- Email: [email protected]
Pustular blastomycosis
Case reports 355
J AM ACAD DERMATOL VOLUME 61, NUMBER 2
advanced stages of primary cutaneous T-cell lymphoma. J Invest Dermatol 2006;126:2217-23. 27. Wong HK, Wilson AJ, Gibson HM, Hafner MS, Hedgcock CJ, Berger CL, et al. Increased expression of CTLA-4 in malignant T cells from patients with mycosis fungoides-cutaneous T-cell lymphoma. J Invest Dermatol 2006;126:212-9. 28. Henney JE. From the Food and Drug Administration. JAMA 2000;283:1131.
29. Zhang C, Hazarika P, Ni X, Weidner DA, Duvic M. Induction of apoptosis by bexarotene in cutaneous T-cell lymphoma cells: relevance to mechanism of therapeutic action. Clin Cancer Res 2002;8:1234-40. 30. Youn HK, Duvic M, Obitz E, Gniadecki R, Iversen L, Osterborg A, et al. Clinical efficacy of zanolimumab (HuMax-CD4): two phase 2 studies in refractory cutaneous T-cell lymphoma. Blood 2007;109:4655-62.
Pustular blastomycosis Kristopher R. Fisher, MD,a Vickie Baselski, PhD,b Gwen Beard, MD,c Thomas M. Chesney, MD,b,d Stephen C. Threlkeld, MD,e and Robert B. Skinner, MDa Memphis, Tennessee
Blastomycosis is an infection caused by the dimorphic fungus Blastomyces dermatitidis. Infection can disseminate to skin, where characteristic ulcerative and verrucous plaques, sometimes studded with pustules, are typically seen. Herein we report 3 patients, two children and one adult, with pustular blastomycosis. Their cutaneous lesions exhibited a pustular morphology at the onset and throughout the course of their illness, without evolution to more typical verrucous or ulcerative plaques. These patients all resided in Memphis, TN, the site of previous case reports of pustular blastomycosis. ( J Am Acad Dermatol 2009;61:355-8.)
B
lastomycosis is an infection caused by the dimorphic fungus Blastomyces dermatitidis, first described by Gilchrist in 1894 and sometimes referred to as Gilchrist disease or North American blastomycosis. Blastomycosis may manifest itself in 3 forms: pulmonary, disseminated, or primary cutaneous. Cutaneous involvement by the organism most frequently occurs in the disseminated form and is the most common site of extrapulmonary involvement.1 Cutaneous lesions usually arise as ulcerated or verrucous plaques, sometimes studded with pustules.2 In the past, we have described disseminated blastomycosis presenting as a widespread pustular eruption.3 With the following 3 cases, we wish to present additional evidence that From the Division of Dermatology, Department of Medicine,a and Department of Pathology and Laboratory Medicine,b University of Tennessee Health Science Center; Memphis Dermatology Clinicc; Trumbull Laboratoriesd; and Infectious Disease Associates.e Funding sources: None. Conflicts of interest: None declared. Reprint requests: Kristopher R. Fisher, MD, Division of Dermatology, Department of Medicine, University of Tennessee Health Science Center, 956 Court Ave, Coleman Bldg, Room D322, Memphis, TN 38163. 0190-9622/$36.00 ª 2008 by the American Academy of Dermatology, Inc. doi:10.1016/j.jaad.2008.12.014
cutaneous blastomycosis may manifest a purely pustular morphology.
CASE REPORTS Case 1 A 68-year-old woman was admitted to the hospital with a 3-week history of fever and progressive dyspnea. She had a medical history significant for vulvar carcinoma status postvulvectomy, bilateral inguinal/femoral lymphadenectomy, whole pelvis radiation, and chemotherapy. Four months before admission, she completed her sixth cycle of cisplatin; she was therefore considered immunocompromised on admission. Physical cutaneous examination revealed widespread pustules on her face, abdomen, and proximal lower extremities (Figs 1 and 2). Radiologic evaluation revealed bilateral pulmonary infiltrates. A skin biopsy specimen was taken, which demonstrated an intraepidermal collection of neutrophils and round organisms (Fig 3, A). On higher magnification aided by Gomori methenamine silver staining, the organisms appeared as thick-walled, broad-based budding yeasts (Fig 3, B). A presumptive diagnosis of blastomycosis was made, and amphotericin B was started. A culture later confirmed B dermatitidis. During her hospitalization, some pustules ruptured, but they never evolved to nodules or verrucous plaques or ulcers. Because of toxicity from
356 Case reports
J AM ACAD DERMATOL AUGUST 2009
Fig 1. Pustules to bilateral cheeks, chin, vermilion, and corners of mouth.
Fig 3. A, Intraepidermal collection of neutrophils and round organisms. B, Broad-based budding yeasts. (A, Hematoxylin-eosin stain; B, Gomori methenamine silver stain; original magnifications: A, 3100; B, 3400.)
Fig 2. Proximal thigh studded with pustules. Biopsy site (bandage) and central venous access appear.
the amphotericin, itraconazole was substituted, but the patient’s clinical course continued to decline. During her stay in the intensive care department, she developed Torulopsis line sepsis, progressive renal insufficiency, deep vein thromboses, anticoagulantassociated gastrointestinal bleeding, and eventually died as a result of acute respiratory distress syndrome. Case 2 A 16-year-old previously healthy boy was seen as an inpatient consultation by our dermatology service. He presented to the hospital with a 5-day history of fever, malaise, and skin lesions. Physical cutaneous examination revealed both minute and bullous pustules, concentrated to the trunk and abdomen (Fig 4). During the course, some pustules ruptured, but never did they evolve to nodules, plaques, or ulcers. We obtained purulent exudate from the lesions and prepared it with potassium hydroxide; this revealed thick-walled yeast organisms, some exhibiting single broad-based budding. Subsequent culture revealed B dermatitidis.
Fig 4. Side of trunk with intact and ruptured pustules.
Amphotericin B was administered intravenously, and the patient fully recovered. Case 3 A 13-year-old previously healthy boy was seen in our outpatient dermatology clinic with a 3-day history of tender skin lesions. Physical cutaneous examination revealed pustules on his forehead, frontotemporal scalp, mucosal lips, and vermilion (Figs 5 and 6). Pustule contents were obtained for Gram staining and culture for bacteria. Although the bacterial culture produced negative findings, the Gram stain revealed broad-based budding organisms (Fig 7). We contacted the patient, who had
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Fig 5. Pustules along forehead and frontotemporal scalp.
Fig 7. Thick-walled yeast organisms. (Gram stain; original magnification: 3600.)
Fig 6. Pustules of vermilion and mucosal lips.
begun to have fever and flu-like symptoms, and he was admitted to the hospital. On admission, a skin biopsy specimen revealed subepidermal collections of neutrophils and large budding yeasts. Computed tomography of the chest demonstrated a left lower lobe pneumonia, and magnetic resonance imaging of the head showed multiple ring enhancing lesions in both cerebral hemispheres. Osteomyelitis of the right first metatarsal and navicular bones was discovered by bone scintigraphy. Tissue culture confirmed B dermatitidis. The pneumonia, encephalitis, and osteomyelitis were all suspected to represent systemic blastomycosis. The patient recovered quickly and fully with intravenously administered amphotericin B.
DISCUSSION B dermatitidis is a thermally dimorphic fungus, existing in mycelial form (masses of hyphae) at 308C and as yeast at 378C. It has been isolated in soil replete with decayed vegetation and rotting wood, and it flourishes in the humid environs of the Mississippi and Ohio River valleys and the Great Lakes region.4 Consequently, both sporadic cases and epidemics are more likely in these regions. Most patients with blastomycosis are immunocompetent,1 but dissemination occurs more frequently in the immunocompromised.5 Although two of our above cases include children, pediatric cases in the literature are limited; one review reported only 70 pediatric cases in the literature between 1939 and 1983.6 In the great majority of cases, infection occurs via inhalation of spores. Cellular immunity primarily controls the organisms once inhaled, but they may disseminate in their more resistant yeast form.
Dissemination most often occurs to the skin, bone, genitourinary system, or central nervous system, in that order of frequency.2 Clinically, the presentation may be variable; this often leads to a delay in diagnosis. This delay can occur even in endemic areas. For example, in a study from the University of Mississippi Medical Center, only 18% of 123 infected patients were initially suspected to have blastomycosis.7 It has been called a great masquerader, with authors pointing to examples of pulmonary blastomycosis being treated with radiation for presumed lung carcinoma.8 This occurs because pulmonary involvement can be particularly variable in presentation, mimicking community-acquired pneumonia, malignancy, or tuberculosis.1,5 With the skin as the most frequent site of extrapulmonary dissemination, the dermatologist can be very helpful in coming to a diagnosis of blastomycosis. Cutaneous lesions are noted in 40% to 80% of disseminated cases.9 Although a primary cutaneous form of blastomycosis may occur after traumatic inoculation, it is very rare, and disseminated cases with cutaneous involvement far outweigh primary cutaneous cases.2 The typical cutaneous lesions of disseminated blastomycosis have been described as two types. One is a verrucous plaque with an atrophic, cribriform center, often studded with pustules at the periphery.2 Another is a pustule that rapidly progresses into an ulcer with heaped borders.10 B dermatitidis is most commonly identified from tissue histology or smears of exudate or sputum. Serology is not useful in everyday clinical practice.1 In one of the cases presented above, the presumptive diagnosis was obtained by potassium hydroxide preparation of lesion exudate; in another, Gram staining of pustule contents suggested the diagnosis. We present the cases herein to provide better appreciation of variability in the cutaneous manifestations of blastomycosis. Pustular blastomycosis was first described by Hashimoto et al11 in 1977. To our
358 Case reports
J AM ACAD DERMATOL AUGUST 2009
knowledge, our 3 patients represent only the fourth to sixth reported cases of pustular blastomycosis. Interestingly, of the 6 total cases, 5 of them, including those of Hashimoto et al,11 all come from Memphis, TN.3,11,12 The ‘‘blasto belt’’ encompasses the Ohio and Mississippi river basins, with most North American cases being reported in the southeastern and south-central United States. We do not know if a genetic or environmental influence has clustered this particular variant here in Memphis, TN. However, we suspect that because of the overall increased disease burden here, atypical presentations are seemingly more likely to arise. Typical presentations of blastomycosis still far outweigh the pustular variant. In conclusion, we present 3 cases of pustular blastomycosis. Dermatologists remain valuable in the diagnosis of blastomycosis, with its protean clinical presentations. Simple, rapid office procedures, such as Gram staining or potassium hydroxide preparation of tissue exudate can be useful in making the diagnosis. Practitioners should consider blastomycosis when faced with a widespread pustular eruption in the appropriate clinical setting. REFERENCES 1. Bradsher RW, Chapman SW, Pappas PG. Blastomycosis. Infect Dis Clin North Am 2003;17:21-40.
2. Mercurio MG, Elewski BE. Cutaneous blastomycosis. Cutis 1992;50:422-4. 3. Friedman R, Henson T, Skinner R. Pustular eruption: blastomycosis. Arch Dermatol 2002;138:1371-6. 4. Klein BS, Vergeront JM, Weeks RJ, Kumar UN, Mathai G, Varkey B, et al. Isolation of Blastomyces dermatitidis in soil associated with a large outbreak of blastomycosis in Wisconsin. N Engl J Med 1986;314:529-34. 5. Chapman SW, Dismukes WE, Proia LA, Bradsher RW, Pappas PG, Threlkeld MG, et al. Clinical practice guidelines for the management of blastomycosis: 2008 update by the Infectious Diseases Society of America. Clin Infect Dis 2008;46: 1801-12. 6. Steele RW, Abernathy RS. Systemic blastomycosis in children. Pediatr Infect Dis 1983;2:304-7. 7. Lemos LB, Baliga M, Guo M. Blastomycosis: the great pretender can also be an opportunist: initial clinical diagnosis and underlying diseases in 123 patients. Ann Diagn Pathol 2002;6: 194-203. 8. Wallace J. Pulmonary blastomycosis: a great masquerader. Chest 2002;121:677-9. 9. Weil M, Mercurio MG, Brodell RT, Elewski BE. Cutaneous lesions provide a clue to mysterious pulmonary process: pulmonary and cutaneous North American blastomycosis infection. Arch Dermatol 1996;132:822-5. 10. Body BA. Cutaneous manifestations of systemic mycoses. Dermatol Clin 1996;14:125-35. 11. Hashimoto K, Kaplan R, Daman LA, Stuart JM, Bernhardt H. Pustular blastomycosis. Int J Dermatol 1977;16:277-80. 12. Sweeney EW, Franks A, Silva-Hunter M. An unusual case of North American blastomycosis in New Jersey: its clinical course and response to amphotericin B. Cutis 1982;30:199-202.
J AM ACAD DERMATOL VOLUME 61, NUMBER 2
advanced stages of primary cutaneous T-cell lymphoma. J Invest Dermatol 2006;126:2217-23. 27. Wong HK, Wilson AJ, Gibson HM, Hafner MS, Hedgcock CJ, Berger CL, et al. Increased expression of CTLA-4 in malignant T cells from patients with mycosis fungoides-cutaneous T-cell lymphoma. J Invest Dermatol 2006;126:212-9. 28. Henney JE. From the Food and Drug Administration. JAMA 2000;283:1131.
29. Zhang C, Hazarika P, Ni X, Weidner DA, Duvic M. Induction of apoptosis by bexarotene in cutaneous T-cell lymphoma cells: relevance to mechanism of therapeutic action. Clin Cancer Res 2002;8:1234-40. 30. Youn HK, Duvic M, Obitz E, Gniadecki R, Iversen L, Osterborg A, et al. Clinical efficacy of zanolimumab (HuMax-CD4): two phase 2 studies in refractory cutaneous T-cell lymphoma. Blood 2007;109:4655-62.
Pustular blastomycosis Kristopher R. Fisher, MD,a Vickie Baselski, PhD,b Gwen Beard, MD,c Thomas M. Chesney, MD,b,d Stephen C. Threlkeld, MD,e and Robert B. Skinner, MDa Memphis, Tennessee
Blastomycosis is an infection caused by the dimorphic fungus Blastomyces dermatitidis. Infection can disseminate to skin, where characteristic ulcerative and verrucous plaques, sometimes studded with pustules, are typically seen. Herein we report 3 patients, two children and one adult, with pustular blastomycosis. Their cutaneous lesions exhibited a pustular morphology at the onset and throughout the course of their illness, without evolution to more typical verrucous or ulcerative plaques. These patients all resided in Memphis, TN, the site of previous case reports of pustular blastomycosis. ( J Am Acad Dermatol 2009;61:355-8.)
B
lastomycosis is an infection caused by the dimorphic fungus Blastomyces dermatitidis, first described by Gilchrist in 1894 and sometimes referred to as Gilchrist disease or North American blastomycosis. Blastomycosis may manifest itself in 3 forms: pulmonary, disseminated, or primary cutaneous. Cutaneous involvement by the organism most frequently occurs in the disseminated form and is the most common site of extrapulmonary involvement.1 Cutaneous lesions usually arise as ulcerated or verrucous plaques, sometimes studded with pustules.2 In the past, we have described disseminated blastomycosis presenting as a widespread pustular eruption.3 With the following 3 cases, we wish to present additional evidence that From the Division of Dermatology, Department of Medicine,a and Department of Pathology and Laboratory Medicine,b University of Tennessee Health Science Center; Memphis Dermatology Clinicc; Trumbull Laboratoriesd; and Infectious Disease Associates.e Funding sources: None. Conflicts of interest: None declared. Reprint requests: Kristopher R. Fisher, MD, Division of Dermatology, Department of Medicine, University of Tennessee Health Science Center, 956 Court Ave, Coleman Bldg, Room D322, Memphis, TN 38163. 0190-9622/$36.00 ª 2008 by the American Academy of Dermatology, Inc. doi:10.1016/j.jaad.2008.12.014
cutaneous blastomycosis may manifest a purely pustular morphology.
CASE REPORTS Case 1 A 68-year-old woman was admitted to the hospital with a 3-week history of fever and progressive dyspnea. She had a medical history significant for vulvar carcinoma status postvulvectomy, bilateral inguinal/femoral lymphadenectomy, whole pelvis radiation, and chemotherapy. Four months before admission, she completed her sixth cycle of cisplatin; she was therefore considered immunocompromised on admission. Physical cutaneous examination revealed widespread pustules on her face, abdomen, and proximal lower extremities (Figs 1 and 2). Radiologic evaluation revealed bilateral pulmonary infiltrates. A skin biopsy specimen was taken, which demonstrated an intraepidermal collection of neutrophils and round organisms (Fig 3, A). On higher magnification aided by Gomori methenamine silver staining, the organisms appeared as thick-walled, broad-based budding yeasts (Fig 3, B). A presumptive diagnosis of blastomycosis was made, and amphotericin B was started. A culture later confirmed B dermatitidis. During her hospitalization, some pustules ruptured, but they never evolved to nodules or verrucous plaques or ulcers. Because of toxicity from
356 Case reports
J AM ACAD DERMATOL AUGUST 2009
Fig 1. Pustules to bilateral cheeks, chin, vermilion, and corners of mouth.
Fig 3. A, Intraepidermal collection of neutrophils and round organisms. B, Broad-based budding yeasts. (A, Hematoxylin-eosin stain; B, Gomori methenamine silver stain; original magnifications: A, 3100; B, 3400.)
Fig 2. Proximal thigh studded with pustules. Biopsy site (bandage) and central venous access appear.
the amphotericin, itraconazole was substituted, but the patient’s clinical course continued to decline. During her stay in the intensive care department, she developed Torulopsis line sepsis, progressive renal insufficiency, deep vein thromboses, anticoagulantassociated gastrointestinal bleeding, and eventually died as a result of acute respiratory distress syndrome. Case 2 A 16-year-old previously healthy boy was seen as an inpatient consultation by our dermatology service. He presented to the hospital with a 5-day history of fever, malaise, and skin lesions. Physical cutaneous examination revealed both minute and bullous pustules, concentrated to the trunk and abdomen (Fig 4). During the course, some pustules ruptured, but never did they evolve to nodules, plaques, or ulcers. We obtained purulent exudate from the lesions and prepared it with potassium hydroxide; this revealed thick-walled yeast organisms, some exhibiting single broad-based budding. Subsequent culture revealed B dermatitidis.
Fig 4. Side of trunk with intact and ruptured pustules.
Amphotericin B was administered intravenously, and the patient fully recovered. Case 3 A 13-year-old previously healthy boy was seen in our outpatient dermatology clinic with a 3-day history of tender skin lesions. Physical cutaneous examination revealed pustules on his forehead, frontotemporal scalp, mucosal lips, and vermilion (Figs 5 and 6). Pustule contents were obtained for Gram staining and culture for bacteria. Although the bacterial culture produced negative findings, the Gram stain revealed broad-based budding organisms (Fig 7). We contacted the patient, who had
J AM ACAD DERMATOL
Case reports 357
VOLUME 61, NUMBER 2
Fig 5. Pustules along forehead and frontotemporal scalp.
Fig 7. Thick-walled yeast organisms. (Gram stain; original magnification: 3600.)
Fig 6. Pustules of vermilion and mucosal lips.
begun to have fever and flu-like symptoms, and he was admitted to the hospital. On admission, a skin biopsy specimen revealed subepidermal collections of neutrophils and large budding yeasts. Computed tomography of the chest demonstrated a left lower lobe pneumonia, and magnetic resonance imaging of the head showed multiple ring enhancing lesions in both cerebral hemispheres. Osteomyelitis of the right first metatarsal and navicular bones was discovered by bone scintigraphy. Tissue culture confirmed B dermatitidis. The pneumonia, encephalitis, and osteomyelitis were all suspected to represent systemic blastomycosis. The patient recovered quickly and fully with intravenously administered amphotericin B.
DISCUSSION B dermatitidis is a thermally dimorphic fungus, existing in mycelial form (masses of hyphae) at 308C and as yeast at 378C. It has been isolated in soil replete with decayed vegetation and rotting wood, and it flourishes in the humid environs of the Mississippi and Ohio River valleys and the Great Lakes region.4 Consequently, both sporadic cases and epidemics are more likely in these regions. Most patients with blastomycosis are immunocompetent,1 but dissemination occurs more frequently in the immunocompromised.5 Although two of our above cases include children, pediatric cases in the literature are limited; one review reported only 70 pediatric cases in the literature between 1939 and 1983.6 In the great majority of cases, infection occurs via inhalation of spores. Cellular immunity primarily controls the organisms once inhaled, but they may disseminate in their more resistant yeast form.
Dissemination most often occurs to the skin, bone, genitourinary system, or central nervous system, in that order of frequency.2 Clinically, the presentation may be variable; this often leads to a delay in diagnosis. This delay can occur even in endemic areas. For example, in a study from the University of Mississippi Medical Center, only 18% of 123 infected patients were initially suspected to have blastomycosis.7 It has been called a great masquerader, with authors pointing to examples of pulmonary blastomycosis being treated with radiation for presumed lung carcinoma.8 This occurs because pulmonary involvement can be particularly variable in presentation, mimicking community-acquired pneumonia, malignancy, or tuberculosis.1,5 With the skin as the most frequent site of extrapulmonary dissemination, the dermatologist can be very helpful in coming to a diagnosis of blastomycosis. Cutaneous lesions are noted in 40% to 80% of disseminated cases.9 Although a primary cutaneous form of blastomycosis may occur after traumatic inoculation, it is very rare, and disseminated cases with cutaneous involvement far outweigh primary cutaneous cases.2 The typical cutaneous lesions of disseminated blastomycosis have been described as two types. One is a verrucous plaque with an atrophic, cribriform center, often studded with pustules at the periphery.2 Another is a pustule that rapidly progresses into an ulcer with heaped borders.10 B dermatitidis is most commonly identified from tissue histology or smears of exudate or sputum. Serology is not useful in everyday clinical practice.1 In one of the cases presented above, the presumptive diagnosis was obtained by potassium hydroxide preparation of lesion exudate; in another, Gram staining of pustule contents suggested the diagnosis. We present the cases herein to provide better appreciation of variability in the cutaneous manifestations of blastomycosis. Pustular blastomycosis was first described by Hashimoto et al11 in 1977. To our
358 Case reports
J AM ACAD DERMATOL AUGUST 2009
knowledge, our 3 patients represent only the fourth to sixth reported cases of pustular blastomycosis. Interestingly, of the 6 total cases, 5 of them, including those of Hashimoto et al,11 all come from Memphis, TN.3,11,12 The ‘‘blasto belt’’ encompasses the Ohio and Mississippi river basins, with most North American cases being reported in the southeastern and south-central United States. We do not know if a genetic or environmental influence has clustered this particular variant here in Memphis, TN. However, we suspect that because of the overall increased disease burden here, atypical presentations are seemingly more likely to arise. Typical presentations of blastomycosis still far outweigh the pustular variant. In conclusion, we present 3 cases of pustular blastomycosis. Dermatologists remain valuable in the diagnosis of blastomycosis, with its protean clinical presentations. Simple, rapid office procedures, such as Gram staining or potassium hydroxide preparation of tissue exudate can be useful in making the diagnosis. Practitioners should consider blastomycosis when faced with a widespread pustular eruption in the appropriate clinical setting. REFERENCES 1. Bradsher RW, Chapman SW, Pappas PG. Blastomycosis. Infect Dis Clin North Am 2003;17:21-40.
2. Mercurio MG, Elewski BE. Cutaneous blastomycosis. Cutis 1992;50:422-4. 3. Friedman R, Henson T, Skinner R. Pustular eruption: blastomycosis. Arch Dermatol 2002;138:1371-6. 4. Klein BS, Vergeront JM, Weeks RJ, Kumar UN, Mathai G, Varkey B, et al. Isolation of Blastomyces dermatitidis in soil associated with a large outbreak of blastomycosis in Wisconsin. N Engl J Med 1986;314:529-34. 5. Chapman SW, Dismukes WE, Proia LA, Bradsher RW, Pappas PG, Threlkeld MG, et al. Clinical practice guidelines for the management of blastomycosis: 2008 update by the Infectious Diseases Society of America. Clin Infect Dis 2008;46: 1801-12. 6. Steele RW, Abernathy RS. Systemic blastomycosis in children. Pediatr Infect Dis 1983;2:304-7. 7. Lemos LB, Baliga M, Guo M. Blastomycosis: the great pretender can also be an opportunist: initial clinical diagnosis and underlying diseases in 123 patients. Ann Diagn Pathol 2002;6: 194-203. 8. Wallace J. Pulmonary blastomycosis: a great masquerader. Chest 2002;121:677-9. 9. Weil M, Mercurio MG, Brodell RT, Elewski BE. Cutaneous lesions provide a clue to mysterious pulmonary process: pulmonary and cutaneous North American blastomycosis infection. Arch Dermatol 1996;132:822-5. 10. Body BA. Cutaneous manifestations of systemic mycoses. Dermatol Clin 1996;14:125-35. 11. Hashimoto K, Kaplan R, Daman LA, Stuart JM, Bernhardt H. Pustular blastomycosis. Int J Dermatol 1977;16:277-80. 12. Sweeney EW, Franks A, Silva-Hunter M. An unusual case of North American blastomycosis in New Jersey: its clinical course and response to amphotericin B. Cutis 1982;30:199-202.