4. SPOROTRICHOSIS
ACUTE OR CHRONIC FUNGAL INFECTION
CAUSED BY SPOROTHRIX SCHENCKII.
BOTH CUTANEOUS AND SYSTEMIC
FORMS EXIST.
SPECIES : S.SCHENCKII ,
S.BRAZILIENSIS , S.MEXICANA
, S.GLOBOSA, S.LUREI.
5. PATHOPHYSIOLOGY
TRAUMA (MINOR/MAJOR) IN
SKIN OR MUCUS MEMBRANE.
SPREAD IN SUBCUTANEOUS
TISSUE , MAY PROGRESS TO
SUBCUTANEOUS LYMPHATICS OR
DISSEMINATE IN BLOODSTREAM.
MIXED GRANULOMATOUS
REACTION WITH NEUTROPHIL
FOCI.
6. CLINICAL FEATURES
• LYMPHANGITIC:
USUALLY OCCURS ON
EXPOSED SKIN.
NODULE OR PUSTULE FORMS
WHICH BREAKS DOWN INTO
SMALL ULCER.
UNTREATED - INVOLVEMENT
OF LYMPHATICS FROM
DRAINING AREA.
• FIXED:
PATHOGEN REMAINS
MORE/LESS LOCALIZED AT
THE POINT OF INOCULATION.
MAY BE
ACNEFORM/NODULAR/ULCER
ATED OR VERRUCOUS.
7.
8. MANAGEMENT
• INVESTIGATIONS:
COLONY- LEATHERY , MOIST AND INITIALLY WHITE OR
CREAM WITH A WRINKLED SURFACE AND LATER MIGHT
BECOME DARK.
MICROSCOPY - PALMATE / FLOWER LIKE ARRANGEMENT OF
CONIDIA AND HYPHAE.
10. MYCETOMA
AKA MADUROMYCOSIS / MADURA
FOOT.
LOCALIZED CHRONIC INFECTION CA
USED BY VARIOUS SPECIES OF FUNGI
/ ACTINOMYCETES.
CHARACTERIZED BY FORMATION OF
AGGREGATES OF GRAINS WITHIN
ABSCESSES, DISCHARGED TO
SURFACE VIA DRAINING SINUSES.
11. • EPIDEMIOLOGY:
• PATHOPHYSIOLOGY :
CRITICAL TO SURVIVAL OF THE FUNGUS OR ACTINOMYCETE IS ITS
ABILITY TO FORM CELL CLUSTERS OR GRAINS.
THESE GRAINS AIDS IN SURVIVAL, VIA PROTECTIVE MATRIX IN CASE OF
ACTINOMYCETES OR CELL WALL THICKENING IN CASE OF FUNGI.
IN CASE OF M.MYCETOMATIS DEPOSTION OF MELANIN IN CELL WALL IS
PROTECTIVE MECHANISM.
EUMYCETOMA MADURELLA
MYCETOMATIS
ACTINOMYCETOMA 1. NOCARDIA
2. STREPTOMYCES
SOMALIENSIS
12. CLINICAL
FEATURES
• EARLY STAGE- firm, painless nodule.
• LATE STAGE- papules and pustules which
break down to form sinuses on skin surface.
• Discharge may be purulent/seropurulent.
Whole area becomes swollen and hard
,without much significant pain.
• COMPLICATIONS- extension to
underlying bone , PERIOSTITIS,
OSTEOMYELITIS,AND ARTHRITIS.
13. MANAGEMENT
• INVESTIGATIONS:
HISTOPATHOLOGY -
v CHRONIC INFLAMMATORY REACTION LEADING
TO FOCAL NEUTROPHIL ABSCESS , SCATTERED
GIANT CELLS AND FIBROSIS.
v GRAINS IN THE FORM OF WHITE, YELLOW RED
OR BLACK GRANULES IN CENTRE
OF INFLAMMATORY RESPONSE AND MAY
BE DISCHARGED THROUGH SURFACE SINUSES.
14. PUS EXAMINATION: FROM PUSTULES/SINUSES THAT
HAVEN'T BEEN RUPTURED YET.
EUMYCETOMA GRAINS
• BLACK IN COLOUR
• WHEN CRUSHED UNDER COVER
SLIP, CONSIST OF MASSES OF
FUNGAL MYCELIUM WITH
HYPHAE OF 2-6um.
• CHLAMYDOCONIDIA AT THE
PERIPHERY OR CENTRE
OF GRAIN
ACTINOMYCETOMA GRAINS
• RED IN COLOUR.
• CONSIST OF MASSES OF MUCH
NARROWER BACTERIAL
FILAMENTS.
15. • FUNGAL CULTURE :
MADURELLA MYCETOMATIS – COLONIES ARE INITIALLY PALE AND
LEATHERY BUT BECOMES OLIVE,OCHRE BROWN OR GREY IN COLOR.
o ON NUTRITIONALLY POOR MEDIA, SPHERICAL CONIDIA MAY BE
FORMED FROM FLASK SHAPED PHIALIDES.
SCEDOSPORIUM APIOSPERMUM: FLOCCOSE GREY/BROQN-GREY
SURFACE COLONIES.
• OTHER: X RAY OF AREA, MRI may be needed.
16. • TREATMENT:
o Localized lesion that can be excised without residual disability are best so treated.
o FOR FUNGAL CAUSES :
KETOCONAZOLE
TRIAL THERAPY WITH GRISEOFULVIN TERBINAFINE ,
VORICONAZOLE OR ITRACONAZOLE
o 2ND LINE : radical surgery.
17. CHROMOBLASTOMYCOSIS
• AKA CHROMOMYCOSIS , VERRUCOUS
DERMATITIS.
• Chronic fungal infection of skin and
subcutaneous tissue caused by
pigmented fungi.
• Produces thick
walled single / multicelled clusters(
sclerotic or muriform bodies) and
charaterised by slow growing exophytic
lesion, usually on feet and legs.
18. • EPIDEMIOLOGY: USUALLY FOUND IN TROPICS, WITH MEDIUM TO
HIGH RAINFALL.
MC IN ADULT MALE AGRICULTURAL WORKERS, CHILDREN CAN BE
AFFECTED.
• PATHOPHYSIOLOGY:
Fungi can be isolated from woods or soil and trauma is the source.
• CAUSATIVE ORGANISM: PHIALOPHORA VERRUCOSA
FONSECAEA PEDROSOI
F.COMPACTA
CLADOPHIALOPHORA CARRIONII
19. CLINICAL FEATURES
• EARLY LESION – Warty papule slowly
enlarges to form hypertrophic plaque . This is
flat and expands slowly with central scarring.
• Lesion can be ulcerative.
• LATE LESION- after months/years large
hyperkeratotic masses upto 3cm thick are
formed and secondary ulceration may occur.
• Usually painless ,if secondary infected -
painful.
• VARIANT- psoriasiform lesions.
20. MANAGEMENT
• D/D- rule out BLASTOMYCOSIS( absent sharp border and pulmonary lesions).
• INVESTIGATIONS:
HISTOPATHOLOGY: o FOREIGN BODY GRANULOMA, WITH
ISOLATED AREAS OF MICROABCESSESS.
o WITHIN GIANT CELL- GROUP OF
FUNGAL CELLS AS CHESTNUT/ GOLDEN
BROWN COLORED IS SEEN
o AKA SCLEROTIC CELLS/MEDLAR
BODIES/COPPER PENNY.
o MARKED PSEUDOEPITHELIOMATOUS
HYPERPLASIA.
21. • COLONIES – colonies of all species are dark grey-green to black and velvety or
downy with a black reverse.
PHIALOPHORA VERRUCOSA- The dominant form of conidiation is FLASK
SHAPED PHIALIDESwith dark collarette at apex.
FONSECAEA PEDROSOI- Dominant form of conidia is SYMPODIAL with
conidia confined to upper part of cell.
CLADOPHIALOPHORA CARRIONII- Acropetal budding is dominant.
24. HISTOPLASMOSIS
• AKA DARLING DISEASE , HISTOPLASMOSIS CAPSULATI
• FUNGUS IS INTRACELLULAR , RESIDING IN
RETICULOENDOTHELIAL SYSTEM.
• CAUSED BY :
1. HISTOPLASMA CAPSULATUM
2. HISTOPLASMA DUBOISII
25. • EPIDEMIOLOGY:
• Infants and children are frequently affected
• Males>females.
• Lymphoma favors infection.
• CAUSATIVE ORGANISM: Saprophytes,isolated from soil contaminated with
bird feathers and droppings.
• In endemic areas , recognised as hazard to cave explorers.
HISTOPLASMA CAPSULATUM WORLDWIDE.
HISTOPLASMA DUBOISII
Aka AFRICAN HISTOPLASMOSIS
FOUND ONLY IN AFRICA.
SKIN LESIONS MORE
COMMONLY SEEN.
26. CLINICAL FEATURES
• PRIMARY SKIN LESION : Following dissemination from primary pulmonary
focus.
Papules , ulcers, nodules, granulomas, abscesses , fistulae ,scars and pigmentary
changes may be seen with often local lymphadenopathy.
Secondary involvement of skin with osteomyelitis may be present.
• CLINICAL VARIANTS: ACUTE PULMONARY HISTOPLASMOSIS
ACUTE DISSEMINATED
CHRONIC PULMONARY HISTOPLASMOSIS
CHRONIC DISSEMINATED
28. MANAGEMENT
• INVESTIGATIONS:
1. BIOPSY- TINY YEAST IS SEEN SEEN WHICH STAINS BLACK WITH
GMS. LARGELY INTRACELLULAR.
2. COLONY – INITIALLY MAY BE WAXY
BUT LATER DEVELOPS TO PRODUCE
WHITE OR TAN COTTONY COLONIES.
30. BLASTOMYCOSIS
• Aka NORTH AMERICAN BLASTOMYCOSIS , GILCHRIST DISEASE.
• Chronic granulomatous and suppurative mycosis caused by
BLASTOMYCES DERMATITIDIS.
• Affects primarily the lungs but disseminating forms also affect skin,
bones, CNS.
31. • EPIDEMIOLOGY:
o Males>females
o Uncommon in pts with HIV/AIDS.
• PATHOPHYSIOLOGY:
o Infection via inhalation of spores from a
saprophytic spores.
o Primary skin infection occurs by direct
inoculation.
32. CLINICAL FEATURES
• PRIMARY CUTANEOUS BLASTOMYCOSIS: Erythematous indurated area with
chancre appears after inoculation within 1-2 weeks.
o Associated lymphangitis and lymphadenopathy may also occur.
• OTHER VARIANTS-
• DIFFERENTIALS -
1. Tuberculosis 3. leprosy
2. Syphilis 4.Pyoderma gangrenosum 5. Drug reactions.
PULMONARY BLASTOMYCOSIS
DISSEMINATED BLASTOMYCOSIS
33. MANAGEMENT
• INVESTIGATION:
1. KOH- Thick walled , rounded, refractile,
broad based spherical yeasts.
2. HISTOPATHOLOGY – Epidermal
hyperplasia ( pseudoepitheliomatous). Intra
and subepidermal polymorphonuclear
abscesses and granulomatous infiltrate are
found in dermis.
3. COLONY: Initial waxy then cottony and
white to tan.
35. COCCIDIOIDOMYCOSIS
• Primary respiratory fungal infection caused by COCCIDIOIDES
IMMITIS and C.POSADASII.
• Endemic in dessert areas and southwest USA.
• More risk of dissemination in pregnant women.
36. • PATHOPHYSIOLOGY: Fungus is a soil inhabitant but infection occurs via
inhalation of fungus laden dust.
• Spreads from lung tissue to form spherules - large ,round, endospore containing
structures.
• Intradermal skin testing with coccidioidin becomes positive between 2-6 weeks after
exposure.
• CLINICAL PRESENTATION- Primary pulmonary form is most common and in
some 3-25% of patients ERYTHEMA MULTIFORME or ERYTHEMA
NODOSUM occurs from third to seventh week .
• Generalized macular rash is seen in 10% of patients.
• Skin lesions may appear as abscesses, granulomas, ulcers/ discharging sinuses.
37. MANAGEMENT
• INVESTIGATION:
1. KOH : Large globular spherules are seen.
2. COLONY : Mycelial, fast growing initially waxy then cottony and white to tan.
3. SEROLOGICAL TESTS: Precipitins develop in 90% of infected individuals
within 2-4 weeks.
4. TREATMENT:
For Localized Infection:
o ORAL ITRACONAZOLE (200-400 mg)
o ORAL FLUCONAZOLE (400-800mg)
2nd Line:
o IV AMPHOTERICIN (0.5-1mg/kg) daily or
o LIPOSOMAL AMPHOTERICIN (3mg/kg) daily.
38. PARACOCCIDIOIDOMYCOSIS
• Chronic granulomatous fungal infection caused by PARACOCCIDIOIDES
BRASILIENSIS.
• Affects skin, mucous membrane , lymph nodes and internal organs.
• Aka SOUTH AMERICAN BLASTOMYCOSIS,
PARACOCCIDIODAL GRANULOMA.
39. • EPIDEMIOLOGY :
o More frequent in rural areas.
o Adult males 20-50 year old most frequently infected.
o Fungus occurs as saprophytes on vegetation and in soils. Infection occurs
via inhalation.
o HLA-A9 susceptibilty may be related.
o CLINICAL FEATURES :
Mucocutaneous lesions might be present along with lung disease or can occur alone .
Oral / circumoral lesions are common and may be localized or diffuse.
40. If mouth is involved – severe, painful ulcerating stomatitis occurs. The ulcer becomes
granulomatous and spreads over mucus membranes – MULBERRY LIKE
EROSION.
Skin lesion may have satellite lesions.
DIFFERENTIALS:
o BLASTOMYCOSIS
o TB, SYPHILIS , ACTINOMYCOSIS , SPOROTRICHOSIS, LEISHMANIASIS.
41. MANAGEMENT
• INVESTIGATIONS:
• KOH- rounded, refractile cells.
• COLONY - Slow and restricted growth. Initially flat or wrinkled and
leathery.
• HISTOPATHOLOGY - Reaction resembles like blastomycosis . Giant cells
are conspicuous and frequently contain budding cells.
42. TREATMENT
• ITRACONAZOLE 200-400 mg daily ; remission in in 3-6 mo is achieved.
or
• KETOCONAZOLE 200mg daily.
• IV AMPHOTERICIN B 0.5-1mg/kg x 2 weeks f/b oral ITRACONAZOLE
200mg daily.
43. CRYPTOCOCCOSIS
• Acute , subacute or chronic infection caused by CRYPTOCOCCUS
NEOFORMANS – an encapsulated yeast.
• Marked predilection for brain and meninges although lung and skin
infection may also occur.
44. EPIEMIOLOGY :
• Particularly associated with AIDS.
• Age - 30-60 years.
• Susceptibility greatly increased in immunodeficiency state .
PATHOPHYSIOLOGY :
• Respiratory tract is portal of entry but primary cutaneous lesion may
occur.
• Skin lesion occur in 10-15% of case of
disseminated cryptococcosis(serotypeD strain)
45. CLINICAL FEATURES
• CNS manifestations usually predominate presenting as chronic meningitis or focal
brain lesion simulating brain tumor.
• Low grade fever persists and coma occurs f/b death.
• In disseminated disease , cutaneous lesion may precede or follow signs of
involvement of CNS and lungs.
• Cutaneous and mucous membrane lesion occur in about 10% and 3% cases
respectively.
• Most frequemt are- firm/cystic,slow growing, subcutaneous,erythema
nodosum like swellings.
• Acneform eruptions in widespread disease, and any of these can ulcerate.
46. • DIFFERENTIALS: Histoplasmosis.
• INVESTIGATIONS:
• KOH – large budding cells.
• COLONY - soft ,cream to pale brown and usually mucoid.
• ASSOCIATION WITH AIDS - multiple skin lesions are seen and high titres
are usually present in these pts.
