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Ecthyma-gangrenosum-like lesions associated with methicillin-resistant Staphylococcus aureus infection
International Journal of Infectious Diseases (2009) 13, e173—e175
http://intl.elsevierhealth.com/journals/ijid
CASE REPORT
Ecthyma-gangrenosum-like lesions associated with methicillin-resistant Staphylococcus aureus infection ¨khan ˙Inangil, Levent S¸ahin, Kamer Dere, Hu ¨seyin S¸en *, Go ¨ zkan, Gu ˘li Sezai O ¨ner Dag Gu ¨lhane Military Medical Academy Haydarpas¸a Training Hospital Medical Faculty, ¨ sku Department of Anaesthesiology and Reanimation, U ¨ dar, Istanbul, Turkey Received 13 May 2008; received in revised form 12 August 2008; accepted 27 September 2008 Corresponding Editor: Sheldon T. Brown
KEYWORDS Ecthyma gangrenosum; Staphylococcus aureus; Bacteremia
Summary Ecthyma gangrenosum (EG) manifests as a skin lesion and is commonly associated with Pseudomonas aeruginosa septicemia in immunocompromised patients. Other viral, fungal and bacterial agents can also cause EG. The first clinical observation is grouped vesicles with surrounding erythema. Within a few days, they evolve into a gangrenous ulcer with a black/gray eschar surrounded by an erythematous halo. Herein, we present a patient with chronic obstructive pulmonary disease who developed EG-like lesions due to methicillin-resistant Staphylococcus aureus infection while he was in the intensive care unit. # 2008 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.
Introduction Ecthyma gangrenosum (EG), which first appears at the skin and mucosa, is a necrotizing vasculitis commonly caused by Pseudomonas aeruginosa. Malnutrition, severe neoplasia or hematological diseases, resulting in immunosuppression, are non-bacterial causes of EG.1 The first clinical observation is grouped vesicles with surrounding erythema; within a few days, they form a gangrenous ulcer with a black/gray eschar surrounded by an erythematous halo.2 In this report, we present a patient with chronic obstructive pulmonary disease * Corresponding author. Gu ¨lhane Military Medical Academy Haydarpas¸a Training Hospital Medical Faculty, Department of Anaesthe¨ sku siology and Reanimation, 34668 U ¨dar, Istanbul, Turkey. Tel.: +90 216 542 2020. E-mail address: [email protected] (H. S¸en).
(COPD) who developed EG-like lesions due to methicillinresistant Staphylococcus aureus (MRSA) infection while he was in the intensive care unit (ICU). To the best of our knowledge, this is the first case in the literature in which MRSA is reported to be the underlying cause of such lesions.
Case report A 69-year-old male, diagnosed with COPD 20 years previously, was admitted to the emergency department for acute dyspnea and confusion possibly due to COPD. His vital signs were as follows: blood pressure 170/95 mmHg; heart rate 98 bpm; body temperature 37.5 8C; and respiratory rate 32/min. He was disoriented and cyanotic. Upon auscultation, respiratory sounds were decreased; rales and wheezing could be detected. Chest radiographs revealed an infiltration at the right middle lobe. Arterial blood gas values were: pO2 68
1201-9712/$36.00 # 2008 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.ijid.2008.09.011
e174
H. S¸en et al. three days and then reduced to 400 mg/day. On the 18th day, his arterial blood pressure decreased and a positive inotropic agent was started. The skin lesions were observed to become necrotic. Laboratory values were WBC count 6200/ml and Hb 7.8 g/dl. The patient then developed hypothermia (34.3—35.4 8C). On the 28th day of his stay in the ICU, the patient died from septic shock.
Discussion
Figure 1 foot.
Dark purple macular lesions on the inner side of the
Figure 2 Several similar lesions on the dorsum of the hand and the fingers with edema.
mmHg; pCO2 80 mmHg; pH 7.31. Laboratory tests yielded: white blood cell (WBC) count 18.7 109/l; hemoglobin (Hb) 16.9 mg/dl; blood urea nitrogen 57 mg/dl; platelet (Plt) 205 000/ml; albumin 2.8 g/dl; C-reactive protein level 68 mg/l; erythrocyte sedimentation rate 93 mm/hour. Other laboratory values were normal. Oxygen (5 l/min) was administered with a nasal cannula. Nebulized ipratropium-bromide/salbutamol and parenteral theophylline were given. As the patient did not improve, he was intubated and transferred to the ICU. The COPD was treated with N-acetylcysteine and methylprednisolone, in addition to the above-mentioned drugs. A combination of tazocin 3 4.5 g/day and amikacin 1 g/day was initiated for concomitant pneumonia. On the 5th day in the ICU, the patient was extubated and his vital signs normalized. Laboratory values were normal (WBC count 9.6 109/l; Hb 9.1 g/dl; Plt 195 000/ml). On the 7th day, antibiotics were stopped. On the 12th day, the patient had an elevated pCO2 and he was again intubated for mechanical ventilation. His WBC count was 13.3 109/l and Plt was 202 000/ml, and he had a temperature of 38.2 8C. On the 15th day, mottled skin lesions on the upper and lower extremities were detected. After a few days, the macular lesions progressed to huge bullae, 3 cm in diameter (Figures 1 and 2). The lesions were erythematous and edematous around the necrotic center, consistent with EG. Cultures taken both from the lesions and from the blood were positive for MRSA. Treatment was administered with ampicillin/sulbactam 4 1 g/day, meropenem 3 1 g/day, and teicoplanin 2 400 mg/day for the first
EG, which can be seen in forms ranging from macula lesions to necrotic ulcers, is commonly observed in patients with malignancy or neutropenia. There are two main types, with bacteremia and without bacteremia, according to its pathogenesis. Skin lesions of the bacteremic type occur by hematological spread and blood cultures are positive. In the nonbacteremic form, lesions occur on the skin where organisms are inoculated. The latter has a better prognosis than the bacteremic form.3 On average, 50% of lesions are located in the gluteal and perineal regions, 30% on the extremities, and 12% on the face and body.4 In our patient, lesions first appeared on the extremities. After invasion of the tunica adventitia of the post-capillary venules, bacterial invasion proceeds to the tunica media and obliterates the vessel,5 causing inflammation and thrombosis of the post-capillary vessels. Arteries also become involved, either directly by bacterial invasion or by venous obliteration, leading to separation of dermis and epidermis and causing bullae formation.6 Bacterial load of the bullae increases, producing a central area of necrosis surrounded by an erythematous halo. In our patient, the lesions eventually became necrotic. EG is typically and most commonly caused by P. aeruginosa. However, EG-like lesions have also been observed in patients with other Gram-negative bacterial (Aeromonas hydrophila, Klebsiella pneumoniae, Serratia marcescens, Xanthomonas maltophilia, Morganella morganii, Escherichia coli, Citrobacter freundii, etc.), fungal (Candida albicans, Aspergillus fumigatus, Fusarium solani, Scytalidium dimidiatum, etc.) and viral (Herpes simplex virus) infections.7—9 To the best of our knowledge, lesions associated with Grampositive bacteria have not been reported in the literature; therefore, our patient seems to be the first case in which EGlike lesions are associated with MRSA sepsis. The clinical scenarios associated with EG-like lesions are reported as leukemia, immunosuppression, chemotherapy, urinary tract infection and pneumonia.9 In our patient, the EG-like lesions were associated with MRSA sepsis due to complications of the COPD during follow-up in the ICU. In conclusion, EG-like skin lesions can occur in immunocompromised patients undergoing long-term treatment in the ICU. Despite the fact that they are commonly associated with pseudomonal sepsis, other bacterial and nonbacterial causes should be kept in mind for the differential diagnosis, and management plans should be tailored accordingly. Conflict of interest: No conflict of interest to declare.
References 1. Greene SL, Su WP, Muller SA. Ecthyma gangrenosum: report of clinical, histopathologic, and bacteriologic aspects of eight cases. J Am Acad Dermatol 1984;11:781—7.
EG-like lesions associated with MRSA 2. Pavithran K. Ecthyma gangrenosum with pseudomonas septicemia. Indian J Dermatol Venereol Leprol 1991;57:192—3. 3. Rodot S, Lacour JP, Elslande L, Castanet J, Desruelles J, Ortonne JP. Ecthyma gangrenosum caused by Klebsiella pneumonia. Int J Dermatol 1995;34:216—7. ¨ zdemir D, Yis U, Ko ¨ ren O, Berktas S. Multiple ˘lu T, O 4. Duman M, O ¨rog erythematous nodules and ecthyma gangrenosum as a manifestation of Pseudomonas aeruginosa sepsis in a previously healthy infant. Pediatr Dermatol 2006;23:243—6. 5. Teplitz C. Pathogenesis of Pseudomonas vasculitis and septic lesions. Arch Pathol 1965;80:297—307.
e175 6. Dorff GJ, Geimer NF, Rosenthal DR. Pseudomonas septicemia. Arch Intern Med 1971;128:591. 7. Ketover BP, Young LS, Armstrong D. Septicemia due to Aeromonas hydrophila: clinical and immunologic aspects. J Infect Dis 1973;127:284—90. 8. Singh N, Devi M, Devi S. Ecthyma gangrenosum: a rare cutaneous manifestation caused by Pseudomonas aeruginosa without bacteremia in a leukemic patient. Indian J Dermatol Venereol Leprol 2005;71:128—9. 9. Reich HL, Fadeyi DW, Naik NS, Honig PJ, Yan AC. Nonpseudomonal ecthyma gangrenosum. J Am Acad Dermatol 2004;50:S114—7.
http://intl.elsevierhealth.com/journals/ijid
CASE REPORT
Ecthyma-gangrenosum-like lesions associated with methicillin-resistant Staphylococcus aureus infection ¨khan ˙Inangil, Levent S¸ahin, Kamer Dere, Hu ¨seyin S¸en *, Go ¨ zkan, Gu ˘li Sezai O ¨ner Dag Gu ¨lhane Military Medical Academy Haydarpas¸a Training Hospital Medical Faculty, ¨ sku Department of Anaesthesiology and Reanimation, U ¨ dar, Istanbul, Turkey Received 13 May 2008; received in revised form 12 August 2008; accepted 27 September 2008 Corresponding Editor: Sheldon T. Brown
KEYWORDS Ecthyma gangrenosum; Staphylococcus aureus; Bacteremia
Summary Ecthyma gangrenosum (EG) manifests as a skin lesion and is commonly associated with Pseudomonas aeruginosa septicemia in immunocompromised patients. Other viral, fungal and bacterial agents can also cause EG. The first clinical observation is grouped vesicles with surrounding erythema. Within a few days, they evolve into a gangrenous ulcer with a black/gray eschar surrounded by an erythematous halo. Herein, we present a patient with chronic obstructive pulmonary disease who developed EG-like lesions due to methicillin-resistant Staphylococcus aureus infection while he was in the intensive care unit. # 2008 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.
Introduction Ecthyma gangrenosum (EG), which first appears at the skin and mucosa, is a necrotizing vasculitis commonly caused by Pseudomonas aeruginosa. Malnutrition, severe neoplasia or hematological diseases, resulting in immunosuppression, are non-bacterial causes of EG.1 The first clinical observation is grouped vesicles with surrounding erythema; within a few days, they form a gangrenous ulcer with a black/gray eschar surrounded by an erythematous halo.2 In this report, we present a patient with chronic obstructive pulmonary disease * Corresponding author. Gu ¨lhane Military Medical Academy Haydarpas¸a Training Hospital Medical Faculty, Department of Anaesthe¨ sku siology and Reanimation, 34668 U ¨dar, Istanbul, Turkey. Tel.: +90 216 542 2020. E-mail address: [email protected] (H. S¸en).
(COPD) who developed EG-like lesions due to methicillinresistant Staphylococcus aureus (MRSA) infection while he was in the intensive care unit (ICU). To the best of our knowledge, this is the first case in the literature in which MRSA is reported to be the underlying cause of such lesions.
Case report A 69-year-old male, diagnosed with COPD 20 years previously, was admitted to the emergency department for acute dyspnea and confusion possibly due to COPD. His vital signs were as follows: blood pressure 170/95 mmHg; heart rate 98 bpm; body temperature 37.5 8C; and respiratory rate 32/min. He was disoriented and cyanotic. Upon auscultation, respiratory sounds were decreased; rales and wheezing could be detected. Chest radiographs revealed an infiltration at the right middle lobe. Arterial blood gas values were: pO2 68
1201-9712/$36.00 # 2008 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.ijid.2008.09.011
e174
H. S¸en et al. three days and then reduced to 400 mg/day. On the 18th day, his arterial blood pressure decreased and a positive inotropic agent was started. The skin lesions were observed to become necrotic. Laboratory values were WBC count 6200/ml and Hb 7.8 g/dl. The patient then developed hypothermia (34.3—35.4 8C). On the 28th day of his stay in the ICU, the patient died from septic shock.
Discussion
Figure 1 foot.
Dark purple macular lesions on the inner side of the
Figure 2 Several similar lesions on the dorsum of the hand and the fingers with edema.
mmHg; pCO2 80 mmHg; pH 7.31. Laboratory tests yielded: white blood cell (WBC) count 18.7 109/l; hemoglobin (Hb) 16.9 mg/dl; blood urea nitrogen 57 mg/dl; platelet (Plt) 205 000/ml; albumin 2.8 g/dl; C-reactive protein level 68 mg/l; erythrocyte sedimentation rate 93 mm/hour. Other laboratory values were normal. Oxygen (5 l/min) was administered with a nasal cannula. Nebulized ipratropium-bromide/salbutamol and parenteral theophylline were given. As the patient did not improve, he was intubated and transferred to the ICU. The COPD was treated with N-acetylcysteine and methylprednisolone, in addition to the above-mentioned drugs. A combination of tazocin 3 4.5 g/day and amikacin 1 g/day was initiated for concomitant pneumonia. On the 5th day in the ICU, the patient was extubated and his vital signs normalized. Laboratory values were normal (WBC count 9.6 109/l; Hb 9.1 g/dl; Plt 195 000/ml). On the 7th day, antibiotics were stopped. On the 12th day, the patient had an elevated pCO2 and he was again intubated for mechanical ventilation. His WBC count was 13.3 109/l and Plt was 202 000/ml, and he had a temperature of 38.2 8C. On the 15th day, mottled skin lesions on the upper and lower extremities were detected. After a few days, the macular lesions progressed to huge bullae, 3 cm in diameter (Figures 1 and 2). The lesions were erythematous and edematous around the necrotic center, consistent with EG. Cultures taken both from the lesions and from the blood were positive for MRSA. Treatment was administered with ampicillin/sulbactam 4 1 g/day, meropenem 3 1 g/day, and teicoplanin 2 400 mg/day for the first
EG, which can be seen in forms ranging from macula lesions to necrotic ulcers, is commonly observed in patients with malignancy or neutropenia. There are two main types, with bacteremia and without bacteremia, according to its pathogenesis. Skin lesions of the bacteremic type occur by hematological spread and blood cultures are positive. In the nonbacteremic form, lesions occur on the skin where organisms are inoculated. The latter has a better prognosis than the bacteremic form.3 On average, 50% of lesions are located in the gluteal and perineal regions, 30% on the extremities, and 12% on the face and body.4 In our patient, lesions first appeared on the extremities. After invasion of the tunica adventitia of the post-capillary venules, bacterial invasion proceeds to the tunica media and obliterates the vessel,5 causing inflammation and thrombosis of the post-capillary vessels. Arteries also become involved, either directly by bacterial invasion or by venous obliteration, leading to separation of dermis and epidermis and causing bullae formation.6 Bacterial load of the bullae increases, producing a central area of necrosis surrounded by an erythematous halo. In our patient, the lesions eventually became necrotic. EG is typically and most commonly caused by P. aeruginosa. However, EG-like lesions have also been observed in patients with other Gram-negative bacterial (Aeromonas hydrophila, Klebsiella pneumoniae, Serratia marcescens, Xanthomonas maltophilia, Morganella morganii, Escherichia coli, Citrobacter freundii, etc.), fungal (Candida albicans, Aspergillus fumigatus, Fusarium solani, Scytalidium dimidiatum, etc.) and viral (Herpes simplex virus) infections.7—9 To the best of our knowledge, lesions associated with Grampositive bacteria have not been reported in the literature; therefore, our patient seems to be the first case in which EGlike lesions are associated with MRSA sepsis. The clinical scenarios associated with EG-like lesions are reported as leukemia, immunosuppression, chemotherapy, urinary tract infection and pneumonia.9 In our patient, the EG-like lesions were associated with MRSA sepsis due to complications of the COPD during follow-up in the ICU. In conclusion, EG-like skin lesions can occur in immunocompromised patients undergoing long-term treatment in the ICU. Despite the fact that they are commonly associated with pseudomonal sepsis, other bacterial and nonbacterial causes should be kept in mind for the differential diagnosis, and management plans should be tailored accordingly. Conflict of interest: No conflict of interest to declare.
References 1. Greene SL, Su WP, Muller SA. Ecthyma gangrenosum: report of clinical, histopathologic, and bacteriologic aspects of eight cases. J Am Acad Dermatol 1984;11:781—7.
EG-like lesions associated with MRSA 2. Pavithran K. Ecthyma gangrenosum with pseudomonas septicemia. Indian J Dermatol Venereol Leprol 1991;57:192—3. 3. Rodot S, Lacour JP, Elslande L, Castanet J, Desruelles J, Ortonne JP. Ecthyma gangrenosum caused by Klebsiella pneumonia. Int J Dermatol 1995;34:216—7. ¨ zdemir D, Yis U, Ko ¨ ren O, Berktas S. Multiple ˘lu T, O 4. Duman M, O ¨rog erythematous nodules and ecthyma gangrenosum as a manifestation of Pseudomonas aeruginosa sepsis in a previously healthy infant. Pediatr Dermatol 2006;23:243—6. 5. Teplitz C. Pathogenesis of Pseudomonas vasculitis and septic lesions. Arch Pathol 1965;80:297—307.
e175 6. Dorff GJ, Geimer NF, Rosenthal DR. Pseudomonas septicemia. Arch Intern Med 1971;128:591. 7. Ketover BP, Young LS, Armstrong D. Septicemia due to Aeromonas hydrophila: clinical and immunologic aspects. J Infect Dis 1973;127:284—90. 8. Singh N, Devi M, Devi S. Ecthyma gangrenosum: a rare cutaneous manifestation caused by Pseudomonas aeruginosa without bacteremia in a leukemic patient. Indian J Dermatol Venereol Leprol 2005;71:128—9. 9. Reich HL, Fadeyi DW, Naik NS, Honig PJ, Yan AC. Nonpseudomonal ecthyma gangrenosum. J Am Acad Dermatol 2004;50:S114—7.