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Derm Dx

What Caused This Abscess and Cellulitis?

Keywords
October 2004

Patient Presentation

A healthy 25-year-old male optometry student working in an operating clinic developed a 15 mm x 10 mm abscess on his left anterolateral thigh that spontaneously ruptured (see photo above). He thought he had been bitten by a spider 4 days earlier. Subsequently, a small painless erythematous macule appeared on his thigh and became progressively larger, tender and fluctuant during the next 2 days. He initially sought medical attention at another clinic and was started on cephalexin (Keflex, Cephalexin). After 2 days of therapy, the lesion continued to enlarge, became cystic and subsequently burst. His past medical history was significant for bronchitis treated with azithromycin (Zithromax) 9 months previously, and acne vulgaris for which he was receiving daily isotretinoin (Accutane). On physical examination, the lesion consisted of a central area of ulceration with a pus-containing exudate at the base, surrounded by cellulitis that extended 6 cm from the ulcer edge. A bacterial culture was performed and results are pending.

Diagnosis: Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CAMRSA) Skin Infection

The occurrence of CAMRSA infections is increasing.1-4 Local outbreaks of CAMRSA skin infections have been reported not only in many cities throughout the United States, but also in several nations throughout the world.4-6 The possibility that infections caused by this pathogen represent an emerging epidemic has been suggested.7

Epidemiology

Recent studies have shown that CAMRSA and nosocomial methicillin-resistant Staphylococcus aureus (MRSA) differ not only demographically and clinically, but also microbiologically at the gene level.3 MRSA is more commonly recognized as a nosocomial pathogen in patients who have infection-associated risk factors, including prior antibiotic use, recent surgical procedures or hospitalization, chronic illness or immunosuppression, intravenous drug abuse, occupation-related risks (healthcare workers), residential-related exposures (long-term care facility residents), and potential social interaction exposures (nursing home resident contacts).4-6 In contrast, CAMRSA infections typically occur in otherwise healthy individuals, many of whom do not have any MRSA-associated risk factors.1,3,5

Clinical Presentation

Cutaneous CAMRSA infection most commonly presents as either an abscess or cellulitis, or both.1,2,5 Lesions are frequently located on the lower extremities. Similar to this patient who initially attributed his lesion as being secondary to a spider bite, 40% of Cohen and Kurzrock’s1-10 CAMRSA patients thought that their cutaneous lesions were also caused by spider bites. Although it is likely that these patients merely misinterpreted their infectious CAMRSA lesions as sites of a spider bite, it is possible that some of the lesions resulted from secondary infection occurring at the bite locations.

Treatment

The diagnosis of MRSA skin infection should be considered in patients whose cutaneous lesions persist or progress while receiving therapy that provides adequate antibiotic coverage for methicillin-sensitive S. aureus (MSSA). More frequent culturing of lesions and susceptibility testing of S. aureus isolates from clinical infections are recommended in cities where MRSA is known to be prevalent.3 Therefore, the clinician should consider performing a bacterial culture at the patient’s initial visit — especially when the cutaneous lesion requires incision and drainage.1,5,7 Starting antimicrobial therapy with an antibiotic to which MRSA is typically susceptible is reasonable in areas where the frequency of CAMRSA is very high.1,3,4,6,7 Alternatively, using antimicrobial therapy directed toward MSSA can be initiated and subsequently altered based upon the reported antibiotic sensitivity in patients whose cultures reveal MRSA.1,5,7 The bacterial culture of this patient demonstrated moderate growth of S. aureus that was resistant to erythromycin, penicillin, and oxacillin. MRSA (often reported as oxacillin-resistant on bacterial cultures) is always resistant to beta-lactam antimicrobials, such as cephalosporins. The patient’s S. aureus isolate was found to be susceptible to ciprofloxacin (Cipro), clindamycin, gentamicin (Gentak), levofloxacin (Levaquin, Quixin), rifampin (Rifadin, Rifamate, Rifatar), trimethoprim-sulfamethoxazole (Bactrim, Septra, Co-trimoxazole), and vancomycin (Vancocin).

Similar to this patient’s causative bacteria, many isolates of MRSA are susceptible to trimethoprim-sulfamethoxazole, clindamycin, and rifampin. Monotherapy with double-strength trimethoprim-sulfamethoxazole (twice daily, usually for at least 10 days) is often effective.1,6-8 Alternatively, clindamycin monotherapy or rifampin in combination with either clindamycin or trimethoprim-sulfamethoxazole has been successfully used.6,8 Some MRSA isolates are susceptible to ciprofloxacin or levafloxacin, or both. However, treatment with these drugs may not be as effective since the bacteria frequently become resistant to quinolones.7 Intravenous vancomycin should be used in critically ill patients with invasive skin and soft tissue MRSA infections.4,8 Alternative systemic antibiotics for these patients include linezolid (Zyvox), dactomycin, quinupristin/dalfopristin (Synercid) and teicoplanin.6,8 Adjuvant topical management for patients may also be helpful. Mupirocin 2% ointment (Bactroban) can be applied to the lesions and the nostrils.7,9 In addition, the involved area can be cleaned daily with a liquid antimicrobial agent: povidone-iodine soap (10% or 7.5% concentration) (Betadine) or 4% chlorhexidine gluconate detergent (Betasept).7,9,10

Precautions to prevent transmission of MRSA to other individuals should be initiated. Patients with cutaneous CAMRSA lesions should limit direct skin-to-skin contact with other people and maximize their personal hygiene, especially with regards to hand washing.2,7,9,10 Also, personal items (such as shaving razors and towels) and public items (such as athletic equipment) that may have become contaminated should be appropriately cleaned or removed.7 Our patient’s initial antibiotic was changed to double-strength trimethoprim-sulfamethoxazole twice daily. In addition, topical treatment was started with daily cleansing of the lesional area using 7.5% povidone-iodine liquid soap and application of 2% mupirocin ointment three times per day to the cutaneous lesion and nostrils. At his follow-up visit 1 week later, the surrounding erythema had resolved, the perilesional induration had markedly decreased, and the ulcer had diminished in size, measuring 12 mm x 5 mm. His oral and topical antibiotics were continued for an additional week, while the frequency of daily application of liquid antimicrobial soap was tapered over the next 3 months.

Dr. Cohen is with the University of Houston Health Center in Houston and the Department of Dermatology at the University of Texas-Houston Medical School in Houston. Dr. Khachemoune, the Section Editor for “Derm DX,” is at The Wellman Center for Photomedicine, Department of Dermatology at Massachusetts General Hospital, Harvard Medical School in Boston, MA.

Patient Presentation

A healthy 25-year-old male optometry student working in an operating clinic developed a 15 mm x 10 mm abscess on his left anterolateral thigh that spontaneously ruptured (see photo above). He thought he had been bitten by a spider 4 days earlier. Subsequently, a small painless erythematous macule appeared on his thigh and became progressively larger, tender and fluctuant during the next 2 days. He initially sought medical attention at another clinic and was started on cephalexin (Keflex, Cephalexin). After 2 days of therapy, the lesion continued to enlarge, became cystic and subsequently burst. His past medical history was significant for bronchitis treated with azithromycin (Zithromax) 9 months previously, and acne vulgaris for which he was receiving daily isotretinoin (Accutane). On physical examination, the lesion consisted of a central area of ulceration with a pus-containing exudate at the base, surrounded by cellulitis that extended 6 cm from the ulcer edge. A bacterial culture was performed and results are pending.

Diagnosis: Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CAMRSA) Skin Infection

The occurrence of CAMRSA infections is increasing.1-4 Local outbreaks of CAMRSA skin infections have been reported not only in many cities throughout the United States, but also in several nations throughout the world.4-6 The possibility that infections caused by this pathogen represent an emerging epidemic has been suggested.7

Epidemiology

Recent studies have shown that CAMRSA and nosocomial methicillin-resistant Staphylococcus aureus (MRSA) differ not only demographically and clinically, but also microbiologically at the gene level.3 MRSA is more commonly recognized as a nosocomial pathogen in patients who have infection-associated risk factors, including prior antibiotic use, recent surgical procedures or hospitalization, chronic illness or immunosuppression, intravenous drug abuse, occupation-related risks (healthcare workers), residential-related exposures (long-term care facility residents), and potential social interaction exposures (nursing home resident contacts).4-6 In contrast, CAMRSA infections typically occur in otherwise healthy individuals, many of whom do not have any MRSA-associated risk factors.1,3,5

Clinical Presentation

Cutaneous CAMRSA infection most commonly presents as either an abscess or cellulitis, or both.1,2,5 Lesions are frequently located on the lower extremities. Similar to this patient who initially attributed his lesion as being secondary to a spider bite, 40% of Cohen and Kurzrock’s1-10 CAMRSA patients thought that their cutaneous lesions were also caused by spider bites. Although it is likely that these patients merely misinterpreted their infectious CAMRSA lesions as sites of a spider bite, it is possible that some of the lesions resulted from secondary infection occurring at the bite locations.

Treatment

The diagnosis of MRSA skin infection should be considered in patients whose cutaneous lesions persist or progress while receiving therapy that provides adequate antibiotic coverage for methicillin-sensitive S. aureus (MSSA). More frequent culturing of lesions and susceptibility testing of S. aureus isolates from clinical infections are recommended in cities where MRSA is known to be prevalent.3 Therefore, the clinician should consider performing a bacterial culture at the patient’s initial visit — especially when the cutaneous lesion requires incision and drainage.1,5,7 Starting antimicrobial therapy with an antibiotic to which MRSA is typically susceptible is reasonable in areas where the frequency of CAMRSA is very high.1,3,4,6,7 Alternatively, using antimicrobial therapy directed toward MSSA can be initiated and subsequently altered based upon the reported antibiotic sensitivity in patients whose cultures reveal MRSA.1,5,7 The bacterial culture of this patient demonstrated moderate growth of S. aureus that was resistant to erythromycin, penicillin, and oxacillin. MRSA (often reported as oxacillin-resistant on bacterial cultures) is always resistant to beta-lactam antimicrobials, such as cephalosporins. The patient’s S. aureus isolate was found to be susceptible to ciprofloxacin (Cipro), clindamycin, gentamicin (Gentak), levofloxacin (Levaquin, Quixin), rifampin (Rifadin, Rifamate, Rifatar), trimethoprim-sulfamethoxazole (Bactrim, Septra, Co-trimoxazole), and vancomycin (Vancocin).

Similar to this patient’s causative bacteria, many isolates of MRSA are susceptible to trimethoprim-sulfamethoxazole, clindamycin, and rifampin. Monotherapy with double-strength trimethoprim-sulfamethoxazole (twice daily, usually for at least 10 days) is often effective.1,6-8 Alternatively, clindamycin monotherapy or rifampin in combination with either clindamycin or trimethoprim-sulfamethoxazole has been successfully used.6,8 Some MRSA isolates are susceptible to ciprofloxacin or levafloxacin, or both. However, treatment with these drugs may not be as effective since the bacteria frequently become resistant to quinolones.7 Intravenous vancomycin should be used in critically ill patients with invasive skin and soft tissue MRSA infections.4,8 Alternative systemic antibiotics for these patients include linezolid (Zyvox), dactomycin, quinupristin/dalfopristin (Synercid) and teicoplanin.6,8 Adjuvant topical management for patients may also be helpful. Mupirocin 2% ointment (Bactroban) can be applied to the lesions and the nostrils.7,9 In addition, the involved area can be cleaned daily with a liquid antimicrobial agent: povidone-iodine soap (10% or 7.5% concentration) (Betadine) or 4% chlorhexidine gluconate detergent (Betasept).7,9,10

Precautions to prevent transmission of MRSA to other individuals should be initiated. Patients with cutaneous CAMRSA lesions should limit direct skin-to-skin contact with other people and maximize their personal hygiene, especially with regards to hand washing.2,7,9,10 Also, personal items (such as shaving razors and towels) and public items (such as athletic equipment) that may have become contaminated should be appropriately cleaned or removed.7 Our patient’s initial antibiotic was changed to double-strength trimethoprim-sulfamethoxazole twice daily. In addition, topical treatment was started with daily cleansing of the lesional area using 7.5% povidone-iodine liquid soap and application of 2% mupirocin ointment three times per day to the cutaneous lesion and nostrils. At his follow-up visit 1 week later, the surrounding erythema had resolved, the perilesional induration had markedly decreased, and the ulcer had diminished in size, measuring 12 mm x 5 mm. His oral and topical antibiotics were continued for an additional week, while the frequency of daily application of liquid antimicrobial soap was tapered over the next 3 months.

Dr. Cohen is with the University of Houston Health Center in Houston and the Department of Dermatology at the University of Texas-Houston Medical School in Houston. Dr. Khachemoune, the Section Editor for “Derm DX,” is at The Wellman Center for Photomedicine, Department of Dermatology at Massachusetts General Hospital, Harvard Medical School in Boston, MA.

Patient Presentation

A healthy 25-year-old male optometry student working in an operating clinic developed a 15 mm x 10 mm abscess on his left anterolateral thigh that spontaneously ruptured (see photo above). He thought he had been bitten by a spider 4 days earlier. Subsequently, a small painless erythematous macule appeared on his thigh and became progressively larger, tender and fluctuant during the next 2 days. He initially sought medical attention at another clinic and was started on cephalexin (Keflex, Cephalexin). After 2 days of therapy, the lesion continued to enlarge, became cystic and subsequently burst. His past medical history was significant for bronchitis treated with azithromycin (Zithromax) 9 months previously, and acne vulgaris for which he was receiving daily isotretinoin (Accutane). On physical examination, the lesion consisted of a central area of ulceration with a pus-containing exudate at the base, surrounded by cellulitis that extended 6 cm from the ulcer edge. A bacterial culture was performed and results are pending.

Diagnosis: Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CAMRSA) Skin Infection

The occurrence of CAMRSA infections is increasing.1-4 Local outbreaks of CAMRSA skin infections have been reported not only in many cities throughout the United States, but also in several nations throughout the world.4-6 The possibility that infections caused by this pathogen represent an emerging epidemic has been suggested.7

Epidemiology

Recent studies have shown that CAMRSA and nosocomial methicillin-resistant Staphylococcus aureus (MRSA) differ not only demographically and clinically, but also microbiologically at the gene level.3 MRSA is more commonly recognized as a nosocomial pathogen in patients who have infection-associated risk factors, including prior antibiotic use, recent surgical procedures or hospitalization, chronic illness or immunosuppression, intravenous drug abuse, occupation-related risks (healthcare workers), residential-related exposures (long-term care facility residents), and potential social interaction exposures (nursing home resident contacts).4-6 In contrast, CAMRSA infections typically occur in otherwise healthy individuals, many of whom do not have any MRSA-associated risk factors.1,3,5

Clinical Presentation

Cutaneous CAMRSA infection most commonly presents as either an abscess or cellulitis, or both.1,2,5 Lesions are frequently located on the lower extremities. Similar to this patient who initially attributed his lesion as being secondary to a spider bite, 40% of Cohen and Kurzrock’s1-10 CAMRSA patients thought that their cutaneous lesions were also caused by spider bites. Although it is likely that these patients merely misinterpreted their infectious CAMRSA lesions as sites of a spider bite, it is possible that some of the lesions resulted from secondary infection occurring at the bite locations.

Treatment

The diagnosis of MRSA skin infection should be considered in patients whose cutaneous lesions persist or progress while receiving therapy that provides adequate antibiotic coverage for methicillin-sensitive S. aureus (MSSA). More frequent culturing of lesions and susceptibility testing of S. aureus isolates from clinical infections are recommended in cities where MRSA is known to be prevalent.3 Therefore, the clinician should consider performing a bacterial culture at the patient’s initial visit — especially when the cutaneous lesion requires incision and drainage.1,5,7 Starting antimicrobial therapy with an antibiotic to which MRSA is typically susceptible is reasonable in areas where the frequency of CAMRSA is very high.1,3,4,6,7 Alternatively, using antimicrobial therapy directed toward MSSA can be initiated and subsequently altered based upon the reported antibiotic sensitivity in patients whose cultures reveal MRSA.1,5,7 The bacterial culture of this patient demonstrated moderate growth of S. aureus that was resistant to erythromycin, penicillin, and oxacillin. MRSA (often reported as oxacillin-resistant on bacterial cultures) is always resistant to beta-lactam antimicrobials, such as cephalosporins. The patient’s S. aureus isolate was found to be susceptible to ciprofloxacin (Cipro), clindamycin, gentamicin (Gentak), levofloxacin (Levaquin, Quixin), rifampin (Rifadin, Rifamate, Rifatar), trimethoprim-sulfamethoxazole (Bactrim, Septra, Co-trimoxazole), and vancomycin (Vancocin).

Similar to this patient’s causative bacteria, many isolates of MRSA are susceptible to trimethoprim-sulfamethoxazole, clindamycin, and rifampin. Monotherapy with double-strength trimethoprim-sulfamethoxazole (twice daily, usually for at least 10 days) is often effective.1,6-8 Alternatively, clindamycin monotherapy or rifampin in combination with either clindamycin or trimethoprim-sulfamethoxazole has been successfully used.6,8 Some MRSA isolates are susceptible to ciprofloxacin or levafloxacin, or both. However, treatment with these drugs may not be as effective since the bacteria frequently become resistant to quinolones.7 Intravenous vancomycin should be used in critically ill patients with invasive skin and soft tissue MRSA infections.4,8 Alternative systemic antibiotics for these patients include linezolid (Zyvox), dactomycin, quinupristin/dalfopristin (Synercid) and teicoplanin.6,8 Adjuvant topical management for patients may also be helpful. Mupirocin 2% ointment (Bactroban) can be applied to the lesions and the nostrils.7,9 In addition, the involved area can be cleaned daily with a liquid antimicrobial agent: povidone-iodine soap (10% or 7.5% concentration) (Betadine) or 4% chlorhexidine gluconate detergent (Betasept).7,9,10

Precautions to prevent transmission of MRSA to other individuals should be initiated. Patients with cutaneous CAMRSA lesions should limit direct skin-to-skin contact with other people and maximize their personal hygiene, especially with regards to hand washing.2,7,9,10 Also, personal items (such as shaving razors and towels) and public items (such as athletic equipment) that may have become contaminated should be appropriately cleaned or removed.7 Our patient’s initial antibiotic was changed to double-strength trimethoprim-sulfamethoxazole twice daily. In addition, topical treatment was started with daily cleansing of the lesional area using 7.5% povidone-iodine liquid soap and application of 2% mupirocin ointment three times per day to the cutaneous lesion and nostrils. At his follow-up visit 1 week later, the surrounding erythema had resolved, the perilesional induration had markedly decreased, and the ulcer had diminished in size, measuring 12 mm x 5 mm. His oral and topical antibiotics were continued for an additional week, while the frequency of daily application of liquid antimicrobial soap was tapered over the next 3 months.

Dr. Cohen is with the University of Houston Health Center in Houston and the Department of Dermatology at the University of Texas-Houston Medical School in Houston. Dr. Khachemoune, the Section Editor for “Derm DX,” is at The Wellman Center for Photomedicine, Department of Dermatology at Massachusetts General Hospital, Harvard Medical School in Boston, MA.

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