CHRONIC Staphylococcus aureus infection - 2014 jan31 - VRSA

50 %
50 %
Information about CHRONIC Staphylococcus aureus infection - 2014 jan31 - VRSA
Health & Medicine

Published on March 3, 2014

Author: necrotonic90



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:

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 Show All 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 firstgeneration 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 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

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

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. References 1. McNamara D. Vancomycin dosing nomograms inadequate for tweens and teens. Medscape Medical News [serial online]. January 13, 2014;Accessed January 20, 2014. Available at 2. Gillon JE, Cassat JE, Di Pentima MC. Validation of two vancomycin nomograms in patients 10 years of age and older. J Clin Pharmacol. Jan 2014;54(1):35-8. [Medline]. 3. Jamal N, Teach SJ. Necrotizing fasciitis. Pediatr Emerg Care. Dec 2011;27(12):1195-9; quiz 1200-2. [Medline]. 4. Jaramillo D. Infection: musculoskeletal. Pediatr Radiol. May 2011;41 Suppl 1:S127-34. [Medline]. 5. Chou H, Teo HE, Dubey N, Peh WC. Tropical pyomyositis and necrotizing fasciitis. Semin Musculoskelet Radiol. Nov 2011;15(5):489-505. [Medline].

6. Lane JW, Tang J, Taggard D, Byun R. Successful use of daptomycin and linezolid, without surgical intervention, in the treatment of extensive epidural abscess and bacteremia due to methicillin-resistant Staphylococcus aureus (MRSA). Infect Dis Clin Pract. Sept 2011;19(5):362-364. 7. Abdel-Haq N, Quezada M, Asmar BI. Retropharyngeal Abscess in Children: The Rising Incidence of Methicillin-Resistant Staphylococcus aureus. Pediatr Infect Dis J. Jul 2012;31(7):696-9. [Medline]. 8. McNeil JC, Hulten KG, Kaplan SL, Mahoney DH, Mason EO. Staphylococcus aureus Infections in Pediatric Oncology Patients: High Rates of Antimicrobial Resistance, Antiseptic Tolerance and Complications. Pediatr Infect Dis J. Sep 11 2012;[Medline]. 9. Elliott DJ, Zaoutis TE, Troxel AB, Loh A, Keren R. Empiric Antimicrobial Therapy for Pediatric Skin and Soft-Tissue Infections in the Era of Methicillin-Resistant Staphylococcus aureus. Pediatrics. Jun 2009;123(6):e959-66. [Medline]. 10. Lee S, Choe PG, Song KH, Park SW, Kim HB, Kim NJ, et al. Is cefazolin inferior to nafcillin for treatment of methicillin-susceptible Staphylococcus aureus bacteremia?. Antimicrob Agents Chemother. Nov 2011;55(11):5122-6. [Medline]. [Full Text]. 11. Williams DJ, Cooper WO, Kaltenbach LA, Dudley JA, Kirschke DL, Jones TF, et al. Comparative Effectiveness of Antibiotic Treatment Strategies for Pediatric Skin and SoftTissue Infections. Pediatrics. Aug 15 2011;[Medline]. 12. [Best Evidence] [Guideline] Liu C, Bayer A, Cosgrove SE, et al. Clinical Practice Guidelines by the Infectious Diseases Society of America for the Treatment of Methicillin-Resistant Staphylococcus Aureus Infections in Adults and Children. Clin Infect Dis. Feb 1 2011;52(3):e18-e55. [Medline]. 13. Kemper AR, Dolor RJ, Fowler VG Jr. Management of skin abscesses by primary care pediatricians. Clin Pediatr (Phila). Jun 2011;50(6):525-8. [Medline]. 14. Sreeramoju P, Porbandarwalla NS, Arango J, Latham K, Dent DL, Stewart RM, et al. Recurrent skin and soft tissue infections due to methicillin-resistant Staphylococcus aureus requiring operative debridement. Am J Surg. Feb 2011;201(2):216-20. [Medline]. 15. Pääkkönen M, Kallio PE, Kallio MJ, Peltola H. Management of Osteoarticular Infections Caused by Staphylococcus aureus Is Similar to That of Other Etiologies: Analysis of 199 Staphylococcal Bone and Joint Infections. Pediatr Infect Dis J. May 2012;31(5):436-8. [Medline]. 16. Boggs W. Daptomycin Treats S. aureus Bacteremia Without Nephrotoxicity. Medscape Medical News. January 8, 2013. Available at Accessed January 15, 2013. 17. von Eiff C, Becker K, Machka K, Stammer H, Peters G. Nasal carriage as a source of Staphylococcus aureus bacteremia. Study Group. N Engl J Med. Jan 4 2001;344(1):11-6. [Medline].

18. van Belkum A, Verkaik NJ, de Vogel CP, Boelens HA, Verveer J, Nouwen JL. Reclassification of Staphylococcus aureus Nasal Carriage Types. J Infect Dis. Jun 15 2009;199(12):1820-6. [Medline]. 19. Wenzel RP, Perl TM. The significance of nasal carriage of Staphylococcus aureus and the incidence of postoperative wound infection. J Hosp Infect. Sep 1995;31(1):13-24. [Medline]. 20. Ruimy R, Angebault C, Djossou F, et al. Are host genetics the predominant determinant of persistent nasal Staphylococcus aureus carriage in humans?. J Infect Dis. Sep 15 2010;202(6):924-34. [Medline]. 21. Chen CJ, Hsu KH, Lin TY, Hwang KP, Chen PY, Huang YC. Factors associated with nasal colonization of methicillin-resistant Staphylococcus aureus among healthy children in Taiwan. J Clin Microbiol. Jan 2011;49(1):131-7. [Medline]. [Full Text]. 22. Nerby JM, Gorwitz R, Lesher L, Juni B, Jawahir S, Lynfield R. Risk Factors for Household Transmission of Community-associated Methicillin-resistant Staphylococcus aureus. Pediatr Infect Dis J. Nov 2011;30(11):927-32. [Medline]. 23. Fritz SA, Krauss MJ, Epplin EK, Burnham CA, Garbutt J, Dunne WM, et al. The natural history of contemporary Staphylococcus aureus nasal colonization in community children. Pediatr Infect Dis J. Apr 2011;30(4):349-51. [Medline]. [Full Text]. 24. Gesualdo F, Bongiorno D, Rizzo C, Bella A, Menichella D, Stefani S, et al. MRSA Nasal Colonization in Children: Prevalence Meta-Analysis, Review of Risk Factors and Molecular Genetics. Pediatr Infect Dis J. Jan 21 2013;[Medline]. 25. Peters PJ, Brooks JT, McAllister SK, Limbago V, Lowery HK, Fosheim G, et al. Methicillin-resistant Staphylococcus aureus colonization of the groin and risk for clinical infection among HIV-infected adults. Emerg Infect Dis. April 2013;19(4):623-629. 26. Faden H, Lesse AJ, Trask J, Hill JA, Hess DJ, Dryja D. Importance of Colonization Site in the Current Epidemic of Staphylococcal Skin Abscesses. Pediatrics. Feb 15 2010;[Medline]. 27. Lee CJ, Sankaran S, Mukherjee DV, Apa ZL, Hafer CA, Wright L. Staphylococcus aureus oropharyngeal carriage in a prison population. Clin Infect Dis. Mar 15 2011;52(6):775-8. [Medline]. 28. Nowrouzian FL, Dauwalder O, Meugnier H, Bes M, Etienne J, Vandenesch F, et al. Adhesin and Superantigen Genes and the Capacity of Staphylococcus aureus to Colonize the Infantile Gut. J Infect Dis. Sep 2011;204(5):714-21. [Medline]. 29. Milstone AM, Song X, Coffin S, Elward A. Identification and eradication of methicillinresistant Staphylococcus aureus colonization in the neonatal intensive care unit: results of a national survey. Infect Control Hosp Epidemiol. Jul 2010;31(7):766-8. [Medline]. [Full Text].

30. Nakamura MM, McAdam AJ, Sandora TJ, Moreira KR, Lee GM. Higher prevalence of pharyngeal than nasal Staphylococcus aureus carriage in pediatric intensive care units. J Clin Microbiol. Aug 2010;48(8):2957-9. [Medline]. 31. Matheson EM, Mainous AG 3rd, Everett CJ, King DE. Tea and coffee consumption and MRSA nasal carriage. Ann Fam Med. Jul-Aug 2011;9(4):299-304. [Medline]. 32. Zanger P, Nurjadi D, Gaile M, Gabrysch S, Kremsner PG. Hormonal Contraceptive Use and Persistent Staphylococcus aureus Nasal Carriage. Clin Infect Dis. Dec 2012;55(12):1625-32. [Medline]. 33. Bartlett AH, Hulten KG. Staphylococcus aureus pathogenesis: secretion systems, adhesins, and invasins. Pediatr Infect Dis J. Sep 2010;29(9):860-1. [Medline]. 34. Tuchscherr L, Heitmann V, Hussain M, Viemann D, Roth J, von Eiff C, et al. Staphylococcus aureus small-colony variants are adapted phenotypes for intracellular persistence. J Infect Dis. Oct 1 2010;202(7):1031-40. [Medline]. 35. Verkaik NJ, Dauwalder O, Antri K, Boubekri I, de Vogel CP, Badiou C. Immunogenicity of toxins during Staphylococcus aureus infection. Clin Infect Dis. Jan 1 2010;50(1):61-8. [Medline]. 36. Aalfs AS, Oktarina DA, Diercks GF, Jonkman MF, Pas HH. Staphylococcal scalded skin syndrome: loss of desmoglein 1 in patient skin. Eur J Dermatol. Jul-Aug 2010;20(4):4516. [Medline]. 37. Bassetti M, Nicco E, Mikulska M. Why is community-associated MRSA spreading across the world and how will it change clinical practice?. Int J Antimicrob Agents. Jul 2009;34 Suppl 1:S15-9. [Medline]. 38. David MZ, Daum RS. Community-associated methicillin-resistant Staphylococcus aureus: epidemiology and clinical consequences of an emerging epidemic. Clin Microbiol Rev. Jul 2010;23(3):616-87. [Medline]. 39. Pickett A, Wilkinson M, Menoch M, Snell J, Yniguez R, Bulloch B. Changing incidence of methicillin-resistant staphylococcus aureus skin abscesses in a pediatric emergency department. Pediatr Emerg Care. Dec 2009;25(12):831-4. [Medline]. 40. Kairam N, Silverman ME, Salo DF, Baorto E, Lee B, Amato CS. Cutaneous MethicillinResistant Staphylococcus aureus in a Suburban Community Hospital Pediatric Emergency Department. J Emerg Med. Nov 2011;41(5):460-5. [Medline]. 41. Boucher HW, Corey GR. Epidemiology of methicillin-resistant Staphylococcus aureus. Clin Infect Dis. Jun 1 2008;46 Suppl 5:S344-9. [Medline]. 42. Tenover FC, Goering RV. Methicillin-resistant Staphylococcus aureus strain USA300: origin and epidemiology. J Antimicrob Chemother. Sep 2009;64(3):441-6. [Medline]. 43. Talan DA, Krishnadasan A, Gorwitz RJ, Fosheim GE, Limbago B, Albrecht V, et al. Comparison of Staphylococcus aureus From Skin and Soft-Tissue Infections in US

Emergency Department Patients, 2004 and 2008. Clin Infect Dis. Jul 2011;53(2):144-149. [Medline]. 44. Long CB, Madan RP, Herold BC. Diagnosis and management of community-associated MRSA infections in children. Expert Rev Anti Infect Ther. Feb 2010;8(2):183-95. [Medline]. 45. Lowy FD. How Staphylococcus aureus adapts to its host. N Engl J Med. May 26 2011;364(21):1987-90. [Medline]. 46. Hay R, Noor NM. Panton-Valentine leucocidin and severe Staphylococcus aureus infections of the skin: sole culprit or does it have accomplices?. Curr Opin Infect Dis. Apr 2011;24(2):97-9. [Medline]. 47. Ritz N, Curtis N. The Role of Panton-Valentine Leukocidin in Staphylococcus aureus Musculoskeletal Infections in Children. Pediatr Infect Dis J. May 2012;31(5):514-8. [Medline]. 48. Mendes RE, Deshpande LM, Smyth DS, Shopsin B, Farrell DJ, Jones RN. Characterization of methicillin-resistant Staphylococcus aureus strains recovered from a phase IV clinical trial for linezolid versus vancomycin for treatment of nosocomial pneumonia. J Clin Microbiol. Nov 2012;50(11):3694-702. [Medline]. [Full Text]. 49. Hermos CR, Yoong P, Pier GB. High levels of antibody to panton-valentine leukocidin are not associated with resistance to Staphylococcus aureus-associated skin and softtissue infection. Clin Infect Dis. Nov 15 2010;51(10):1138-46. [Medline]. 50. Grundmeier M, Tuchscherr L, Bruck M, Viemann D, Roth J, Willscher E. Staphylococcal strains vary greatly in their ability to induce an inflammatory response in endothelial cells. J Infect Dis. Mar 15 2010;201(6):871-80. [Medline]. 51. Strandberg KL, Rotschafer JH, Vetter SM, Buonpane RA, Kranz DM, Schlievert PM. Staphylococcal superantigens cause lethal pulmonary disease in rabbits. J Infect Dis. Dec 1 2010;202(11):1690-7. [Medline]. 52. Li M, Cheung GY, Hu J, Wang D, Joo HS, Deleo FR, et al. Comparative analysis of virulence and toxin expression of global community-associated methicillin-resistant Staphylococcus aureus strains. J Infect Dis. Dec 15 2010;202(12):1866-76. [Medline]. 53. Torres VJ, Stauff DL, Pishchany G, Bezbradica JS, Gordy LE, Iturregui J, et al. A Staphylococcus aureus regulatory system that responds to host heme and modulates virulence. Cell Host Microbe. Apr 19 2007;1(2):109-19. [Medline]. [Full Text]. 54. Pishchany G, McCoy AL, Torres VJ, Krause JC, Crowe JE Jr, Fabry ME, et al. Specificity for human hemoglobin enhances Staphylococcus aureus infection. Cell Host Microbe. Dec 16 2010;8(6):544-50. [Medline]. [Full Text]. 55. Kobayashi SD, Malachowa N, Whitney AR, Braughton KR, Gardner DJ, Long D, et al. Comparative Analysis of USA300 Virulence Determinants in a Rabbit Model of Skin and Soft Tissue Infection. J Infect Dis. Sep 2011;204(6):937-41. [Medline]. [Full Text].

56. Hota B, Lyles R, Rim J, Popovich KJ, Rice T, Aroutcheva A. Predictors of clinical virulence in community-onset methicillin-resistant Staphylococcus aureus infections: the importance of USA300 and pneumonia. Clin Infect Dis. Oct 2011;53(8):757-65. [Medline]. 57. Peyrani P, Allen M, Wiemken TL, Haque NZ, Zervos MJ, Ford KD, et al. Severity of disease and clinical outcomes in patients with hospital-acquired pneumonia due to methicillin-resistant Staphylococcus aureus strains not influenced by the presence of the Panton-Valentine Leukocidin gene. Clin Infect Dis. Oct 2011;53(8):766-71. [Medline]. 58. Kebaier C, Chamberland RR, Allen IC, Gao X, Broglie PM, Hall JD. Staphylococcus aureus a-Hemolysin Mediates Virulence in a Murine Model of Severe Pneumonia Through Activation of the NLRP3 Inflammasome. J Infect Dis. Mar 2012;205(5):807-17. [Medline]. 59. Rudkin JK, Edwards AM, Bowden MG, Brown EL, Pozzi C, Waters EM. Methicillin Resistance Reduces the Virulence of Healthcare-Associated Methicillin-Resistant Staphylococcus aureus by Interfering With the agr Quorum Sensing System. J Infect Dis. Mar 2012;205(5):798-806. [Medline]. 60. Sharma-Kuinkel BK, Ahn SH, Rude TH, Zhang Y, Tong SY, Ruffin F, et al. Presence of genes encoding panton-valentine leukocidin is not the primary determinant of outcome in patients with hospital-acquired pneumonia due to Staphylococcus aureus. J Clin Microbiol. Mar 2012;50(3):848-56. [Medline]. [Full Text]. 61. Soong G, Chun J, Parker D, Prince A. Staphylococcus aureus Activation of Caspase 1/Calpain Signaling Mediates Invasion Through Human Keratinocytes. J Infect Dis. May 2012;205(10):1571-9. [Medline]. 62. Otto M. How Staphylococcus aureus Breaches Our Skin to Cause Infection. J Infect Dis. May 2012;205(10):1483-5. [Medline]. 63. Wehrhahn MC, Robinson JO, Pascoe EM, Coombs GW, Pearson JC, O'Brien FG. Illness Severity in Community-Onset Invasive Staphylococcus aureus Infection and the Presence of Virulence Genes. J Infect Dis. Jun 2012;205(12):1840-8. [Medline]. 64. Garofalo A, Giai C, Lattar S, Gardella N, Mollerach M, Kahl BC. The Length of the Staphylococcus aureus Protein A Polymorphic Region Regulates Inflammation: Impact on Acute and Chronic Infection. J Infect Dis. Jul 2012;206(1):81-90. [Medline]. 65. Shallcross LJ, Fragaszy E, Johnson AM, Hayward AC. The role of the Panton-Valentine leucocidin toxin in staphylococcal disease: a systematic review and meta-analysis. Lancet Infect Dis. Jan 2013;13(1):43-54. [Medline]. [Full Text]. 66. Suryadevara M, Clark AE, Wolk DM, Carman A, Rosenbaum PF. Molecular characterization of invasive Staphylococcus aureus infection in central New York children: importance of two clonal groups and inconsistent presence of selected virulence determinants. J Pediatr Infect Dis Soc. March 2013;2(1):30-39.

67. Schneider-Lindner V, Quach C, Hanley JA, Suissa S. Antibacterial Drugs and the Risk of Community-Associated Methicillin-Resistant Staphylococcus aureus in Children. Arch Pediatr Adolesc Med. Aug 1 2011;[Medline]. 68. Smith TL, Pearson ML, Wilcox KR, et al. Emergence of vancomycin resistance in Staphylococcus aureus. Glycopeptide-Intermediate Staphylococcus aureus Working Group. N Engl J Med. Feb 18 1999;340(7):493-501. [Medline]. 69. Zheng X, Qi C, Arrieta M, O'Leary A, Wang D, Shulman ST. Lack of increase in vancomycin resistance of pediatric methicillin-resistant Staphylococcus aureus Isolates from 2000 to 2007. Pediatr Infect Dis J. Sep 2010;29(9):882-4. [Medline]. 70. Cameron DR, Ward DV, Kostoulias X, Howden BP, Moellering RC Jr, Eliopoulos GM. Serine/Threonine Phosphatase Stp1 Contributes to Reduced Susceptibility to Vancomycin and Virulence in Staphylococcus aureus. J Infect Dis. Jun 2012;205(11):1677-87. [Medline]. 71. Cheung A, Duclos B. Stp1 and Stk1: The Yin and Yang of Vancomycin Sensitivity and Virulence in Vancomycin-Intermediate Staphylococcus aureus Strains. J Infect Dis. Jun 2012;205(11):1625-7. [Medline]. 72. Shore AC, Deasy EC, Slickers P, et al. Detection of Staphylococcal Cassette Chromosome mec Type XI Encoding Highly Divergent mecA, mecI, mecR1, blaZ and ccr Genes in Human Clinical Clonal Complex 130 Methicillin-Resistant Staphylococcus aureus. Antimicrob Agents Chemother. Jun 2 2011;[Medline]. 73. García-Álvarez L, Holden MT, Lindsay H, et al. Meticillin-resistant Staphylococcus aureus with a novel mecA homologue in human and bovine populations in the UK and Denmark: a descriptive study. Lancet Infect Dis. Jun 2 2011;[Medline]. 74. Cameron DR, Howden BP, Peleg AY. The interface between antibiotic resistance and virulence in Staphylococcus aureus and its impact upon clinical outcomes. Clin Infect Dis. Sep 2011;53(6):576-82. [Medline]. 75. [Guideline] CDC. Interim guidelines for prevention and control of Staphylococcal infection associated with reduced susceptibility to vancomycin. MMWR Morb Mortal Wkly Rep. Jul 11 1997;46(27):626-8, 635. [Medline]. 76. Iwamoto M, Mu Y, Lynfield R, Bulens SN, Nadle J, Aragon D, et al. Trends in Invasive Methicillin-Resistant Staphylococcus aureus Infections. Pediatrics. Oct 2013;132(4):e817-e824. [Medline]. 77. Laidman J. Community-Associated MRSA Incidence on the Rise in Children. Medscape [serial online]. Available at Accessed September 30, 2013. 78. Helwick C. MRSA Rising in Children With Musculoskeletal Infections. Medscape [serial online]. Available at Accessed November 4, 2013.

79. Saravolatz LD, Pawlak J, Johnson LB. In vitro susceptibilities and molecular analysis of vancomycin-intermediate and vancomycin-resistant Staphylococcus aureus isolates. Clin Infect Dis. Aug 2012;55(4):582-6. [Medline]. 80. Frei CR, Makos BR, Daniels KR, Oramasionwu CU. Emergence of community-acquired methicillin-resistant Staphylococcus aureus skin and soft tissue infections as a common cause of hospitalization in United States children. J Pediatr Surg. Oct 2010;45(10):196774. [Medline]. 81. Hadler JL, Petit S, Mandour M, Cartter ML. Trends in Invasive Infection with Methicillin-Resistant Staphylococcus aureus, Connecticut, USA, 2001-2010. Emerg Infect Dis. Jun 2012;18(6):917-24. [Medline]. [Full Text]. 82. Suryadevara M, Moro MR, Rosenbaum PF, Kiska D, Riddell S, Weiner LB. Incidence of invasive community-onset Staphylococcus aureus infections in children in Central New York. J Pediatr. Jan 2010;156(1):152-154.e1. [Medline]. 83. Landrum ML, Neumann C, Cook C, Chukwuma U, Ellis MW, Hospenthal DR. Epidemiology of Staphylococcus aureus Blood and Skin and Soft Tissue Infections in the US Military Health System, 2005-2010Staphylococcus aureus in US Military. JAMA. Jul 4 2012;308(1):50-9. [Medline]. 84. Hsiang MS, Shiau R, Nadle J, Chan L, Lee B, Chambers HF, et al. Epidemiologic similarities in pediatric community-associated methicillin-resistant and methicillinsensitive Staphylococcus aureus in the San Francisco Bay area. J Pediatr Infect Dis Soc. September 2012;1(3):200-211. 85. Reyes J, Rincon S, Diaz L, et al. Dissemination of methicillin-resistant Staphylococcus aureus USA300 sequence type 8 lineage in Latin America. Clin Infect Dis. Dec 15 2009;49(12):1861-7. [Medline]. [Full Text]. 86. Saxena S, Thompson P, Birger R, Bottle A, Spyridis N, Wong I. Increasing Skin Infections and Staphylococcus aureus Complications in Children, England, 1997-2006. Emerg Infect Dis. Mar 2010;16(3):530-533. [Medline]. 87. Otter JA, French GL. Molecular epidemiology of community-associated meticillinresistant Staphylococcus aureus in Europe. Lancet Infect Dis. Apr 2010;10(4):227-239. [Medline]. 88. Lessa FC, Mu Y, Davies J, Murray M, Lillie M, Pearson A. Comparison of incidence of bloodstream infection with methicillin-resistant Staphylococcus aureus between England and United States, 2006-2007. Clin Infect Dis. Oct 15 2010;51(8):925-8. [Medline]. 89. Golding GR, Levett PN, McDonald RR, Irvine J, Quinn B, Nsungu M. High rates of Staphylococcus aureus USA400 infection, Northern Canada. Emerg Infect Dis. Apr 2011;17(4):722-5. [Medline]. 90. Golding GR, Levett PN, McDonald RR, Irvine J, Nsungu M, Woods S, et al. A comparison of risk factors associated with community-associated methicillin-resistant

and -susceptible Staphylococcus aureus infections in remote communities. Epidemiol Infect. May 2010;138(5):730-7. [Medline]. 91. Kim J, Ferrato C, Golding GR, Mulvey MR, Simmonds KA, Svenson LW, et al. Changing epidemiology of methicillin-resistant Staphylococcus aureus in Alberta, Canada: population-based surveillance, 2005-2008. Epidemiol Infect. Sep 21 2010;1-10. [Medline]. 92. Matlow A, Forgie S, Pelude L, Embree J, Gravel D, Langley JM, et al. National surveillance of methicillin-resistant Staphylococcus aureus among hospitalized pediatric patients in Canadian acute care facilities, 1995-2007. Pediatr Infect Dis J. Aug 2012;31(8):814-20. [Medline]. 93. Alesana-Slater J, Ritchie SR, Heffernan H, Camp T, Richardson A, Herbison P. Methicillin-resistant Staphylococcus aureus, Samoa, 2007-2008. Emerg Infect Dis. Jun 2011;17(6):1023-9. [Medline]. 94. Suzuki M, Yamada K, Nagao M, Aoki E, Matsumoto M, Hirayama T, et al. Antimicrobial Ointments and Methicillin-Resistant Staphylococcus aureus USA300. Emerg Infect Dis. Oct 2011;17(10):1917-20. [Medline]. 95. Tong SY, Bishop EJ, Lilliebridge RA, et al. Community-associated strains of methicillinresistant Staphylococcus aureus and methicillin-susceptible S. aureus in indigenous Northern Australia: epidemiology and outcomes. J Infect Dis. May 15 2009;199(10):1461-70. [Medline]. 96. Salmenlinna S, Lyytikainen O, Vainio A, Myllyniemi AL, Raulo S, Kanerva M, et al. Human Cases of Methicillin-Resistant Staphylococcus aureus CC398, Finland. Emerg Infect Dis. Oct 2010;16(10):1626-9. [Medline]. 97. Tappe D, Schulze MH, Oesterlein A, Turnwald D, Müller A, Vogel U, et al. PantonValentine leukocidin-positive Staphylococcus aureus infections in returning travelers. Am J Trop Med Hyg. Oct 2010;83(4):748-50. [Medline]. [Full Text]. 98. Chua K, Laurent F, Coombs G, Grayson ML, Howden BP. Not Community-Associated Methicillin-Resistant Staphylococcus aureus (CA-MRSA)! A Clinician's Guide to Community MRSA - Its Evolving Antimicrobial Resistance and Implications for Therapy. Clin Infect Dis. Jan 2011;52(1):99-114. [Medline]. 99. Nickerson EK, Wuthiekanun V, Kumar V, Amornchai P, Wongdeethai N, Chheng K. Emergence of Community-Associated Methicillin-Resistant Staphylococcus aureus Carriage in Children in Cambodia. Am J Trop Med Hyg. Feb 2011;84(2):313-7. [Medline]. 100. Hamdan-Partida A, Sainz-Espuñes T, Bustos-Martínez J. Characterization and persistence of Staphylococcus aureus strains isolated from the anterior nares and throats of healthy carriers in a Mexican community. J Clin Microbiol. May 2010;48(5):1701-5. [Medline].

101. Muttaiyah S, Coombs G, Pandey S, Reed P, Ritchie S, Lennon D, et al. Incidence, risk factors, and outcomes of Panton-Valentine leukocidin-positive methicillinsusceptible Staphylococcus aureus infections in Auckland, New Zealand. J Clin Microbiol. Oct 2010;48(10):3470-4. [Medline]. [Full Text]. 102. Adler A, Givon-Lavi N, Moses AE, Block C, Dagan R. Carriage of communityassociated methicillin-resistant Staphylococcus aureus in a cohort of infants in southern Israel: risk factors and molecular features. J Clin Microbiol. Feb 2010;48(2):531-8. [Medline]. [Full Text]. 103. Vaska VL, Grimwood K, Gole GA, Nimmo GR, Paterson DL, Nissen MD. Community-associated Methicillin-resistant Staphylococcus aureus Causing Orbital Cellulitis in Australian Children. Pediatr Infect Dis J. Nov 2011;30(11):1003-1006. [Medline]. 104. Marra F, Patrick DM, Chong M, McKay R, Hoang L, Bowie WR. Populationbased study of the increased incidence of skin and soft tissue infections and associated antimicrobial use. Antimicrob Agents Chemother. Dec 2012;56(12):6243-9. [Medline]. [Full Text]. 105. Jenkins TC, Sabel AL, Sarcone EE, Price CS, Mehler PS, Burman WJ. Skin and soft-tissue infections requiring hospitalization at an academic medical center: opportunities for antimicrobial stewardship. Clin Infect Dis. Oct 15 2010;51(8):895-903. [Medline]. 106. Spellberg B. Skin and soft-tissue infections: modern evolution of an ancient problem. Clin Infect Dis. Oct 15 2010;51(8):904-6. [Medline]. [Full Text]. 107. Carrillo-Marquez MA, Hulten KG, Hammerman W, Lamberth L, Mason EO, Kaplan SL. Staphylococcus aureus Pneumonia in Children in the Era of Communityacquired Methicillin-resistance at Texas Children's Hospital. Pediatr Infect Dis J. Jul 2011;30(7):545-50. [Medline]. 108. Vander Have KL, Karmazyn B, Verma M, Caird MS, Hensinger RN, Farley FA. Community-associated methicillin-resistant Staphylococcus aureus in acute musculoskeletal infection in children: a game changer. J Pediatr Orthop. Dec 2009;29(8):927-31. [Medline]. 109. Fretzayas A, Moustaki M, Tsagris V, Brozou T, Nicolaidou P. MRSA blistering distal dactylitis and review of reported cases. Pediatr Dermatol. Jul-Aug 2011;28(4):4335. [Medline]. 110. Carrillo-Marquez MA, Hulten KG, Hammerman W, Mason EO, Kaplan SL. USA300 is the predominant genotype causing Staphylococcus aureus septic arthritis in children. Pediatr Infect Dis J. Dec 2009;28(12):1076-80. [Medline]. 111. Carrillo-Marquez MA, Hulten KG, Mason EO, Kaplan SL. Clinical and Molecular Epidemiology of Staphylococcus aureus Catheter-Related Bacteremia in Children. Pediatr Infect Dis J. May 2010;29(5):410-4. [Medline].

112. Jacobson JA, Kasworm E, Daly JA. Risk of developing toxic shock syndrome associated with toxic shock syndrome toxin 1 following nongenital staphylococcal infection. Rev Infect Dis. Jan-Feb 1989;11 Suppl 1:S8-13. [Medline]. 113. John CC, Niermann M, Sharon B, Peterson ML, Kranz DM, Schlievert PM. Staphylococcal toxic shock syndrome erythroderma is associated with superantigenicity and hypersensitivity. Clin Infect Dis. Dec 15 2009;49(12):1893-6. [Medline]. [Full Text]. 114. Ramirez-Schrempp D, Dorfman DH, Baker WE, Liteplo AS. Ultrasound softtissue applications in the pediatric emergency department: to drain or not to drain?. Pediatr Emerg Care. Jan 2009;25(1):44-8. [Medline]. 115. Sivitz AB, Lam SH, Ramirez-Schrempp D, Valente JH, Nagdev AD. Effect of bedside ultrasound on management of pediatric soft-tissue infection. J Emerg Med. Nov 2010;39(5):637-43. [Medline]. 116. Corey GR. Staphylococcus aureus bacteremia and endocarditis: the role of diagnostic evaluation. Infect Dis Clin Pract. 2011/09;19(5):307-312. 117. Kaasch AJ, Fowler VG Jr, Rieg S, Peyerl-Hoffmann G, Birkholz H, Hellmich M, et al. Use of a simple criteria set for guiding echocardiography in nosocomial Staphylococcus aureus bacteremia. Clin Infect Dis. Jul 1 2011;53(1):1-9. [Medline]. [Full Text]. 118. Soriano A, Mensa J. Is transesophageal echocardiography dispensable in hospitalacquired Staphylococcus aureus bacteremia?. Clin Infect Dis. Jul 1 2011;53(1):10-2. [Medline]. 119. Patel Wylie F, Kaplan SL, Mason EO, Allen CH. Needle aspiration for the etiologic diagnosis of children with cellulitis in the era of community-acquired methicillin-resistant Staphylococcus aureus. Clin Pediatr (Phila). Jun 2011;50(6):503-7. [Medline]. 120. Duong M, Markwell S, Peter J, Barenkamp S. Randomized, controlled trial of antibiotics in the management of community-acquired skin abscesses in the pediatric patient. Ann Emerg Med. May 2010;55(5):401-7. [Medline]. 121. Lee MC, Rios AM, Aten MF, Mejias A, Cavuoti D, McCracken GH Jr, et al. Management and outcome of children with skin and soft tissue abscesses caused by community-acquired methicillin-resistant Staphylococcus aureus. Pediatr Infect Dis J. Feb 2004;23(2):123-7. [Medline]. 122. Rajendran PM, Young D, Maurer T, Chambers H, Perdreau-Remington F, Ro P. Randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in a population at risk for community-acquired methicillinresistant Staphylococcus aureus infection. Antimicrob Agents Chemother. Nov 2007;51(11):4044-8. [Medline].

123. Ruhe JJ, Smith N, Bradsher RW, Menon A. Community-onset methicillinresistant Staphylococcus aureus skin and soft-tissue infections: impact of antimicrobial therapy on outcome. Clin Infect Dis. Mar 15 2007;44(6):777-84. [Medline]. 124. Karchmer AW. Staphylococcus aureus bacteremia and native valve endocarditis: the role of antimicrobial therapy. Infect Dis Clin Pract. March 2012;20(2):100-108. 125. Chen AE, Carroll KC, Diener-West M, Ross T, Ordun J, Goldstein MA, et al. Randomized controlled trial of cephalexin versus clindamycin for uncomplicated pediatric skin infections. Pediatrics. Mar 2011;127(3):e573-80. [Medline]. 126. McNamara WF, Hartin CW Jr, Escobar MA, Yamout SZ, Lau ST, Lee YH. An alternative to open incision and drainage for community-acquired soft tissue abscesses in children. J Pediatr Surg. Mar 2011;46(3):502-6. [Medline]. 127. Nailor MD, Sobel JD. Antibiotics for gram-positive bacterial infections: vancomycin, teicoplanin, quinupristin/dalfopristin, oxazolidinones, daptomycin, dalbavancin, and telavancin. Infect Dis Clin N Am. Dec 2009;23(4):965-82. 128. Thwaites GE, Edgeworth JD, Gkrania-Klotsas E, Kirby A, Tilley R, Török ME. Clinical management of Staphylococcus aureus bacteraemia. Lancet Infect Dis. Mar 2011;11(3):208-222. [Medline]. 129. Weisman LE, Thackray HM, Steinhorn RH, Walsh WF, Lassiter HA, Dhanireddy R, et al. A randomized study of a monoclonal antibody (pagibaximab) to prevent staphylococcal sepsis. Pediatrics. Aug 2011;128(2):271-9. [Medline]. 130. Jimenez-Truque N, Thomsen I, Saye E, Creech CB. Should higher vancomycin trough levels be targeted for invasive community-acquired methicillin-resistant Staphylococcus aureus infections in children?. Pediatr Infect Dis J. Apr 2010;29(4):36870. [Medline]. 131. Aguado JM, San-Juan R, Lalueza A, Sanz F, Rodríguez-Otero J, GómezGonzalez C, et al. High Vancomycin MIC and Complicated Methicillin-Susceptible Staphylococcus aureus Bacteremia. Emerg Infect Dis. Jun 2011;17(6):1099-102. [Medline]. 132. Lubin AS, Snydman DR, Ruthazer R, Bide P, Golan Y. Predicting high vancomycin minimum inhibitory concentration in methicillin-resistant Staphylococcus aureus bloodstream infections. Clin Infect Dis. Apr 15 2011;52(8):997-1002. [Medline]. 133. Kullar R, Davis SL, Levine DP, Rybak MJ. Impact of vancomycin exposure on outcomes in patients with methicillin-resistant Staphylococcus aureus bacteremia: support for consensus guidelines suggested targets. Clin Infect Dis. Apr 15 2011;52(8):975-81. [Medline]. 134. Patel N, Pai MP, Rodvold KA, Lomaestro B, Drusano GL, Lodise TP. Vancomycin: we can't get there from here. Clin Infect Dis. Apr 15 2011;52(8):969-74. [Medline].

135. van Hal SJ, Lodise TP, Paterson DL. The Clinical Significance of Vancomycin Minimum Inhibitory Concentration in Staphylococcus aureus Infections: A Systematic Review and Meta-analysis. Clin Infect Dis. Mar 2012;54(6):755-71. [Medline]. 136. Deresinski S. Methicillin-Resistant Staphylococcus aureus and Vancomycin: Minimum Inhibitory Concentration Matters. Clin Infect Dis. Mar 2012;54(6):772-4. [Medline]. 137. Wunderink RG, Niederman MS, Kollef MH, Shorr AF, Kunkel MJ, Baruch A, et al. Linezolid in Methicillin-Resistant Staphylococcus aureus Nosocomial Pneumonia: A Randomized, Controlled Study. Clin Infect Dis. Mar 2012;54(5):621-9. [Medline]. 138. Ramirez P, Fernández-Barat L, Torres A. New therapy options for MRSA with respiratory infection/pneumonia. Curr Opin Infect Dis. Apr 2012;25(2):159-65. [Medline]. 139. Morales G, Picazo JJ, Baos E, Candel FJ, Arribi A, Pelaez B. Resistance to linezolid is mediated by the cfr gene in the first report of an outbreak of linezolidresistant Staphylococcus aureus. Clin Infect Dis. Mar 15 2010;50(6):821-5. [Medline]. 140. Sanchez Garcia M, De la Torre MA, Morales G, et al. Clinical outbreak of linezolid-resistant Staphylococcus aureus in an intensive care unit. JAMA. Jun 9 2010;303(22):2260-4. [Medline]. 141. Prokocimer P, De Anda C, Fang E, Mehra P, Das A. Tedizolid phosphate vs linezolid for treatment of acute bacterial skin and skin structure infections: the ESTABLISH-1 randomized trial. JAMA. Feb 13 2013;309(6):559-69. [Medline]. 142. Prokocimer P, Bien P, Deanda C, Pillar CM, Bartizal K. In vitro activity and microbiological efficacy of tedizolid (TR-700) against Gram-positive clinical isolates from a phase 2 study of oral tedizolid phosphate (TR-701) in patients with complicated skin and skin structure infections. Antimicrob Agents Chemother. Sep 2012;56(9):460813. [Medline]. [Full Text]. 143. Saravolatz LD, Stein GE, Johnson LB. Telavancin: a novel lipoglycopeptide. Clin Infect Dis. Dec 15 2009;49(12):1908-14. [Medline]. 144. Moellering RC, Jr, Ferraro MJ. Oritavancin for the treatment of serious grampositive infections. Clin Infect Dis. April 2012 15;54(Suppl 3):S201-S243. 145. Corey GR, Wilcox M, Talbot GH, et al. Integrated analysis of CANVAS 1 and 2: phase 3, multicenter, randomized, double-blind studies to evaluate the safety and efficacy of ceftaroline versus vancomycin plus aztreonam in complicated skin and skin-structure infection. Clin Infect Dis. Sep 15 2010;51(6):641-50. [Medline]. 146. Saravolatz LD, Stein GE, Johnson LB. Ceftaroline: a novel cephalosporin with activity against methicillin-resistant Staphylococcus aureus. Clin Infect Dis. May 2011;52(9):1156-63. [Medline].

147. Gums JG. Ceftaroline fosamil: a broad-spectrum cephalosporin with methicillinresistant Staphylococcus aureus activity. Infect Dis Clin Pract. March 2012;20(2):122130. 148. Farrell DJ, Castanheira M, Mendes RE, Sader HS, Jones RN. In vitro activity of ceftaroline against multidrug-resistant Staphylococcus aureus and Streptococcus pneumoniae: a review of published studies and the AWARE Surveillance Program (2008-2010). Clin Infect Dis. Sep 2012;55 Suppl 3:S206-14. [Medline]. 149. Sader HS, Flamm RK, Farrell DJ, Jones RN. Activity analyses of staphylococcal isolates from pediatric, adult, and elderly patients: AWARE Ceftaroline Surveillance Program. Clin Infect Dis. Sep 2012;55 Suppl 3:S181-6. [Medline]. 150. Jones RN, Mendes RE, Sader HS, Castanheira M. In vitro antimicrobial findings for fusidic acid tested against contemporary (2008-2009) gram-positive organisms collected in the United States. Clin Infect Dis. Jun 2011;52 Suppl 7:S477-86. [Medline]. 151. Craft JC, Moriarty SR, Clark K, Scott D, Degenhardt TP, Still JG. A randomized, double-blind phase 2 study comparing the efficacy and safety of an oral fusidic acid loading-dose regimen to oral linezolid for the treatment of acute bacterial skin and skin structure infections. Clin Infect Dis. Jun 2011;52 Suppl 7:S520-6. [Medline]. 152. Fernandes P, Pereira D. Efforts to support the development of fusidic acid in the United States. Clin Infect Dis. Jun 2011;52 Suppl 7:S542-6. [Medline]. 153. Lee AS, Macedo-Vinas M, François P, Renzi G, Schrenzel J, Vernaz N. Impact of combined low-level mupirocin and genotypic chlorhexidine resistance on persistent methicillin-resistant Staphylococcus aureus carriage after decolonization therapy: a casecontrol study. Clin Infect Dis. Jun 15 2011;52(12):1422-30. [Medline]. 154. US Food and Drug Administration. FDA Drug Safety Communication: Serious CNS reactions possible when linezolid (Zyvox®) is given to patients taking certain psychiatric medications. Available at Accessed July 27, 2011. 155. Jain R, Kralovic SM, Evans ME, et al. Veterans Affairs initiative to prevent methicillin-resistant Staphylococcus aureus infections. N Engl J Med. Apr 14 2011;364(15):1419-30. [Medline]. 156. Robotham JV, Graves N, Cookson BD, Barnett AG, Wilson JA, Edgeworth JD. Screening, isolation, and decolonisation strategies in the control of meticillin resistant Staphylococcus aureus in intensive care units: cost effectiveness evaluation. BMJ. 2011;343:d5694. [Medline]. 157. Simor AE. Staphylococcal decolonisation: an effective strategy for prevention of infection?. Lancet Infect Dis. Dec 2011;11(12):952-62. [Medline]. 158. Fritz SA, Hogan PG, Hayek G, Eisenstein KA, Rodriguez M, Epplin EK, et al. Household Versus Individual Approaches to Eradication of Community-Associated

Staphylococcus aureus in Children: A Randomized Trial. Clin Infect Dis. Mar 2012;54(6):743-51. [Medline]. [Full Text]. 159. Miller LG. Where We Are With Community-Associated Staphylococcus aureus Prevention--And in the Meantime, What Do We Tell Our Patients?. Clin Infect Dis. Mar 2012;54(6):752-4. [Medline]. 160. Kling J. PCR screening cuts in-hospital infection. Medscape Medical News [serial online]. May 14, 2013;Accessed May 19, 2013. Available at 161. Milstone AM, Goldner BW, Ross T, Shepard JW, Carroll KC, Perl TM. Methicillin-resistant Staphylococcus aureus colonization and risk of subsequent infection in critically ill children: importance of preventing nosocomial methicillin-resistant Staphylococcus aureus transmission. Clin Infect Dis. Nov 2011;53(9):853-9. [Medline]. [Full Text]. 162. Huang SS, Septimus E, Kleinman K, Moody J, Hickok J, Avery TR, et al. Targeted versus Universal Decolonization to Prevent ICU Infection. N Engl J Med. May 29 2013;[Medline]. 163. Edmond MB, Wenzel RP. Screening Inpatients for MRSA - Case Closed. N Engl J Med. May 29 2013;[Medline]. 164. Laidman J. MRSA: Universal Decolonization Beats Screening and Isolation. Medscape Medical News. Available at Accessed June 11, 2013. 165. Shenoy ES, Kim J, Rosenberg ES, Cotter JA, Lee H, Walensky RP, et al. Discontinuation of Contact Precautions for Methicillin-Resistant Staphylococcus aureus: A Randomized Controlled Trial Comparing Passive and Active Screening With Culture and Polymerase Chain Reaction. Clin Infect Dis. Jul 2013;57(2):176-84. [Medline]. [Full Text]. 166. Lin Y-C, Peterson ML. New insights into the prevention of staphylococcal infections and toxic shock syndrome. Expert Rev Clin Pharmacol. 2010;3:753-767. 167. Huda T, Nair H, Theodoratou E, Zgaga L, Fattom A, El Arifeen S, et al. An evaluation of the emerging vaccines and immunotherapy against staphylococcal pneumonia in children. BMC Public Health. Apr 13 2011;11 Suppl 3:S27. [Medline]. [Full Text]. 168. Daum RS, Spellberg B. Progress Toward a Staphylococcus aureus Vaccine. Clin Infect Dis. Feb 2012;54(4):560-7. [Medline]. 169. Theilacker C, Kropec A, Hammer F, Sava I, Wobser D, Sakinc T. Protection Against Staphylococcus aureus by Antibody to the Polyglycerolphosphate Backbone of Heterologous Lipoteichoic Acid. J Infect Dis. Apr 2012;205(7):1076-85. [Medline]. 170. Proctor RA. Challenges for a Universal Staphylococcus aureus Vaccine. Clin Infect Dis. Apr 2012;54(8):1179-86. [Medline].

171. Anderson AS, Scully IL, Timofeyeva Y, Murphy E, McNeil LK, Mininni T, et al. Staphylococcus aureus Manganese Transport Protein C Is a Highly Conserved Cell Surface Protein That Elicits Protective Immunity Against S. aureus and Staphylococcus epidermidis. J Infect Dis. Jun 2012;205(11):1688-96. [Medline]. [Full Text]. 172. Fritz SA, Tiemann KM, Hogan PG, Epplin EK, Rodriguez M, Al-Zubeidi DN, et al. A Serologic Correlate of Protective Immunity Against Community-Onset Staphylococcus aureus Infection. Clin Infect Dis. Jun 2013;56(11):1554-61. [Medline]. [Full Text]. 173. McNeil JC, Hulten KG, Kaplan SL, Mahoney DH, Mason EO. Staphylococcus aureus Infections in Pediatric Oncology Patients: High Rates of Antimicrobial Resistance, Antiseptic Tolerance and Complications. Pediatr Infect Dis J. Feb 2013;32(2):124-8. [Medline]. 174. Creel AM, Durham SH, Benner KW, Alten JA, Winkler MK. Severe invasive community-associated methicillin-resistant Staphylococcus aureus infections in previously healthy children. Pediatr Crit Care Med. May 2009;10(3):323-7. [Medline]. 175. Vergnano S, Menson E, Smith Z, Kennea N, Embleton N, Clarke P. Characteristics of Invasive Staphylococcus aureus in United Kingdom Neonatal Units. Pediatr Infect Dis J. Oct 2011;30(

Add a comment

Related presentations

Related pages

Vancomycin - Intermediate/Resistant Staphylococcus Aureus ...

... resistant Staphylococcus aureus (MRSA). VISA and VRSA are ... Vancomycin - Intermediate/Resistant Staphylococcus Aureus ... VRSA infections ...
Read more

MRSA: MedlinePlus - National Library of Medicine

MRSA stands for methicillin-resistant Staphylococcus aureus. It causes a staph infection ... Staphylococcus aureus (MRSA) ... 2014 ...
Read more

Methicillin-resistant Staphylococcus aureus (MRSA) Infections

Methicillin-resistant Staphylococcus aureus ... Staph and MRSA can cause a variety of problems ranging from are skin infections and sepsis to pneumonia to ...
Read more

Staphylococcal Infections: MedlinePlus - U.S. National ...

... but Staphylococcus aureus causes most staph infections ... VISA/VRSA (Vancomycin ... STAPHYLOCOCCUS AUREUS... Staphylococcal Infections ...
Read more

Causes and Symptoms of Staphylococcus aureus - Minnesota ...

Staphylococcus aureus ... Methicillin-resistant Staphylococcus aureus infections have been associated with hospitalization or ... 2014 at 02 :38PM ...
Read more

MRSA Symptoms, Infection Pictures, Treatment & Causes

Learn MRSA infection causes ... Chronic Pain; Cold & Flu; Depression; ... Staphylococcus aureus (Staph aureus, S. aureus, ...
Read more

Healthcare-associated Infections (HAIs) - CDC

... of their Role in the Search and Containment of ... resistant Staphylococcus aureus (VRSA) infection since ... infection, chronic ...
Read more


ODH-IDCM STAPHYLOCOCCUS AUREUS Page1/Section 3 Revised 1/2014 STAPHYLOCOCCUS AUREUS Vancomycin Intermediate Resistant Staphylococcus aureus (VISA);
Read more