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Community-acquired methicillin-resistant Staphylococcus aureus infection
This month’s selected commentary
Community-acquired methicillin-resistant Staphylococcus aureus infection Warren R. Heymann, MD Based on a dialogue between Jennifer Trent, MD and Maurice Thew, MD Dialogues in Dermatology, a monthly audio program from the American Academy of Dermatology, contains discussions between dermatologists on timely topics. Commentaries from the Dialogues Editor-inChief, Warren R. Heymann, MD, are provided after each discussion as a topic summary and are provided here as a special service to readers of the Journal of the American Academy of Dermatology. ( J Am Acad Dermatol 2005;53:318-9.)
M
ethicillin-resistant Staphylococcus aureus (MRSA) is currently the most commonly identified antibiotic-resistant pathogen in US hospitals. According to Deresinski,1 although 25.9% of S aureus strains isolated from outpatients were methicillin-resistant, most of these strains were recovered from individuals who were likely to have acquired them in the health care environment. Their association with health care, however, may have been indirect; household contacts of individuals with hospital-acquired MRSA (HA-MRSA) are at significantly increased risk for MRSA colonization. In a recent and dramatic development, however, infection with novel community-acquired strains of MRSA (CA-MRSA) in previously healthy people without direct or indirect association with health care facilities has emerged as a significant health problem. S aureus strains that cause infection in children are often separated into hospital- and communityacquired types, based on both molecular and epidemiologic differences. The mechanism of resistance to the b-lactams in these strains is the presence of a novel transpeptidase. The function of the transpeptidases, also known as penicillin-binding proteins (PBPs), is peptidoglycan linking in the formation of the cell wall. The novel PBP that exists in MRSA is PBP2a, which has an altered binding site for the b-lactams that is distinct from that present in strains of methicillin-susceptible S aureus (MSSA). Both HA-MRSA and CA-MRSA have this same resistance
The statements and opinions expressed in this commentary are those of the Editor-in-Chief of Dialogues in Dermatology.
318
mechanism. The gene encoding PBP2a, mecA, is carried on the mobile staphylococcal antibiotic resistance gene cassette, SCCmec, which also has the ability to carry multiple antibiotic resistance genes. HA-MRSA strains typically carry SCCmec I, II, or III. These relatively large cassettes often carry resistance to clindamycin, macrolides, and aminoglycosides. By contrast, the newly emergent strains of CA-MRSA have a much smaller gene cassette, SCCmec IV, carrying only the mecA resistance determinant.2 Patterns of resistance may differ geographically. Chen et al3 observed that in Taiwan, CA-MRSA isolates were multiresistant and genetically associated with hospital-acquired isolates. A 62% increase in community-acquired S aureus infections was noted in the year between 2001-2002 and 2002-2003 at Texas Children’s Hospital.4 Mirkinson5 details the case of a woman with erythematous pustules of the lower extremities and a 3 cm 3 3 cm abscess of the leg. Kazakova et al6 reported that during the 2003 football season, 8 MRSA skin infections were noted in 5 of 58 St. Louis Rams players (9%). All isolates carried the gene for PantoneValentine leukocidin and the gene complex for staphylococcal-cassette chromosome mec type IVa. This issue is not only of academic interest. Indeed, during the past week alone in my practice, I encountered 2 patients with CA-MRSA— a young woman with furunculoid lesions and a girl with secondarily infected atopic dermatitis (unpublished data). Although the majority of infections with community-acquired Staphylococcal infections are limited to the skin and soft tissues, infection may
J AM ACAD DERMATOL VOLUME 53, NUMBER 2
be life-threatening. Gonzalez et al7 reported on 14 adolescents with severe community-acquired S aureus infection requiring admission to the pediatric intensive care unit. Twelve patients had CA-MRSA and 2 were infected with MSSA. Thirteen patients had pulmonary involvement and/or bone and joint infection; 4 patients developed deep vein thrombosis and 3 patients died. It is imperative that clinicians be vigilant for the presence of CA-MRSA. According to Cohen and Grossman,8 MRSA should be suspected when infectious skin lesions do not respond to initial antimicrobial therapy that is directed toward MSSA. Bacterial cultures and sensitivities should then be performed. The authors recommend incision and drainage when appropriate, oral trimethoprim/sulfamethoxisole, topical mupirocin ointment to the lesions and intranasally, and daily bathing using povidine-iodine soap. For patients with sulfa allergy or microbial resistance to these agents, combination therapy with clindamycin and rifampin is recommended. Linezolid should be considered for patients who have failed other treatments. Severe infections may require intravenous vancomycin or daptomycin.8 The streptogramins quinupristin and dalfopristin are not approved by the US Food and Drug Administrations for use in children. Oritavancin and dalbavancin, glycopeptide antibiotics structurally related to vancomycin and teicoplanin, are currently undergoing clinical trials in adults. Several companies have developed cephalosporins with the capability to bind PBP2a, the mec gene product that makes S aureus methicillin- and cephalosporinresistant. It is anticipated that some of these drugs may enter clinical trials.2 The rapidity of changing antibiotic-resistance patterns mandates that clinicians keep abreast of the dynamic nature of CA-MRSA. REFERENCES 1. Deresinski S. Methicillin-resistant Staphylococcus aureus: an evolutionary, epidemiologic, and therapeutic odyssey. Clin Infect Dis 2005;40:562-73.
Dialogues in Dermatology 319
2. Bradley JS. Newer antistaphylococcal agents. Curr Opin Pediatr 2005;17:71-7. 3. Chen C-J, Huang YC, Chiu CH, Su LH, Lin TY. Clinical features and genotyping analysis of community-acquired methicillinresistant Staphylococcus aureus infections in Taiwanese children. Pediatr Infect Dis J 2005;24:40-5. 4. Mishaan AM, Mason EO Jr, Martinez-Aguilar G, Hammerman W, Propst JJ, Lupski JR, et al. Emergence of a predominant clone of community-acquired Staphylococcus aureus among children in Houston, Texas. Pediatr Infect Dis J 2005;24: 201-6. 5. Mirkinson LJ. A 16 year-old female with persistent lower extremity lesions and community-acquired methicillinresistant Staphylococcus aureus. Pediatr Emerg Care 2005;21: 134-6. 6. Kazakova SV, Hageman JC, Matava M, Srinivasan A, Phelan L, Garfinkel B, et al. A clone of methicillin-resistant Staphylococcus aureus among professional football players. New Engl J Med 2005;352:468-75. 7. Gonzalez BE, Martinez-Aguilar G, Hulten KG, Hammerman WA, Coss-Bu J, Avalos-Mishaan A, et al. Severe Staphylococcal sepsis in adolescents in the era of community-acquired methicillin-resistant Staphylococcus aureus. Pediatrics 2005; 115:642-8. 8. Cohen PR, Grossman ME. Management of cutaneous lesions associated with an emerging epidemic: Community-acquired methicillin-resistant Staphylococcus aureus skin infections. J Am Acad Dermatol 2004;51:132-5.
Additional topics from the July 2005 issue of the Dialogues in Dermatology: 1. Topical anesthesia for dermatologic procedures Drs Anthony Benedetto and Richard Scher 2. Adjuntive therapy for atopic dermatitis Drs Richard Antaya and Joel Barkoff Dialogues in Dermatology is published monthly by the American Academy of Dermatology in both audio cassette and CD formats. Corporate and editorial offices: 930 E. Woodfield Dr, Schaumburg, IL 60173-4729. 2005 subscription rates: $150 for individuals in the United States, Canada, and Mexico; $200 International. ª 2005 by the American Academy of Dermatology, Inc. Subscriptions are available by calling toll-free: 866-503-7546 or faxing 847-240-1859. Additional information is available in the Marketplace section of www. aad.org.
Community-acquired methicillin-resistant Staphylococcus aureus infection Warren R. Heymann, MD Based on a dialogue between Jennifer Trent, MD and Maurice Thew, MD Dialogues in Dermatology, a monthly audio program from the American Academy of Dermatology, contains discussions between dermatologists on timely topics. Commentaries from the Dialogues Editor-inChief, Warren R. Heymann, MD, are provided after each discussion as a topic summary and are provided here as a special service to readers of the Journal of the American Academy of Dermatology. ( J Am Acad Dermatol 2005;53:318-9.)
M
ethicillin-resistant Staphylococcus aureus (MRSA) is currently the most commonly identified antibiotic-resistant pathogen in US hospitals. According to Deresinski,1 although 25.9% of S aureus strains isolated from outpatients were methicillin-resistant, most of these strains were recovered from individuals who were likely to have acquired them in the health care environment. Their association with health care, however, may have been indirect; household contacts of individuals with hospital-acquired MRSA (HA-MRSA) are at significantly increased risk for MRSA colonization. In a recent and dramatic development, however, infection with novel community-acquired strains of MRSA (CA-MRSA) in previously healthy people without direct or indirect association with health care facilities has emerged as a significant health problem. S aureus strains that cause infection in children are often separated into hospital- and communityacquired types, based on both molecular and epidemiologic differences. The mechanism of resistance to the b-lactams in these strains is the presence of a novel transpeptidase. The function of the transpeptidases, also known as penicillin-binding proteins (PBPs), is peptidoglycan linking in the formation of the cell wall. The novel PBP that exists in MRSA is PBP2a, which has an altered binding site for the b-lactams that is distinct from that present in strains of methicillin-susceptible S aureus (MSSA). Both HA-MRSA and CA-MRSA have this same resistance
The statements and opinions expressed in this commentary are those of the Editor-in-Chief of Dialogues in Dermatology.
318
mechanism. The gene encoding PBP2a, mecA, is carried on the mobile staphylococcal antibiotic resistance gene cassette, SCCmec, which also has the ability to carry multiple antibiotic resistance genes. HA-MRSA strains typically carry SCCmec I, II, or III. These relatively large cassettes often carry resistance to clindamycin, macrolides, and aminoglycosides. By contrast, the newly emergent strains of CA-MRSA have a much smaller gene cassette, SCCmec IV, carrying only the mecA resistance determinant.2 Patterns of resistance may differ geographically. Chen et al3 observed that in Taiwan, CA-MRSA isolates were multiresistant and genetically associated with hospital-acquired isolates. A 62% increase in community-acquired S aureus infections was noted in the year between 2001-2002 and 2002-2003 at Texas Children’s Hospital.4 Mirkinson5 details the case of a woman with erythematous pustules of the lower extremities and a 3 cm 3 3 cm abscess of the leg. Kazakova et al6 reported that during the 2003 football season, 8 MRSA skin infections were noted in 5 of 58 St. Louis Rams players (9%). All isolates carried the gene for PantoneValentine leukocidin and the gene complex for staphylococcal-cassette chromosome mec type IVa. This issue is not only of academic interest. Indeed, during the past week alone in my practice, I encountered 2 patients with CA-MRSA— a young woman with furunculoid lesions and a girl with secondarily infected atopic dermatitis (unpublished data). Although the majority of infections with community-acquired Staphylococcal infections are limited to the skin and soft tissues, infection may
J AM ACAD DERMATOL VOLUME 53, NUMBER 2
be life-threatening. Gonzalez et al7 reported on 14 adolescents with severe community-acquired S aureus infection requiring admission to the pediatric intensive care unit. Twelve patients had CA-MRSA and 2 were infected with MSSA. Thirteen patients had pulmonary involvement and/or bone and joint infection; 4 patients developed deep vein thrombosis and 3 patients died. It is imperative that clinicians be vigilant for the presence of CA-MRSA. According to Cohen and Grossman,8 MRSA should be suspected when infectious skin lesions do not respond to initial antimicrobial therapy that is directed toward MSSA. Bacterial cultures and sensitivities should then be performed. The authors recommend incision and drainage when appropriate, oral trimethoprim/sulfamethoxisole, topical mupirocin ointment to the lesions and intranasally, and daily bathing using povidine-iodine soap. For patients with sulfa allergy or microbial resistance to these agents, combination therapy with clindamycin and rifampin is recommended. Linezolid should be considered for patients who have failed other treatments. Severe infections may require intravenous vancomycin or daptomycin.8 The streptogramins quinupristin and dalfopristin are not approved by the US Food and Drug Administrations for use in children. Oritavancin and dalbavancin, glycopeptide antibiotics structurally related to vancomycin and teicoplanin, are currently undergoing clinical trials in adults. Several companies have developed cephalosporins with the capability to bind PBP2a, the mec gene product that makes S aureus methicillin- and cephalosporinresistant. It is anticipated that some of these drugs may enter clinical trials.2 The rapidity of changing antibiotic-resistance patterns mandates that clinicians keep abreast of the dynamic nature of CA-MRSA. REFERENCES 1. Deresinski S. Methicillin-resistant Staphylococcus aureus: an evolutionary, epidemiologic, and therapeutic odyssey. Clin Infect Dis 2005;40:562-73.
Dialogues in Dermatology 319
2. Bradley JS. Newer antistaphylococcal agents. Curr Opin Pediatr 2005;17:71-7. 3. Chen C-J, Huang YC, Chiu CH, Su LH, Lin TY. Clinical features and genotyping analysis of community-acquired methicillinresistant Staphylococcus aureus infections in Taiwanese children. Pediatr Infect Dis J 2005;24:40-5. 4. Mishaan AM, Mason EO Jr, Martinez-Aguilar G, Hammerman W, Propst JJ, Lupski JR, et al. Emergence of a predominant clone of community-acquired Staphylococcus aureus among children in Houston, Texas. Pediatr Infect Dis J 2005;24: 201-6. 5. Mirkinson LJ. A 16 year-old female with persistent lower extremity lesions and community-acquired methicillinresistant Staphylococcus aureus. Pediatr Emerg Care 2005;21: 134-6. 6. Kazakova SV, Hageman JC, Matava M, Srinivasan A, Phelan L, Garfinkel B, et al. A clone of methicillin-resistant Staphylococcus aureus among professional football players. New Engl J Med 2005;352:468-75. 7. Gonzalez BE, Martinez-Aguilar G, Hulten KG, Hammerman WA, Coss-Bu J, Avalos-Mishaan A, et al. Severe Staphylococcal sepsis in adolescents in the era of community-acquired methicillin-resistant Staphylococcus aureus. Pediatrics 2005; 115:642-8. 8. Cohen PR, Grossman ME. Management of cutaneous lesions associated with an emerging epidemic: Community-acquired methicillin-resistant Staphylococcus aureus skin infections. J Am Acad Dermatol 2004;51:132-5.
Additional topics from the July 2005 issue of the Dialogues in Dermatology: 1. Topical anesthesia for dermatologic procedures Drs Anthony Benedetto and Richard Scher 2. Adjuntive therapy for atopic dermatitis Drs Richard Antaya and Joel Barkoff Dialogues in Dermatology is published monthly by the American Academy of Dermatology in both audio cassette and CD formats. Corporate and editorial offices: 930 E. Woodfield Dr, Schaumburg, IL 60173-4729. 2005 subscription rates: $150 for individuals in the United States, Canada, and Mexico; $200 International. ª 2005 by the American Academy of Dermatology, Inc. Subscriptions are available by calling toll-free: 866-503-7546 or faxing 847-240-1859. Additional information is available in the Marketplace section of www. aad.org.