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Infective Pyomyositis and Myositis in Children in the Era of Community-Acquired, Methicillin-Resistant Staphylococcus aureus Infection

  1. Pia S. Pannaraj,
  2. Kristina G. Hulten,
  3. Blanca E. Gonzalez,
  4. Edward O. Mason Jr., and
  5. Sheldon L. Kaplan
  1. Section of Infectious Diseases, Department of Pediatrics, Baylor College of Medicine and Texas Children's Hospital, Houston, Texas
  1. Reprints or correspondence: Dr. Pia S. Pannaraj, Dept. of Pediatrics, Baylor College of Medicine, One Baylor Plaza, Rm. 302A, Houston, TX 77030 (pannaraj{at}bcm.tmc.edu).
 
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Abstract

Background. Cases of pyomyositis and myositis have been increasing in frequency at Texas Children's Hospital (Houston) since 2000. The increase appears to correlate with the emergence of community-acquired methicillin-resistant Staphylococcus aureus (MRSA).

Methods. The medical records of patients with pyomyositis and myositis hospitalized at Texas Children's Hospital during the period from January 2000 through December 2005 were reviewed. Available S. aureus isolates were obtained for susceptibility testing, to determine the presence of pvl (lukS-PV and lukF-PV), and for pulsed-field gel electrophoresis analysis.

Results. Forty-five previously healthy children with bacterial pyomyositis or myositis were analyzed. The causes were S. aureus (in 57.8% of children) and Streptococcus pyogenes (in 2.2%); 40.0% of children had negative culture results. The number of cases increased between 2000 and 2005, primarily as a result of an increase in the prevalence of community-acquired MRSA. The mean patient age was 5.5 years (range, 0.06–15 years). The thigh (40.0% of children) and pelvis (28.9%) were the most commonly affected sites. The mean abscess diameter was 3.5 cm. Eighteen children required at least 1 muscle drainage procedure. Of the 24 available S. aureus isolates (15 community-acquired MRSA isolates and 9 community-acquired, methicillin-susceptible S. aureus [MSSA] isolates), 16 were found to be USA300 by pulsed-field gel electrophoresis, and 17 carried pvl. Patients with community-acquired MRSA, USA300, and/or pvl-positive strains required more drainage procedures than did those with community-acquired MSSA, non-USA300, and/or pvl-negative strains (81% vs. 40% [P =.05], 82% vs. 29% [P =.02], and 81% vs. 38% [P =.07], respectively).

Conclusions. Community-acquired MRSA is an increasing cause of pyomyositis and myositis in children. Community-acquired MRSA, USA300, pvl-positive S. aureus isolates caused more severe disease than did community-acquired MSSA, non-USA300, and pvl-negative isolates, respectively.

Pyomyositis is an acute bacterial infection of skeletal muscle with localized abscess formation. This infection, which is also known as “tropical pyomyositis,” is endemic in tropical countries, accounting for 2.2%–4% of surgical admissions [1, 2]. Staphylococcus aureus accounts for 75%–90% of these infections [3, 4]. Pyomyositis is much less common in temperate climates, such as North America, where only 98 such cases were reported during 1972–1992 [5]. In this and in more recent descriptions of pyomyositis [6, 7], more than one-half of patients in temperate climates had underlying conditions, and only one-third were children. S. aureus constituted two-thirds of the isolates.

Acute bacterial myositis is an infection within the muscle, but inflammation extends diffusely through ⩾1 muscle group without distinct abscesses. Reports of acute bacterial myositis are less common than reports of pyomyositis and more frequently involve adult patients. Most cases have been due to Streptococcus pyogenes [8]. However, cases caused by S. aureus also have been reported [9].

The number of S. aureus infections has increased substantially at Texas Children's Hospital (Houston, TX) since 2001. Currently, >75% of community-acquired staphylococcal infections at Texas Children's Hospital are caused by methicillin-resistant S. aureus (MRSA) [10]. More than 90% of community-acquired MRSA isolates and 25% of community-acquired methicillin-susceptible S. aureus (MSSA) isolates have PFGE patterns identical or closely related to the USA300 clone [11, 12].

Panton-Valentine leukocidin (PVL) is a staphylococcal virulence factor associated with severe pneumonia, skin and soft-tissue infections, and bone and joint infections [13–16]. Fibronectin-binding proteins encoded by fnbA and fnbB are in the family of adhesins known as microbial surface components recognizing adhesive matrix molecules. Fibronectin-binding proteins mediate S. aureus adherence and invasion into host cells and have been associated with infection in humans and animal models [17–19]. Their roles in muscle infection have not been established.

Cases of pyomyositis and bacterial myositis have increased in frequency in pediatric patients since 2000 at Texas Children's Hospital. The increase appears to correlate with the emergence of community-acquired MRSA. This study describes demographic, clinical, and microbiological characteristics of children with pyomyositis and myositis during a 6-year period. We postulated that presentation, hospital course, and outcome would differ among patients with disease caused by community-acquired MRSA, compared with those with disease due to community-acquired MSSA, and that the clonality and presence or absence of certain genes (pvl, fnbA, and fnbB) would be associated with different clinical manifestations and outcomes.

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Methods

Patients. From 1 January 2000 through 31 December 2005, patients admitted to Texas Children's Hospital with infective pyomyositis or myositis were identified from medical records (International Classification of Diseases, Ninth Revision, code 728.0), the infectious diseases consultation database, and our S. aureus database [10]. Pyomyositis was defined as acute bacterial infection of skeletal muscle with abscess formation. Acute bacterial myositis was defined as infection within the muscle, with inflammation extending diffusely through ⩾1 muscle group but without abscess formation. Since August 2001, all S. aureus strains isolated by the Texas Children's Hospital clinical microbiology laboratory have been collected as part of prospective surveillance. Demographic and clinical characteristics of these patients are maintained in a computer database.

The medical records and imaging study findings for each patient with pyomyositis and myositis were reviewed. Diagnosis was based on compatible clinical presentation and ultrasound examination, CT or MRI, and/or surgical exploration. Patients who did not have a bacterial pathogen isolated from culture were included if they received a diagnosis of and treatment for a bacterial infection and if they had an abscess noted on an imaging study or had a single site of infection, with an admission WBC count >10,000 cells/mm3. All patients with concurrent osteomyelitis or septic arthritis were excluded. From the medical record, we obtained demographic information, dates of admission and discharge, size and location of muscle infection, associated infections, predisposing factors, symptoms, febrile days, laboratory values, surgical drainage procedures, antimicrobial treatment, and complications. Our criteria for categorizing an infection as community acquired have been described elsewhere [11]. The Institutional Review Board of Baylor College of Medicine (Houston, TX) approved the study. Informed consent was not required.

Laboratory methods. The Texas Children's Hospital clinical microbiology laboratory identified bacterial isolates by standard methods. Antimicrobial susceptibilities were determined by disk diffusion testing using CLSI methods and interpretation guidelines [20]. S. aureus isolates were frozen at -80°C in horse blood in the Infectious Disease Research Laboratory.

Molecular analysis. DNA isolation, SCCmec typing, and PCR (for pvl [luk-S-PV and luk-F-PV], fnbA and fnbB) was performed as previously described [11, 21]. Genetic relatedness was determined by PFGE [22].

Statistical analysis. Mann-Whitney U test (for continuous variables) and χ2 test or Fisher's exact test (for dichotomous variables) were performed to compare differences between groups. Trend analysis was conducted using the χ2 test for trend. SPSS for Windows software, version 10.0 (SPSS), was used. All analyses were 2-tailed, and P <.05 was considered statistically significant.

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Results

Patients. Pyomyositis or myositis was identified in 182 patients admitted to Texas Children's Hospital during the period from 1 January 2000 through 31 December 2005. Patients with chronic underlying illnesses, such as spina bifida or cerebral palsy (10 patients), hematologic or oncologic disease (9 patients), chronic skin disease (4 patients), immunodeficiencies or chronic immunosuppression (4 patients), congenital heart disease (4 patients), and extreme prematurity (1 patient), were excluded. Five patients with infection resulting from an open wound or a medical procedure and 9 patients with viral myositis (influenza A in 3 patients and unknown etiology in 6) also were excluded.

Of the remaining 136 patients, 55 (41%) had an associated osteomyelitis, 10 (7%) had concomitant septic arthritis, and 25 (18%) had osteomyelitis and septic arthritis. One patient had primary endocarditis with septic emboli. Thus, 45 patients (43%) with primary muscle infection were included in the analysis.

Bacterial etiologies. Among the 45 children with primary muscle infection, S. aureus was isolated from blood and/or muscle cultures in 26 patients (58%), and group A streptococci were isolated from blood culture in 1 patient (2%). Of the 26 S. aureus isolates, 16 were community-acquired MRSA, and 10 were community-acquired MSSA. No organism was isolated from 18 patients (40%); of these, 9 had muscle abscesses revealed by MRI or ultrasound, and 9 had single sites of infection with elevated WBC counts.

Epidemiology. The frequency of cases increased from 5 cases in 2000 to 10 cases in 2005 (P =.07) (figure 1). Community-acquired MRSA accounted for most of the increase, compared with community-acquired MSSA and other etiologies, but this difference was not statistically significant (P =.12). Although more patients were affected from May through October, cases were observed throughout the year (figure 2).

Figure 1
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Figure 1

Number of children with primary pyomyositis and myositis admitted to Texas Children's Hospital (Houston) annually during 2000–2005. GAS, group A streptococci; MRSA, methicillin-resistant Staphylococcus aureus; MSSA, methicillin-susceptible S. aureus.

Figure 2
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Figure 2

Monthly distribution of children with pyomyositis and myositis at Texas Children's Hospital (Houston).

Male children were affected more frequently than female children (31 [69%] vs. 14 [31%], respectively; P =.01). Mean age among patients was 5.5 years (range, 22 days to 15 years). Community-acquired MRSA-affected patients were younger than children infected with community-acquired MSSA (P =.04) (table 1).

Figure 3
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Figure 3

Clonality of Staphylococcus aureus strains isolated from 24 patients with pyomyositis or myositis.

Table 1
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Table 1

Characteristics of 26 patients with pyomyositis or myositis due to community-acquired, methicillin-resistant Staphylococcus aureus (MRSA) or methicillin-susceptible S. aureus (MSSA).

Presentation. The most common presenting signs and symptoms were pain (100%), fever (93%), limp (89% of lower extremity and pelvic infections), and swelling (58%). The mean duration of symptoms was 2.7 days before the first presentation for medical evaluation and 3.7 days before hospital admission. Eight children experienced a specific injury, and 4 performed vigorous activity that affected the site of infection before the onset of infection. In the 10 patients who were able to recall, the event occurred an average of 5.4 days before admission. Twenty-two patients (49%) had skin barrier penetration secondary to insect bites, minor lacerations, or excoriations. Twenty-one (47%) took an anti-inflammatory medication before presentation. Thirteen patients (29%) were given antibiotics before admission; 10 received a cephalosporin or amoxicillin, with or without clavulanate, 2 received clindamycin, and 1 received an unknown antibiotic. Thirty-four patients (76%) and 9 patients (20%) had an admission body weight greater than the 50th and 90th percentile for age, respectively.

The proximal lower extremity and pelvis were the most commonly affected sites (table 2). Disease involved the right side in 20 (44%), the left side in 19 (42%), and both sides in 6 (13%). The percentages of patients with multifocal disease caused by community-acquired MRSA, compared with cases due to community-acquired MSSA, were similar. Thirty patients (67%) had pyomyositis, and 15 (33%) had myositis. The etiologies of pyomyositis versus myositis were similar.

Table 2
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Table 2

Sites of muscle infection.

Laboratory and imaging studies. Laboratory study findings are presented in table 3. Interestingly, creatine kinase levels were in the normal range for patients with bacterial muscle infection (mean level, 149 U/L) and were significantly lower than the levels in the 9 patients who were excluded with the diagnosis of viral myositis (mean level, 5591 U/L; P =.006). Bacteria were isolated from 27 patients (60%); they were isolated from blood cultures alone from 8 (30%), from muscle cultures alone from 18 (67%), and from both blood and muscle cultures from 1 (4%). Nine (21%) of 42 patients were bacteremic for a mean period of 3.2 days (range, 1–7 days).

Table 3
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Table 3

Hospital course and outcome of children with pyomyositis and myositis caused by all etiologies.

Muscle abnormalities were well defined in all 36 patients who underwent MRI. Abnormalities were less distinct but observed in 8 (100%) of 8 CT scans, 10 (59%) of 17 ultrasounds, and 15 (73%) of 33 plain radiographs.

Diagnosis, treatment, and complications. The diagnosis of pyomyositis or myositis was made after an average of 1.8 days in the hospital. In 2 patients (4%), muscle infection was associated with septic shock. The first patient had pyomyositis in the latissimus dorsi and trapezius muscles and developed bacteremia, septic shock, and pleocytosis of the CSF, with community-acquired MRSA (USA300 and pvl positive) isolated from CSF broth culture only. She was treated for CNS infection with vancomycin (60 mg/kg/day). For the second patient, blood and triceps abscess culture yielded community-acquired MRSA. Extramuscular complications occurred in 1 patient each with mediastinitis (who had a pvl-positive, USA300 strain of community-acquired MRSA) extending from sternocleidomastoid pyomyositis, poststreptococcus glomerulonephritis (no organism isolated, but the antistreptolysin O titer was 6400), or contiguous epidural fat inflammation from paraspinous myositis (no organism isolated).

Details of hospital course and drainage procedures are shown in table 3. Samples obtained from all 5 children who required a second drainage procedure grew S. aureus. Initial antibiotic regimens included vancomycin or clindamycin in 41 patients (91%). Four patients were initially treated with nafcillin before the emergence of community-acquired MRSA was widely appreciated. One patient with community-acquired MRSA infection did not initially receive appropriate coverage; the child underwent drainage on the second day of hospitalization, without adverse effects. Antimicrobial therapy was tailored to the causative organism once susceptibility data were known (table 4). Patients received intravenous antibiotics for a mean duration of 12.8 days, followed by 11.3 days of oral antibiotic treatment. The switch from intravenous to oral antibiotics was made on the basis of improvement in fever, examination, and inflammatory markers and was at the discretion of the primary or consulting infectious diseases physician. The average length of total treatment was 20.4 days. Fifteen patients (33%) and 6 patients (13%) required inpatient and outpatient physical therapy, respectively; all but 1 recovered without complications. One patient with community-acquired MSSA infection was readmitted for drainage of recurrent pyomyositis; the abscess was not drained during the first admission.

Table 4
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Table 4

Antimicrobial treatment of pyomyositis and myositis due to community-acquired, methicillin-resistant Staphylococcus aureus, to methicillin-susceptible S. aureus (MSSA), or with an unknown etiology.

Molecular analysis. Fifteen community-acquired MRSA and 9 community-acquired MSSA isolates were available for molecular analysis. All 15 community-acquired MRSA isolates carried the SCCmec type IV gene. pvl genes were present in 13 (81%) of 15 community-acquired MRSA strains and 4 (44%) of 9 community-acquired MSSA strains (P =.06). fnbA and fnbB were present in 23 (96%) and 22 (92%) of S. aureus isolates, respectively.

All 15 available community-acquired MRSA isolates were USA300; 10 of them corresponded to the predominant PFGE type (USA300.0114). One of 9 community-acquired MSSA isolates was USA300; 8 displayed divergent patterns. Figure 3 shows the increase in number of USA300 isolates over the 5-year period, although this trend was not statistically significant (P =.13). More USA300 isolates than non-USA300 isolates carried pvl (88% vs. 38%; P =.02).

Comparison of clinical features. Hospital course and outcome of the 26 patients with S. aureus pyomyositis and myositis are presented in table 5. Three comparisons are shown: community-acquired MRSA versus community-acquired MSSA strains, pvl-positive versus pvl-negative isolates, and USA300 clones versus other clones. Presenting signs and symptoms were similar in these groups; however, interestingly, trauma was more common in patients infected with pvl-negative than pvl-positive strains (67% vs. 12%; P =.038). Children with fnbA- and fnbB-containing strains showed no significant differences in clinical presentation or hospital course.

Table 5
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Table 5

Hospital courses for 26 children with pyomyositis and myositis caused by Staphylococcus aureus.

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Discussion

The number of cases of infective pyomyositis and myositis in children has increased substantially in our community. Although several case studies of pyomyositis in children and adults have been published since 1979 [3–5, 23–25], many of the patients described in those reports had underlying conditions, such as immunodeficiency or diabetes mellitus. Our patient series is, to our knowledge, the largest case study of otherwise healthy pediatric patients with pyomyositis and myositis, and it covered 6 years in a nontropical region.

Several factors may explain the increasing incidence of muscle infection in our community. Since 2000, there has been a heightened awareness of the severity of diseases caused by community-acquired MRSA. However, some primary care physicians have continued to use antibiotics that are not active against MRSA as first-line treatment, and this may have allowed the progression of infection. Physicians may obtain MRIs, which best define muscle infections, to evaluate for osteomyelitis and septic arthritis more frequently than in the past. Houston has average daily high temperatures of 34°C in July and 17°C in January (http://www.weather.com, accessed on 8 June 2006); however, the incidence of muscle infection has increased over the past 6 years, despite there being no changes in weather patterns. Our data show that the increased frequency and severity of disease are associated with the recent emergence of community-acquired MRSA, pvl-positive strains, and the predominance of the USA300 clone in the Houston area.

Children with community-acquired MRSA infection had a shorter duration of bacteremia than did those with community-acquired MSSA infection. Nevertheless, community-acquired MRSA infections were associated with larger abscesses and required more drainage procedures than did community-acquired MSSA infection, suggesting that community-acquired MRSA can attack muscle and form abscesses more readily than community-acquired MSSA. Community-acquired MRSA affected patients at a younger age, but other clinical parameters were similar. The same findings were seen with the USA300 clone, compared with other clones. Almost 70% of the S. aureus isolates recovered from patients with pyomyositis or myositis were USA300 isolates. The frequency of isolation of this clone has increased since 2000 at our institution and throughout the United States, indicating that it may have a selective advantage for becoming the predominant community pathogen [11, 12, 26–28].

Several genes likely contribute to the virulence of community-acquired MRSA and the USA300 clone. The pvl genes are associated with the predominant USA300 clone at our institution and are less associated with the other clones isolated from children with myositis/pyomyositis in this study. PVL is an exotoxin that forms pores and induces polymorphonuclear leukocyte death by apoptosis [29, 30]. Several recent studies have confirmed the association between PVL and the development of deep-seated furunculosis [14, 31, 32]. We found that S. aureus strains that carried pvl were associated with increased levels of inflammatory markers, longer hospitalizations, and more complications than were pvl-negative isolates in patients with osteomyelitis [16, 33].

Muscle infections are postulated to occur when transient bacteremia seeds a site of local muscle injury [34]. Almost one-half of the patients in our study had skin barrier penetration that could have been the site of bacteria introduction. Approximately 30% of patients recalled a specific incident of trauma or strenuous activity. Interestingly, fewer patients with pvl-positive isolates than with pvl-negative isolates experienced trauma. Although parents often may neglect to notice minor trauma in children, this suggests that pvl may encode for or be closely associated with a virulence factor with a propensity to damage normal muscle tissue. Furthermore, pvl emerged as a significant predictor of need for a drainage procedure and a higher number of surgical interventions, indicating that PVL (or an associated factor) likely contributes to the severity of muscle disease caused by S. aureus.

Empirical antimicrobial therapy for pyomyositis and myositis will depend upon local epidemiologic and susceptibility patterns. However, as seen in our study, an increase in the prevalence of community-acquired MRSA is contributing to an increase in frequency of cases. Thus, one should strongly consider coverage for MRSA in the empirical treatment regimen, which, in our area, currently consists primarily of vancomycin or clindamycin. MRI is the optimal imaging modality to demonstrate muscle inflammation and/or the presence of a muscle abscess. Drainage of the abscess expedites healing and is helpful in isolating the causative pathogen. Muscle abscess culture yielded the pathogen in 94% of patients who underwent drainage. Antimicrobial therapy then can be tailored on the basis of the causative pathogen and susceptibility results. The majority of our patients who were infected with community-acquired MRSA were treated with clindamycin. However, linezolid is an option for oral or intravenous therapy for treatment of community-acquired MRSA infections caused by clindamycin-resistant isolates. The duration of therapy depends on clinical improvement. In cases of primary muscle infection without bone or joint involvement, treatment with an intravenous agent followed by an oral agent (when clinical improvement has occurred) for a total of 3 weeks seems to be appropriate.

As the frequency of community-acquired MRSA has increased in our community, cases of infective myositis and pyomyositis have risen appreciably. Infection caused by community-acquired MRSA, USA300 related clones, and pvl-positive strains are more likely to cause severe disease than MSSA, non-USA300 clones, and pvl-negative strains. Additional studies are important to examine virulence factors associated with community-acquired MRSA and their roles in the pathogenesis of muscle infections.

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Acknowledgments

Financial support. Pfizer (to S.L.K.).

Potential conflicts of interest. S.L.K. received a grant from Pfizer. All other authors: no conflicts.

  • Received April 14, 2006.
  • Accepted June 16, 2006.
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References

  1. ↵
    1. Feigin RD,
    2. Cherry JD,
    3. Demmler GJ,
    4. Kaplan SL
    1. Grose C
    . Pyomyositis and bacterial myositis. In: Feigin RD, Cherry JD, Demmler GJ, Kaplan SL, editors. Textbook of pediatric infectious diseases. 5th ed. Philadelphia: Saunders; 2004. p. 737-41.
  2. ↵
    1. Horn CV,
    2. Master S
    . Pyomyositis tropicans in Uganda. East Afr Med J 1968;45:463-71.
    Medline
  3. ↵
    1. Ameh EA
    . Pyomyositis in children: analysis of 31 cases. Ann Trop Paediatr 1999;19:263-5.
    CrossRefMedlineWeb of Science
  4. ↵
    1. Chiedozi LC
    . Pyomyositis: review of 205 cases in 112 patients. Am J Surg 1979;137:255-9.
    CrossRefMedlineWeb of Science
  5. ↵
    1. Christin L,
    2. Sarosi GA
    . Pyomyositis in North America: case reports and review. Clin Infect Dis 1992;15:668-77.
    Abstract/FREE Full Text
  6. ↵
    1. Ruiz ME,
    2. Yohannes S,
    3. Wladyka CG
    . Pyomyositis caused by methicillin-resistant Staphylococcus aureus. N Engl J Med 2005;352:1488-9.
    CrossRefMedlineWeb of Science
  7. ↵
    1. Evans JA,
    2. Ewald MB
    . Pyomyositis: a fatal case in a healthy teenager. Pediatr Emerg Care 2005;21:375-7.
    CrossRefMedlineWeb of Science
  8. ↵
    1. Adams EM,
    2. Gudmundsson S,
    3. Yocum DE,
    4. Haselby RC,
    5. Craig WA,
    6. Sundstrom WR
    . Streptococcal myositis. Arch Intern Med 1985;145:1020-3.
    Abstract/FREE Full Text
  9. ↵
    1. Adamski GB,
    2. Garin EH,
    3. Ballinger WE,
    4. Shulman ST
    . Generalized nonsuppurative myositis with staphylococcal septicemia. J Pediatr 1980;96:694-7.
    CrossRefMedlineWeb of Science
  10. ↵
    1. Kaplan SL,
    2. Hulten KG,
    3. Hammerman WA,
    4. et al
    . Three-year surveillance of community-acquired Staphylococcus aureus infections in children. Clin Infect Dis 2005;40:1785-91.
    Abstract/FREE Full Text
  11. ↵
    1. Avalos-Mishaan AM,
    2. Mason EO,
    3. Martinez-Aguilar G,
    4. et al
    . Emergence of a predominant clone of community-acquired Staphylococcus aureus among children in Houston, Texas. Pediatr Infect Dis J 2005;24:201-6.
    CrossRefMedlineWeb of Science
  12. ↵
    1. McDougal LK,
    2. Steward CD,
    3. Killgore GE,
    4. Chaitram JM,
    5. McAllister SK,
    6. Tenover FC
    . Pulse-field gel electrophoresis typing of oxacillin-resistant Staphylococcus aureus isolates from the United States: establishing a national database. J Clin Microbiol 2003;41:5113-20.
    Abstract/FREE Full Text
  13. ↵
    1. Gonzalez BE,
    2. Hulten KG,
    3. Dishop MK,
    4. et al
    . Pulmonary manifestations in children with invasive community-acquired Staphylococcus aureus infection. Clin Infect Dis 2005;41:583-90.
    Abstract/FREE Full Text
  14. ↵
    1. Lina G,
    2. Piemont Y,
    3. Godail-Gamot F,
    4. et al
    . Involvement of Panton-Valentine leukocidin-producing Staphylococcus aureus in primary skin infections and pneumonia. Clin Infect Dis 1999;29:1128-32.
    Abstract/FREE Full Text
    1. Diep BA,
    2. Sensabaugh GF,
    3. Somboona NS,
    4. Carleton HA,
    5. Perdreau-Remington F
    . Widespread skin and soft tissue infections due to two methicillin-resistant Staphylococcus aureus strains harboring genes for Panton-Valentine leukocidin. J Clin Microbiol 2004;42:2080-4.
    Abstract/FREE Full Text
  16. ↵
    1. Martinez-Aguilar G,
    2. Avalos-Mishaan A,
    3. Hulten K,
    4. Hammerman W,
    5. Mason EO,
    6. Kaplan SL
    . Community-acquired, methicillin-resistant Staphylococcus aureus musculoskeletal infections in children. Pediatr Infect Dis J 2004;23:701-6.
    MedlineWeb of Science
  17. ↵
    1. Sinha B,
    2. Francois P,
    3. Que YA,
    4. et al
    . Heterologously expressed Staphylococcus aureus fibronectin-binding proteins are sufficient for invasion of host cells. Infect Immun 2000;68:6871-8.
    Abstract/FREE Full Text
    1. Palmqvist N,
    2. Foster T,
    3. Fitzgerald JR,
    4. Josefsson E,
    5. Tarkowski A
    . Fibronectin-binding proteins and fibrinogen-binding clumping factors play distinct roles in Staphylococcus arthritis and systemic inflammation. J Infect Dis 2005;191:791-8.
    Abstract/FREE Full Text
  19. ↵
    1. Mongodin E,
    2. Bajolet O,
    3. Cutrona J,
    4. et al
    . Fibronectin-binding proteins of Staphylococcus aureus are involved in adherence to human airway epithelium. Infect Immun 2002;70:620-30.
    Abstract/FREE Full Text
  20. ↵
    CLSI. Performance standards for antimicrobial disk susceptibility testing: 15th informational supplement. Wayne, PA: CLSI; 2005.
  21. ↵
    1. Okuma K,
    2. Iwakawa K,
    3. Turnidge JD,
    4. et al
    . Dissemination of new methicillin-resistant Staphylococcus aureus clones in the community. J Clin Microbiol 2002;40:4289-94.
    Abstract/FREE Full Text
  22. ↵
    1. Hulten KG,
    2. Kaplan SL,
    3. Gonzalez BE,
    4. et al
    . Three-year surveillance of community onset health care-associated Staphylococcus aureus infections in children. Pediatr Infect Dis J 2006;25:349-53.
    CrossRefMedlineWeb of Science
  23. ↵
    1. Sirinavin S,
    2. McCracken GH
    . Primary suppurative myositis in children. Am J Dis Child 1979;133:263-5.
    Abstract/FREE Full Text
    1. Spiegel DA,
    2. Meyer JS,
    3. Dormans JP,
    4. Flynn JM,
    5. Drummond DS
    . Pyomyositis in children and adolescents: report of 12 cases and review of the literature. J Pediatr Orthop 1999;19:143-50.
    CrossRefMedlineWeb of Science
  25. ↵
    1. Gubbay AJ,
    2. Isaacs D
    . Pyomyositis in children. Pediatr Infect Dis J 2000;19:1009-13.
    CrossRefMedlineWeb of Science
  26. ↵
    1. Buckingham SC,
    2. McDougal LK,
    3. Cathey LD,
    4. et al
    . Emergence of community-associated methicillin-resistant Staphylococcus aureus at a Memphis, Tennessee Children's Hospital. Pediatr Infect Dis J 2004;23:619-24.
    MedlineWeb of Science
    1. Miller LG,
    2. Perdreau-Remington F,
    3. Rieg G,
    4. et al
    . Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureus in Los Angeles. N Engl J Med 2005;352:1445-53.
    CrossRefMedlineWeb of Science
  28. ↵
    1. Biep BA,
    2. Gill AR,
    3. Chang RF,
    4. et al
    . Complete genome sequence of USA300, an epidemic clone of community-acquired methicillin-resistant Staphylococcus aureus. Lancet 2006;367:731-9.
    CrossRefMedlineWeb of Science
  29. ↵
    1. Panton PN,
    2. Valentine FCO
    . Staphylococcal toxin. Lancet 1932;i:506-8.
  30. ↵
    1. Genestier AL,
    2. Michallet MC,
    3. Prevost G,
    4. et al
    . Staphylococcus aureus Panton-Valentine leukocidin directly targets mitochondria and induces Bax-independent apoptosis of human neutrophils. J Clin Invest 2005;115:3117-27.
    CrossRefMedlineWeb of Science
  31. ↵
    1. Baggett HC,
    2. Hennessey TW,
    3. Rudolph K,
    4. et al
    . Community-onset methicillin resistant Staphylococcus aureus associated with antibiotic use and the cytotoxin Panton-Valentine leukocidin during a furunculosis outbreak in rural Alaska. J Infect Dis 2004;189:1565-73.
    Abstract/FREE Full Text
  32. ↵
    1. Yamasaki O,
    2. Kaneko J,
    3. Morizane S,
    4. et al
    . The association between Staphylococcus aureus strains carrying Panton-Valentine leucocidin genes and the development of deep-seated follicular infection. Clin Infect Dis 2005;40:381-5.
    Abstract/FREE Full Text
  33. ↵
    1. Bocchini CE,
    2. Hulten KG,
    3. Mason EO,
    4. Gonzalez BE,
    5. Hammerman WA,
    6. Kaplan SL
    . Panton-Valentine leukocidin genes are associated with enhanced inflammatory response and local disease in acute Staphylococcus aureus osteomyelitis in children. Pediatrics 2006;117:433-40.
    Abstract/FREE Full Text
  34. ↵
    1. Miyake H
    . Beitrage zur kenntnis der sogenannten myositis infectiosa. Mitt Grenageb Med Chir 1904;13:155-98.
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  1. Clin Infect Dis. (2006) 43 (8): 953-960. doi: 10.1086/507637
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