Staphylococcus aureus are ubiquitous environmental organisms, with a predilection for skin, particularly of the face, nose and hands-and are routinely found in one-third of adults as normal flora. Nasal carriage is mediated by teichoic acid, and as many as 50% of the population are intermittent carriers. Staphylococcal carriage rates as high as 90% have been found in health care workers, in those with dermatologic disease, dialysis patients, intravenous drug users and diabetics. Hospital spread in surgical units, intensive care units, nurseries and burn units are well-documented. 1
Production of abscesses is the trademark of S. aureus clinical infection and involvements of skin and skin structures and of lymph nodes are most commonly encountered. Invasive disease involving lungs, liver, bones and joints, kidney, endocardium and foreign body devices are potentially life-threatening.
S. aureus organisms are easily recognized in the laboratory by their tendency to produce classic golden pigmented colonies with beta-hemolysis on blood agar and the appearance of clustered, grape-like Gram-positive cocci on Gram staining. Distinguished from other staphylococcal species by the production of coagulase, heat resistance to endonucleases, anaerobic acid fermentation of mannitol and the presence of protein A, these organisms also feature the production of a variety of biologically active components including enzymes, hemolysins, leukocidins, toxins and cell surface proteins and cell wall components. These organisms have the ability to produce toxins including enterotoxins A–E which are associated with food poisoning and toxic shock syndrome (TSS), the epidermolytic toxins A and B which are implicated in cases of scalded skin syndrome and toxic shock syndrome toxin-1 which is associated with most cases of TSS. Transposons and plasmids are responsible for virulence and the development of antimicrobial resistance.
Global pandemic staphylococcal disease was well-reported through the 1950s and 1960s when the first reports of methicillin-resistant S. aureus (MRSA) emerged. By the late 1970s MRSA was clearly established as an important nosocomial pathogen. 1 Within the last decade virtually all hospitals have identified MRSA within their facilities and have recognized nosocomial spread and subsequent infection in high risk hospitalized patients.
The changing epidemiology of MRSA became evident in the 1990s when community-acquired MRSA cases were first reported. Embil et al. 2 reported that 63% of MRSA isolates were identified within 72 h of admission in a review of five Canadian university hospitals from 1990 to 1992. Moreno et al. 3 also reported a high rate of community MRSA cases (99 of 170; 58%) with an incidence of 0.2 per 1000 patient days. No risk factors differentiated patients with community MRSA from methicillin-susceptible S. aureus (MSSA), and pulse field gel electrophoresis confirmed that 68% had unique pulse field gel electrophoresis patterns. Whereas Layton et al. 4 noted that community MRSA acquisition was associated with recent hospitalization, previous antimicrobial therapy, nursing home residence and iv drug use, they also observed that 22% of patients had no discernible risk factors. Warshawsky et al. 5 also identified hospital contact as a risk factor for MRSA acquisition and suggested that community spread was directly related to this acquisition.
MRSA Epidemiology in Children
The prevalence of community-acquired MRSA in hospitalized children was recently evaluated by Herold et al. 6 Data from 1988–1990 were compared with those from 1998–1999 and demonstrated a significant increase in prevalence from 10 per 100,000 admissions to 208 per 100,000 admissions. Moreover a greater proportion of isolates was associated with clinical infection in children with no traditional predisposing risk factors for MRSA carriage. Gorak et al. 7 also noted that the majority of children hospitalized with community-acquired MRSA infection had no risk factors. Investigators have noted that community-acquired MRSA infections were more likely to be susceptible to clindamycin, and the types of clinical infections encountered were similar to that of MSSA.
Although MRSA disease has been increasingly recognized in children without traditional risk factors, it is not clear to what extent MRSA colonization has become more pervasive in the community at large. S. aureus colonization was evaluated in 500 children visiting a midwestern emergency department where increasing MRSA disease had been noted. 8 Overall 130 (26%) children carried S. aureus; 11 carried MRSA and only 4 had no traditional risk factors for MRSA colonization. Although the number of children evaluated was small, data from 2 Texas day-care centers after the introduction of an index case demonstrated that spread from the index case to other children did occur, particularly in toddlers. 9 Shahin et al. 10 also documented transmission in the day-care center and noted that throat and perianal site cultures had better sensitivity than specimens obtained from nares.
Treatment Issues in Staphylococcal Infection
Empiric treatment of healthy outpatients. Empiric treatment of skin and soft tissue infections with standard antistaphylococcal therapy is still adequate for the majority of patients. Treatment failure will result if an antistaphylococcal beta-lactam antibiotic is used for therapy of MRSA infection. In cases of treatment failure, identification of a specific isolate is important, allowing appropriate antibiotic treatment adjustments to be made on the basis of antimicrobial susceptibility testing.
Empiric treatment of invasive infection. Where staphylococci may be involved in more extensive infections, the empiric use of clindamycin provides appropriate coverage, including the majority of community-acquired MRSA strains.
In severe, invasive staphylococcal infections, such as severe pneumonia or toxic shock syndrome, inclusion of vancomycin in an empiric antibiotic regimen may be prudent initially, particularly among children with predisposing risk factors for MRSA carriage.
Unfortunately the increasing prevalence of MRSA will inevitably increase vancomycin use, adding further to the problem of antimicrobial resistance. Thus it is important that vancomycin be discontinued if no MRSA is identified and that suitable antibiotic therapy be substituted based on susceptibilities.
MRSA risk factors should be delineated in all cases in which MRSA is documented. Those factors include prior hospitalization, surgery or antimicrobials within the last 6 months, day-care center attendance and/or day-care or household contact with health care workers, or those with chronic underlying diseases. Recent data within our institution show that day-care or household contact with a health care worker or an individual with a chronic underlying illness is commonly overlooked as a risk factor for MRSA colonization among healthy children. 11 Such contacts may to some extent account for increasing resistance rates. Careful interview of families of otherwise healthy children with MRSA infection and no perceived risk factors should focus on common contacts.
Reducing the Spread of MRSA
The role of decolonization among children with MRSA colonization is controversial. Previously reported regimens including intranasal and topical mupirocin, either alone or in combination with oral antibiotics and antibacterial soaps, have shown success in eliminating MRSA carriage. 12 The duration of this decolonization effect is uncertain. Those favoring decolonization cite the opportunity to limit further transmission of MRSA and suggest that consideration be given to decolonization of patients who require lengthy hospitalizations. Concerns regarding further development of antimicrobial resistance, particularly involving mupirocin, form the foundation of the argument opposing decolonization efforts.
Appropriately applied contact precautions, including masks in the case of MRSA pneumonia, are deemed adequate to prevent MRSA transmission among hospitalized patients. Contact precautions include: a private room; use of gowns and gloves at all times, removing them before leaving the patient’s environment; and hand antisepsis before and after glove removal or any contact. 13
With the recognition of increased community acquisition of MRSA, the judicious use of antibiotics is a mainstay in the strategy to reduce MRSA spread. Limiting broad spectrum antibiotic use will minimize the antibiotic pressure that favors selection of resistant strains. Attention to personal hygiene, particularly involving open wounds or skin lesions, is also prudent in our attempts to limit MRSA involvement.
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2. Embil J, et al. Infect Control Hosp Epidemiol 1994; 15: 646–51.
3. Moreno F, et al. Clin Infect Dis 1995; 21: 1308–12.
4. Layton MC, et al. Infect Control Hosp Epidemiol 1995; 16: 12–17.
5. Warshawsky B, et al. Infect Control Hosp Epidemiol 2000; 21: 724–7.
6. Herold BC, et al. JAMA 1998; 279: 593–8.
7. Gorak EJ, et al. Clin Infect Dis 1999; 29: 797–800.
8. Suggs AH, et al. Pediatr Infect Dis J 1999; 18: 410–14.
9. Adcock PM, et al. J Infect Dis 1998; 179: 577–80.
10. Shahin R, et al. Arch Pediatr Adoles Med 1999; 153: 864–8.
11. Bratcher D, et al. 39th Annual Meeting of the Infectious Diseases Society of America, 2001;Abstract 310.
12. Rao N, et al. Infect Control Hosp Epidemiol 1988; 9: 255–60.
13. American Academy of Pediatrics. Pickering LK, ed. 2000 Red Book: Report of the Committee on Infectious Diseases. 25th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2000:523–4.