1. Mycetoma is a chronic subcutaneous infection characterized by painless swelling, sinuses, and discharge of characteristic grains. It is mostly caused by fungi (eumycetoma) or bacteria (actinomycetoma) transmitted through skin trauma in tropical areas. 2. Chromoblastomycosis presents as verrucous plaques or nodules that may ulcerate, caused by dematiaceous fungi transmitted through skin abrasions in tropical regions. Phaeohypomycosis is a related fungal infection characterized by subcutaneous cysts. 3. Other fungal infections described include sporotrichosis causing ulcerative nodules along lymphatics, lobomy

1. Dr. Jerriton, 1st Year PG, DVL,
SVMCH, Pondy.
11.09.18

2. SUBCUTANEOUS MYCOSIS
• Infections limited to skin & subcutaneous tissue
• Rarely spreading to internal organs
• Caused by fungi with saprophytic existence in nature
• Usual mode of transmission by inoculation
DEFINITION

4. EYMYCE
-TOMA
CHROMO-
MYCOSIS
PHAEOHYP
OMYCOSIS
SPOROTRI-
CHOSIS
LOBOMYC-
OSIS
SC
ZYGOMYC-
OSIS
RHINOSPO
-RIDIASIS
ETIOLOGY M.
mycetomat
is
C. carrionii,
F. pedrosoi
E.
jeanselmei
, P.
verrucosa
S. schenkii Lacazia
loboi
Basidiobol
us,
conidiobol
us spp.
R. seebri
CLINICAL
FEATURES
Painless SC
swelling +
sinus +
discharging
granules
Verrucous
plaques or
nodules +
ulceration
Subcutane
ous cysts
Ulcerated
nodules
along
lymphatics
Polymorph
ic; keloidal
& painless
Painless SC
masses –
bathsuit,
monstrous
face
Painless
friable
warty
outgrowth
with
ulceration
DIAGNOSIS Granules Sclerotic
bodies
Melanin Asteroid
bodies
Round
cells,
tubular
projections
, bifringent
memb.
Mixed
inflammat
ory cells
with fungal
elements
Sporangia
with
endospore
s
TREATMENT Surgery +
Antifungals
Antifungals Surgery +
Antifungals
SSKI +
Antifungals
Surgery +
Clofazimin
e +
Antifungals
SSKI +
Antifungals
Surgery

5. MYCETOMA
Definition
• Chronic, suppurative, granulomatous disease of subcutaneous (SC) tissue
& bones.
• It’s a triad of:
a) Painless SC Tumefaction
b) Sinuses
c) Discharge of granules

6. MYCETOMA
Etiology
• Bacteria (Actinomycotic Mycetoma) – M/C in India
 Actinomadura madurae (M/C)
• Fungi (Eumycotic Mycetoma)
 Madurella mycetomatis (M/C in South India)
Brown grain – M. mycetomatis White grain – A. madurae

7. MYCETOMA
HISTORY & TRANSMISSION
• John Gill in 1842 described “Madura Foot” first.
• Mycetoma means fungal tumor.
• The organisms are soil / plant saprophytes.
• Entry is by abrasion / implantation.
• More common in tropics.

8. MYCETOMA
EPIDEMIOLOGY
• 20 and 40 years, mostly in developing countries.
• Tropics and sub-tropics.
• Barefoot walkers.
• Low socioeconomic status.

9. MYCETOMA
CLINICAL FEATURES
• Begins as small, painless SC nodule at site of injury.
• Nodules increase in number, ulcerate & drain through sinuses.
• Discharge will have the characteristic granules.
• Surrounding skin becomes swollen, indurated & deformed.
• Spreads by direct contiguity along facial planes.
• Spares tendons till late stage.
• Becomes painful if bones are involved / 2° infection.
• Bones show punched out lytic lesions.
• Ankylosis can happen.

10. MYCETOMA
MACROSCOPIC COLOR OF GRAINS
• Black Grains – Eumycotic
• Red Grains – Actinomadura pelletierii
• White Grains – Eumycotic / Actinomycotic
DIAGNOSIS

11. MYCETOMA
• Granules microscopy (KOH / Gram stain) of discharge are characteristic:
1) Actinomycetomas – Fine, branching interlacing filaments with no
chlamydospores
2) Eumycetomas – Thick walled septate hyphae with chalmydospores
MICROSCOPY OF DISCHARGE
DIAGNOSIS
HPE
• Initially – Acute suppurative reaction
• Later – Suppurative granuloma (peripheral epithelioid histiocytes and
MNGs with central PMNs)
• Characteristic granules can be seen within central abscess of granuloma

12. MYCETOMA
EUMYCETOMA GRAIN

13. EUMYCETOMA
EUMYCETOMA GRAIN
A: Ulcerated, indurated plaque of
eumycotic mycetoma on the foot.
B: H&E staining shows a “sulfur granule”
in a purulent area of granulation tissue.
C: The sulfur granule is composed largely
of septate hyphae of P. boydii (GMS stain).

14. MYCETOMA
TREATMENT
ACTINOMYCETOMA
1. Modified Welsch Regimen (3-4 cycles)
Amikacin
15 mg/Kg IV x 21 days with 15 day intervals
PLUS
Co-trimoxazole
35 mg/Kg oral daily
PLUS
Rifampicin
10 mg/day oral daily

15. MYCETOMA
TREATMENT
ACTINOMYCETOMA
1. Modified Two – Step Regimen
Gentamycin
80 mg IV 12 hourly
PLUS
Co-trimoxazole
320 mg/1600 mg oral BD x 4 weeks
FOLLOWED BY
Maintenance doses
Co-trimoxazole & Doxy 100 mg oral BD
Continued 6 months till after healing

16. MYCETOMA
TREATMENT
EUMYCETOMA
• Ketaconazole
• Terbinafine
• Irraconazole 400 mg/day for 3 months f/b 200 mg/day for 9 months
• Voriconazole 300 mg BD doe 16 months
• Posaconazole for refractory cases

17. MYCETOMA
TREATMENT
ROLE OF SURGERY
• Exploration & drainage of sinus tracts
• Debridement of diseased tissue
• Removal of bone cysts
• They help healing faster

18. CHROMOBLASTOMYCOSIS
DEFINITION
• Chronic granulomatous infection, usually of exposed areas,
characterised by verrucous plaques or nodules that ulcerate.

19. CHROMOBLASTOMYCOSIS
ETIOLOGY
• Dematiaceous (brown-pigmented) fungi
1. Cladophialophora carrionii
2. Fonsecaea pedrosoi
• Saprophytes of soil, decaying vegetation and rotting wood
• Enter skin through abrasion
• Most common in tropics and subtropics

20. CHROMOBLASTOMYCOSIS
CLINICAL FEATURES
• 3 clinical forms exist:
1. Localized
2. Multiple with satellite lesions
3. Sporotrichoid
• Begins as a verrucous papule ->
verrucous plaque, which may have
central atrophy / scarring
• Seen mostly at exposed sites
• Complications include elephantiasis, 2° infection, ulceration &
malignant change

21. CHROMOBLASTOMYCOSIS
DIAGNOSIS
• KOH of skin scraping, crusts, aspiration, biopsy tissue
Sclerotic bodies / muriform cells

22. CHROMOBLASTOMYCOSIS
DIAGNOSIS
• H & E stain of biopsy specimen
Sclerotic bodies / muriform cells

23. CHROMOBLASTOMYCOSIS
DIAGNOSIS
• Culture for species identification
Sabouraud dextrose agar
• Serology if culture is not possible

24. CHROMOBLASTOMYCOSIS
TREATMENT
• Systemic antifungals
Itraconazole 200-400 mg / day
PLUS
Terbinafine 250-500 mg / day
X 6 – 12 months

25. CHROMOBLASTOMYCOSIS
TREATMENT
• Other treatment options
1. Iodides, Fluconazole, posiconazole
2. Surgical excision, cryotherapy, local heat

26. PHAEOHYPOMYCOSIS
DEFINITION
• Infections other than chromoblastomycosis and eumycetoma caused
by dematiaceous (melanized / phaeoid) fungi
• They do not have grains or sclerotic bodies that characterized
mycetoma and chromomycosis respectively.
• This entity is characterized by dark septate hyphae, pseudohyphae,
yeast or their combinations.

27. PHAEOHYPOMYCOSIS
ETIOLOGY
• Most common are:
1. Exophiala jeanselmei
2. Wangiella dermatitidis
3. Phialophora verrucosa
4. Bipolaris spp.
• They live in decaying vegetation, bird nests and soil
• They are seen mostly in tropics and subtropics
• Infection is by local trauma by abrasion or inhalation

28. PHAEOHYPOMYCOSIS
PATHOGENESIS
• DHN melanin – fungal armor in cell wall
1. Scavenges free radicals
2. Prevents action of hydrolytic enzymes
• Thermotolerance – can cause deep invasive cerebral lesions

29. PHAEOHYPOMYCOSIS
CLASSIFICATION
1. Superficial: black piedra and tinea nigra
2. Cutaneous: dermatomycosis and onychomycosis
3. Mycotic keratitis
4. Subcutaneous phaeohypomycosis
5. Invasive, systemic & cerebral

30. PHAEOHYPOMYCOSIS
CLINICAL FEATURES
• Classical presentation: SC cyst.
• Begins as small papule -> evolves into SC cyst
• Usually single
• M/C site: extremities
• Children: face

31. PHAEOHYPOMYCOSIS
DIAGNOSIS
• KOH of pus, drainage or skin scrapings
Pigmented yeasts, pseudohyphae and hyphae
• Biopsy
1. Foreign body granuloma
2. Pigmented fungi seen within granuloma
3. Splendore-Hoeppli reaction +/-
4. Fontana Masson stain for melanin is diagnostic
• FNAC
Pigmented fungi with inflammatory cells

32. PHAEOHYPOMYCOSIS
TREATMENT
• Triple antifungal combinations give best results for refractory cases
Amphotericin B, glucytosine and itraconazole
• Localised lesion: excision f/b pre & post op antifungal therapy
• Antifungals used:
• Flucytosine 150 mg/kg/day
• Itraconazole 200 mg/day
• Ketoconazole 200 mg/day
• IV / ILS Amphotericin B

33. SPOROTRICHOSIS
DEFINITION
• Subacute or chronic infection caused by dimorphic fungi, S. schenckii
• Characterized by nodular and ulcerative lesions along lymphatics

34. SPOROTRICHOSIS
ETIOLOGY
S. schenkii
• Dimorphic fungi
• Mycelia at 26°C and yeast at 37°C
• Mycelia bears conidia resembling flower
• Grows in common agar
• Produces creamy white colonies
• Turns black later
• It is a saprophyte in dead plants
• Introduced by trauma to skin

35. SPOROTRICHOSIS
HISTOLOGY
• HPE shows three granulomatous patterns observed
1. Sporotrichotic (central suppuration seen)
2. Tuberculoid (central suppuration seen)
3. Foreign body (no central suppuration)
• Asteroid bodies are characteristic
Round basophilic yeast-like body with surrounding
elongated radiating eosinophilic material (a type of
Splendore – Hoeppli reaction)

37. SPOROTRICHOSIS
CLINICAL FEATURES
• Cutaneous
1. Lymphocutaneous
2. Localized
• Extra cutaneous
1. Pulmonary
2. Disseminated

38. SPOROTRICHOSIS
CLINICAL FEATURES
Lymphocutaneous form
• M/C seen in exposed site of upper extremity
• Small nodule / pustule develops at site of trauma
• Nodule breaks to form ulcer
• New nodules form along lymphatics at few days interval
• Ulcerated nodules connect by cord-like swollen lymphatics
• Heals with scarring and new nodules develop at other sites
• These secondary lesions are gummatous and persist for years

39. SPOROTRICHOSIS
CLINICAL FEATURES
Lymphocutaneous form

40. SPOROTRICHOSIS
CLINICAL FEATURES
Localized cutaneous form
• Primary lesion is restricted to site of injury
• It can be ulcerative, verrucous, acneiform or scaly plaque
• Does not involve local lymphatics
• Mucous membrane can be involved
• Pain is predominant complaint

41. SPOROTRICHOSIS
INVESTIGATIONS
• Sporotrichin skin test
• 0.1 mL of intradermal sporotrichin M (mycelia) is injected
into their forearm and the reading is ascertained at 48
hours, using the same criterion as for the tuberculin skin
test.
• Induration ≥ 0.8 cm is positive.
• Serology – for extra-cutaneous forms

42. SPOROTRICHOSIS
INVESTIGATIONS
• Culture – definitive diagnosis
1. Sabouraud’s dextrose agar at 26°C and 37°C
2. Conversion to yeast form at 37°C is important
• Animal innoculation
1. Gram positive cigar bodies in pus

43. SPOROTRICHOSIS
TREATMENT
• SSKI
1. Given orally in milk
2. Initial dose: 5 drops (1 ml) TID after meals
3. Increased by 1 drop / dose till 40 drops TID
4. Continued till signs of active disease are gone
5. Then dose decreased by 1 drop / dose till 5 drops
6. Then discontinued
• Itraconazole 100-200 mg/day
• Terbinafine 250 mg/day
• Thermotherapy / pocket warmer

44. LOBOMYCOSIS
DEFINITION
Also known as keloidal blastomycosis, pseudoleprosy. It is
characterized by pleomorphic lesions.

45. LOBOMYCOSIS
ETIOLOGY
• Caused by fungi, Lacazia loboi
• Has a saprophytic phase in vegetation, soil & water
• Infection is acquired through trauma
• Farmers, gold miners, fishermen and hunters are affected
• Dolphin to human transmission is reported
• No person-to-person transmission

46. LOBOMYCOSIS
CLINICAL FEATURES
• Pleomorphic lesions
• Nodules or plaques (hypopigmented / hyperpigmented)
• Ulcers
• Sclerodermoid
• Keloidal
• Verrucous
• Legs, outer ears and arms are commonly affected
• Single or multiple, become confluent
• Generally painless, occasionally painless

47. LOBOMYCOSIS
INVESTIGATIONS
• Direct microscopy
• KOH shows round yeast-like organisms, singly or in chains
connected by short tubular projections.
• They have bifringngent membrane with central granules
• HPE
• Granulomatous infiltrate without suppuration
• Grenz zone +/-
• Asteroid bodies +/-
• Fungal forms seen at different levels of epidermis (TEE)

48. LOBOMYCOSIS
TREATMENT
• Medical:
1. Clofazimine 300 mg/day initial dose with maintainance
dose of 100 mg/day for 2 years
2. Ketoconazole, Itraconazole, Posaconazole
• Surgical excision
• Electrocautery
• Cryosurgery

49. SUBCUTANEOUS ZYGOMYCOSIS
DEFINITION
• Chronic subcutaneous infection characterized by woody
swelling of SC tissue

50. SUBCUTANEOUS ZYGOMYCOSIS
ETIOLOGY & CLASSIFICATION
FEATURES ENTOMOPHTHORALES
(Basidiobolus, conidiobolus)
MUCORALES
Host Immunocompetent Immunocompromised
Distribution Tropics and subtropics Worldwide
Transmission Traumatic implantation Inhalation of spores
Systems involved SC mycosis and sinusitis RS, CNS, GIT, skin
Histopathology Chronic inflammatory
response
Angioinvasion,
thrombosis,tissue necrosis
Splendore-Hoeppli Characteristic Rarely seen
Septation More common Less common
Dissemination Uncommon Common

51. SUBCUTANEOUS ZYGOMYCOSIS
EPIDEMIOLOGY & TRANSMISSION
BASIDIOBOLUS
• Children less than 20 years
• Male > Female
• Africa > India
• Transmitted by minor trauma / insect bite / contaminated toilet
leaves (bathing suit distribution)
• Also transmitted through soil and vegetation containing
contaminated animal faeces

52. SUBCUTANEOUS ZYGOMYCOSIS
EPIDEMIOLOGY & TRANSMISSION
CONIDIOBOLUS
• Young adults
• Male > female
• Africa > India
• Identified in soil & plant debris, M/C c. coronatus
• Transmitted by inhalation of fungal spores / frequent nose
pricking habits
• Leads to monstrous disfigurement of face

53. SUBCUTANEOUS ZYGOMYCOSIS
PATHOGENESIS
BASIDIOBOLUS
• Produces extracellular proteinases and lipases
 Phospholipase A hydrolizes lecithin, which destroyed
membranes of blood, skin & muscle cells
 Once lipase liberates cellular protein components,
proteinases digest them as its nutrients
• Thermotolerant – grows poorly at 37°C

54. SUBCUTANEOUS ZYGOMYCOSIS
PATHOGENESIS
CONIDIOBOLUS
• Produces elastase, esterase, collagenase and lipase
 Proteinase is secreted first – breaks down proteins to amino acids
 Lipase is produced later – hydrolizes fatty materials in SC tissue
• Thermophilic – grows readily at 37°C

55. SUBCUTANEOUS ZYGOMYCOSIS
CLINICAL FEATURES
BASIDIOBOLOMYCOSIS
• M/C site: limb girdles / proximal limbs
• Bathing suit distribution
• Painless well-circumcized, firm to hard, smooth, rounded SC masses
that can be raised by inserting fingers underneath it (freely mobile)
• Satellite lesions may be seen at advancing margins
• May encompass part / whole of limb
• Overlying skin may be tense, edematous, desquamating,
hyperpigmented or normal
• Non-pitting oedema +/-
• Underlying muscle / visceral involvement can occur

56. SUBCUTANEOUS ZYGOMYCOSIS
CLINICAL FEATURES
CONIDIOBOLOMYCOSIS
• Begins as swelling of inferior nasal turbinates
• Stuffiness, discharge, epistaxis, nasal obstruction are symptoms
• Diffuse erythematous infiltration with skin thickening on nose, cheeks,
forehead and lips – monstrous disfigurement, facial elephantiasis,
palatal perforation, orbital cellulitis, saddle nose deformity
• Phase 1 – nose, paranasal sinuses & pharynx
• Phase 2 – frontal region and lips
• Phase 3 – muscle, bones & viscera

57. SUBCUTANEOUS ZYGOMYCOSIS
DIAGNOSIS
HPE
• Mixed inflammatory infiltrate
• Fungal hyphal elements with surrounding dense eosinophilic granular
aterial (Splenndore-Hoeppli phenomenon)
MICROSCOPY
• KOH from scrapings show broad, septate branching hypahe
CULTURE
• Basidiobolus – flat & furrowed, yellowish grey color with musty odor
• Conidiobolus – white surface, becomes beige to brown, no odor

58. SUBCUTANEOUS ZYGOMYCOSIS
TREATMENT
• Itraconazole / SSKI – 1st line choices
• Treated continuously for 1-2 months after clinical cure

59. RHINOSPORIDIOSIS
DEFINITION
• Chronic granulomatous disease of mucocutaneous tissue
• Characterized by development of polypoid tumors or pedunculated /
sessile polyps

60. RHINOSPORIDIOSIS
ETIOLOGY & EPIDEMIOLOGY
• Caused by Rhinosporidium seeberi – protistan parasite of class
Mesomycetozoea
• Common pond bathing with buffalos is a risk factor
• Disease is endemic in Kerela, Tamil nadu and Chandigarh

61. RHINOSPORIDIOSIS
HISTOLOGY
• Thick walled sporangia with endospores

62. RHINOSPORIDIOSIS
CLINICAL FEATURES
CUTANEOUS RHINOSPORIDIOSIS
• Associated with mucosal disease
• Begin as tiny papules and enlarge to become wart like / tumorous
growth
• They are friable and have crenated surface, often ulcerated - & painless

63. RHINOSPORIDIOSIS
DIAGNOSIS
• KOH / HPE for sporangia with endospores
TREATMENT
• Surgical excision
• Electrocoagulation

64. REFERENCES
1. Rook’s Textbook of Surgery
2. IADVL Textbook of Dermatology
3. Fitzpatrick Textbook of Dermatology
4. Lever’s Histopathology
5. Weedon’s Histopathology
6. Online journals