DOI: 10.1111/j.1610-0387.2010.07453.

x Academy 619

CME

Subcutaneous mycoses: chromoblastomycosis,

sporotrichosis and mycetoma
Alexandro Bonifaz1, Denisse Vázquez-González1, Ana María Perusquía-Ortiz2
(1) Departamento de Micología, Servicio de Dermatología, Hospital General de México, Ciudad de México
(2) Department of Dermatology, University of Münster, Germany

Section Editor
Prof. Dr. Jan C. Simon,
JDDG; 2010 • 8:619–628 Submitted: 6. 3. 2010 | Accepted: 17. 4. 2010 Leipzig

Keywords Summary
• chromoblastomycosis Subcutaneous mycoses are common in subtropical and tropical regions of the
• sporotrichosis world. They are rarely observed in Europe. These mycoses are heterogeneous,
• mycetoma but all are caused by penetrating trauma of the skin. Most cases in Europe are
• subcutaneous mycoses observed in returning travelers, aid workers, archaeologists and immigrants.
• treatment Therefore, a careful, thorough history is essential in order to reach a proper
diagnosis. We provide up-to-date epidemiological, clinical, diagnostic, and ther-
apeutic data on the three most important imported subcutaneous mycoses in
Europe: chromoblastomycosis, sporotrichosis and mycetoma.

Introduction
Chromoblastomycosis, sporotrichosis and mycetoma all develop at sites of penetrat-
ing injuries, but differ in epidemiology, clinical findings and treatment.

The two main pathogens causing chro-
moblastomycosis are Fonsecaea pe-
drosoi and Cladophialophora carrionii.
The disease occurs predominantly in
tropical and subtropical regions.
Chromoblastomycosis
Etiology and pathogenesis
Chromoblastomycosis is caused by various pigmented or dematiaceous fungi. Two main
pathogens are: Fonsecaea pedrosoi and Cladophialophora carrionii (Table 1) [1–3]. The
disease occurs predominantly in tropical and subtropical regions.
Fungi such as F. pedrosoi are found in hot and humid climate zones in the soil, in
plants and woods, in decaying plant material, in compost. This explains dissemination
in farmer and agricultural workers. Fungal infections caused by C. carrionii are found,
in contrast, most frequently in semiarid zones (Cactaceae). Chromoblastomycosis has
a worldwide distribution, especially in Madagascar, Brazil and Costa Rica, occasionally
on the American continent in the USA, Mexico, Venezuela, the Dominican Republic
and Colombia; in Asia in Japan, China and Malaysia; in Europe in Russia, the Czech
Republic, Romania and in Eastern Germany [4, 5]. Infection usually occurs in
adulthood between the age of 20 and 40 years [2, 4, 6]. Occurrence in childhood is
exceptional [1, 6]. Men are preferentially infected (m:f 4:1), which may reflect
occupational activities instead of hormonal factors [1, 2 4]. Affected individuals are
generally immunocompetent.

Clinically characteristic are initially uni- Clinical findings

lateral and asymmetric scaling erythem-
tous cutaneous-subcutaneous nodules,
especially on the limbs. Sometimes
psoriasis-like erythematosquamous
plaques or tumor-like lesions appear.
The disease takes a chronic course. It is practically limited to subcutaneous tissue,
only rarely involves bone or spreads lymphatically [1–4]. Clinically characteristic are
initially unilateral and asymmetric scaling erythematous cutaneous-subcutaneous
nodules, especially on the limbs; later verrucous lesions, vegetating plaques, scaling
cauliflower-like tumors, ulcers and crusts develop. The size of the lesions ranges from

© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0808 JDDG | 8 ˙2010 (Band 8)
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Table 1: Principal etiologic agents
of chromoblastomycosis [2, 4].
• Fonsecaea pedrosoi
• Cladophialophora carrionii
• Phialophora verrucosa
• Exophiala dermatitidis
• Rhinocladiella aquaspersa
• Cladophialophora yegresii
• Fonsecaea monophora
In direct microscopy (KOH examina-
tion) “fumagoid” cells are characteris-
tic. Cultures in Sabouraud dextrose
and Sabouraud yeast agar as routine
detection test confirm the species.
Treatment results are often unsatis-
factory.
Physical methods: Cryosurgery has
shown the best results.
Chemotherapy: best results with itra-
conazole (200–400 mg daily) and
terbinafine (500 mg daily) with a
treatment duration between 6 and
12 months.
JDDG | 8 ˙2010 (Band 8)
Figure 1: Widespread chromoblastomycosis (a). Dermatopathology: “copper bodies” (H&E, 40X)
(b). Micromorphology: Fonsecaea pedrosoi (erythrosine, 60X) (c).
a few millimeters up to several centimeters. Sometimes psoriasis-like erythematosqua-
mous plaques or tumor-like lesions appear (Figure 1a) [2–4]. Complications of the
chronic inflammation are particularly fibrosis and lymphedema. Lymphedema also
facilitates bacterial superinfection. Occasionally chronic disease with alternating ulcer-
ation and scarring leads to squamous cell carcinomas [1, 3–6].
Diagnostic approach
Laboratory diagnosis is made on the basis of mycological and histological criteria. In
direct microscopy (KOH examination) “fumagoid” cells are seen. These are coffee-
colored, thick-walled cells with a double membrane and central septum (“like coffee
beans”). Cultures on Sabouraud dextrose and Sabouraud yeast agar as routine detec-
tion test confirm the species: slowly growing pigmented dematiaceous fungi that can
be identified micromorphologically and by genetic sequencing (Figure 1b, c) [1, 4].
Histology: The epidermis often displays pseudoepitheliomatous hyperplasia. In the
papillary and reticular dermis lymphohistocytic infiltrates and tuberculoid granulo-
mas with epitheloid cells, giant cells of the Langerhans and foreign body type are
observed. “Fumagoid” cells can readily be differentiated in routine hematoxylin-
eosin staining (HE) in the stratum corneum, in granulation tissue or giant cells
[2–4]. As these can often be found in the stratum corneum the mycological diagno-
sis is often made by direct microscopy using a tape stripping technic.
Therapy
The treatment of chromoblastomycosis depends on the pathogens, the severity and
extent of lesions (fibrosis, impaired lymphatic drainage) and the choice of medica-
tion [7, 8]. Treatment results are often unsatisfactory. The recurrence rate is high par-
ticularly in long-lasting and extensive involvement. Physical methods, chemo- and
combination therapy are employed (Table 2) [2].
Physical methods: 1. Cryosurgery has shown the best results. Here open spray or con-
tact probes, together with measure of tissue temperature, are employed, especially for
small lesions. 2. Local hyperthermia with heating of the skin surface to a mean tem-
perature of 43 °C. The results are variable. 3. Surgical excision or curettage and elec-
trodesiccation for small and sharply well-delineated lesions [2, 4, 6].
Chemotherapy: A multitude of substances have been tried with variable success: cal-
ciferol, potassium iodide, 5-fluorocytosine, ketoconazole, fluconazole, ampho-
tericin B. The best results were observed with intraconazole and terbinafine with a
treatment duration between 6 and 12 months [2–4, 6].
For itraconazole high doses of 200–400 mg daily are recommended. With this com-
plete cure was observed in 42 % of cases after an average of 7.2 months. This drug
© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0808
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Table 2: Chromoblastomycosis: Therapy of choice [2, 4, 6].

Physical methods Chemotherapy Combination therapy

• Excision
• 5-Fluorocytosine • Itraconazole + cryosurgery
• Cryosurgery and
• Itraconazole • Terbinafine + cryosurgery
curettage
• Terbinafine • Itraconazole + terbinafine
• Local hyperthermia

can be used alone or in combination with cryosurgery [2, 4, 6]. The good results are
based on the high sensitivity of the etiologic agents to this drug, due to their low
minimum inhibitory concentrations (MICs) [2, 4].
Terbinafine is employed in doses of 250–500 mg daily. Several reports exist of suc-
cessful treatment with lower doses (250 mg daily) [2, 4, 6], but 500 mg daily is
viewed as more adequate. Queiroz-Tellez et al. [2] achieved clinical and mycological
cure in 74.2 % after twelve months of treatment. Terbinafine is particularly effective
and well-tolerated with only few drug interactions [2, 6].
Due to the high recurrence rate, chemotherapeutic agents have often been combined.
Gupta et al. [7] reported good results for a combination of itraconazole with
terbinafine in chronic cases where amphotericin B and various oral antifungal agents
had not been effective. They suspect synergistic effects of the two drugs on the basis
of differing actions on ergosterol synthesis.

Sporotrichosis
Etiology and pathogenesis
This subcutaneous or deep cutaneous fungal infection with a subacute to chronic Sporotrichosis is caused by the
course is caused by dimorphous fungi of the Sporothrix schenckii complex. Primarily dimorphous fungi of the Sporothrix
skin and lymphatic vessels are involved in the form of subcutaneous nodules or gum- schenckii complex. Primarily skin and
mata, only rarely bone, joints or internal organs [1, 4, 8]. Recently, Marimon et al. lymphatic vessels are involved in the
[9] have described the Sporothrix schenckii complex, which includes in addition to form of subcutaneous nodules.
Sporothrix schenckii sensu stricto four other species: S. albicans, S. brasiliensis,
S. globosa and S. mexicana. There are current reports of epidemics in domestic ani-
mals, so that sporotrichosis can be viewed as a zoonosis [4, 8].
It occurs on all continents, but most cases are seen in the Americas (Peru, Mexico,
Colombia, Brazil, Uruguay, Guatemala). It has been observed in almost all of
Europe, especially in Spain, France and Germany. The pathogens of the Sporothrix
schenckii complex develop in plants, wood, decaying plant materials in climates with
an average temperature of 20–25 °C and humidity over 90 %. They also occur in
cats, dogs, birds, rodents and reptiles [4, 5, 8]. Inoculation usually occurs by injury
with contaminated splinters or animal bites. The incubation period is variable (7 to
30 days). Most in danger are farmers, gardeners, livestock breeders and flower grow-
ers, miners, veterinarians, packers etc. There is no sexual preference (m:f 1:1).
Children are frequently infected (5 to 15 years, about 30 % of cases), especially
young adults (16–35 years, 50 %) [1, 3, 8].
In highly endemic regions the fungus can gain access to the airways and incite primary
pulmonary forms with usually asymptomatic cavitary disease. Immunosuppression of
all kinds can facilitate spread of the disease to other organs. The differences between
the various Sporothrix species relate mainly to their sensitivity to different antifungal
agents [4, 5, 8].

Clinical findings
Sporotrichosis appears in different clinical forms:
Lymphocutaneous sporotrichosis: the most common form (70 %) affects the extremi-
ties and the face with erythematous-violet, often ulcerated, gumma-like, subcuta-
neous, nodular lesions along lymphatic vessels up to the regional lymph nodes
(Figure 2a). This is associated with slight pruritus and pain. In exceptional cases lym-
phatic drainage may be impaired. In children it is located in the face uni- or bilater-
ally in 40 % of cases [1, 4, 8].

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The two most common clinical vari-
ants of sporotrichosis are lymphocu-
taneous (70 %) and fixed cutaneous
(25 %).
Disseminated, hematogenous cuta-
neous and extracutaneous variants of
sporotrichosis usually occur in im-
munosuppressed patients.
The diagnosis is confirmed by isolat-
ing Sporothrix schenckii from exudates
of cutaneous lesions or sputum in
Sabouraud culture media.
Sporothrichosis has a benign course and
responds well to various treatments.
JDDG | 8 ˙2010 (Band 8)
Figure 2: Lymphangitic cutaneous sporotrichosis (a). Fixed cutaneous sporotrichosis (b).
Macromorphology: Sporothrix schenckii (Sabouraud dextrose agar) (c). Micromorphology: Sporothrix
schenckii (Cotton blue stain, 60X) (d).
Fixed cutaneous sporotrichosis: This chronic form (25 % of cases) is characterized by
a single vegetating or verrucous, sharply delineated plaque with an erythematous-
violet border, covered by scales and crusts and usually asymptomatic (Figure 2b).
It is the most limited of the clinical forms and occurs in immunocompetent patients
[1, 4, 5, 8].
Disseminated cutaneous sporotrichosis: This form consists of erythematous, violet and pru-
ritic plaques. It usually affects only the face, usually in immunosuppressed patients [4, 8].
Hematogenous cutaneous sporotrichosis: This rarest form (1–2 %) manifests with
gumma-like subcutaneous nodular lesions, ulcers and verrucous plaques with pruri-
tus and pain. They appear on the skin as well as mucous membranes. They are asso-
ciated with a poor prognosis and occur in immunosuppressed patients. It is thought
that the fungus behaves as an opportunistic pathogen.
Extracutaneous sporotrichosis: In immunosuppressed patients it is caused by
hematogenous dissemination in internal organs, bone, joints etc. or by primary inoc-
ulation of the pathogen in the lungs [5, 8].
Diagnostic approach
Diagnosis is made by isolating Sporothrix schenckii from exudate of cutaneous lesions
or sputum in common culture media (Sabouraud dextrose agar with antibiotics). The
colonies are well-circumscribed, membranous, ray-like, beige to coffee-colored.
Microscopically the pathogen produces conidia, hyphae and conidiophores (sympo-
dulae) often in the form of a “daisy flower” (Figure 2c, d). Direct microscopy and
staining are of little help, as these yeasts are difficult to observe.
Histology: Tuberculoid granulomas with extensive necroses. In exceptional cases
“asteroid bodies” or the Splendore-Hoeppli phenomenon (antigen-antibody com-
plexes and cell detritus of inflammatory cells or plasma cells, histiocytes, lymphocytes
and eosinophils) can be found. To detect yeast cells and elongated blastoconidia
staining with periodic acid-Schiff (PAS) stain or methenamine silver is needed.
Further useful diagnostic methods include intradermal reaction to sporotrichin, spe-
cific for lymphocutaneous and fixed cutaneous sporotrichosis, as well as serological
(precipitin, agglutinin, complement fixation) and molecular tests (polymerase chain
reaction to chitin synthetase gen ChS1 and gen 26S rDNA) [1, 3–5, 8].
Therapy
Spontaneous involution has been reported occasionally. The disease usually has
a benign course and responds well to various treatments. In regions where
© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0808
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Table 3: Principal etiologic agents of mycetoma [4, 12].

Mycetoma types Causative pathogens

• Nocardia asteroides, N. brasiliensis, N. otitidiscaviarum
(form yellow-white grains)
Actinomycetoma
• Actinomadura madurae, A. pelletieri (form red grains)
• Streptomyces somaliensis
Eumycetoma • Madurella mycetomatis, M. grisea
by Dematiaceae • Leptosphaeria senegalensis, Leptosphaeria tompkinsii
or phaeohy- • Pyrenochaeta romeroi
phomycetes (form • Curvularia lunata, Curvularia geniculata
black grains) • Exophiala jeanselmei
• Pseudallescheria boydii (Scedosporium apiospermum)
Eumycetoma
• Acremonium falciforme, Acremonium recifei
by white fungi or
• Neotestudina rosatii
hyalohy-
• Fusarium moniliform (Fusarium subglutinans),
phomycetes (form
Fusarium solanii
white grains)
• Aspergillus nidulans

Sporothrix sp. are endemic, potassium iodide is favored due to good efficacy, safety In endemic regions oral potassium io-
and low costs; it is administered orally (1–3 g daily in children, 3–6 g daily in dide is therapy of choice (1–3 g daily
adults). The duration of therapy in uncomplicated sporotrichosis (lymphocuta- in children, 3–6 g daily in adults for
neous and fixed form) is on average 4 months. Potassium iodide is usually well-tol- 4 months).
erated. The most frequent side effect is gastritis. Less frequent are rhinitis, bronchi-
As an alternative therapy itraconazole
tis, urticaria, erythema nodosum. As an alternative therapy oral antifungal agents
(5 mg /kg daily in children, 200–300
can be administered with good results: itraconazole (5 mg/kg daily in children,
mg daily in adults) or terbinafine
200–300 mg daily in adults) or terbinafine 250–500 mg daily for 3–4 months. In
250–500 mg daily for 3–4 months can
severe and disseminated cases amphotericin B (0.25–0.75 mg/kg daily) should be
be administered.
used [4, 8, 10].

Mycetoma
Etiology and pathogenesis
The term encompasses two different groups of chronic inflammatory swelling with The clinical symptom complex “myce-
deformity of the involved region and fistulization with granules (grains) in the fistulas. toma” encompasses chronic inflam-
Actinomycetomas or actinomycetic mycetomas are caused by aerobic and gram- matory swelling with deformity of the
positive filamentous actinomycetes (microsiphonated). Usually three genera are involved region and fistulas which
responsible: Nocardia, Actinomadura and Streptomyces. The most common discharge granules (grains).
pathogens are the species Nocardia brasiliensis and Actinamadura madurae [3, 4].
One must distinguished between
The cervicofacial variety of actinomycosis is always caused by a mixed infection
actinomycetomas and eumycetomas.
with other anaerobic bacteria [4, 11].
Eumycetomas or eumycetic mycetomas are caused by septated pigmented or hyaline
and white filamentous fungi (macrosiphonated) from several genera including
pigmented dematiaceae such as Madurella, Pyrenochaeta, Exophiala, Leptosphaeria
and Curvularia. The most common species are Madurella mycetomatis, Madurella
grisea and several white fungi such as Pseudallescheria, Acremonium and Fusarium,
particularly Pseudallescheria boydii (Table 3) [1, 4, 12, 13].
Mycetomas are quite frequent in an area parallel to the Tropic of Cancer, where spe-
cial climatic conditions prevail: a juxtaposition of subtropical and tropical climate
(“mycetoma belt”). The highest prevalence is found in Africa (Sudan, Somalia,
Senegal, Nigeria, Chad and Niger), in India and America (Mexico, Venezuela,
Brazil). Only scattered cases are reported in Europe and the USA [4, 12, 13]. The
microorganisms which live in the soil, on plants, thorns, splinters etc. are inoculat-
ed into the skin by small injuries or splinters. The primary lesion slowly spreads to
surrounding tissue, invades the subcutis and finally even muscles, connective tissue
and bone [4, 5 13].

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The lower limbs are most of often
affected, especially the feet (50 %).
Mycetomas can involve subcutaneous
tissue, aponeurosis, muscle, perios-
teum and bone as well as internal
organs.
The diagnosis is confirmed by direct
microscopy of typical grains in fistula
content.
Biopsy is essential for the diagnsosis.
Histology: pseudoepitheliomatous hy-
perplasia overlying chronic purulent
liquefying granulation tissue, some-
times of the foreign body type; in the
dermis granulomatous infiltrate with
polymorphonuclear granulocytes in
microabscesses, macrophages, plasma
cells and lymphocytes. Grains are
usually found in the center of the
microabscesses.
JDDG | 8 ˙2010 (Band 8)
Figure 3: Actinomycetoma caused by Nocardia brasiliensis (a). Dermatopathology: grain of Nocardia
sp. (H&E, 40 X) (b). Eumycetoma caused by Madurella mycetomatis (c). Dermatopathology: grain of
Madurella mycetomatis (H&E, 10X) (d).
Mycetomas are more common in men (4 : 1) which reflects occupational exposure.
Actinomycetic as well as eumycetic mycetomas affect farmers, gardeners, housewives
working in the fields and people working in very primitive conditions, which is why
young people and adults are more frequently infected than children [4, 5].
Clinical findings
The lower limbs, especially feet (50 %), ankles, knees, flexures of knees and perineal
region, are affected most strongly [1, 4, 12]. Other often involved areas are the back,
nape of neck and upper limbs. This chronic disorder manifests with swelling and
deformity of the involved area as well as the development of nodular lesions with
fistulas secreting a viscous seropurulent or stringy exudate that contains the “para-
sitic forms” or grains (microscopically similar to the genus Nocardia sp., macroscop-
ically as in true fungi) (Figure 3a, c). Mycetomas can involve subcutaneous tissue,
aponeurosis, muscle, periosteum and bone as well as internal organs [1, 4, 12, 13].
In contrast to actinomycetomas eumycetomas generally cause less fistulization and
more fibrosis. Frequent symptoms are pruritus and pain on palpation, but many
cases cause few complaints.
Diagnostic approach
Diagnosis is confirmed by direct microscopy of fistula contents obtained by suction
with a narrow-bore cannula with the addition of Lugol iodine solution or 10 %
potassium hydroxide (KOH). Grains can be recognized microscopically (< 1 µm) as
in the genus Nocardia or macroscopically (> 1 µm) as in A. madurae and the eumyce-
tomas [4, 5, 12, 13].
The pathogens can be cultured on media (Sabouraud dextrose and Sabouraud yeast
agar). Some Species of the actinomycetes (A. madurae and Streptomyces somaliensis)
grow only on media such as Löwenstein-Jensen culture medium. Suitable media
for eumycetomas are Sabouraud dextrose or Sabouraud yeast agar [4, 5].
Histology: Biopsy is essential for the diagnsosis. Independent of the causative
pathogen, histological features are almost identical: purulent liquefying granulomas,
sometimes of the foreign body type under an epidermis with pseudoepitheliomatous
hyperplasia; deep in the dermis granulomatous infiltrate with polymorphonuclear
microabscesses, macrophages, plasma cells and lymphocytes. Grains usually appear
in the center of microabscesses and are gram- as well as Grocott-positive (Figure 3b,
d) [1, 3–5, 13].
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Table 4: Principal differential diagnoses of subcutaneous mycoses.

Chromoblastomycosis Sporotrichosis Mycetoma

• Tuberculosis cutis verrucosa • Tuberculosis cutis colliquativa and verrucosa • Osteomyelitis
• Sporotrichosis • Leishmaniasis • Tuberculosis colliquativa
• Leishmaniasis • Mycetoma • Sporotrichosis
• Paracoccidioidomycosis • Tularemia • Coccidioidomycosis
• Coccidioidomycosis • Chromoblastomycosis • Actinomycosis
• Blastomycosis • Atypical mycobacterioses • Hidrosadenitis
• Syphilis III • Squamous cell carcinoma • Furuncle
• Squamous cell carcinoma • Orf (ecthyma contagiosum)
• Psoriasis
• Bowen disease

Therapy
Actinomycetomas are treated with antibacterial antibiotics and eumycetomas with
antifungal agents.
Mycetomas caused by Nocardia sp. (N. brasiliensis) ares usually treated according to
the following scheme: diaminodiphenylsulfone (DDS) 100–200 mg daily and Nocardia sp. are treated with diamin-
trimethroprim-sulfamethoxazole 80/400 to 160/800 mg each daily. Treatment is odiphenylsulfone (DDS) 100–200 mg
continued over a longer period of time depending on the clinical course. In myce- daily and trimethoprim-sulfamethoxa-
tomas with a complex location (back, thorax, visceral involvement) amikacin is addi- zole 80/400 to 160/800 mg each daily.
tionally administered intravenously in doses of 15 mg/kg daily in cycles of 15 to
21 days each (3 to 5 cycles). After completion of the cycles DDS and/or trimetho- In mycetomas with a complex location
prim-sulfamethoxazole should be continued for a longer period of time [4, 5]. (back, thorax, visceral involvement)
Another widely employed scheme is: amoxicillin (875 mg) + clavulanic acid amikacin is additionally administered
(125 mg) twice daily for 3–6 months [4]. intravenously in doses of 15 mg/kg
Mycetomas due to A. madurae are resistant or not sensitive to most therapies; the daily in cycles of 15 to 21 days each (3
same holds true for cases caused by Streptomyces somaliensis and A. pelletieri. Here, the to 5 cycles).
best results are achieved with streptomycin (1 g daily) + trimethoprim-sulfamethox-
azole (80/400–160/800 mg daily) or DDS (100–200 mg daily). The total dose of
streptomycin should not exceed 50 g [4, 5, 12]. Surgical measures are considered
contraindicated, as they can lead to spread of infection. Surgical measures are considered con-
In eumycetomas therapeutic results are variable; the cure rates are low. Infection traindicated in actinomycetomas, as
with M. mycetomatis and M. grisea can be controlled by itraconazole in doses of they can lead to spread of infection.
200–300 mg daily or also by terbinafine 250–500 mg daily over a mean time period
of one and an half year. Griseofulvin and ketoconazole have also been employed, but
are no longer used due to poor results and side effects. Amphotericin B 5–30 mg
every three days achieves not very consistent results. Depending on location eumyce-
tomas can also be treated surgically, e. g. by amputation; they spread less than actin-
For eumycetomas depending on
omycetomas [1, 3–5, 13].
location surgical measures (e. g. ampu-
The differential diagnoses of the three diseases are different depending on the clini-
tation) can be considered, as they
cal form; especially other cutaneous fungal infections, bacterial diseases and tumors
spread less than actinomycetomas.
must be excluded (Table 4). In Table 5 the features of the depicted fungal infections
are summarized.

Conclusions
Clinical features of chromoblastomycosis, sporotrichosis and mycetoma are highly
variable; it is therefore often difficult to recognize and treat them early. Most
causative pathogens respond to itraconazole and terbinafine. The infection is often
initiated by a penetrating injury of the skin. Protective measures such as wearing stur-
dy and high boots during work with soil and plant materials reduce the danger of
infection. <<<

Conflict of interest
None.

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Table 5: Principal features of subcutaneous mycoses.

Chromoblastomycosis Sporotrichosis Mycetoma

Eumycetoma: black and
Most frequent Fonsecaea pedrosoi,
white filamentous fungi
causative Cladophialophora Sporothrix schenckii complex
Actinomycetoma: aerobic
pathogens carrionii
actinomycetes
Eumycetoma: black and
Causative hyaline filamentous fungi
Dematiaceae Dimorphous fungi
pathogen types Actinomycetoma: aerobic
gram-positive actinomycetes
Gumma-like, nodular
Swelling, deformity and
Clinical features Verrucous plaques subcutaneous lesions and
fistulization
verrucous plaques
Involved body sites Lower and upper limbs Lower and upper limbs Back and lower limbs

“Asteroid bodies” and Filamentous grains (micro-

Parasitic form “Fumagoid” cells
elongated yeast cells and macrosiphonated)

Tuberculoid granuloma Purulent chronic granuloma,

Histology Purulent granuloma with grains
with “fumagoid” cells rarely with “asteroid bodies”

Eumycetoma: itraconazole, terbinafine

Actinomycetoma: trimethoprim-
Itraconazole, terbinafine, Potassium iodide,
Treatment sulfamethoxazole, diaminodiphenyl-
cryosurgery itraconazole, terbinafine
sulfone, amikacin, amoxicillin +
clavulanic acid
Response to Eumycetoma: satisfactory
Satisfactory Very good
treatment Actinomycetoma: good

Alexandro Bonifaz

Correspondence to
Ana María Perusquía Ortiz, M. D.
Center for Innovative Dermatology (ZiD)
Department of Dermatology
University of Münster
Von-Esmarch-Straße 58
D-48149 Münster, Germany
Tel.: +49-251-83-56558
Fax: +49-251-83-57296
E-mail: anamaria.perusquiaortiz@ukmuenster.de

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References
1 Hay JH. Cutaneus and subcutaneous mycoses. In: Anaissie EJ, McGinnis MR, Pfaller
MA: Clinical Mycology. Philadelphia PA: Churchill Livingstone, 2003: 456–73.
2 Queiroz-Telles F, Esterre P, Perez-Blanco M, Vitale RG, Salgado CG, Bonifaz A. Chro-
moblastomycosis: an overview of clinical manifestations, diagnosis and treatment. Med
Mycol 2009; 47: 3–15.
3 Arenas R. Micología médica ilustrada. 3ª edición, McGraw-Hill, México D.F., 2008.
4 Bonifaz A. Micología médica básica. 3ª edición, McGraw-Hill, México D.F., 2009.
5 Dismukes WE, Pappas PG, Sobel JD. Clinical mycology. Oxford University press,
New York, 2003.
6 Bonifaz A, Carrasco-Gerard E, Saúl A. Chromoblastomycosis: a clinical and mycolog-
ical experience of 51 cases. Mycoses 2001; 44: 1–7.
7 Gupta AK, Taborda PR, Sanzovo AD. Alternate week and combination itraconazole
and terbinafine therapy for chromoblastomycosis caused by Fonsecaea pedrosoi in
Brazil. Med Mycol 2002; 40: 529–34.
8 Arenas R. Sporotrichosis. In: Merz WG, Hay R, Eds: Topley & Wilsongs Microbiology
and Microbial infections. 10th ed. London: Hodder-Arnold, 2005: 367–84.
9 Marimon R, Cano J, Gené J, Sutton DA, Kawasaki M, Guarro J. Sporothrix brasiliensis,
S. globosa, and S. mexicana, three new Sporothrix species of clinical interest. J Clin
Microbiol 2007; 45: 3198–206.
10 Kauffman CA, Hajjeh R, Chapman SW. Practice guidelines for the management of pa-
tients with sporotrichosis. For the Mycoses Study Group. Infectious Diseases Society of
America. Clin Infect Dis 2000; 30: 684–7.
11 Stein E, Schaal KP. Die Aktinomykosen. In: Hornstein OP, Hundeiker M, Schönfeld J
(Hrsg.): Neue Entwicklungen in der Dermatologie, Bd. 2. Berlin, Heidelberg, New
York: Springer Verlag, 1987: 137–41.
12 Lichon V, Khachemoune A. Mycetoma: a review. Am J Clin Dermatol 2006; 7:
315–21.
13 Fahal AH. Mycetoma: A thorn in the flesh. Trans R Soc Trop Med Hyg 2004; 98:
3–11.

© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0808 JDDG | 8 ˙2010 (Band 8)
628 Academy
Fragen zur Zertifizierung durch die DDA
1. Die beiden wichtigsten ätiologi-
schen Erreger der Chromoblastomy-
kose sind:
a) Fonsecaea pedrosoi und Cladophia-
lophora carrionii
b) Nocardia brasiliensis und
Actinomadura madurae
c) Sporothrix schenkii und Sporothrix
globosa
d) Madurella mycetomatis und
Nocardia brasiliensis
e) Madurella grisea und
Pseudallescheria boydii
2. Was beobachten Sie bei der
Chromoblastomykose in dem
Nativpräparat mit KOH?
a) vesikulöse makroskopische Drusen
b) mikroskopische Drusen
c) „fumagoide“ Zellen
d) „asteroid bodies“ und elongierte
Hefen
e) Blastokonidien und Pilzfilamente
3. Eines der bevorzugten
chemotherapeutischen Schemata
bei der Chromoblastomykose ist:
a) Kaliumhydroxid 3 g/d über
3 Monate
b) Itraconazol 200–400 mg/d über 7
Monate
c) Ketoconazol 200 mg/d über 8
Monate
d) Trimethoprim-Sulfamethoxazol
800/160 mg/d über 12 Monate
e) Amikacin 15 mg/kg/d, 3 Zyklen
von jeweils 21 Tagen
4. Eine klinische Variante der
Sporotrichose, die an den
Lymphbahnen entlang gummös-
knotenartige Läsionen bis zum
Liebe Leserinnen und Leser,
der Einsendeschluss an die DDA für diese Ausgabe ist der 17. September 2010.
Die richtige Lösung zum Thema „Systematisches Vorgehen bei Frauen mit Haarausfall“ in Heft 4 (April 2010) ist:
1c, 2d, 3e, 4d, 5b, 6e, 7a, 8a, 9d, 10d.
Bitte verwenden Sie für Ihre Einsendung das aktuelle Formblatt auf der folgenden Seite oder aber geben Sie Ihre Lösung online
unter http://jddg.akademie-dda.de ein.
JDDG | 8 ˙2010 (Band 8)
regionalen Lymphknoten bildet,
ist die:
a) fixe kutane Sporotrichose
b) lymphokutane Sporotrichose
c) disseminierte kutane
Sporotrichose
d) lymphatische osteoartikuläre
Sporotrichose
e) hämatogene kutane Sporotrichose
5. Die endgültige diagnostische
Methode bei der Sporotrichose ist:
a) Nativpräparat in 10 % Kaliumhy-
droxid (KOH)
b) serologische Untersuchung
(Komplementfixation)
c) Nativpräparat mit Gram- und
PAS-Färbungen
d) Hautbiopsie
e) Wachstum in Sabouraud-
Kulturmedien
6. Achtjähriger männlicher Patient
mit lymphokutaner Sporotrichose
im Gesicht: Welche Behandlung
wird bevorzugt?
a) Diaminodiphenylsulfon 100 mg/d
über 1 Jahr
b) Trimethoprim-Sulfamethoxazol
160/800 mg über 1 Jahr
c) Kaliumjodid 1–3 g/d über
3–4 Monate
d) Kaliumjodid 6–9 g/d über
2 Monate
e) Amphotericin B 0,25–0,75
mg/kg/d
7. Die bevorzugte klinische
Lokalisation des Myzetoms ist
im Allgemeinen:
a) obere Extremitäten
b) Kopf und Nacken
© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0808
c) Rumpf
d) untere Extremitäten
e) anogenitaler Bereich
8. Welche Struktur findet man im
Nativpräparat eines aktinomyzeti-
schen Myzetoms?
a) vesikulöse makroskopische Drusen
b) „fumagoide“ Zellen
c) mikroskopische Drusen mit
mikrosiphonierten Myzelien
d) „asteroid bodies“ und elongierte
Hefen
e) Endosporen in Sphärulen
9. Das Therapieschema mit Amikacin
in Zyklen von 21 Tagen zusammen
mit Trimethoprim-Sulfamethoxazol
oder Diaminodiphenylsulfon ist vor
allem indiziert bei:
a) Myzetom durch N. brasiliensis an
Thorax, Abdomen und Kopf
b) Eumyzetom durch schwarze Pilze
c) Eumyzetom durch weiße Pilze
d) Actinomadura madurae, mit
Resistenz gegen konventionelle
Behandlung
e) Patienten mit einer assoziierten
oberflächlichen Mykose
10. Die bevorzugte Behandlung
bei Aktinomyzetom durch
Actinomadura madurae ist:
a) Amoxicillin + Clavulansäure
b) Streptomycin + Trimethoprim-
Sulfamethoxazol oder Diaminodi-
phenylsulfon
c) Amikacin in 21-Tage-Zyklen +
Trimethoprim-Sulfamethoxazol
d) Trimethoprim-Sulfamethoxazol +
Diaminodiphenylsulfon
e) Fosfomycin + Linezolid