MRSA: From the hospital to your office

Once considered a nosocomial pathogen, methicillin-resistant Staphylococcus aureus is a growing community problem. Make sure you know the signs.

An 18-year-old wrestler presents with a spontaneous, rapidly evolving, 2-cm abscess on the thigh. A culture is performed. What is the most likely diagnosis, and how should it be treated?

Out of the hospital and into the community

Most cutaneous staphylococcal abscesses are caused by methicillin-sensitive staphylococci, but the history of a rapidly evolving spontaneous abscess in an athlete suggests infection with a virulent strain of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) (see photo above). These strains typically contain the Panton-Valentine leukocidin virulence factor. About 75% of CA-MRSA infections present as skin infections, typically a furuncle that rapidly evolves to an abscess. A minority of patients present with a syndrome that has no cutaneous lesions but features necrotizing pneumonitis with or without osteolytic bone lesions.¹

CA-MRSA tends to infect young, previously healthy individuals, especially athletes and children in day care. Other risk groups include prison inmates, military personnel, IV drug users, the homeless, homosexuals, Native Americans, and Pacific Islanders.² CA-MRSA frequently colonizes family members and other close contacts of the infected patient, and colonization often progresses to clinical infection.

Outbreaks of CA-MRSA infection have become common across North America, but individual outbreaks may be restricted to very small geographic areas. In Massachusetts, 182 cases of CA-MRSA infection were largely restricted to a single isolated community; 27 of 33 patients proved to be from a single town, mostly within a single 1.96-km²area.³

The typical CA-MRSA strain in the United States is associated with the type IV staphylococcal chromosomal cassette (SCC)mec that codes for methicillin resistance but does not code for resistance to other drugs. This is in sharp contrast to health-care-associated strains, which are typically resistant to multiple antibiotics. Some health-care-associated strains even demonstrate resistance to vancomycin and linezolid.

Infections with CA-MRSA now frequently outnumber those with health-care-associated strains. In a Texas children's hospital, 93% of MRSA cases were caused by CA-MRSA.⁴

In the San Francisco Bay area, the incidence of CA-MRSA infections more than quadrupled between 1998 and 2002, and more than half of cultured skin and soft-tissue infections seen in Oakland, Calif., emergency departments are now caused by CA-MRSA.¹ CA-MRSA has also caused outbreaks in rural communities in Alaska and Wisconsin. Although the terminology remains “community-acquired” MRSA, strains have crossed over into health-care settings and been associated with nosocomial neonatal, postpartum, and prosthetic joint infections. CA-MRSA strains now account for about 30% of hospital MRSA infections.⁵

Most important intervention: incision and drainage

The primary treatment for any abscess is drainage. Abscesses that are appropriately drained will usually heal, regardless of the antibiotic chosen. Laboratory-based sentinel surveillance data from 1,647 cases of CA-MRSA infection gathered by the CDC indicate that 77% of the infections presented as skin infection; only 6% involved invasive disease. Although 73% of the patients received an antibiotic to which the organism was resistant, such therapy was not associated with adverse outcomes if the abscess was appropriately incised and drained.6 Data from two other studies led to a similar conclusion that antibiotic therapy may not be required in patients with CA-MRSA abscesses if appropriate drainage is done.^7,8 Failure to drain the abscess may have devastating consequences. One report noted bilateral blindness from orbital CA-MRSA cellulitis that began as a pustule on the nose. Effective antibiotic therapy had been administered, but drainage was delayed.⁹

When an antibiotic is needed

Many patients will also require an antibiotic. Sulfa drugs and tetracyclines remain the most cost-effective choices. There was concern that the use of sulfa for Pneumocystis prophylaxis in areas with large HIV-positive populations would result in sulfa resistance among CA-MRSA, but isolates in an Oakland, Calif., study remained susceptible to sulfa.²

The use of lincosamide antibiotics, e.g., clindamycin, is problematic. Staphylococcal strains with inducible clindamycin resistance will appear to be clindamycin-susceptible in routine testing but will test as erythromycin-resistant. In the D-test, a clindamycin disk is placed next to an erythromycin disk. If inducible resistance is present, the zone of inhibition around the clindamycin disk is shaped like a capital D, with bacterial growth seen on the side next to the erythromycin disk. Rates of inducible lincosamide resistance can be as high as 94%.¹⁰

Serious infections, such as MRSA pneumonitis, myositis, or infection associated with systemic toxicity, may require vancomycin, fluoroquinolones, linezolid, daptomycin, quinupristin/dalfopristin, or the newer-generation carbapenems. Vancomycin must be administered parenterally.

Fluoroquinolones may be administered orally and provide adequate coverage for some CA-MRSA isolates. However, resistance is emerging, and overuse of fluoroquinolones clearly promotes emergence of MRSA strains in the community. Linezolid is an oxazolidinone that is generally well tolerated but is quite expensive. In some instances, it may outperform vancomycin. Daptomycin must be given parenterally. Daptomycin resistance has been reported, and standard disk diffusion testing may fail to predict clinical failures.

Many MRSA isolates are susceptible to quinupristin-dalfopristin, but resistance has been reported. Newer carbapenems have demonstrated activity against MRSA and synergism with vancomycin. Tigecycline, a derivative of minocycline, may be effective against some MRSA isolates resistant to other tetracyclines. Treatment guidelines have been issued by the CDC (www.cdc.gov/ncidod/dhqp/pdf/ar /CAMRSA_ExpMtgStrategies.pdf. Accessed May 12, 2006).

Whichever agent is used, antibiotic susceptibilities must be monitored, as some CA-MRSA isolates in Asia have demonstrated resistance to multiple antibiotics. In 2004, a multidrug-resistant SCCmec IV CA-MRSA strain was isolated from a Japanese athlete's abscess. Other Asian CA-MRSA isolates carry a different SCCmec cassette that codes for resistance to multiple antibiotics.

Addressing recurrent infections

Recurrent CA-MRSA infections are common. To prevent these, we must address nasal and skin-surface colonization. Skin-surface colonization may respond to such topical antiseptics as chlorhexidine, triclosan, Dakin's solution, and povidone-iodine. Chlorhexidine gluconate is commonly used; hand disinfectants containing both alcohol and chlorhexidine are more effective than those containing chlorhexidine alone. In a study comparing chlorhexidine gluconate, povidone-iodine, ethanol, and benzalkonium chloride, 70% ethanol was the most effective agent.¹¹ Some MRSA isolates exhibiting low-level resistance to chlorhexidine have also shown resistance to the quaternary ammonium compounds.

Mupirocin is commonly used for nasal carriage, but resistant strains have emerged. An earlier study found nasal eradication in only 44% of mupirocin-treated patients.

Dr. Elston is attending staff dermatologist/dermatopathologist at Geisinger Medical Center in Danville, Pa.

References

1. Frazee BW, Lynn J, Charlebois ED, et al. High prevalence of methicillin-resistant Staphylococcus aureus in emergency department skin and soft tissue infections. Ann Emerg Med. 2005;45:311-320.

2. Weber JT. Community-associated methicillin-resistant Staphylococcus aureus. Clin Infect Dis. 2005;41 Suppl 4:S269-S272.

3. Tirabassi MV, Wadie G, Moriarty KP, et al. Geographic information system localization of community-acquired MRSA soft tissue abscesses. J Pediatr Surg. 2005;40:962-965.

4. Purcell K, Fergie J. Epidemic of community-acquired methicillin-resistant Staphylococcus aureus infections: a 14-year study at Driscoll Children's Hospital. Arch Pediatr Adolesc Med. 2005;159:980-985.

5. Salgado CD, Farr BM, Calfee DP. Community-acquired methicillin-resistant Staphylococcus aureus: a meta-analysis of prevalence and risk factors. Clin Infect Dis. 2003;36:131-139.

6. Fridkin SK, Hageman JC, Morrison M, et al. Active Bacterial Core Surveillance Program of the Emerging Infections Program Network. Methicillin-resistant Staphylococcus aureus disease in three communities. N Engl J Med. 2005;352:1436-1444.

7. Young DM, Harris HW, Charlebois ED, et al. An epidemic of methicillin-resistant Staphylococcus aureus soft tissue infections among medically underserved patients. Arch Surg. 2004;139:947-951.

8. Lee MC, Rios AM, Aten MF, 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. 2004;23:123-127.

9. Rutar T, Zwick OM, Cockerham KP, Horton JC. Bilateral blindness from orbital cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus. Am J Ophthalmol. 2005;140:740-742.

10. Frank AL, Marcinak JF, Mangat PD, et al. Clindamycin treatment of methicillin-resistant Staphylococcus aureus infections in children. Pediatr Infect Dis J. 2002;21:530-534.

11. Suzuki J, Komatsuzawa H, Kozai K, Nagasaka N. In vitro susceptibility of Staphylococcus aureus including MRSA to four disinfectants. ASDC J Dent Child. 1997;64:260-263.