Community-Acquired Methicillin-Resistant Staphylococcus Aureus: Skin Infection Presenting as an Axillary Abscess With Cellulitis in a College Athlete

Philip R. Cohen, MD


Skinmed. 2005;4(2):115-118. 

A healthy 19-year-old black man without any methicillin-resistant Staphylococcus aureus risk factors developed axillary boils after he began lifting weights at the university gym in Houston, TX. He presented with a large tender erythematous fluctuant abscess of his right axillae and a superiorly located smaller painful red indurated nodule; the surrounding cellulitis extended into the adjacent tissue (Figure 1). The abscess was incised, drained, and cultured. Empiric treatment with cephalexin 500 mg q.i.d. was given for 7 days. The culture grew methicillin-resistant S. aureus. Susceptibility testing of the S. aureus isolate was performed by Laboratory Corp. of America (Houston, TX); the Vitek system (Biomerieux, Hazelwood, MO) was used, and the specimen was incubated for 8 hours. Confirmation of methicillin resistance was performed using a methicillin-resistant S. aureus plate and the specimen was incubated for 24 hours. In addition to resistance to methicillin, the bacterial isolate was also resistant to ciprofloxacin, erythromycin, and penicillin. The S. aureus strain had intermediate susceptibility to levofloxacin and was susceptible to clindamycin, gentamicin, rifampin, tetracycline, trimethoprim/sulfamethoxazole, and vancomycin. The infection persisted and the antibiotic was changed to double strength trimethoprim/ sulfamethoxazole, taken twice daily for 15 days. In addition, topical care included lesional and intranasal application of mupirocin 2% ointment and daily cleaning of the area with 10% povidone-iodine liquid soap. The skin infection completely resolved without recurrence within 2 weeks.

The right axilla of a weight lifter shows cutaneous community-acquired methicillin- resistant infection presenting as a tender red abscess inferiorly with a painful erythematous nodule superiorly and cellulitis of the adjacent tissue.

Community-acquired methicillin-resistant Staphylococcus aureus (CAMRSA) bacterial isolates are different from hospital-acquired methicillin-resistant S. aureus (MRSA) strains.[1] Methicillin resistance is encoded by the mec A gene which is located on staphylococcal chromosomal cassettes.[2,3] Hospital-acquired (also referred to as nosocomial or health care-associated) MRSA strains of bacteria are characterized by having type I, II, and III staphylococcal chromosomal cassettes.[4,5] In contrast to hospital-acquired MRSA bacterial strains, isolates of CAMRSA not only carry type IV staphylococcal chromosomal cassettes, but also have the Panton-Valentine leukocidin locus which encodes for a leukocyte-killing toxin; this latter feature has specifically been associated with the bacteria's ability to cause skin and soft tissue infections.[6,7]

CAMRSA skin infection has been reported not only in many cities throughout the United States, but also in several countries throughout the world.[2,5,8,9] The most common clinical presentations of cutaneous CAMRSA infection are abscess and cellulitis[8,10,11,12,13,14]; however, infectious lesions of CAMRSA have appeared as crusted plaques and erythematous pustules, papules, and nodules.[2,8]

Risk factors for CAMRSA infection have been previously defined as including prior antibiotic use, day care attendance, health care visits, hospitalization, IV drug abuse, invasive indwelling devices, long-term care facility residency, long-term hemodialysis, surgical procedures, and underlying chronic illness or immunosuppression.[11,15] CAMRSA skin infection often occurs in healthy individuals who do not have any of the risk factors typically associated with the development of MRSA infection.[1,2,8,9,14] Similar to the student reported, outbreaks of cutaneous CAMRSA has recently been observed in athletic participants of competitive sports such as fencing, football, rugby, volleyball, and wrestling.[8,15,16,17,18]

The management of cutaneous CAMRSA infection is dependent upon considering the diagnosis.[15] In the community, methicillin-sensitive Staphylococcus aureus (MSSA) infection is still more common than MRSA infection; hence, a diagnosis of cutaneous MSSA infection is likely to be entertained in a healthy individual without MRSA-associated risk factors who presents with infectious skin lesions[2,8,15]; however, similar to the reported patient, MRSA skin infection usually persists or worsens when the individual is treated with antimicrobials that are directed toward MSSA infection.[8,14] Therefore, when a patient presents with skin lesions that are suspected to be secondary to S. aureus, bacterial culture of the lesions at the initial office visit is recommended ( Table 1 ).[1,15] Alternatively, if a bacterial culture was not initially performed, it should be considered if the patient returns with progressive or unresolving cutaneous infection.[15]

Treatment of cutaneous CAMRSA infection should optimally be based upon the culture-determined susceptibility of the bacterial strain ( Table 1 ).[2,15] MRSA strains are not susceptible to cephalosporins.[14]Also, MRSA isolate often rapidly develop resistance to quinolones; hence, even for susceptible isolates, ciprofloxacin or levofloxacin may not be an optimal therapeutic choice.[15,16] If the bacterial isolate is resistant to erythromycin, there is the possibility that the bacterial strain will develop resistance to monotherapy with clindamycin.[9,13,15] Most bacterial strains of CAMRSA are susceptible to trimethoprim/sulfamethoxazole, or clindamycin, or both.[8,9,14,15] Therefore, infection may be treated with either agent alone or in combination with rifampin.[15]

Most CAMRSA strains are also susceptible to vancomycin, linezolid, daptomycin, quinupristin/dalfopristin, and teicoplanin ( Table 1 ). These antimicrobials may be used as second-line therapy for immunocompetent patients with more severe skin and soft tissue infections and with infections involving not only the skin, but also other sites such as the blood stream, bone, heart, lung, and meninges, and for those patients who do not respond to first-line therapy. These antimicrobials may also be considered as first-line therapy for immunosuppressed patients. In addition, some investigators recommend these antimicrobials as first-line therapy for previously healthy individuals with no medical comorbidities.[11]

Topical treatment should also be initiated ( Table 1 ). The topical treatments should be considered as adjuvant therapeutic modalities to be used in patients who are also concurrently receiving local treatment and/or systemic treatment.

Mupirocin 2% ointment three times daily can be applied not only to the skin lesions to treat the infection, but also intranasally to treat potential bacterial colonization at this site.[14,15,19,20] In addition to soaking the lesions in warm water, daily bathing with either povidone-iodine liquid soap (10% or 7.5%) or 4% chlorhexidine gluconate liquid detergent is helpful for treating MRSA infection and colonization.[14,15,19,20]

In conclusion, CAMRSA is a pathogen of increasing global prevalence that is genetically distinct from hospital-acquired strains of MRSA. Cutaneous CAMRSA infection often occurs in healthy people without MRSA risk factors and typically appears as abscess or cellulitis, or both. CAMRSA skin infection is being recognized with increasing frequency in athletic participants. Antimicrobial therapy should be based upon bacterial susceptibility since the skin infection frequently worsens when antibiotics directed toward MSSA are used.


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