increasing prevalence of CA-MRSA infections, increasing proportions of community-associated S. aureus infections that are MRSA, and increasing proportions of MRSA that are CA-MRSA [9,17,25,28,55,71,72]. The prevalence of CA-MRSA infections in children in the United States and other countries increased until approximately 2010 and then appears to have declined in some populations [34,64,73-76]. In the United States in 2020, the incidence of invasive CA-MRSA was <5 per 100,000 for children younger than 1 year of age, 1 year of age, 2 to 4 years of age, and 5 to 17 years of age [68].

Most CA-MRSA infections are noninvasive. Community outbreaks of skin and soft tissue infection have been reported in multiple settings, including Native American, including Alaska Native, communities [43,77], sports teams [78-81], child-care centers [10,82], military personnel [83,84], men who have sex with men [85], and prison inmates and guards [81,84,86,87]. In national surveys of athletic trainers, the prevalence of CA-MRSA was greater in football players and wrestlers than in other student athletes [88].

Analysis of CA-MRSA outbreaks indicates several risk factors that have a relatively poor predictive value for CA-MRSA [5]:

Skin trauma (eg, "turf burns," lacerations or abrasions, cosmetic body shaving, body piercing, tattoo placement) [79,89,90]

Frequent skin-to-skin contact [79]

Sharing potentially contaminated personal items or equipment that is not cleaned or laundered between users (eg, razors, sports equipment, towels) [79]

Crowding

Challenges in maintaining personal cleanliness and hygiene

Limited access to health care [91]

Frequent exposure to antimicrobial agents [92,93]

Thus, in most areas of the United States, CA-MRSA should be considered in any child presenting in the community with an infection for which S. aureus is a potential etiology.

TRANSMISSION — MRSA transmission requires contact with a colonized individual or a contaminated surface. Adherence to infection control measures is critical for interrupting MRSA transmission. (See "Infection prevention: Precautions for preventing transmission of infection" and "Methicillin-resistant Staphylococcus aureus (MRSA) in children: Prevention and control", section on 'Infection control'.)

Three major reservoirs of MRSA are patients, health care workers, and perhaps the inanimate environment. Patients are the greatest source of transmission in the health care setting. Term and late-preterm infants may acquire infection from their mothers, some other source in the community, or possibly the nursery [16,54,94-96].

Colonized individuals — Individuals colonized with MRSA serve as a reservoir for transmission. MRSA can colonize the skin and nares of hospitalized patients, health care workers, and healthy individuals [69,97-99].

Sites of colonization – The anterior nares is the most common site of MRSA colonization, although in patients presenting with skin and soft tissue infections the groin is colonized with S. aureus as frequently as or more frequently than the anterior nares [100-104]. The durability of MRSA colonization can vary from a few days or weeks to up to several years [102,105]. In one report of patients requiring readmission to a hospital, the median length of colonization was 40 months [102].

Up to 30 percent of individuals with nasal colonization are also colonized on other areas of intact skin, including the hands, axillae, perineum, and umbilicus (in infants) [100,106-110]. Other potential sites of MRSA colonization include surgical wounds, decubitus ulcers, intravascular catheter sites, throat, sputum, stool, and genitourinary tract. The throat was the second-most colonized site (after the nose) in one study [111].

Epidemiology and predisposing factors – Surveillance during the National Health and Nutrition Survey indicates that the overall prevalence of nasal colonization among children (age 1 to 19 years) in the United States during 2003 to 2004 was 1.3 percent (increased from 0.6 percent in 2001 to 2002) [112]. Colonization rates were increased in children >5 years compared with those aged one to five years.

The prevalence of nasal colonization with MRSA varies depending upon the population, with rates of approximately 10 percent among healthy children in the United States attending health maintenance visits in 2004 [113], 22 percent among children admitted to a single children's hospital in the United States in 2005 [114], and <1 percent among hospitalized children in Switzerland and healthy schoolchildren in Germany [58,115]. The prevalence of nasal MRSA colonization also varies over time. In an observational study of children admitted to a single children's hospital, the rate of MRSA colonization decreased from 22 percent in 2005 to 3 percent in 2016 [116].

In a given region, colonization rates may vary from practice to practice. Multipractice surveillance among children presenting for health maintenance or acute care visits in a single metropolitan area of the United States during 2005 to 2006 demonstrated colonization rates ranging from 0 to 9 percent [117].

Nasal colonization appears to be increased in children who have been immunized with the conjugate pneumococcal vaccine, probably due to competition between vaccine-type pneumococci and S. aureus [118,119]. It also may be related to exposure to amoxicillin-clavulanate in the preceding three months [93].

Infection in colonized individuals – Colonization with S. aureus is a risk factor for subsequent infection [69,120-124]. In a review of 758 hospitalized patients, MRSA colonization was observed in 3.4 percent of admissions and acquired in an additional 3 percent; the rates of MRSA infection within one year in these groups were 19 and 25 percent (relative risks 9.5 and 13 compared with patients with no colonization or methicillin-susceptible S. aureus [MSSA] colonization, respectively) [69]. In a meta-analysis of 18 studies reporting data from 1999 to 2011, the prevalence of MRSA colonization at admission to a neonatal or pediatric intensive care unit (NICU or PICU) was 1.9 percent (95% CI 1.3-2.6) and the acquisition rate was 4.1 percent (95% CI 1.2-8.6) [123]. Neonates who were admitted to the NICU after discharge from the birth hospitalization were more likely to be colonized than those who had never left the NICU (5.8 versus 0.2 percent). The risk of MRSA infection during hospitalization was increased among colonized patients (relative risk 24.2, 95% CI 8.9-66.0).

Transmission by colonized individuals – Colonization can occur in the following ways [100,105,125]:

Contact with contaminated wounds or dressings of infected patients

Contact with another individual's colonized intact skin

Contact with contaminated inanimate objects (see 'Contaminated surfaces' below)

Inhalation of aerosolized droplets from chronic nasal carriers

Individuals with nasal MRSA carriage transmit MRSA more readily in the setting of concomitant sinus infection or upper respiratory infection [125,126]. Health care workers with dermatitis that is infected or colonized with MRSA are particularly prone to transmitting the organism [127,128].

Contaminated surfaces — MRSA-contaminated surfaces also can serve as reservoirs for MRSA transmission [129-132]. Health care workers who touch contaminated surfaces may contaminate their gloves (or presumably their hands) with MRSA [129]. The extent to which contaminated environmental surfaces contribute to transmission of MRSA to patients has not been established.

The risk of contamination of inanimate surfaces in patient rooms may depend upon the patient's site of MRSA infection. In a prospective culture survey of a 200-bed hospital, cultures obtained from inanimate surfaces in the hospital rooms of MRSA-infected patients were positive more frequently in the setting of wound infections or urinary tract infections than in the setting of MRSA infection at other sites (36 versus 6 percent) [129].

MRSA also may be transmissible through contact with medical equipment (eg, tourniquets, stethoscopes, blood pressure cuffs) [129-131,133]. In a study of cultures from 200 stethoscope ear tips, 80 percent were contaminated with microorganisms. Among the positive cultures, 58 percent were Staphylococcus species and 17 percent were MRSA [130].

Contaminated surfaces that may play a role in the transmission of MRSA in the community include surfaces to which people have bare skin contact [22,92,134,135]. These include towels, razors, sauna benches, sports equipment, and exercise mats, as well as multiple household surfaces such as remote controls or sink faucet handles [136].

CLINICAL SPECTRUM — The clinical spectrum of MRSA infection ranges from asymptomatic colonization, to skin and soft tissue infection (SSTI), to life-threatening invasive infection [22]. Colonization is discussed above. (See 'Colonized individuals' above.)

Health care-associated infections — Between 30 and 60 percent of hospitalized patients who are colonized with MRSA develop an overt infection [137].

Health care-associated MRSA (HA-MRSA) is associated with severe, invasive disease in hospitalized patients [11,14,17,62,138,139]. MRSA is one of the few pathogens routinely implicated in nearly every type of health care-associated infection. This is probably related to its capacity for biofilm formation on health care-associated foreign devices (eg, endotracheal tubes, urinary catheters, intravascular catheters).

The body sites most frequently affected by HA-MRSA are wounds, skin, and bloodstream, followed by the lower respiratory tract and urinary tract [11,17,21,71]. During 14 years of surveillance at a single children's hospital (1990 to 2003), 74 children developed HA-MRSA infection, of which 66 percent were invasive (primarily of the lungs and bloodstream) [17]. In six years of surveillance (2001 to 2007) at another children's hospital, more than one-half of the HA-MRSA infections were SSTIs, including postoperative wound infections. The majority of invasive MRSA infections were central line-associated bloodstream infections [140]. In population surveillance from the United States Centers for Disease Control and Prevention, rates of hospital-onset MRSA bloodstream infections declined between 2005 and 2016 [141].

Patients with MRSA infection have higher mortality, longer hospital stays, and higher health care costs than patients with methicillin-susceptible S. aureus (MSSA) infection [139,142-146].

Community infections — Community-associated MRSA (CA-MRSA) isolates are most often associated with SSTI. However, CA-MRSA is a significant cause of invasive disease.

SSTI — CA-MRSA isolates are most often associated with SSTI, which have accounted for up to 96 percent of cases of CA-MRSA infection in various series limited to children [17,54,71,147]. The predilection of CA-MRSA strains to cause SSTI may be related at least in part to the presence of Panton-Valentine leukocidin [148].

CA-MRSA strains have been cultured from pustules, furuncles (abscessed hair follicles or "boils"), carbuncles (coalesced masses of furuncles), and skin abscesses [22]. The role of MRSA in cellulitis is less clear since cultures are rarely obtained [22]. Staphylococcal SSTI may be confused with recluse spider bites by both patients and clinicians [22]. CA-MRSA SSTI are far more prevalent than spider bites. (See "Bites of recluse spiders", section on 'Differential diagnosis'.)

The evaluation and management of MRSA SSTI are discussed separately. (See "Skin and soft tissue infections in children >28 days: Evaluation and management".)

Invasive disease — CA-MRSA is an important cause of invasive disease, although less frequently than of SSTI [11,48,149-154]. Invasive disease may occur spontaneously in patients without previous infections, but often with minor skin disruptions or as a complication of SSTI [22,154]. Disseminated disease may occur as a consequence of bacteremia.

Invasive disease occurs more often in children with risk factors for HA-MRSA than in children without such risk factors (32 versus 5 percent in one study) [14,17]. Acute hematogenous osteomyelitis is the most common invasive disease caused by CA-MRSA in children [48,155]. (See "Hematogenous osteomyelitis in children: Epidemiology, pathogenesis, and microbiology", section on 'Staphylococcus'.)

Other types of invasive MRSA disease reported in children include [11]:

Septic arthritis [156]

Bacteremia without a focus [150,157]

Pneumonia (often necrotizing) and empyema, sometimes as a fatal complication of influenza [149,152-154,158,159] (see "Pneumonia in children: Epidemiology, pathogenesis, and etiology", section on 'Community-acquired pneumonia')

Meningitis [160]

Pyomyositis and necrotizing fasciitis [30,48,161-163]

Sinusitis (associated complications such as epidural abscess)

Deep neck space infections, including retropharyngeal abscess and Lemierre syndrome [164,165] (see "Retropharyngeal infections in children" and "Lemierre syndrome: Septic thrombophlebitis of the internal jugular vein")

Lymphadenitis

Orbital cellulitis [166]

Endocarditis

Sepsis (with or without Waterhouse-Friderichsen syndrome) [30,31]

Other sites of infection include:

Otitis media [167] and otitis externa

Urinary tract infection (which is invasive if it affects the upper urinary tract [ie, pyelonephritis])

Compared with community-associated MSSA (CA-MSSA) invasive disease, CA-MRSA invasive disease is associated with increased severity and complications [30,74,155,168]. This was illustrated in a series of 158 cases of acute osteoarticular infection from a single institution in which MRSA infections were associated with increased rate of subperiosteal abscess formation (71 versus 38 percent), increased need for surgical drainage (91 versus 62 percent) and increased median hospital stay (10 versus 7 days) [155].

The treatment of invasive MRSA infections in children is discussed separately. (See "Staphylococcus aureus in children: Overview of treatment of invasive infections".)

In young infants — The clinical spectrum of community-associated S. aureus infections in term and late-preterm previously healthy infants younger than 30 days of age was described in a series of 126 infants from a single institution [147]. Two-thirds of isolates were MRSA. There were 43 cases of pustulosis, 68 of cellulitis/abscess, and 15 invasive infections. As in older children, the morbidity of CA-MRSA compared with CA-MSSA infections in neonates appears to be increased [169].

SUMMARY

Classification – Methicillin-resistant Staphylococcus aureus (MRSA) has traditionally been classified into health care-associated (HA-MRSA) and community-associated (CA-MRSA). (See 'Classification' above.)

Microbiologic characteristics

HA-MRSA – HA-MRSA strains tend to have multidrug resistance and carry staphylococcal cassette chromosome type II (SCCmec type II) or SCCmec type III. HA-MRSA strains are typified by a USA100 or USA200 pulse-field gel electrophoresis (PFGE) pattern. (See 'HA-MRSA strains' above.)

CA-MRSA – CA-MRSA strains are usually susceptible to nonbeta-lactam antibiotics, although local susceptibility patterns vary. CA-MRSA strains typically carry SCCmec type IV or V and have a USA300 or USA400 PFGE pattern. They also frequently carry genes for Panton-Valentine leukocidin (PVL). (See 'CA-MRSA strains' above.)

Community-onset HA-MRSA – MRSA strains isolated from children with risk factors for HA-MRSA and onset of infection in the community (CO HA-MRSA) share features of HA-MRSA and CA-MRSA. Similar to CA-MRSA, most CO HA-MRSA strains carry the SCCmec type IV cassette. However, they have greater diversity in PFGE patterns, are less likely to contain sequences for PVL, and are more likely to be resistant to ≥3 classes of antibiotics than CA-MRSA. (See 'Community-onset HA-MRSA strains' above.)

Epidemiology and risk factors – Risk factors for CA-MRSA include skin trauma, crowding, frequent skin-to-skin contact, sharing potentially contaminated personal items or equipment, and frequent exposure to antimicrobial agents. However, they have a relatively poor ability to distinguish MRSA from methicillin-sensitive S. aureus infection, and CA-MRSA should be considered in any child presenting in the community with an infection for which S. aureus is a potential etiology. (See 'Epidemiology and risk factors' above.)

Transmission – MRSA transmission requires contact with a colonized individual or a contaminated surface. (See 'Transmission' above.)

Clinical spectrum – The clinical spectrum of MRSA infection ranges from asymptomatic colonization, to skin and soft tissue infection, to life-threatening invasive infection. (See 'Clinical spectrum' above.)

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Topic 6065 Version 29.0

References

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