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Tender Annular Plaque on the Thigh
Author(s)
Bao Vincent K. Ho, BS
Spyros M. Siscos, MD
Jace Rickstrew, MD
Garth Fraga, MD
Ting A. Wang-Weinman, MD, PhD

The Diagnosis: Ecthyma Gangrenosum

Histopathology revealed basophilic bacterial rods around necrotic vessels with thrombosis and edema (Figure). Blood and tissue cultures grew Pseudomonas aeruginosa. Based on the histopathology and clinical presentation, a diagnosis of P aeruginosa–associated ecthyma gangrenosum (EG) was made. The patient’s symptoms resolved with intravenous cefepime, and he later was transitioned to oral levofloxacin for outpatient treatment.

Histopathology showed basophilic bacterial rods around necrotic vessels (arrows) with thrombosis and edema (H&E, original magnification ×200).

Ecthyma gangrenosum is an uncommon cutaneous manifestation of bacteremia that most commonly occurs secondary to P aeruginosa in immunocompromised patients, particularly patients with severe neutropenia in the setting of recent chemotherapy.1,2 Ecthyma gangrenosum can occur anywhere on the body, predominantly in moist areas such as the axillae and groin; the arms and legs, such as in our patient, as well as the trunk and face also may be involved.3 Other causes of EG skin lesions include methicillin-resistant Staphylococcus aureus, Citrobacter freundii, Escherichia coli, fungi such as Candida, and viruses such as herpes simplex virus.2,4-6 Common predisposing conditions associated with EG include neutropenia, leukemia, HIV, diabetes mellitus, extensive burn wounds, and a history of immunosuppressive medications. It also has been known to occur in otherwise healthy, immunocompetent individuals with no difference in clinical manifestation.2

The diagnosis is clinicopathologic, with initial evaluation including blood and wound cultures as well as a complete blood cell count once EG is suspected. An excisional or punch biopsy is performed for confirmation, showing many gram-negative, rod-shaped bacteria in cases of pseudomonal EG.7 Histopathology is characterized by bacterial perivascular invasion that then leads to secondary arteriole thrombosis, tissue edema, and separation of the epidermis.7,8 Resultant ischemic necrosis results in the classic macroscopic appearance of an erythematous macule that rapidly progresses into a central necrotic lesion surrounded by an erythematous or violaceous halo after undergoing a hemorrhagic bullous stage.1,9 A Wood lamp can be used to expedite the diagnosis, as Pseudomonas bacteria excretes a pigment (pyoverdine) that fluoresces yellowish green.10

Ecthyma gangrenosum can be classified as a primary skin lesion that may or may not be followed by bacteremia or as a lesion secondary to pseudomonal bacteremia.11 Bacteremia has been reported in half of cases, with hematogenous metastasis of the infection, likely in manifestations with multiple bilateral lesions.2 Our patient’s presentation of a single lesion revealed a positive blood culture result. Lesions also can develop by direct inoculation of the epidermis causing local destruction of the surrounding tissue. The nonbacteremic form of EG has been associated with a lower mortality rate of around 15% compared to patients with bacteremia ranging from 38% to 96%.12 The presence of neutropenia is the most important prognostic factor for mortality at the time of diagnosis.13

Prompt empiric therapy should be initiated after obtaining wound and blood cultures in those with infection until the causative organism and its susceptibility are identified. Pseudomonal infections account for 4% of all cases of hospital-acquired bacteremia and are the third leading cause of gram-negative bloodstream infection.7 Initial broad-spectrum antibiotics include antipseudomonal β-lactams (piperacillin-tazobactam), cephalosporins (cefepime), fluoroquinolones (levofloxacin), and carbapenems (imipenem).1,7 Medical therapy alone may be sufficient without requiring extensive surgical debridement to remove necrotic tissue in some patients. Surgical debridement usually is warranted for lesions larger than 10 cm in diameter.3 Our patient was treated with intravenous cefepime with resolution and was followed with outpatient oral levofloxacin as appropriate. A high index of suspicion should be maintained for relapsing pseudomonal EG infection among patients with AIDS, as the reported recurrence rate is 57%.14

Clinically, the differential diagnosis of EG presenting in immunocompromised patients or individuals with underlying malignancy includes pyoderma gangrenosum, papulonecrotic tuberculid, and leukemia cutis. An erythematous rash with central necrosis presenting in a patient with systemic symptoms is pathognomonic for erythema migrans and should be considered as a diagnostic possibility in areas endemic for Lyme disease in the United States, including the northeastern, mid-Atlantic, and north-central regions.15 A thorough history, physical examination, basic laboratory studies, and histopathology are critical to differentiate between these entities with similar macroscopic features. Pyoderma gangrenosum histologically manifests as a noninfectious, deep, suppurative folliculitis with leukocytoclastic vasculitis in 40% of cases.16 Although papulonecrotic tuberculid can present with dermal necrosis resulting from a hypersensitivity reaction to antigenic components of mycobacteria, there typically are granulomatous infiltrates present and a lack of observed organisms on histopathology.17 Although leukemia cutis infrequently occurs in patients diagnosed with leukemia, its salient features on pathology are nodular or diffuse infiltrates of leukemic cells in the dermis and subcutis with a high nuclear-to-cytoplasmic ratio, often with prominent nucleoli.18 Lyme disease can present in various ways; however, cutaneous involvement in the primary lesion is histologically characterized by a perivascular lymphohistiocytic infiltrate containing plasma cells at the periphery of the expanding annular lesion and eosinophils present at the center.19

References
  1. Abdou A, Hassam B. Ecthyma gangrenosum [in French]. Pan Afr Med J. 2018;30:95. doi:10.11604/pamj.2018.30.95.6244
  2. Vaiman M, Lazarovitch T, Heller L, et al. Ecthyma gangrenosum and ecthyma-like lesions: review article. Eur J Clin Microbiol Infect Dis. 2015;34:633-639. doi:10.1007/s10096-014-2277-6
  3. Vaiman M, Lasarovitch T, Heller L, et al. Ecthyma gangrenosum versus ecthyma-like lesions: should we separate these conditions? Acta Dermatovenerol Alp Pannonica Adriat. 2015;24:69-72. doi:10.15570 /actaapa.2015.18
  4. Reich HL, Williams Fadeyi D, Naik NS, et al. Nonpseudomonal ecthyma gangrenosum. J Am Acad Dermatol. 2004;50(5 suppl): S114-S117. doi:10.1016/j.jaad.2003.09.019
  5. Hawkley T, Chang D, Pollard W, et al. Ecthyma gangrenosum caused by Citrobacter freundii [published online July 27, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220996
  6. Santhaseelan RG, Muralidhar V. Non-pseudomonal ecthyma gangrenosum caused by methicillin-resistant Staphylococcus aureus (MRSA) in a chronic alcoholic patient [published online August 3, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220983m
  7. Bassetti M, Vena A, Croxatto A, et al. How to manage Pseudomonas aeruginosa infections [published online May 29, 2018]. Drugs Context. 2018;7:212527. doi:10.7573/dic.212527
  8. Llamas-Velasco M, Alegría V, Santos-Briz Á, et al. Occlusive nonvasculitic vasculopathy. Am J Dermatopathol. 2017;39:637-662. doi:10.1097/DAD.0000000000000766
  9. Sarkar S, Patra AK, Mondal M. Ecthyma gangrenosum in the periorbital region in a previously healthy immunocompetent woman without bacteremia. Indian Dermatol Online J. 2016;7:36-39. doi:10.4103/2229-5178.174326
  10. Ponka D, Baddar F. Wood lamp examination. Can Fam Physician. 2012;58:976.
  11. Van den Broek PJ, Van der Meer JWM, Kunst MW. The pathogenesis of ecthyma gangrenosum. J Infect. 1979;1:263-267. doi:10.1016 /S0163-4453(79)91329-X
  12. Downey DM, O’Bryan MC, Burdette SD, et al. Ecthyma gangrenosum in a patient with toxic epidermal necrolysis. J Burn Care Res. 2007;28:198-202. doi:10.1097/BCR.0B013E31802CA481
  13. Martínez-Longoria CA, Rosales-Solis GM, Ocampo-Garza J, et al. Ecthyma gangrenosum: a report of eight cases. An Bras Dermatol. 2017;92:698-700. doi:10.1590/abd1806-4841.20175580
  14. Khan MO, Montecalvo MA, Davis I, et al. Ecthyma gangrenosum in patients with acquired immunodeficiency syndrome. Cutis. 2000;66:121-123.
  15. Nadelman RB, Wormser GP. Lyme borreliosis. Lancet. 1998; 352:557-565.
  16. Su WP, Schroeter AL, Perry HO, et al. Histopathologic and immunopathologic study of pyoderma gangrenosum. J Cutan Pathol. 1986;13:323-330. doi:10.1111/j.1600-0560.1986.tb00466.x
  17. Tirumalae R, Yeliur IK, Antony M, et al. Papulonecrotic tuberculidclinicopathologic and molecular features of 12 Indian patients. Dermatol Pract Concept. 2014;4:17-22. doi:10.5826/dpc.0402a03
  18. Obiozor C, Ganguly S, Fraga GR. Leukemia cutis with lymphoglandular bodies: a clue to acute lymphoblastic leukemia cutis [published online August 15, 2015]. Dermatol Online J. 2015;21:13030/qt6m18g35f
  19. Vasudevan B, Chatterjee M. Lyme borreliosis and skin. Indian J Dermatol. 2013;58:167-174. doi:10.4103/0019-5154.110822
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Author and Disclosure Information

From the Division of Dermatology, University of Kansas Medical Center, Kansas City.

The authors report no conflict of interest.

Correspondence: Spyros M. Siscos, MD, Division of Dermatology, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160 ([email protected]).

Issue
Cutis - 108(4)
Publications
MDedge Dermatology
Cutis
Clinician Reviews
Topics
Dermatopathology
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E11-E13
Sections
Photo Challenge
Author(s)
Bao Vincent K. Ho, BS
Spyros M. Siscos, MD
Jace Rickstrew, MD
Garth Fraga, MD
Ting A. Wang-Weinman, MD, PhD
Author(s)
Bao Vincent K. Ho, BS
Spyros M. Siscos, MD
Jace Rickstrew, MD
Garth Fraga, MD
Ting A. Wang-Weinman, MD, PhD
Author and Disclosure Information

From the Division of Dermatology, University of Kansas Medical Center, Kansas City.

The authors report no conflict of interest.

Correspondence: Spyros M. Siscos, MD, Division of Dermatology, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160 ([email protected]).

Author and Disclosure Information

From the Division of Dermatology, University of Kansas Medical Center, Kansas City.

The authors report no conflict of interest.

Correspondence: Spyros M. Siscos, MD, Division of Dermatology, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160 ([email protected]).

Article PDF
ct108004011_e.pdf
Article PDF
ct108004011_e.pdf
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The Diagnosis: Ecthyma Gangrenosum

Histopathology revealed basophilic bacterial rods around necrotic vessels with thrombosis and edema (Figure). Blood and tissue cultures grew Pseudomonas aeruginosa. Based on the histopathology and clinical presentation, a diagnosis of P aeruginosa–associated ecthyma gangrenosum (EG) was made. The patient’s symptoms resolved with intravenous cefepime, and he later was transitioned to oral levofloxacin for outpatient treatment.

Histopathology showed basophilic bacterial rods around necrotic vessels (arrows) with thrombosis and edema (H&E, original magnification ×200).

Ecthyma gangrenosum is an uncommon cutaneous manifestation of bacteremia that most commonly occurs secondary to P aeruginosa in immunocompromised patients, particularly patients with severe neutropenia in the setting of recent chemotherapy.1,2 Ecthyma gangrenosum can occur anywhere on the body, predominantly in moist areas such as the axillae and groin; the arms and legs, such as in our patient, as well as the trunk and face also may be involved.3 Other causes of EG skin lesions include methicillin-resistant Staphylococcus aureus, Citrobacter freundii, Escherichia coli, fungi such as Candida, and viruses such as herpes simplex virus.2,4-6 Common predisposing conditions associated with EG include neutropenia, leukemia, HIV, diabetes mellitus, extensive burn wounds, and a history of immunosuppressive medications. It also has been known to occur in otherwise healthy, immunocompetent individuals with no difference in clinical manifestation.2

The diagnosis is clinicopathologic, with initial evaluation including blood and wound cultures as well as a complete blood cell count once EG is suspected. An excisional or punch biopsy is performed for confirmation, showing many gram-negative, rod-shaped bacteria in cases of pseudomonal EG.7 Histopathology is characterized by bacterial perivascular invasion that then leads to secondary arteriole thrombosis, tissue edema, and separation of the epidermis.7,8 Resultant ischemic necrosis results in the classic macroscopic appearance of an erythematous macule that rapidly progresses into a central necrotic lesion surrounded by an erythematous or violaceous halo after undergoing a hemorrhagic bullous stage.1,9 A Wood lamp can be used to expedite the diagnosis, as Pseudomonas bacteria excretes a pigment (pyoverdine) that fluoresces yellowish green.10

Ecthyma gangrenosum can be classified as a primary skin lesion that may or may not be followed by bacteremia or as a lesion secondary to pseudomonal bacteremia.11 Bacteremia has been reported in half of cases, with hematogenous metastasis of the infection, likely in manifestations with multiple bilateral lesions.2 Our patient’s presentation of a single lesion revealed a positive blood culture result. Lesions also can develop by direct inoculation of the epidermis causing local destruction of the surrounding tissue. The nonbacteremic form of EG has been associated with a lower mortality rate of around 15% compared to patients with bacteremia ranging from 38% to 96%.12 The presence of neutropenia is the most important prognostic factor for mortality at the time of diagnosis.13

Prompt empiric therapy should be initiated after obtaining wound and blood cultures in those with infection until the causative organism and its susceptibility are identified. Pseudomonal infections account for 4% of all cases of hospital-acquired bacteremia and are the third leading cause of gram-negative bloodstream infection.7 Initial broad-spectrum antibiotics include antipseudomonal β-lactams (piperacillin-tazobactam), cephalosporins (cefepime), fluoroquinolones (levofloxacin), and carbapenems (imipenem).1,7 Medical therapy alone may be sufficient without requiring extensive surgical debridement to remove necrotic tissue in some patients. Surgical debridement usually is warranted for lesions larger than 10 cm in diameter.3 Our patient was treated with intravenous cefepime with resolution and was followed with outpatient oral levofloxacin as appropriate. A high index of suspicion should be maintained for relapsing pseudomonal EG infection among patients with AIDS, as the reported recurrence rate is 57%.14

Clinically, the differential diagnosis of EG presenting in immunocompromised patients or individuals with underlying malignancy includes pyoderma gangrenosum, papulonecrotic tuberculid, and leukemia cutis. An erythematous rash with central necrosis presenting in a patient with systemic symptoms is pathognomonic for erythema migrans and should be considered as a diagnostic possibility in areas endemic for Lyme disease in the United States, including the northeastern, mid-Atlantic, and north-central regions.15 A thorough history, physical examination, basic laboratory studies, and histopathology are critical to differentiate between these entities with similar macroscopic features. Pyoderma gangrenosum histologically manifests as a noninfectious, deep, suppurative folliculitis with leukocytoclastic vasculitis in 40% of cases.16 Although papulonecrotic tuberculid can present with dermal necrosis resulting from a hypersensitivity reaction to antigenic components of mycobacteria, there typically are granulomatous infiltrates present and a lack of observed organisms on histopathology.17 Although leukemia cutis infrequently occurs in patients diagnosed with leukemia, its salient features on pathology are nodular or diffuse infiltrates of leukemic cells in the dermis and subcutis with a high nuclear-to-cytoplasmic ratio, often with prominent nucleoli.18 Lyme disease can present in various ways; however, cutaneous involvement in the primary lesion is histologically characterized by a perivascular lymphohistiocytic infiltrate containing plasma cells at the periphery of the expanding annular lesion and eosinophils present at the center.19

The Diagnosis: Ecthyma Gangrenosum

Histopathology revealed basophilic bacterial rods around necrotic vessels with thrombosis and edema (Figure). Blood and tissue cultures grew Pseudomonas aeruginosa. Based on the histopathology and clinical presentation, a diagnosis of P aeruginosa–associated ecthyma gangrenosum (EG) was made. The patient’s symptoms resolved with intravenous cefepime, and he later was transitioned to oral levofloxacin for outpatient treatment.

Histopathology showed basophilic bacterial rods around necrotic vessels (arrows) with thrombosis and edema (H&E, original magnification ×200).

Ecthyma gangrenosum is an uncommon cutaneous manifestation of bacteremia that most commonly occurs secondary to P aeruginosa in immunocompromised patients, particularly patients with severe neutropenia in the setting of recent chemotherapy.1,2 Ecthyma gangrenosum can occur anywhere on the body, predominantly in moist areas such as the axillae and groin; the arms and legs, such as in our patient, as well as the trunk and face also may be involved.3 Other causes of EG skin lesions include methicillin-resistant Staphylococcus aureus, Citrobacter freundii, Escherichia coli, fungi such as Candida, and viruses such as herpes simplex virus.2,4-6 Common predisposing conditions associated with EG include neutropenia, leukemia, HIV, diabetes mellitus, extensive burn wounds, and a history of immunosuppressive medications. It also has been known to occur in otherwise healthy, immunocompetent individuals with no difference in clinical manifestation.2

The diagnosis is clinicopathologic, with initial evaluation including blood and wound cultures as well as a complete blood cell count once EG is suspected. An excisional or punch biopsy is performed for confirmation, showing many gram-negative, rod-shaped bacteria in cases of pseudomonal EG.7 Histopathology is characterized by bacterial perivascular invasion that then leads to secondary arteriole thrombosis, tissue edema, and separation of the epidermis.7,8 Resultant ischemic necrosis results in the classic macroscopic appearance of an erythematous macule that rapidly progresses into a central necrotic lesion surrounded by an erythematous or violaceous halo after undergoing a hemorrhagic bullous stage.1,9 A Wood lamp can be used to expedite the diagnosis, as Pseudomonas bacteria excretes a pigment (pyoverdine) that fluoresces yellowish green.10

Ecthyma gangrenosum can be classified as a primary skin lesion that may or may not be followed by bacteremia or as a lesion secondary to pseudomonal bacteremia.11 Bacteremia has been reported in half of cases, with hematogenous metastasis of the infection, likely in manifestations with multiple bilateral lesions.2 Our patient’s presentation of a single lesion revealed a positive blood culture result. Lesions also can develop by direct inoculation of the epidermis causing local destruction of the surrounding tissue. The nonbacteremic form of EG has been associated with a lower mortality rate of around 15% compared to patients with bacteremia ranging from 38% to 96%.12 The presence of neutropenia is the most important prognostic factor for mortality at the time of diagnosis.13

Prompt empiric therapy should be initiated after obtaining wound and blood cultures in those with infection until the causative organism and its susceptibility are identified. Pseudomonal infections account for 4% of all cases of hospital-acquired bacteremia and are the third leading cause of gram-negative bloodstream infection.7 Initial broad-spectrum antibiotics include antipseudomonal β-lactams (piperacillin-tazobactam), cephalosporins (cefepime), fluoroquinolones (levofloxacin), and carbapenems (imipenem).1,7 Medical therapy alone may be sufficient without requiring extensive surgical debridement to remove necrotic tissue in some patients. Surgical debridement usually is warranted for lesions larger than 10 cm in diameter.3 Our patient was treated with intravenous cefepime with resolution and was followed with outpatient oral levofloxacin as appropriate. A high index of suspicion should be maintained for relapsing pseudomonal EG infection among patients with AIDS, as the reported recurrence rate is 57%.14

Clinically, the differential diagnosis of EG presenting in immunocompromised patients or individuals with underlying malignancy includes pyoderma gangrenosum, papulonecrotic tuberculid, and leukemia cutis. An erythematous rash with central necrosis presenting in a patient with systemic symptoms is pathognomonic for erythema migrans and should be considered as a diagnostic possibility in areas endemic for Lyme disease in the United States, including the northeastern, mid-Atlantic, and north-central regions.15 A thorough history, physical examination, basic laboratory studies, and histopathology are critical to differentiate between these entities with similar macroscopic features. Pyoderma gangrenosum histologically manifests as a noninfectious, deep, suppurative folliculitis with leukocytoclastic vasculitis in 40% of cases.16 Although papulonecrotic tuberculid can present with dermal necrosis resulting from a hypersensitivity reaction to antigenic components of mycobacteria, there typically are granulomatous infiltrates present and a lack of observed organisms on histopathology.17 Although leukemia cutis infrequently occurs in patients diagnosed with leukemia, its salient features on pathology are nodular or diffuse infiltrates of leukemic cells in the dermis and subcutis with a high nuclear-to-cytoplasmic ratio, often with prominent nucleoli.18 Lyme disease can present in various ways; however, cutaneous involvement in the primary lesion is histologically characterized by a perivascular lymphohistiocytic infiltrate containing plasma cells at the periphery of the expanding annular lesion and eosinophils present at the center.19

References
  1. Abdou A, Hassam B. Ecthyma gangrenosum [in French]. Pan Afr Med J. 2018;30:95. doi:10.11604/pamj.2018.30.95.6244
  2. Vaiman M, Lazarovitch T, Heller L, et al. Ecthyma gangrenosum and ecthyma-like lesions: review article. Eur J Clin Microbiol Infect Dis. 2015;34:633-639. doi:10.1007/s10096-014-2277-6
  3. Vaiman M, Lasarovitch T, Heller L, et al. Ecthyma gangrenosum versus ecthyma-like lesions: should we separate these conditions? Acta Dermatovenerol Alp Pannonica Adriat. 2015;24:69-72. doi:10.15570 /actaapa.2015.18
  4. Reich HL, Williams Fadeyi D, Naik NS, et al. Nonpseudomonal ecthyma gangrenosum. J Am Acad Dermatol. 2004;50(5 suppl): S114-S117. doi:10.1016/j.jaad.2003.09.019
  5. Hawkley T, Chang D, Pollard W, et al. Ecthyma gangrenosum caused by Citrobacter freundii [published online July 27, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220996
  6. Santhaseelan RG, Muralidhar V. Non-pseudomonal ecthyma gangrenosum caused by methicillin-resistant Staphylococcus aureus (MRSA) in a chronic alcoholic patient [published online August 3, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220983m
  7. Bassetti M, Vena A, Croxatto A, et al. How to manage Pseudomonas aeruginosa infections [published online May 29, 2018]. Drugs Context. 2018;7:212527. doi:10.7573/dic.212527
  8. Llamas-Velasco M, Alegría V, Santos-Briz Á, et al. Occlusive nonvasculitic vasculopathy. Am J Dermatopathol. 2017;39:637-662. doi:10.1097/DAD.0000000000000766
  9. Sarkar S, Patra AK, Mondal M. Ecthyma gangrenosum in the periorbital region in a previously healthy immunocompetent woman without bacteremia. Indian Dermatol Online J. 2016;7:36-39. doi:10.4103/2229-5178.174326
  10. Ponka D, Baddar F. Wood lamp examination. Can Fam Physician. 2012;58:976.
  11. Van den Broek PJ, Van der Meer JWM, Kunst MW. The pathogenesis of ecthyma gangrenosum. J Infect. 1979;1:263-267. doi:10.1016 /S0163-4453(79)91329-X
  12. Downey DM, O’Bryan MC, Burdette SD, et al. Ecthyma gangrenosum in a patient with toxic epidermal necrolysis. J Burn Care Res. 2007;28:198-202. doi:10.1097/BCR.0B013E31802CA481
  13. Martínez-Longoria CA, Rosales-Solis GM, Ocampo-Garza J, et al. Ecthyma gangrenosum: a report of eight cases. An Bras Dermatol. 2017;92:698-700. doi:10.1590/abd1806-4841.20175580
  14. Khan MO, Montecalvo MA, Davis I, et al. Ecthyma gangrenosum in patients with acquired immunodeficiency syndrome. Cutis. 2000;66:121-123.
  15. Nadelman RB, Wormser GP. Lyme borreliosis. Lancet. 1998; 352:557-565.
  16. Su WP, Schroeter AL, Perry HO, et al. Histopathologic and immunopathologic study of pyoderma gangrenosum. J Cutan Pathol. 1986;13:323-330. doi:10.1111/j.1600-0560.1986.tb00466.x
  17. Tirumalae R, Yeliur IK, Antony M, et al. Papulonecrotic tuberculidclinicopathologic and molecular features of 12 Indian patients. Dermatol Pract Concept. 2014;4:17-22. doi:10.5826/dpc.0402a03
  18. Obiozor C, Ganguly S, Fraga GR. Leukemia cutis with lymphoglandular bodies: a clue to acute lymphoblastic leukemia cutis [published online August 15, 2015]. Dermatol Online J. 2015;21:13030/qt6m18g35f
  19. Vasudevan B, Chatterjee M. Lyme borreliosis and skin. Indian J Dermatol. 2013;58:167-174. doi:10.4103/0019-5154.110822
References
  1. Abdou A, Hassam B. Ecthyma gangrenosum [in French]. Pan Afr Med J. 2018;30:95. doi:10.11604/pamj.2018.30.95.6244
  2. Vaiman M, Lazarovitch T, Heller L, et al. Ecthyma gangrenosum and ecthyma-like lesions: review article. Eur J Clin Microbiol Infect Dis. 2015;34:633-639. doi:10.1007/s10096-014-2277-6
  3. Vaiman M, Lasarovitch T, Heller L, et al. Ecthyma gangrenosum versus ecthyma-like lesions: should we separate these conditions? Acta Dermatovenerol Alp Pannonica Adriat. 2015;24:69-72. doi:10.15570 /actaapa.2015.18
  4. Reich HL, Williams Fadeyi D, Naik NS, et al. Nonpseudomonal ecthyma gangrenosum. J Am Acad Dermatol. 2004;50(5 suppl): S114-S117. doi:10.1016/j.jaad.2003.09.019
  5. Hawkley T, Chang D, Pollard W, et al. Ecthyma gangrenosum caused by Citrobacter freundii [published online July 27, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220996
  6. Santhaseelan RG, Muralidhar V. Non-pseudomonal ecthyma gangrenosum caused by methicillin-resistant Staphylococcus aureus (MRSA) in a chronic alcoholic patient [published online August 3, 2017]. BMJ Case Rep. doi:10.1136/bcr-2017-220983m
  7. Bassetti M, Vena A, Croxatto A, et al. How to manage Pseudomonas aeruginosa infections [published online May 29, 2018]. Drugs Context. 2018;7:212527. doi:10.7573/dic.212527
  8. Llamas-Velasco M, Alegría V, Santos-Briz Á, et al. Occlusive nonvasculitic vasculopathy. Am J Dermatopathol. 2017;39:637-662. doi:10.1097/DAD.0000000000000766
  9. Sarkar S, Patra AK, Mondal M. Ecthyma gangrenosum in the periorbital region in a previously healthy immunocompetent woman without bacteremia. Indian Dermatol Online J. 2016;7:36-39. doi:10.4103/2229-5178.174326
  10. Ponka D, Baddar F. Wood lamp examination. Can Fam Physician. 2012;58:976.
  11. Van den Broek PJ, Van der Meer JWM, Kunst MW. The pathogenesis of ecthyma gangrenosum. J Infect. 1979;1:263-267. doi:10.1016 /S0163-4453(79)91329-X
  12. Downey DM, O’Bryan MC, Burdette SD, et al. Ecthyma gangrenosum in a patient with toxic epidermal necrolysis. J Burn Care Res. 2007;28:198-202. doi:10.1097/BCR.0B013E31802CA481
  13. Martínez-Longoria CA, Rosales-Solis GM, Ocampo-Garza J, et al. Ecthyma gangrenosum: a report of eight cases. An Bras Dermatol. 2017;92:698-700. doi:10.1590/abd1806-4841.20175580
  14. Khan MO, Montecalvo MA, Davis I, et al. Ecthyma gangrenosum in patients with acquired immunodeficiency syndrome. Cutis. 2000;66:121-123.
  15. Nadelman RB, Wormser GP. Lyme borreliosis. Lancet. 1998; 352:557-565.
  16. Su WP, Schroeter AL, Perry HO, et al. Histopathologic and immunopathologic study of pyoderma gangrenosum. J Cutan Pathol. 1986;13:323-330. doi:10.1111/j.1600-0560.1986.tb00466.x
  17. Tirumalae R, Yeliur IK, Antony M, et al. Papulonecrotic tuberculidclinicopathologic and molecular features of 12 Indian patients. Dermatol Pract Concept. 2014;4:17-22. doi:10.5826/dpc.0402a03
  18. Obiozor C, Ganguly S, Fraga GR. Leukemia cutis with lymphoglandular bodies: a clue to acute lymphoblastic leukemia cutis [published online August 15, 2015]. Dermatol Online J. 2015;21:13030/qt6m18g35f
  19. Vasudevan B, Chatterjee M. Lyme borreliosis and skin. Indian J Dermatol. 2013;58:167-174. doi:10.4103/0019-5154.110822
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A 58-year-old man who was receiving gilteritinib therapy for relapsed acute myeloid leukemia presented to the emergency department with a painful, rapidly enlarging lesion on the right medial thigh of 2 days’ duration that was accompanied by fever (temperature, 39.2 °C) and body aches. Physical examination revealed a tender annular plaque with a dark violaceous halo overlying a larger area of erythema and induration. Laboratory evaluation revealed a white blood cell count of 600/μL (reference range, 4500–11,000/μL) and an absolute neutrophil count of 200/μL (reference range, 1800–7000/μL). A biopsy was performed.

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