A 6-year-old Boy with "Spider Bites"

Educational Objectives

After reading this article and answering the review questions, the reader will be able to:

1. Recognize common clinical presentations of staphylococcal skin infections in children and adolescents
2. Understand when systemic antibiotic treatment is recommended for skin and soft tissue infections
3. Know the major strategies for prevention and control of Staphylococcus aureus colonization and infection in the household and community

Case

A 6-year-old boy presents to the office with a complaint of bumps on his upper left thigh. He was in his usual state of health until two days ago when his mother noticed a "spider bite" on his leg. It did not seem to bother him at the time and his mother put some "anti-itch" cream on it. This morning, the bump seemed to suddenly grow and is now very red and painful to touch. Two new bumps have also appeared next to the large one. He continues to walk without difficulty, has no fever and no change in appetite or activity. His 4-year-old sister has been treated with antibiotics twice in the past six months for similar bumps. The only other household members are the patient's mother and father. On physical examination, the child has a temperature of 36.8°F, respiratory rate of 22 breaths/min, and pulse of 92 bpm. He is playful and cooperative. The most notable finding on examination is a 1.5 x 2 cm erythematous, warm mass on his left posteriolateral thigh that is tender to palpation. It is mobile and fluctuant but without drainage. There is surrounding erythema that is 3 cm in diameter. There are also two small pustular lesions within 3 cm of the larger one. He has no inguinal adenopathy. He is able to move his hip and knee through full range without resistance.

The boy in this scenario has a skin abscess caused by Staphylococcus aureus (S. aureus). This clinical presentation has become commonplace in the offices of general practitioners because S. aureus skin and soft tissue infections have become much more prevalent over the past decade, especially among children.

Background

S. aureus is a gram-positive bacterium that is part of the natural skin flora of humans. Throughout history it has also caused significant morbidity and mortality. Originally sensitive to all b-lactam antibiotics, S. aureus developed resistance to penicillin via penicillinase (a specific b-lactamase that disrupts the beta-lactam ring and converts penicillin to a compound with no antibiotic activity) soon after this antibiotic was introduced. Penicillinase-stable drugs (methicillin and nafcillin) were thus developed to better combat this organism. Then, in the early 1960s, presence of methicillin-resistant S. aureus (MRSA) was first reported. These strains carried genes for resistance to multiple classes of antibacterial agents and were almost exclusively associated with infections acquired in healthcare settings (HA-MRSA). The mechanism of resistance for MRSA is an alteration of penicillin binding proteins.

In the late 1990s, new stains of S. aureus emerged which were frequently associated with skin and soft tissue infections (SSTIs) in people who had no history of contact with the health care setting. These strains are commonly referred to as community-aquired MRSA (CA-MRSA). In the United States (US), the predominant strain of S. aureus causing CA-MRSA infection is called US 300. It carries a distinct gene conferring methicillin-resistance (SCCmecA IV). Unlike HA-MRSA, this strain does not have multi-drug resistant antibiograms and, therefore, remains sensitive to several other antibiotic classes. The majority of CA-MRSA strains also carry the Panton Valentine Leukocidin gene (pvl) which has been associated with SSTIs as well as more invasive musculoskeletal infections, bacteremia, sepsis, endocarditis, and pneumonia. A survey of MRSA isolates from national databases of hospital discharges over a 10-year period from 1998-2007 indicated a 16-fold increase in hospitalization rates for CA-MRSA infections in children. The proportion of S. aureus abscesses caused by the CA-MRSA phenotype increased from 8.7 to 60.3 percent over this same time period¹.

Clinical Presentation

A SSTI due to CA-MRSA may present in a variety of ways. Common presentations include impetigo, folliculitis, furuncles (abscess of one hair follicle), carbuncles, (the coalescence of multiple furuncles, also known as boils, see Figure), frank abscess or cellulitis. The patient may often describe the initial lesion as being a red, raised, pinpoint lesion resembling a spider bite. There are usually no associated systemic symptoms, though low-grade fevers and lymphadenitis have been described. Severe invasive infections such as bacteremia, osteomyelitis, pyomyositis, necrotizing fasciitis, endocarditis or necrotizing pneumonia are becoming more common although this varies by geographic location.

Figure 1. Carbuncle of the chin caused by Methicillin-Resistant Staphylococcus aureus. Note the multiple surrounding furuncles. Several have coalesced to form an abscess that is now draining.

Management of Skin and Soft Tissue Infections (SSTIs)

There are several different presentations of Staphylococcal SSTI, the majority of which can be treated in the outpatient setting (See Figure 2).

Folliculitis or furuncles may often respond to warm, moist compresses alone. Topical 2% mupirocin may be effective treatment for these as well as impetigo or superinfected skin lesions such as eczema. Once carbuncles or abscesses develop, the definitive treatment is incision and drainage (I&D). This is likely to be adequate treatment alone. Cultures should be obtained whenever possible. Although the role of systemic antibiotics after I&D of a simple abscess has not been completely defined, in general, systemic antibiotics are not required after adequate drainage unless there is a wide area of cellulitis surrounding the abscess.² This recommendation is supported by several reports that indicate resolution of a drained abscess in the presence of empiric antibiotics that turned out to be inappropriate based on the sensitivities of the cultured bacteria. When drainage is performed, a culture of the material obtained is necessary to guide management if there is no response to therapy, progression occurs or for management of subsequent infections.

Systemic antibiotic therapy is indicated in the presence of cellulitis, severe, extensive or rapidly progressive disease, or if there has been no response to topical therapy or I&D. Other indications are listed in Figure 3.

Though CA-MRSA is the predominant strain causing SSTI in children throughout the U.S., there are pvl-positive methicillin-susceptible strains (MSSA) that cause SSTI as well as invasive, necrotizing infections.³ Therefore a β-lactam antibiotic can still be considered first-line empiric therapy in children without systemic toxicity. It would be important to have close follow-up in these children to enable antibiotic change in the absence of improvement or if culture results indicate the presence of MRSA.

In regions of the country where there is a high-prevalence of MRSA or when a child has failed to respond to β-lactam therapy, it is prudent to choose an alternative treatment such as clindamycin, trimethoprim-sulfamethoxasole, doxycycline (in patients over 7-years-old) or linezolid. However, there are specific considerations for each antibiotic choice in children. There are increasing rates of inducible clindamycin resistance in both MSSA and MRSA isolates. Although most clinical laboratories now routinely test for the presence of the gene that induces resistance, it is important for practitioners to ascertain whether the microbiology laboratory processing the specimen does test for and report inducible clindamycin resistance before starting clindamycin based on culture results. More than 90% of strains are susceptible to trimethoprim-sulfamethoxasole though failures have been documented and there is concern of decreased penetration into abscesses. Doxycycline should not be used in children < 8-years-old and linezolid is an expensive alternative. Though the majority of isolates are sensitive to rifampin, this antibiotic should not be used alone due to the rapid development of resistance.

When cellulitis is present, empiric antibiotics should be selected to cover both S. aureus and β-hemolytic streptococci. This may include clindamycin alone, linezolid alone or a β-lactam such as penicillin (to cover Streptococcus pyogenes) in combination with trimethoprim-sulfamethoxasole (to cover MRSA and MSSA).^4,5 The recommended duration of therapy for SSTI is 5 to 10 days, but can be adjusted based on the patient's clinical response.

Cellulitis associated with lymphadenitis may also be treated as an outpatient if the patient is stable. In general, severe invasive infections such as bacteremia, osteomyelitis, pyomyositis, necrotizing fasciitis, endocarditis or necrotizing pneumonia require hospitalization and systemic antibiotic therapy.

Transmission and Prevention

S. aureus is part of the endogenous flora of humans. Twenty to forty percent of people carry S. aureus in their anterior nares. Primary sites of skin colonization are the axilla and groin. Transmission is primarily through person-to-person skin contact but also through contact with contaminated environmental surfaces. Thus, one of the major risk factors for infection with CA-MRSA is close contact with someone who is a carrier of CA-MRSA or has infected wounds. In the early 2000s outbreaks were identified among groups of people who were in close contact with others (i.e., prisoners, wrestlers and military recruits). Young children presenting with SSTIs are most likely to be in close contact with household members, caregivers and other children in daycare. Participation in contact-sports becomes more of a risk factor for older children and adolescents.

The primary method of prevention of transmission is personal and environmental hygiene. The practitioner can assist preventive efforts by informing patients and families of the mechanisms of transmission and encouraging meticulous attention to hygiene. Regular bathing, hand-washing or the use of alcohol-based gels, and covering of infected, draining wounds can reduce the risk of person-to-person transmission. Family members should avoid sharing potentially contaminated objects such as towels, linens or razors. Environmental hygiene includes the regular cleaning of frequently handled objects in the home such as doorknobs, remote control devices or telephones. Further guidance for prevention in the community setting (i.e. schools) may be found on the Wisconsin Department of Health Services website.⁶

Nasal screening and Decolonization

Nasal screening for MRSA carriers has been used in the healthcare setting to identify patients and staff at risk of transmitting MRSA. Several reports have demonstrated that once nasal carriers are identified, there is efficacy in decolonizing the anterior nares by applying the antibiotic mupirocin intranasally.⁷ Decolonization has had a role in controlling outbreaks in healthcare settings. However, with the high-prevalence of CA-MRSA in the community, routine nasal screening and decolonization is not recommended. The vast majority of CA-MRSA carriers are asymptomatic and often the MRSA strains are replaced within months by other bacteria, including MSSA, without intervention. Additionally, judicious use of mupirocin is necessary as mupirocin-resistant bacteria are emerging.

Routine screening and decolonization is also not recommended for household members or close contacts of a child with a single episode of SSTI due to S. aureus. Decolonization may only be indicated to reduce the overall Staphylococcal burden in a household when SSTIs occur in multiple members of a household, or if one person has multiple recurrences. In these situations, one approach is to screen all members of the household by culturing anterior nares and only decolonizing those who are positive. Given the variability in sensitivity of detection tests for MRSA in the nares and the possibility of falsely negative screens, another, more comprehensive approach would be to decolonize all household members at the same time without the time and expense of nasal screening. A survey of Pediatric Infectious Disease providers regarding their approach to decolonization demonstrated that there is not a consensus opinion regarding this issue.8 However, in general, protocols include antibiotic application with mupirocin to the nares with or without the addition of baths with topical scrubs or bleach. A representative protocol (see Figure 4) includes multiple interventions occurring simultaneously to reduce the burden of S. aureus in the household.

Summary

CA-MRSA has become more prevalent over the past decade, with a concurrent rise in SSTIs due to this organism. The majority of SSTIs can be treated with warm soaks or I&D. Systemic antibiotics are often not necessary in cases of folliculitis, furuncles or simple abscesses. However, when antibiotics are used, there are often several choices available. MSSA is also often isolated from SSTIs and in some communities, such as in Wisconsin, a β-lactam antibiotic may be used as first line therapy with close monitoring of the patient and cultures.

Prevention of transmission is primarily through personal and environmental hygiene. Routine nasal screening and decolonization in the community setting is not recommended although there are rare instances in which this may be necessary. If you have concerns or questions about children with recurrent or complicated SSTIs in themselves or household members please contact the UW Pediatric Infectious Disease Clinic (608) 263-0946 for consultation.

Further guidance on the evaluation, management and prevention of CA-MRSA beyond SSTI can be found at the following websites:

• The Wisconsin Department of Health Services
• The American Academy of Pediatrics  

Go to CME questions

References

1. Mera, RM, Suaya, JA, Amrine-Madsen, H et. al. Increasing role of Staphylococcus aureus and Community-Acquired Methicillin-Resistant Staphylococcus aureus Infections in the United States: A 10-Year Trend of Replacement and Expansion Microbial Drug Resistance 2011; 17:321-328.
2. 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 2010; 55:401-407
3. McCaskill, ML, Mason, EO, Kaplan, SL et. al. Increase of the USA300 Clone Among community-Acquired Methicillin-Susceptible Staphylococcus aureus Causing Invasive Infections. Ped Inf Dis J. 2007; 26: 1122-1127
4. Borlaug, G, Davis, JP and Fox, BC. Community Associated Methicillin Resistant Staphylococcus aureus (CA MRSA) Guidelines for the Clinical Management and Control of Transmission. Wisconsin Department of Public Health. http://www.dhs.wisconsin.gov/communicable/MRSA/index.htm.
5. 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 Chldren. Clinical Infectious Diseases 2011; 52(3) e18-e55.
6. Borlaug, G. Community Associated Methicillin Resistant Staphylococcus aureus (CA MRSA). Guidelines for Controlling Transmission among Students and Athletes. Wisconsin Department of Health Services. 2007; http://www.dhs.wisconsin.gov/communicable/resources/pdffiles/CAMRSA_SchoolGuidePPH42179_1007.pdf
7. Chen, SF. Staphylococcus aureus Decolonization. Ped Inf Dis J. 2005; 24:79-81
8. Creech CB, Beekmann SE, Chen, Y and Polgreen PM. Variability among pediatric Infectious disease specialists in the treatment and prevention of methicillin-resistant Staphylococcus aureus skin and soft tissue infections. Ped Inf Dis J. 2008; 27: 270-272

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