Letters
Author Affiliations: University of Michigan Medical School, Ann Arbor (Tran); Department of Dermatology, University of Michigan, Ann Arbor (Egbers, Lowe, Helfrich, Wang); Department of Pathology, University of Michigan, Ann Arbor, Michigan (Lowe). Corresponding Author: Frank Wang, MD, Department of Dermatology, University of Michigan Health System, 1910 Taubman Center, 1500 E Medical Center Dr, Ann Arbor, MI 48109 ([email protected]). Published Online: June 11, 2014. doi:10.1001/jamadermatol.2013.8846. Conflict of Interest Disclosures: None reported. Additional Contributions: We are indebted to Laura VanGoor, BFA, for assistance with graphic material. Ms VanGoor is an employee of the Department of Dermatology at the University of Michigan Medical School. 1. Pennington M, Yeager J, Skelton H, Smith KJ. Cholesterol embolization syndrome: cutaneous histopathological features and the variable onset of symptoms in patients with different risk factors. Br J Dermatol. 2002;146(3): 511-517. 2. Donohue KG, Saap L, Falanga V. Cholesterol crystal embolization: an atherosclerotic disease with frequent and varied cutaneous manifestations. J Eur Acad Dermatol Venereol. 2003;17(5):504-511.
Most reports of A baumannii infection, both nosocomial and community-acquired (CA) SSTI, involve cellulitis of peau d’orange appearance with overlying vesicles that, when untreated, progress to necrotizing fasciitis with coalescent bullae.2 The condition is uncommon and has been reported solely in compromised hosts.3 To our knowledge, A baumannii has never been reported as a cause of CA-SSTI in a healthy patient. However, unpublished and anecdotal cases of increasingly drug-resistant A baumannii presenting as SSTI in healthy patients are known to exist. Molecular typing experiments reveal community and nosocomial A baumannii isolates to be genetically distinct, existing as separate reservoirs with unique virulence and resistance patterns. Until recently, multidrug resistance was considered a hospital-based phenomenon.4 We report herein the case of a healthy woman with CA multidrugresistant A baumannii.
Acinetobacter baumannii Emerging as a Multidrug-Resistant Skin and Soft-Tissue Pathogen: Parallels to Methicillin-Resistant Staphylococcus aureus
Report of a Case | A woman in her 50s with no comorbidities or history of hospitalization presented with tender, violaceous, indurated dermal plaques with central ulceration and peripheral erythema and edema (Figure, A) that had progressively enlarged over the previous 7 to 8 months. Tissue culture results were specific for A baumannii with sensitivity to polymyxin B and tigecycline. The patient was admitted for treatment with intravenous tigecycline and discharged to home with an inpatient-administered peripherally inserted central catheter to facilitate a subsequent 2 weeks of treatment. Following treatment, the patient underwent extensive wound care for 6 months prior to reepithelialization with resulting scarring, dyschromia, and neuropathic pain (Figure, B).
Over the last 30 years, the gram-negative coccobacillus Acinetobacter baumannii has risen to microbiologic notoriety for its ability to successfully evade nearly all available antibiotics. It is now a well-established source of nosocomial bacteremia and pneumonia, known to cause hospital outbreaks, particularly in the intensive care unit. Less often it represents a source of nosocomial skin and soft-tissue infection (SSTI) in the setting of war wounds, surgical sites, and burns.1
Discussion | The evolution of A baumannii infection bears a striking similarity to the now established methicillin-resistant Staphylococcus aureus (MRSA) epidemic; MRSA was initially regarded as a nosocomial pathogen transmitted between health care facilities and limited to a small number of strains with distinct virulence patterns. While the first CA cases occurred in those with predisposing risk factors, it eventually began ap-
3. Belenfant X, Meyrier A, Jacquot C. Supportive treatment improves survival in multivisceral cholesterol crystal embolism. Am J Kidney Dis. 1999;33(5):840-850. 4. Falanga V, Fine MJ, Kapoor WN. The cutaneous manifestations of cholesterol crystal embolization. Arch Dermatol. 1986;122(10):1194-1198. 5. Gore I, Collins DP. Spontaneous atheromatous embolization: review of the literature and a report of 16 additional cases. Am J Clin Pathol. 1960;33:416-426. 6. Tunick PA, Nayar AC, Goodkin GM, et al; NYU Atheroma Group. Effect of treatment on the incidence of stroke and other emboli in 519 patients with severe thoracic aortic plaque. Am J Cardiol. 2002;90(12):1320-1325.
Figure. Clinical Images of Community-Acquired, Extensively Drug-Resistant Acinetobacter baumannii Skin and Soft-Tissue Infection A
B
A, Left pretibial lower extremity at presentation. B, Left pretibial lower extremity after antibiotic therapy and wound care. jamadermatology.com
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Copyright 2014 American Medical Association. All rights reserved.
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905
Letters
pearing in healthy patients. Over time, CA-MRSA incorporated new virulence patterns, acquiring large-scale antibiotic resistance, while maintaining a unique genetic profile compared with nosocomial isolates. Better appreciated through a retrospective lens, this CA form rivals its hospital-based counterpart and can aptly be considered an epidemic.5 A baumannii has the potential to evolve in a pattern similar to that of MRSA and should be monitored for growing resistance and virulence. Epidemiologic history has demonstrated how quickly an organism can evolve from benign commensal to resistant pathogen and highlights the need for intense vigilance with regard to infection control and treatment development.1 With continued accrual of pathogenicity and antibiotic resistance, A baumannii is offering new diagnostic and therapeutic challenges. Enhanced awareness is paramount to control this growing threat as the practice gap continues to widen. Brandon L. Adler, BA Aimee Krausz, BA Adam J. Friedman, MD Author Affiliations: Department of Medicine, Division of Dermatology, Albert Einstein College of Medicine, Bronx, New York (Adler, Krausz, Friedman); Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York (Friedman). Corresponding Author: Adam J. Friedman, MD, Division of Dermatology, Montefiore Medical Center, 111 E 210th St, Bronx, NY 10467 ([email protected]). Published Online: June 18, 2014. doi:10.1001/jamadermatol.2013.8855. Conflict of Interest Disclosures: None reported. Funding/Support: This study was supported in part by the Dermatology Foundation. Role of the Sponsors: The Dermatology Foundation had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Additional Information: Mr Adler and Ms Krausz contributed equally to this work. 1. Munoz-Price LS, Weinstein RA. Acinetobacter infection. N Engl J Med. 2008; 358(12):1271-1281. 2. Guerrero DM, Perez F, Conger NG, et al. Acinetobacter baumannii–associated skin and soft-tissue infections: recognizing a broadening spectrum of disease. Surg Infect (Larchmt). 2010;11(1):49-57.
which usually appears in young adults and regresses spontaneously; and a secondary form, lymphoma-associated follicular mucinosis (LAFM),2 which mostly occurs in elderly patients. Most cases of LAFM are related to cutaneous T-cell lymphomas (especially mycosis fungoides), although some cases of Hodgkin disease3 and chronic lymphocytic leukemia4 have also been reported. Report of a Case | A man in his 60s initially presented with a history of an intermittently pruritic eruption on the chest and proximal limbs. Two skin biopsies were performed on the neck and the back. The lesions were reported as primary, cutaneous, low-grade, B-cell lymphoma favoring marginal B-cell lymphoma. The peripheral blood sample test results and the bonemarrow core biopsy findings were normal. Computed tomographic scans did not reveal any abnormality. The patient was never treated and did not come back because the lesions disappeared spontaneously. Eight years later, he presented with multiple, millimetric, pruritic, skin-colored papules with a follicular pattern on the chest, back, and upper extremities (Figure 1). He did not have any constitutional symptoms. Two biopsies performed on the chest and the abdomen revealed dense lymphocytic infiltrate in the reticular dermis, centered around and within hair follicles, which showed cavities filled with abundant mucinous material (Figure 2A). Small and irregular lymphocytes were admixed with large lymphocytes, plasma cells, and eosinophils. Atypical cells expressed CD20, CD43, CD79α and BCL6. Some intraepithelial lymphocytes tested positive for CD3 and CD4, but most of them expressed CD20 (Figure 2B). Polymerase chain reaction revealed a monoclonal rearrangement of the heavy chain immunoglobulin IgH gene with a peak at 160 base pairs. A reactive lymphoid T cell (CD3, CD43 and CD4 positive) infiltrate was found surrounding the neoplastic cells. The patient was finally diagnosed as having primary cutaneous follicle center lymphoma associated with follicular mucinosis. At last follow-up 4 months later, the lesions and the Figure 1. A Case of Primary Cutaneous Follicle Center Lymphoma With a Very Unusual Miliary Clinical Presentation
3. Howard A, O’Donoghue M, Feeney A, Sleator RD. Acinetobacter baumannii: an emerging opportunistic pathogen. Virulence. 2012;3(3):243-250. 4. Farrugia DN, Elbourne LD, Hassan KA, et al. The complete genome and phenome of a community-acquired Acinetobacter baumannii. PLoS One. 2013;8 (3):e58628. 5. Otter JA, French GL. Community-associated methicillin-resistant Staphylococcus aureus: the case for a genotypic definition. J Hosp Infect. 2012; 81(3):143-148.
Primary Cutaneous Follicle Center Lymphoma With Follicular Mucinosis Follicular mucinosis (FM) is defined as the accumulation of a mucinous material within the hair follicle. Since its first description by Pinkus1 in 1957 in the setting of alopecia mucinosa, 2 main forms have been classically recognized: a benign idiopathic form, primary follicular mucinosis (PFM), 906
Multiple, diffuse, pruritic, skin-colored papules show a follicular pattern on the chest.
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Copyright 2014 American Medical Association. All rights reserved.
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Author Affiliations: University of Michigan Medical School, Ann Arbor (Tran); Department of Dermatology, University of Michigan, Ann Arbor (Egbers, Lowe, Helfrich, Wang); Department of Pathology, University of Michigan, Ann Arbor, Michigan (Lowe). Corresponding Author: Frank Wang, MD, Department of Dermatology, University of Michigan Health System, 1910 Taubman Center, 1500 E Medical Center Dr, Ann Arbor, MI 48109 ([email protected]). Published Online: June 11, 2014. doi:10.1001/jamadermatol.2013.8846. Conflict of Interest Disclosures: None reported. Additional Contributions: We are indebted to Laura VanGoor, BFA, for assistance with graphic material. Ms VanGoor is an employee of the Department of Dermatology at the University of Michigan Medical School. 1. Pennington M, Yeager J, Skelton H, Smith KJ. Cholesterol embolization syndrome: cutaneous histopathological features and the variable onset of symptoms in patients with different risk factors. Br J Dermatol. 2002;146(3): 511-517. 2. Donohue KG, Saap L, Falanga V. Cholesterol crystal embolization: an atherosclerotic disease with frequent and varied cutaneous manifestations. J Eur Acad Dermatol Venereol. 2003;17(5):504-511.
Most reports of A baumannii infection, both nosocomial and community-acquired (CA) SSTI, involve cellulitis of peau d’orange appearance with overlying vesicles that, when untreated, progress to necrotizing fasciitis with coalescent bullae.2 The condition is uncommon and has been reported solely in compromised hosts.3 To our knowledge, A baumannii has never been reported as a cause of CA-SSTI in a healthy patient. However, unpublished and anecdotal cases of increasingly drug-resistant A baumannii presenting as SSTI in healthy patients are known to exist. Molecular typing experiments reveal community and nosocomial A baumannii isolates to be genetically distinct, existing as separate reservoirs with unique virulence and resistance patterns. Until recently, multidrug resistance was considered a hospital-based phenomenon.4 We report herein the case of a healthy woman with CA multidrugresistant A baumannii.
Acinetobacter baumannii Emerging as a Multidrug-Resistant Skin and Soft-Tissue Pathogen: Parallels to Methicillin-Resistant Staphylococcus aureus
Report of a Case | A woman in her 50s with no comorbidities or history of hospitalization presented with tender, violaceous, indurated dermal plaques with central ulceration and peripheral erythema and edema (Figure, A) that had progressively enlarged over the previous 7 to 8 months. Tissue culture results were specific for A baumannii with sensitivity to polymyxin B and tigecycline. The patient was admitted for treatment with intravenous tigecycline and discharged to home with an inpatient-administered peripherally inserted central catheter to facilitate a subsequent 2 weeks of treatment. Following treatment, the patient underwent extensive wound care for 6 months prior to reepithelialization with resulting scarring, dyschromia, and neuropathic pain (Figure, B).
Over the last 30 years, the gram-negative coccobacillus Acinetobacter baumannii has risen to microbiologic notoriety for its ability to successfully evade nearly all available antibiotics. It is now a well-established source of nosocomial bacteremia and pneumonia, known to cause hospital outbreaks, particularly in the intensive care unit. Less often it represents a source of nosocomial skin and soft-tissue infection (SSTI) in the setting of war wounds, surgical sites, and burns.1
Discussion | The evolution of A baumannii infection bears a striking similarity to the now established methicillin-resistant Staphylococcus aureus (MRSA) epidemic; MRSA was initially regarded as a nosocomial pathogen transmitted between health care facilities and limited to a small number of strains with distinct virulence patterns. While the first CA cases occurred in those with predisposing risk factors, it eventually began ap-
3. Belenfant X, Meyrier A, Jacquot C. Supportive treatment improves survival in multivisceral cholesterol crystal embolism. Am J Kidney Dis. 1999;33(5):840-850. 4. Falanga V, Fine MJ, Kapoor WN. The cutaneous manifestations of cholesterol crystal embolization. Arch Dermatol. 1986;122(10):1194-1198. 5. Gore I, Collins DP. Spontaneous atheromatous embolization: review of the literature and a report of 16 additional cases. Am J Clin Pathol. 1960;33:416-426. 6. Tunick PA, Nayar AC, Goodkin GM, et al; NYU Atheroma Group. Effect of treatment on the incidence of stroke and other emboli in 519 patients with severe thoracic aortic plaque. Am J Cardiol. 2002;90(12):1320-1325.
Figure. Clinical Images of Community-Acquired, Extensively Drug-Resistant Acinetobacter baumannii Skin and Soft-Tissue Infection A
B
A, Left pretibial lower extremity at presentation. B, Left pretibial lower extremity after antibiotic therapy and wound care. jamadermatology.com
JAMA Dermatology August 2014 Volume 150, Number 8
Copyright 2014 American Medical Association. All rights reserved.
Downloaded From: http://archderm.jamanetwork.com/ by a Nanyang Technological University User on 06/09/2015
905
Letters
pearing in healthy patients. Over time, CA-MRSA incorporated new virulence patterns, acquiring large-scale antibiotic resistance, while maintaining a unique genetic profile compared with nosocomial isolates. Better appreciated through a retrospective lens, this CA form rivals its hospital-based counterpart and can aptly be considered an epidemic.5 A baumannii has the potential to evolve in a pattern similar to that of MRSA and should be monitored for growing resistance and virulence. Epidemiologic history has demonstrated how quickly an organism can evolve from benign commensal to resistant pathogen and highlights the need for intense vigilance with regard to infection control and treatment development.1 With continued accrual of pathogenicity and antibiotic resistance, A baumannii is offering new diagnostic and therapeutic challenges. Enhanced awareness is paramount to control this growing threat as the practice gap continues to widen. Brandon L. Adler, BA Aimee Krausz, BA Adam J. Friedman, MD Author Affiliations: Department of Medicine, Division of Dermatology, Albert Einstein College of Medicine, Bronx, New York (Adler, Krausz, Friedman); Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York (Friedman). Corresponding Author: Adam J. Friedman, MD, Division of Dermatology, Montefiore Medical Center, 111 E 210th St, Bronx, NY 10467 ([email protected]). Published Online: June 18, 2014. doi:10.1001/jamadermatol.2013.8855. Conflict of Interest Disclosures: None reported. Funding/Support: This study was supported in part by the Dermatology Foundation. Role of the Sponsors: The Dermatology Foundation had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Additional Information: Mr Adler and Ms Krausz contributed equally to this work. 1. Munoz-Price LS, Weinstein RA. Acinetobacter infection. N Engl J Med. 2008; 358(12):1271-1281. 2. Guerrero DM, Perez F, Conger NG, et al. Acinetobacter baumannii–associated skin and soft-tissue infections: recognizing a broadening spectrum of disease. Surg Infect (Larchmt). 2010;11(1):49-57.
which usually appears in young adults and regresses spontaneously; and a secondary form, lymphoma-associated follicular mucinosis (LAFM),2 which mostly occurs in elderly patients. Most cases of LAFM are related to cutaneous T-cell lymphomas (especially mycosis fungoides), although some cases of Hodgkin disease3 and chronic lymphocytic leukemia4 have also been reported. Report of a Case | A man in his 60s initially presented with a history of an intermittently pruritic eruption on the chest and proximal limbs. Two skin biopsies were performed on the neck and the back. The lesions were reported as primary, cutaneous, low-grade, B-cell lymphoma favoring marginal B-cell lymphoma. The peripheral blood sample test results and the bonemarrow core biopsy findings were normal. Computed tomographic scans did not reveal any abnormality. The patient was never treated and did not come back because the lesions disappeared spontaneously. Eight years later, he presented with multiple, millimetric, pruritic, skin-colored papules with a follicular pattern on the chest, back, and upper extremities (Figure 1). He did not have any constitutional symptoms. Two biopsies performed on the chest and the abdomen revealed dense lymphocytic infiltrate in the reticular dermis, centered around and within hair follicles, which showed cavities filled with abundant mucinous material (Figure 2A). Small and irregular lymphocytes were admixed with large lymphocytes, plasma cells, and eosinophils. Atypical cells expressed CD20, CD43, CD79α and BCL6. Some intraepithelial lymphocytes tested positive for CD3 and CD4, but most of them expressed CD20 (Figure 2B). Polymerase chain reaction revealed a monoclonal rearrangement of the heavy chain immunoglobulin IgH gene with a peak at 160 base pairs. A reactive lymphoid T cell (CD3, CD43 and CD4 positive) infiltrate was found surrounding the neoplastic cells. The patient was finally diagnosed as having primary cutaneous follicle center lymphoma associated with follicular mucinosis. At last follow-up 4 months later, the lesions and the Figure 1. A Case of Primary Cutaneous Follicle Center Lymphoma With a Very Unusual Miliary Clinical Presentation
3. Howard A, O’Donoghue M, Feeney A, Sleator RD. Acinetobacter baumannii: an emerging opportunistic pathogen. Virulence. 2012;3(3):243-250. 4. Farrugia DN, Elbourne LD, Hassan KA, et al. The complete genome and phenome of a community-acquired Acinetobacter baumannii. PLoS One. 2013;8 (3):e58628. 5. Otter JA, French GL. Community-associated methicillin-resistant Staphylococcus aureus: the case for a genotypic definition. J Hosp Infect. 2012; 81(3):143-148.
Primary Cutaneous Follicle Center Lymphoma With Follicular Mucinosis Follicular mucinosis (FM) is defined as the accumulation of a mucinous material within the hair follicle. Since its first description by Pinkus1 in 1957 in the setting of alopecia mucinosa, 2 main forms have been classically recognized: a benign idiopathic form, primary follicular mucinosis (PFM), 906
Multiple, diffuse, pruritic, skin-colored papules show a follicular pattern on the chest.
JAMA Dermatology August 2014 Volume 150, Number 8
Copyright 2014 American Medical Association. All rights reserved.
Downloaded From: http://archderm.jamanetwork.com/ by a Nanyang Technological University User on 06/09/2015
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