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Blastomycoid sporotrichosis
Blastomycoid sporotrichosis* Response to low-dose amphotericin B James F. Dolezal, M.D. Council Bluffs, fA A patient is described with a large verrucous lesion of sporotrichosis of 7 years' duration, resembling North American blastomycosis. The observed change over two untreated years is described. The patient responded to significantly less than recommended doses of amphotericin B. (J AM ACAD DERMATOL 4:523-527, 1981.)
Sporotrichosis is a fungal infection which usually affects the skin in a characteristic manner. A nodule or ulcer develops, followed by the appearance of a chain of nodules proximally following the drainage course of the local lymphatic system. The most common cause for this pattern is sporotrichosis, yet many other diseases can cause an identical pattern. To encourage complete and proper diagnostic investigation, such an arrangement of nodules or ulcers is often referred to as being "sporotrichoid. " This description is retained if an organism other than Sporothrix schenckii is causative, but it is discarded in true cases of sporotrichosis. This pattern of infection is called the ascending lymphangitic type. Less commonly, sporotrichosis may be restricted to the site of inoculation and is called the localized cutaneous (fixed) type. It has been suggested that this reaction is more likely to occur in patients who have been previously sensitized to S. Schenckii.' The localized cutaneous form of sporotrichosis may mimic patterns usually associated with other organisms or disease processes. Patients with localized cutaneous sporotrichosis have been described as having lesions resembling acne.! actinomycosis," bromoderma," chromo-
Reprints not available. *Owen Laboratories, Dallas, TX, financed the cost of the color reproductions.
0190-9622/81/050523+05$00.50/0 © 1981 Am Acad Dennatol
blastomycosis.v" coccidioidomycosis," dermatophyte granulomas (Majocchi's granuloma) ,7 gummatous syphilis, 3.8.9 iododerma," leishmaniasis,' North American blastomycosis, 10 paracoccidioidomycosis.!' psoriasis;" pyogenic granuloma," sarcoidosis," and tuberculosis verrucosa cutis.!" Wood splinters, marsh and prairie hay, barberry and rose thoms, sphagnum moss, straw, and dried grass are among the fomites implicated'! in the transmission of this disease by primary cutaneous inoculation. Cutaneous inoculation most commonly is followed by the ascending lymphangitic form, but it may result in the localized cutaneous form. The disseminated type may develop from hematogenous spread of either of the primary cutaneous types, or from primary cutaneous inoculation without obvious lesion formation. The inhalation of spores may cause primary pulmonary sporotrichosis, which may also result in hematogenous spread to skin as well as other organ systems. I have recently followed a patient with a lO-cm blastomycoid lesion of sporotrichosis spanning 7 years before resolution. CASE REPORT
A 21-year-old Iowa man was seen concerning a recent tear in a lesion which had been in the right axilla for 5 years. While roughhousing with a friend, the lesion tore duringapplication of a wrestling hold. He said the lesion had been diagnosed previously as a "ring-
523
524 Dolezal
worm. " Since several different medications prescribed for the condition were ineffective, he had not treated it for the preceding 3 years. The lesion was occasionally pruritic and tended to restrict the raising of his arm. The onset of the lesion followed a summer spent on a Kansas farm. About 4 months prior to the onset, he noticed a "sore" on his right elbow and enlarged nodes in the right axilla. At about the time this' 'sore" and the adenopathy resolved, he noticed the lesion in the skin of the right axilla. The cutaneous lesion gradually enlarged, but as it progressed inferiorly previously involved areas healed with scarring. Occasionally, similar-appearing but smaller lesions would come and go. There was no history of iodide or bromide ingestion. Review of medical records from the time of onset indicated he consulted his physician with a lesion described as an abscess with lymphangitis as well as generalized adenopathy. At that time, the complete blood count was unremarkable, the Monospot test was negative, and a 2-hour glucose tolerance test showed no abnormalities. Three weeks later a cervical node biopsy showed only nonspecific reactive hyperplasia. Outing the next 6 weeks, reference was made to continuing lymphangitis. Although various internal and external antibiotics were ordered during this period, records indicated that the patient did not obtain or take the prescribed medications. The patient was seen several more times shortly thereafter for unrelated problems. No further reference was made in his old medical records to the abscess or lymphadenopathy. Physical examination. Located immediately inferior to the right axilla was a 10 x 6-cm crescentshaped lesion with a verrucous, violaceous surface which superiorly blended into a scar, and inferiorly had a raised, sharply marginated border. A 3-cm plaque with similar surface characteristics was located on the posterosuperior aspect of the crescent and was divided with a hemorrhagic fissure (Fig. 1). In the right inguinal crease was a 1.5x 1.0-cm indurated plaque with a verrucous surface. There was a 4-cm streak of erythema overlying the inguinal crease, emanating from the lesion (Fig. 3). A similar but smaller lesion was present in the left inguinal crease. Scattered about these areas as well as over the back were acneiform pustules. Open and closed comedones were abundant over the upper back. Body weight was 73 kg. The remainder of the physical examination was either negative or noncontributory . Laboratory examination. Punch biopsies were taken from the active border of the axillary lesion on two separate occasions. Each biopsy was divided, with one half being prepared for histologic examination,
Journal of the American Academy of Dermatology
while the other half was submitted for culture. S. schenckii was identified in each of the cultures from the biopsy material. Histologic examination showed pseudoepitheliomatous hyperplasia, intraepidermal neutrophilic abscesses, a dense polymorphous upper dermal infiltrate with numerous multinucleated giant cells without vacuolation. Periodic acid-Schiff (PAS) with diastase and Gomori's methenamine silver stains did not demonstrate fungal organisms. The paraffin block containing tissue from the cervical node biopsy was located. Fungal stains on recut material failed to reveal fungal organisms. Sporotrichosis antibody titers from serum were positive. The latex agglutination titer was 1: 16 and the tube agglutination titer was 1: 32, as reported by the Center for Disease Control. The CDC reports that latex agglutination titers of 1 :8 and tube agglutination titers of 1: 16 or greater are considered presumptive evidence of sporotrichosis. The blastomycosis complement fixation titer and VDRL were negative. The chest roentgenogram was unremarkable. The serum bromide was less than 10 mg of sodium bromide/ dl. The histoplasmosis complement fixation titer was positive at 1: 8. Immunologic studies were normal. The T and B lymphocyte enumeration counted 62% T lymphocytes and 33% B lymphocytes. Lymphocyte transformation responses to concanavalin A, phytohemagglutinin, and pokeweed mitogen were in the normal range. The hemolytic activity of whole complement for 50% of sheep erythrocytes was 50 D/ml (normal, 49-103). C3 was 113 mg/dl (normal, 88-244), and C4 was 16.5 mg/dl (normal, 12-66). Course. Treatment was begun with oral potassium iodide given in the saturated solution (SSKI). He noted a flare of the acne shortly thereafter and discontinued the SSKI. Reestablishment and adjustment of the dosage of the SSKI, as well as management of the acne, was complicated by the patient's poor compliance with reporting andlor follow-up visits. Recommendations for local applications of heat on a regular basis were similarly unheeded. Two years after establishment of the diagnosis the axillary lesion had advanced (Fig. 4), but the inguinal lesions had resolved. Considering his poor response, and the difficulty in establishing an effective therapeutic program, he consented to treatment with amphotericin B (Fungizone). Following extended discussion of the potential difficulties associated with the administration of amphotericin B, the patient agreed to a short hospitalization. He remained in the hospital approximately 30 hours, receiving two doses of am-
Volume 4 Number 5 May, 1981
Blastomycoid sporotrichosis
Fig. 1. The tear in the posterosuperior portion of the lesion prompted the patient to seek
medical care. Fig. 2. Six weeks later, the tear had healed, with an apparent resolution of the process in
the traumatized area. Fig. 3. Verrucous lesion in the right inguinal crease. Fig. 4. The lesion 2 years after Fig. 1, immediately prior to treatment with amphotericin B. It had advanced inferiorly and posteriorly. Fig. 5. The lesion 24 days after Fig. 4. At this time 485 mg of amphotericin B had been infused. There was resolution of the verrucous surface and the color was less vivid. Fig. 6. Seven months after stopping the amphotericin B, the patient remained free of disease, with scar tissue as the only apparent sequela.
525
Journal of the American Academy of Dermatology
526 Dolezal
photericin B, 24 hours apart, 35 mg and 50 mg, respectively. He experienced no difficulties, but left the hospital without notice. Arrangements were made for continuing treatment at the outpatient department. A total dosage of at least 1.5 gm was planned. The patient made arrangements to receive the infusion at night while sleeping. He received 50 mg nightly for three nights, skipped a night, then began to appear for treatment at erratic and ever-increasing intervals. His dose was gradually increased to 100 mg. The last interval before he stopped treatment was 9 days. During this time his blood urea nitrogen rose from a pretreatment level of 6 mg/dl to 25 mg/ dl. The total dosage of amphotericin B was 685 mg. During this period of treatment, the lesion was visibly improving (Fig. 5). When next seen, 7 months later, a flattened scar was the only apparent residual (Fig. 6). The patient reported that maximum resolution was obtained within about 2 weeks of cessation of treatment. DISCUSSION
Generally patients with the localized cutaneous type of sporotrichosis have lesions less than 6 em in diameter and are diagnosed and treated within 18 months of onset. 10 However, there are several notable exceptions. 4.10 The patient of Carr et apo had a 21-year duration of extensive blastomycoid lesions over a buttock and thigh. There are no reports describing blastomycoid or verrucous lesions evolving following a sporotrichotic ascending lymphangitic infection. Relatively little is known about the immune status of patients with sporotrichosis. 16 It is interesting to speculate that the poorly resolving abscess with lymphangitis actually represented the primary lesion of sporotrichosis in this patient. Although biopsy or culture of the verrucous lesions in the inguinal creases was not done, the clinical similarity to the axillary lesion suggests that these also represented cutaneous lesions of sporotrichosis. Although difficulty in follow-up prevented in vivo immunologic studies, the in vitro studies indicated a normal immunologic system. This patient may have experienced three forms of sporotrichosis: the ascending lymphangitic, the localized cutaneous, and, disregarding the possibility of self-inoculation, the hematogenous with dissemination (to skin only). The localized cuta-
neous lesion had a very unusual clinical presentation, was unusually large, and was present for an unusual length of time. When other measures have failed, the dose of amphotericin B usually recommended for cutaneous sporotrichosis is similar to that recommended for systemic sporotrichosis, 1.5 to 2.5 gm.J" No controlled studies have confirmed that this is the optimal dosage for treatment of sporotrichosis. Lynch et aP7 reported two patients with systemic sporotrichosis who responded to 725 mg and 1,000 mg of amphotericin B and remained free of disease at 9- and 8-month follow-up. Amphotericin B must be administered intravenously and is often associated with significant side effects, many of which are dose-related. In this patient, less than half the recommended dose of amphotericin B nevertheless resulted in successful treatment. If the total dosage of amphotericin B can be lowered in other patients with localized disease, then the requirement for hospitalization as well as the potential for side effects will be lowered. Whether this observation will have application in other patients remains to be determined. REFERENCES 1. Rippon JW: Medical mycology. Philadelphia, 1974, W. B. Saunders Co., pp. 252-253. 2. Silva M: Sporotrichosis in Columbia. Arch Dermatol 65:355-356, 1952. 3. Smith LM: Sporotrichosis: Report of four clinically atypical cases. South Med J 38:505-509, 1945. 4. Restrepo MA, Calle Velez G, et al: Esporotricosis epidermica atipica. Gac Sanit 22:98-102, 1967. 5. Hughes WT: Chromoblastomycosis versus sporotrichosis. J Pediatr 73:253-254, 1968. 6. Wilson JW, Smith CE, Plunkett OA: Primary cutaneous coccidioidomycosis-the criteria for diagnosis and a report of a case. Calif Med 79:233-239, 1953. 7. Schiff BL: Solitary sporotrichotic granuloma. Arch Dermatol 65:353-355, 1952. 8. Moore M, Kile RL: Generalized subcutaneous gummatous ulcerating sporotrichosis. Arch Derrnatol 31:672685, 1935. 9. Gluckman I: Sporotrichosis in children. S Afr Med J 39:991-992, 1965. 10. Carr RD, Storkan MA, Wilson JW, Swatek FE: Extensive verrucous sporotrichosis of long duration. Arch Dermato189:124-130, 1964. 11. Alvarado ERG, Seminarro C, Negri T: Generalized verrucose sporotrichosis. Prensa Med Argent 22: 110·113. 1935.
Volume 4 Number 5 May, 198\
12. Nicholas L, Shaffer B: Sporotrichosis; psoriasis (case presentation). Arch Dermatol 61:166-167, 1950. 13. McFarland RB, Goodman SB: Sporotrichosis and sarcoidosis. Arch Intern Med 112:760-765, 1963. 14. Elsenstaedt JS: Sporotrichosis resembling tuberculosis cutis. JAMA 71:726-728,1918. 15. Laur WE, Posey RE, Waller JD: A family epidemic of
Blastomycoid sporotrichosis
527
cutaneous sporotrichosis occurring in North Texas. Cutis 23:205-208, 1979. 16. Utz JP: Sporotrichosis, in Hoeprich P; Infectious diseases, ed. 2. Hagerstown, MD, 1977, Harper & Row, Publishers, Inc., p. 850. 17. Lynch PJ, Voorhees JJ, Harrell ER: Systemic sporotrichosis. Ann Intern Med 73:23-30, 1970.
Sporotrichosis is a fungal infection which usually affects the skin in a characteristic manner. A nodule or ulcer develops, followed by the appearance of a chain of nodules proximally following the drainage course of the local lymphatic system. The most common cause for this pattern is sporotrichosis, yet many other diseases can cause an identical pattern. To encourage complete and proper diagnostic investigation, such an arrangement of nodules or ulcers is often referred to as being "sporotrichoid. " This description is retained if an organism other than Sporothrix schenckii is causative, but it is discarded in true cases of sporotrichosis. This pattern of infection is called the ascending lymphangitic type. Less commonly, sporotrichosis may be restricted to the site of inoculation and is called the localized cutaneous (fixed) type. It has been suggested that this reaction is more likely to occur in patients who have been previously sensitized to S. Schenckii.' The localized cutaneous form of sporotrichosis may mimic patterns usually associated with other organisms or disease processes. Patients with localized cutaneous sporotrichosis have been described as having lesions resembling acne.! actinomycosis," bromoderma," chromo-
Reprints not available. *Owen Laboratories, Dallas, TX, financed the cost of the color reproductions.
0190-9622/81/050523+05$00.50/0 © 1981 Am Acad Dennatol
blastomycosis.v" coccidioidomycosis," dermatophyte granulomas (Majocchi's granuloma) ,7 gummatous syphilis, 3.8.9 iododerma," leishmaniasis,' North American blastomycosis, 10 paracoccidioidomycosis.!' psoriasis;" pyogenic granuloma," sarcoidosis," and tuberculosis verrucosa cutis.!" Wood splinters, marsh and prairie hay, barberry and rose thoms, sphagnum moss, straw, and dried grass are among the fomites implicated'! in the transmission of this disease by primary cutaneous inoculation. Cutaneous inoculation most commonly is followed by the ascending lymphangitic form, but it may result in the localized cutaneous form. The disseminated type may develop from hematogenous spread of either of the primary cutaneous types, or from primary cutaneous inoculation without obvious lesion formation. The inhalation of spores may cause primary pulmonary sporotrichosis, which may also result in hematogenous spread to skin as well as other organ systems. I have recently followed a patient with a lO-cm blastomycoid lesion of sporotrichosis spanning 7 years before resolution. CASE REPORT
A 21-year-old Iowa man was seen concerning a recent tear in a lesion which had been in the right axilla for 5 years. While roughhousing with a friend, the lesion tore duringapplication of a wrestling hold. He said the lesion had been diagnosed previously as a "ring-
523
524 Dolezal
worm. " Since several different medications prescribed for the condition were ineffective, he had not treated it for the preceding 3 years. The lesion was occasionally pruritic and tended to restrict the raising of his arm. The onset of the lesion followed a summer spent on a Kansas farm. About 4 months prior to the onset, he noticed a "sore" on his right elbow and enlarged nodes in the right axilla. At about the time this' 'sore" and the adenopathy resolved, he noticed the lesion in the skin of the right axilla. The cutaneous lesion gradually enlarged, but as it progressed inferiorly previously involved areas healed with scarring. Occasionally, similar-appearing but smaller lesions would come and go. There was no history of iodide or bromide ingestion. Review of medical records from the time of onset indicated he consulted his physician with a lesion described as an abscess with lymphangitis as well as generalized adenopathy. At that time, the complete blood count was unremarkable, the Monospot test was negative, and a 2-hour glucose tolerance test showed no abnormalities. Three weeks later a cervical node biopsy showed only nonspecific reactive hyperplasia. Outing the next 6 weeks, reference was made to continuing lymphangitis. Although various internal and external antibiotics were ordered during this period, records indicated that the patient did not obtain or take the prescribed medications. The patient was seen several more times shortly thereafter for unrelated problems. No further reference was made in his old medical records to the abscess or lymphadenopathy. Physical examination. Located immediately inferior to the right axilla was a 10 x 6-cm crescentshaped lesion with a verrucous, violaceous surface which superiorly blended into a scar, and inferiorly had a raised, sharply marginated border. A 3-cm plaque with similar surface characteristics was located on the posterosuperior aspect of the crescent and was divided with a hemorrhagic fissure (Fig. 1). In the right inguinal crease was a 1.5x 1.0-cm indurated plaque with a verrucous surface. There was a 4-cm streak of erythema overlying the inguinal crease, emanating from the lesion (Fig. 3). A similar but smaller lesion was present in the left inguinal crease. Scattered about these areas as well as over the back were acneiform pustules. Open and closed comedones were abundant over the upper back. Body weight was 73 kg. The remainder of the physical examination was either negative or noncontributory . Laboratory examination. Punch biopsies were taken from the active border of the axillary lesion on two separate occasions. Each biopsy was divided, with one half being prepared for histologic examination,
Journal of the American Academy of Dermatology
while the other half was submitted for culture. S. schenckii was identified in each of the cultures from the biopsy material. Histologic examination showed pseudoepitheliomatous hyperplasia, intraepidermal neutrophilic abscesses, a dense polymorphous upper dermal infiltrate with numerous multinucleated giant cells without vacuolation. Periodic acid-Schiff (PAS) with diastase and Gomori's methenamine silver stains did not demonstrate fungal organisms. The paraffin block containing tissue from the cervical node biopsy was located. Fungal stains on recut material failed to reveal fungal organisms. Sporotrichosis antibody titers from serum were positive. The latex agglutination titer was 1: 16 and the tube agglutination titer was 1: 32, as reported by the Center for Disease Control. The CDC reports that latex agglutination titers of 1 :8 and tube agglutination titers of 1: 16 or greater are considered presumptive evidence of sporotrichosis. The blastomycosis complement fixation titer and VDRL were negative. The chest roentgenogram was unremarkable. The serum bromide was less than 10 mg of sodium bromide/ dl. The histoplasmosis complement fixation titer was positive at 1: 8. Immunologic studies were normal. The T and B lymphocyte enumeration counted 62% T lymphocytes and 33% B lymphocytes. Lymphocyte transformation responses to concanavalin A, phytohemagglutinin, and pokeweed mitogen were in the normal range. The hemolytic activity of whole complement for 50% of sheep erythrocytes was 50 D/ml (normal, 49-103). C3 was 113 mg/dl (normal, 88-244), and C4 was 16.5 mg/dl (normal, 12-66). Course. Treatment was begun with oral potassium iodide given in the saturated solution (SSKI). He noted a flare of the acne shortly thereafter and discontinued the SSKI. Reestablishment and adjustment of the dosage of the SSKI, as well as management of the acne, was complicated by the patient's poor compliance with reporting andlor follow-up visits. Recommendations for local applications of heat on a regular basis were similarly unheeded. Two years after establishment of the diagnosis the axillary lesion had advanced (Fig. 4), but the inguinal lesions had resolved. Considering his poor response, and the difficulty in establishing an effective therapeutic program, he consented to treatment with amphotericin B (Fungizone). Following extended discussion of the potential difficulties associated with the administration of amphotericin B, the patient agreed to a short hospitalization. He remained in the hospital approximately 30 hours, receiving two doses of am-
Volume 4 Number 5 May, 1981
Blastomycoid sporotrichosis
Fig. 1. The tear in the posterosuperior portion of the lesion prompted the patient to seek
medical care. Fig. 2. Six weeks later, the tear had healed, with an apparent resolution of the process in
the traumatized area. Fig. 3. Verrucous lesion in the right inguinal crease. Fig. 4. The lesion 2 years after Fig. 1, immediately prior to treatment with amphotericin B. It had advanced inferiorly and posteriorly. Fig. 5. The lesion 24 days after Fig. 4. At this time 485 mg of amphotericin B had been infused. There was resolution of the verrucous surface and the color was less vivid. Fig. 6. Seven months after stopping the amphotericin B, the patient remained free of disease, with scar tissue as the only apparent sequela.
525
Journal of the American Academy of Dermatology
526 Dolezal
photericin B, 24 hours apart, 35 mg and 50 mg, respectively. He experienced no difficulties, but left the hospital without notice. Arrangements were made for continuing treatment at the outpatient department. A total dosage of at least 1.5 gm was planned. The patient made arrangements to receive the infusion at night while sleeping. He received 50 mg nightly for three nights, skipped a night, then began to appear for treatment at erratic and ever-increasing intervals. His dose was gradually increased to 100 mg. The last interval before he stopped treatment was 9 days. During this time his blood urea nitrogen rose from a pretreatment level of 6 mg/dl to 25 mg/ dl. The total dosage of amphotericin B was 685 mg. During this period of treatment, the lesion was visibly improving (Fig. 5). When next seen, 7 months later, a flattened scar was the only apparent residual (Fig. 6). The patient reported that maximum resolution was obtained within about 2 weeks of cessation of treatment. DISCUSSION
Generally patients with the localized cutaneous type of sporotrichosis have lesions less than 6 em in diameter and are diagnosed and treated within 18 months of onset. 10 However, there are several notable exceptions. 4.10 The patient of Carr et apo had a 21-year duration of extensive blastomycoid lesions over a buttock and thigh. There are no reports describing blastomycoid or verrucous lesions evolving following a sporotrichotic ascending lymphangitic infection. Relatively little is known about the immune status of patients with sporotrichosis. 16 It is interesting to speculate that the poorly resolving abscess with lymphangitis actually represented the primary lesion of sporotrichosis in this patient. Although biopsy or culture of the verrucous lesions in the inguinal creases was not done, the clinical similarity to the axillary lesion suggests that these also represented cutaneous lesions of sporotrichosis. Although difficulty in follow-up prevented in vivo immunologic studies, the in vitro studies indicated a normal immunologic system. This patient may have experienced three forms of sporotrichosis: the ascending lymphangitic, the localized cutaneous, and, disregarding the possibility of self-inoculation, the hematogenous with dissemination (to skin only). The localized cuta-
neous lesion had a very unusual clinical presentation, was unusually large, and was present for an unusual length of time. When other measures have failed, the dose of amphotericin B usually recommended for cutaneous sporotrichosis is similar to that recommended for systemic sporotrichosis, 1.5 to 2.5 gm.J" No controlled studies have confirmed that this is the optimal dosage for treatment of sporotrichosis. Lynch et aP7 reported two patients with systemic sporotrichosis who responded to 725 mg and 1,000 mg of amphotericin B and remained free of disease at 9- and 8-month follow-up. Amphotericin B must be administered intravenously and is often associated with significant side effects, many of which are dose-related. In this patient, less than half the recommended dose of amphotericin B nevertheless resulted in successful treatment. If the total dosage of amphotericin B can be lowered in other patients with localized disease, then the requirement for hospitalization as well as the potential for side effects will be lowered. Whether this observation will have application in other patients remains to be determined. REFERENCES 1. Rippon JW: Medical mycology. Philadelphia, 1974, W. B. Saunders Co., pp. 252-253. 2. Silva M: Sporotrichosis in Columbia. Arch Dermatol 65:355-356, 1952. 3. Smith LM: Sporotrichosis: Report of four clinically atypical cases. South Med J 38:505-509, 1945. 4. Restrepo MA, Calle Velez G, et al: Esporotricosis epidermica atipica. Gac Sanit 22:98-102, 1967. 5. Hughes WT: Chromoblastomycosis versus sporotrichosis. J Pediatr 73:253-254, 1968. 6. Wilson JW, Smith CE, Plunkett OA: Primary cutaneous coccidioidomycosis-the criteria for diagnosis and a report of a case. Calif Med 79:233-239, 1953. 7. Schiff BL: Solitary sporotrichotic granuloma. Arch Dermatol 65:353-355, 1952. 8. Moore M, Kile RL: Generalized subcutaneous gummatous ulcerating sporotrichosis. Arch Derrnatol 31:672685, 1935. 9. Gluckman I: Sporotrichosis in children. S Afr Med J 39:991-992, 1965. 10. Carr RD, Storkan MA, Wilson JW, Swatek FE: Extensive verrucous sporotrichosis of long duration. Arch Dermato189:124-130, 1964. 11. Alvarado ERG, Seminarro C, Negri T: Generalized verrucose sporotrichosis. Prensa Med Argent 22: 110·113. 1935.
Volume 4 Number 5 May, 198\
12. Nicholas L, Shaffer B: Sporotrichosis; psoriasis (case presentation). Arch Dermatol 61:166-167, 1950. 13. McFarland RB, Goodman SB: Sporotrichosis and sarcoidosis. Arch Intern Med 112:760-765, 1963. 14. Elsenstaedt JS: Sporotrichosis resembling tuberculosis cutis. JAMA 71:726-728,1918. 15. Laur WE, Posey RE, Waller JD: A family epidemic of
Blastomycoid sporotrichosis
527
cutaneous sporotrichosis occurring in North Texas. Cutis 23:205-208, 1979. 16. Utz JP: Sporotrichosis, in Hoeprich P; Infectious diseases, ed. 2. Hagerstown, MD, 1977, Harper & Row, Publishers, Inc., p. 850. 17. Lynch PJ, Voorhees JJ, Harrell ER: Systemic sporotrichosis. Ann Intern Med 73:23-30, 1970.