Fungal Infections

Professor Dr.Abdulhamid Elorfi

Consultant Dermatology
2019
 Classification of fungal infections

A-SUPERFICIAL → stratum corneum, hair and nails

I-Non-Inflammatory
1-COMMENSAL :Pityriasis versicolor,Pityrosporum folliculitis
2-INFECTIOUS : Tinea nigra - Black piedra & White piedra
II-Inflammatory
1-Dermatophyte infections : Tinea (capitis -barbae -faciei -corporis -cruris
-manuum
-pedis -unguium (onychomycosis)
2-Candida :Mucocutaneous candidiasis
B-SUBCUTANEOUS→ dermis or subcutaneous tissue→implantation - Mycetoma –
Sporotrichosis, Chromoblastomycosis .
C-SYSTEMIC(DEEP)
1-True pathogens→ dermis or subcutaneous tissue hematogenous spread or
extension from underlying structures : Histoplasmosis - Coccidioidomycosis
2-Opportunistic→1ry or 2ry skin lesions in→↓immunity :Candidiasis, Aspergillosis -
Zygomycosis - Cryptococcosis (where there are pigeon droppings) - Trichosporon
beigelii -Pseudallescheria boydii
 Pityriasis versicolor
Cause:-Dimorphic yeast( Malassezia furfur)(Pathogenic filamentous
form of normal flora(Pityrosporum).Other Yeast :
M.globosa,M.sympodialis,M.nana.Under predisposing conditions
change from commensal to pathogenic mycelial form .
Young adults(20-35).,Both sexes,Children in tropics.Neonates also seen.
Family history in about 18%.
Clinically:-Asymptomatic (itch may be moderate). Sharp round or oval
macules,coverd with fine branny scales easily scraped off.Size varies
from small macules to large confluent > 30 cm
large areas,scattered patches,light-brown to pink to hypo-pigmented
white.Spontaneous remission may occur in winter &re-ocurr in
summer
Sites:-Upper trunk,neck,upper arms.In tropics→face.
Inverse Pit.versicolor rare(axilla,groin,face)
 Predisposing factors
1.Genetic predisposition
2.↓ immunity
3.Corticosteroids→→↑↑yeast growth
4.Cushing disease
5.Humidity & Warm(Hot,Humid tropical).
6.Hyperhidrosis →sweat→sticked organisms together
7.Bath Oils and oily creams application(in children)→substrate for yeast
growth
8.Sunlight→modifies fungus metabolism →↑ azelaic acid
9.Malnutrition
 Clinical types
1-(Hyperpigmented )Brown type ( Enlarged melanosomes ,Thick stratum corneum
,Hyperaemia in response to infection )
2-(Hypopigmented)White type :
Ø Sun expousre→+ azelaic acid (decarboxylic )→ diffuses &Inhibits tyrosinase
Ø Damage to melanocytes→ explain why repigmentation take months to years after
treatment.
Ø Melanosomes → small size & numbers decreased
Ø Blocking of UV→lipid-like material accumulating in stratum corneum
→ not explained in non-sun-exposed skin
3-(Erythematous)Pink type → inflamed→ due to dermatitis(hyperkeratosis)→ induced
by malassezia or its metabolites +/- seborrhoeic dermatitis.Also large No.of
organism ,superficial lymphocytic infiltrate& macromelanosomes
4-Follicular (Pityrosporum folliculitis) due to Deep follicular infection manifest
as
perifollicular, erythematous itchy papules & pustules involving back, the
chest, and
the extremities
5-Inversus( affecting flexures ,face ) more in immuncompromizd.
6-Achromia parasitica .
7-Atrophic. 8. Trichrome.
Hypopigmented Type
 DD
1.Hypopigmented type: Vitiligo,Pityriasis alba,Leprosy,
progressive macular hypomelanosis (due to Prop.acnes)
2.Pityriasis rosea
3.Inversus type : Seb. Dermatitis, Erythrasma,candidiasis
dermatophytes,flexural psoriasis
4.Epidermodysplasia veruciformis
5. Secondary syphilis and Pinta
6.Confluent and Reticulate papillomatosis
7.Guttate psoriasis
8.MF.
 Diagnosis
1.Clinical
2.Wood’s lamp→yellow fluorescence
3.Direct KOH or cellophane tape with methylene blue→spherical thick
-wall budding cells &short hyphea(Spaghatti &meat balls)or (bacon &
eggs) or (bananas & grapes ).Mycelium is diagnostic .
Histo.:- Hyperkeratosis,acanthosis,perivascular lymphocytic
infiltration,plasma cells,histiocytes.PAS stain or methenamine sliver
stain →hyphea&round budding cellular fungi in strat.corneum.
Culture:- Difficult to grow yeasts in a laboratory ,need enriched media
with fat(natural sterile olive oil).Rarely done.
Pityriasis Versicolor Microscope
Pityriasis Versicolor – Woods Light

Yellow White
 Management
Patients should be informed:
• → fungus normally present on the skin surface and
is therefore not considered contagious.
• → skin color alterations resolve → within 1-2
months after treatment
• →Vigorous exercise an hour after taking the
medication.
• → Avoid bathing for a few hours after treatment
A.Topical:-(Relapse rate (60%-80%)
1.Selenium sulfide 2.5% for 10-15 minutes then washed off. For 2
weeks .(Irritant),Not on face.
2.Ketoconazole shampoo. Left 10 min.before rinsing /twice per wk/2-4w
3.Imidazoles:-miconazole,isoconazole,tioconazole,ketoconazole 2%
sertaconazole.(→ every night for 2 weeks then Weekly → to prevent
recurrence)
4.Ciclopiroxolamine 0.1%
5.Allylamines(Naftifine,terbinafine)
6.Zinc pyrithione 2% shampoo.5 min application nightly for 2weeks
7.Sodium thiosulphate 25% once /day at night(offensive)
8.Sodium sulfacetamide 20%
9.Propylene glycol 50% in water.BD for 2 weeks .
10.Retinoic acid cream BD for 2 weeks (cure fungus & help re-pigmentn)
B.Systemic therapy : For patients convenience
→ less time consuming than topical treatment
→extensive lesions.
→If topical agents have failed.
1.Fluconazole →single 150- to 300-mg weekly repeat after 2-4 weeks
2.Itraconazole →200 mg/d for 7 days.
3.Pramiconazole→ 200 mg/d for 2-3 days or 200-400mg once.
4.ketoconazole:-Single dose of 400mg.(!!! Liver!!!)
Recurrences
Relapse prevention:- monthly 300mg fluconazole in summer (6
months) ± ketoconazole shampoo twice/wk
Topical antifungals →Weekly → prevent recurrence
Antifungal shampoo →one to three days each month.
Treatment of post-inflamm hypopigmentd lesions:-
UVB, Topical steroids,PUVA.
Other diseases with Malassezia:-
1.Seb.dermat.
2.Atopic dermatitis.
3.Pityrosporum folliculitis:- pruritic perifollicular erythematous 2-3mm
papules or pustules on upper trunk,neck,arms,in hot
,humid,occlusion,DM,immunosupp.(yeast form found in hair
follicles).(® oral itraconazol or selsun or nizoral shampoo)
4.Confluent & reticulate papillomatosis(Gougerot-Carteaud syndrom):-
Girls,after puberty,Gray brown confluent
papules,intermammary,interscapular,M.furfur cells found in lesions.
Some responde to Antifungal,some responde to Minocycline
5.Sebopsoriasis.
6.Neonatal cephalic pustulosis (Neonatal acne) .
7.Scalp psoriasis.
 Candidiasis
Candidiasis : Acute or chronic, Skin,MM , rare internal organs
Commonly by Candida albicans→ is an oval yeast 2-6 µm in diameter
It is Yeast like fungs, exist in: -
1. Budding yeast(commensal)
2. Mycelial (pathogenic)
Commensal in mouth,intestine,rectum,vagina.
Ø Not of normal flora except in areas near orifices or inter-triginous
areas.
Ø Not commensal in body fluids except in urine.
Isolation from skin lesions is pathogenic.
The genus Candida includes more than 150 species. Candida tropicalis,
Candida parapsilosis, Candida guilliermondi, Candida krusei, Candida
kefyr, Candida zeylanoides, and Candida glabrata (formerly
Torulopsis glabrata) are less common causes of human disease.
Candida albicans virulence factors:-
1.Adhesion factors(cell wall mannan or protein components) lead to
colonization of epithelial surfaces.
2.Proteinase enzymes
3.Hyphae formation
4.Contact sensing of hyphae→deeper penetration into epithelial
5.Surface hydrophobicity
6.Rapid switching of its phenotype.
Predisposing factors:-
1.Lack of bacterial flora(prolong Antibiotic therapy,mouth of neonate, in
DM,G-ve bacteria in web spaces→co-pathogen enhance yeast
pathogenicity.
2.Local tissue damage:- friction,dentures,maceration,humidity
3.↓ofCMI(Steroid,Immsup,Leukem,lymphoma,AIDS,Endocrines.
(Cushing,addisons,chronic mucocutan.candidaisis)
4.Serum transferrin:- Of newborn & in patient with leukemia is highly
saturated with iron and has lower unbound iron binding capacity
than normal adults, so more free iron for growth of candida.
5.Pregnancy & oral pills:- Increase estrogen→increase glycogen in
vaginal mucosa(extra nutrition for candida)
Diagnosis:-
1.KOH of skin scraping,Vaginal disharge stain with Gram stain→gram +ve blastospore
yeast and pseudo or true hyphea
2.Culture on Sabouraud’s glucose agar:- Colonies appear 1-3 days at room
temperature(white creamy colonies,moist)
3.Chromogenic agars:- Candida colonies are blue and other yeast are cream or
white(Biomerieux agar),while on Becton &Dickinson agar colonies are
green,tropicalis are blue,krusei are pink.
4.Depleted media as corn meal agar or rice extract agar:-
Supplemented with Tween 80.Candida albicans produce rounded refractile
chlamydospore within 104 days at 26°C.
5.Serum tube test:- Candida albicans produce filaments when grow in serum for 2-3
hours at 37°C
6.Commensall yeast identification system:- API 20C and Auxa-color
7.Sero-diagnosis:- agglutinating,precipitating antibodies.(of little value)
8. PCR.
Histopathology: ( using gomoris methylamine sliver stains (GMS). mycelia in
strat.corneum.,subcorneal pustules,spongiform pustules in epidermis.Dermal
infiltration with lymphocytes,plasma,histiocytes.
Candidal granuloma:-Hyperkeratosis,acanthosis,dense mixed infiltrate, giant cells
in
dermis.
 Clinical types of candidiasis
1.C.intertrigo
2.Genital candidiasis
3.Chronic paronychia
4.Napkin
5. Oral candidiasis:- A.Oral thrush:-
B.Acute atrophic C.(Candidal glossitis):-
C. Chronic atrophic C.:-
D.Perleche(angular chelitis)
E.C.leukoplakia
F.Black hairy tongue:-
6.Congenital candidosis :
7.Chronic mucocutaneous C.(CMC):-
Subgroups of CMC:-
A. Chronic oral C.(Denture stomatits,HIV-associated
B. CMC with polyendrocrinopathy
C. Localized CMC(sporadic):-
D. Diffuse CMC(AR)
E. CMC with thymoma:-
8.Systemic candidiasis:-
candidiasis
9.Other forms
Clinical Types of candidiasis:-

1.C.intertrigo(Flexural)Skin
(Flexural) folds, in obese,itchy,moist,intense
erythematous ,well defined border,pustules rupture leaving
erosions.satellite lesions outside the lesion.
Erosio-interdigitalis blastomycetica:- between ring &middle
fingers,pruritic marked macerated with scaly border.
Perianal canididiasis:- Intense nocturnal itching & burning
or lesion of candida.
2.Genital candidiasis:
Male: A.Balanoposthitis : inflamm.of glans &prepuce ,usually involv
corona l sulcus
B. Allergic form: Allergic reaction of partner from infected
woman(itching,burning,vesicles,erosion) after intercourse
Female: A.Valvovaginitis(CVV): scanty thick white cheesy discharge
B.Dysuria,dyspareunia,intense pruritus.
3.Chronic paronychia:- In house wifes,facilitated by pedicures.→→→
nail fold tender,red, swollen,loss of cuticle ,detachment of nail fold
from dorsal surface of plate,discharge of thick white pus.
Cand.Onychomycosis:- thick nail,rough,yellow,irregular ridges with
periungual inflammation.
4.Napkin dermatitis(Diaper dermatitis):-
dermatitis
Newborn&infants,confluent intense erythema with irregular sharp
border,papules,pustules satallite lesions.
Nodular or granulomatous candidiasis:- Bluish or brown
nodules,similar to kaposi sarcoma in napkin area.
Topical steroid should be avoided
Oral & paronychia candidiasis may occur with Acrodermatitis
Enteropathica.
Erosio-interdigitalis blastomycetica
Dry, red, superficially scaly, pruritic macules and
patches on the penis represent candidal balanitis
Vaginal canididosis
Candidal paronychia
 5. Oral candidiasis:-
A.Oral thrush:- The most common form of oral Candidiasis.
In Newborn in first weeks of life or AIDS or deblitating.Affecting Buccal
mucosa,tongue,gum.Presents as Sharp defined creamy gray-white
patches & plaques on mucous membranes(Pseudomembrane) with
reddish macerated base and/or smooth-surfaced bright red tongue
(atrophic papillae) . On removal leaves eroded erythematous base.
B.Acute atrophic C.(Candidal glossitis):-
In Elderly,As beefy, red smooth glistening tongue (sore,tender on eating
).With use of broad spectrum antibiotics,topical,inhaled steroid.
C. Chronic atrophic C.:-
Chronic erythema,edema of mucosa on hard & soft palat of denture
wearers.
D.Perleche(angular cheilitis or angular stomatitis)
Fissuring, sometimes with crusting at angle of mouth.(Strepto. infect.,
Vitamin. Deficn.,licking, are factores),
E.C.leukoplakia:- Multiple,white, adherent,firm plaques
with red margin.On tongue or buccal mucosa,(NOT RUB-OFF, as Oral
thrush),more in smokers,Malignancy may develop ,
F.Black hairy tongue:-In heavy smokers,Antibiotics use
Granuloma gluteale infantum. Multiple dark red
papules and nodules in an infant
6.Congenital Cutaneous C.
At birth ,skin,birth membranes due to I.U.infection
7.Chronic mucocutaneous C.(CMC):-
Heterogenous group of clinical syndromes( chronic or recurrent C. of
skin,MM,nails.Start in Infancy or early childhood.
Subgroups of CMC:-
1.Chronic oral C.(Denture stomatits,HIV-associated C.,Inhaled steroid
therapy)
2.CMC with polyendrocrinopathy:-
Hypoparath.,hypothyrod,hypoadrenalism(other Autoimmun
dis(vitiligo,pern.anam)
3.Localized CMC(sporadic):- sever ,children,Multiple hyperkeratotic
crusted on face,scalp.
4.Diffuse CMC(AR) multiple erythem.serpigin. Lesion
5.CMC with thymoma:- In adults.
Asssociated diseases with CMC:-
1.infections:-Dermatophytosis,viral(HPV)
2.Skin diseases:-Vitiligo,AA,Seb.dermat.
3.Systemic dis.:-malabsorption,hepatitis,Pern anem.,myopathy,Cancer.
8.Systemic candidiasis:-In
candidiasis serious diseases(leukemia) .Candid.come
from GIT,or I.V. infusion
Triad of :-Fever,Diffuse muscle tenderness,Erythematous papules or
nodules with pale center.Candida can be culture from blood in 25%
Candidal allergic reaction:- Pruritic eczematous,on trunk,&/or hands
&feet or erythema annular centrifugum or chronic urticaria.
Treatment of Candidiasis:-
1.Avoid predisposing factors:-
Drying, ventilation of skin,napkin change,better hygiene
Use cotton undercloths,open footwear, removal of dentures with care
of mouth hygien,oral nystatin
2.Topical:- G.violet 2%,Nystatin,Imidazoles for 2 weeks
3.Systemic :-itraconazole or Fluconazole in CMC,recurrent
VVC,paronychia,onychomycosis,immunsuppre.,Systemic candidiasis.
Oral Candid.:-Nystatin suspension 2ml /4 times/d. remain in mouth as
long as possible before swallow.
Aqueous G.violet 1%,Systemic antifungal.
CMC:- Detect immun.defect,prolong ® antifungal,Endocrin.check
Oral C. in HIV:-Flucon.100-200mg/d/14d.Itraconazole
200mg/d/3wk,Resistanc→IV.amphoteric± oral flucytocin.
 Deep mycoses
A.Subcutaneous :- Sporotrichosis
Chromoblastomycosis
Mycetoma
B.Systemic Mycosis :- Blastomycosis
Coccidiodomycosis
Histoplasmosis
Africans histoplasmosis
Paracoccodioidomycosis
Penicilliosis
C.Opportunistic :- Cryptococcosis
Mucormycosis
Aspergillosis
Fusarium infection
 Sporotrichosis
Chronic lymphatic S.C. fungal infection-Rose gardener’s disease
Sporothrix schenckii, dimorphic aerobic fungus in soil
Introduced into skin by trauma( thorns &woods) and direct inoculation.(I.P.1-3 wks)
In tropical areas in south &central America,Canada, Mexico,South Africa ,Australia
Adults male.mine workers ,gardeners.In Brazil reported in Cats.
Clinical forms:-
1.Cutaneous forms:-
forms
A.Lymphocutaneous:- Commonst,Sporotrichotic chancre, on exposed skin,upper
limbs, as nodules or pustules break down into ulcer. Involvement of lymphatics
proximally lead to chain of lymphatic nodules ,soften and ulcerate and connected
by hard lymphatic cords.
Regional LN rarely swollen and break down.Primary lesion may heal spontanously
leaving LN enlarged.G.C.good
DD.:-Atypical Mb.,leishmaniasis,Tb,Pyogenic bact.infections,Cat scratch dis.
B.Endemic(fixed) type:-
Pathogen localized to point of inoculation→acneiform,nodular,ulcer,extensive
verucous Or infiltrated plaques.High immunity.
C.The disseminated cutaneous form.
D.The disseminated extracutaneous forms.
Lymphocutaneous sporotrichosis
Lymphocutaneous sporotrichosis showing typical elevated
subcutaneous nodules developing along the regional
lymphatics of the forearm.
Fixed cutaneous sporotrichosis
Cut.Sporotrichosis After trauma from bones of
marine cat-fish that were in aquarium
Sporotrichosis begins as an erythematous papule, nodule, or
ulcerated nodule located at the site of inoculation. New
lesions may then spread proximally
Sporotrichosis involving finger
Sporotrichosis
Fixed cutaneous verrucous-type sporotrichosis of the
wrist and hand
 A.Localized cut. Type involving face
B.Localized Scurflodermic type involving face

A B
cutaneous disseminated sporotrichosis in a
patient with AIDS before and after therapy
Disseminated cutaneous sporotrichosis
 Presentation Features
Skin disease qPatients are typically well without fever
qLesion develops at the site of a trauma
qNodules appear under the skin along the
lymphatic channels

Lung disease qPatients usually have severe underlying

chronic lung disease and present with
pneumonia
qThey may or may not have skin lesions

Bones & joint disease qPatients typically present with a subacute

or chronic inflammatory arthritis involving
one or more joints
qThey may or may not have skin lesions

Disseminated disease qPatients present with skin lesions but may

have other organ involvement including the
eye, prostate, oral mucosa, larynx and brain
qSpreading usually occurs only in people with
a weakened immune system, e.g. HIV or AIDS
patient
 Differential diagnosis
Ø The diagnosis must be considered in all cases when the initial
lesions have followed an injury.
Ø Lymphocutaneous sporotrichosis :- pyoderma, atypical
Mycobacterium and Nocardia infection , leishmaniasis .
Ø The fixed form :- pyoderma, paracoccidioidomycosis,
chromoblastomycosis, cutaneous tuberculosis, atypical
mycobacteria, tertiary syphilis, leishmaniasis, skin cancer ,Cutaneous
anthrax :Ulcer with eschar is painless and surrounded by
characteristic non-pitting edema , Lymphatic vessel is not involved
Ø The disseminated cutaneous form :- Other deep mycosis, such as
paracoccidioidomycosis or histoplasmosis, or atypical mycobacteria
and noninfectious granulomatous diseases.
Ø The disseminated extracutaneous forms are diagnosed differently
according to the affected organ. Other fungal conjunctivitis,
bacterial osteomyelitis, pulmonary fungal infections, tuberculosis
and sarcoidosis should also be considered
Diagnosis:-
Direct microscopy of clinical material is of little or no value in confirming a
diagnosis because its presence may easily be source of overlooked.
► (source of diagnostic materials smear,exudate,biopsies)
1.KOH : Not helpful
2. Fluorescent Antibody technique successfully employed in locating the pathogenic
phase in vivo but with inter-laboratory variability in sensitivity and specificity
3. Culture:- Culture of pus, joint fluid, sputum, or a skin biopsy specimen is
preferred
.At room tempret. Compact moist white with wrinkled surface. Later aerial
mycelium and colonies →darker.Microscopically as narrow hyphae with small
oval or triangular conidia.
At 25 ᵒ C : Rapid -growing ,glabrous white to brown mould that become firm
wrinkled and more darkly pigmented overtime .
Microscopically : delicate conidia at the ends of conidiophores
(specialized hyphae)
At 37ᵒ C : Slow-growing ,whitish ,pasty, yeast like colonies.
Microscopically : Cigar –shaped budding yeasts.
4.Biopsy:- Full-thickness skin biopsy: Culture of exuded pus from
cutaneous lesions can be diagnostic; however, full-thickness skin
biopsy for histology and culture may improve diagnostic yield.
Mixed granulomatous reaction , neutrophils microabscess.
As small cigar-shaped or oval yeast that may surrounded by thick
radiating eosinophilic fringe forming ( using methenamine silver
stain)
5.PCR: not available for routine use
 Cytologic preparation from a case of
sporotrichosis; phagocytic cells show
numerous variably-shaped yeast forms within
 Sporotrichosis: tissue section stained with haematoxylin
and eosin. Organisms are usually very scanty but asteroid
bodies, representing a foreign body tissue reaction, may be
observed
Photomicrograph that shows the conidiophores and
conidia of the fungus Sporothrix schenckii.
 Sporothrix schenckii on Sabouraud's dextrose agar grown at 25oC
colonies are moist and glabrous, with a wrinkled and folded surface.
Pigmentation may vary from white to cream to black
 Microscopic morphology of the saprophytic or mycelial form of
Sporothrix schenckii when grown on Sabouraud's dextrose agar at
25oC. Note clusters of ovoid conidia produced sympodially on short
conidiophores arising at right angles from the thin septate hyphae
Microscopic morphology of the parasitic or yeast form of Sporothrix
schenckii when grown on brain heart infusion agar containing blood
and incubated at 370C. Note budding yeast cells.
 Treatment
• Cases have been described where spontaneous remission
has been seen to occur
• Treatment of sporotrichosis depends on the severity and
location of the disease.
• Treatment can be prolonged but should continue until all
lesions have resolved. This may take months or years, and
scars may remain at the original site of infection.
However, most people can expect a full recovery
Ø The orally available azole antifungals are the drugs of
choice for cutaneous or lymphocutaneous sporotrichosis
in developed nations
Ø Systemic or disseminated sporotrichosis is usually more
difficult to treat and in some cases life-threatening for
people with weakened immune systems
® :-Cutaneous and lymphocutaneous sporotrichosis
Ø Oral itraconazole 200 mg/d .upto 2-4 weeks after all lesions have resolved,
(usually for a total of 3-6 months). It is the drug of choice for all types of
sporotrichosis but not CNS and disseminated sporotrichosis
Ø Patients who do not respond should be given one of the following:
Ø (1) oral itraconazole 200 mg twice daily,
Ø (2) oral terbinafine 500 mg twice daily (no comparative data with itraconazole
therapy exist), or
Ø (3)(SSKI ) Saturated potassium iodide solution : Old treatment, inexpensive,
its mechanism is unknown,poorly tolerated by many due to
nausea,hypersalivation
Ø SSKI :- in oral droplet form can cure cutaneous sporotrichosis. (initially
using a
standard eye dropper) A recommended schedule is five drops , ( 1 ml) initially
increased gradually upto to( 50 drops) 4–6 mL of saturated potassium iodide
/3 times/d over 2-3 wk . This usually requires 3 to 6 months of treatment. and
should be continued for 3–4 weeks after clinical cure.
Ø Fluconazole(400-800mg/d/6m) and cotinue for 2-4 wk after healing.
Fluconazole is less effective than itraconazole
Ø Ketoconazole is less effective & is no longer indicated
 ®:Sporotrichosis in pregnant women
• Local hyperthermia can be used to treat cutaneous
sporotrichosis that does not require urgent therapy.
For sporotrichosis that must be treated during
pregnancy, liposomal amphotericin B 3-5 mg/kg/d
should be used.
• Systemic antifungal (Azoles )should be avoided
 Prognosis
• Cutaneous or lymphocutaneous sporotrichosis: Complete recovery without
scarring is the expected outcome with appropriate treatment; however, the
therapy is protracted and expensive.
• Pulmonary sporotrichosis Limited data are available on the response to
treatment; however, evidence suggests that most cases of pulmonary
sporotrichosis respond to itraconazole therapy. Those who do not respond
to itraconazole require treatment with amphotericin B.
• Pulmonary sporotrichosis contributes to declined respiratory function in
patients with COPD.
• Osteoarticular sporotrichosis: More than 70% of patients with
osteoarticular sporotrichosis have a clinical response to itraconazole
therapy. Relapse may occur. Severe disability can result from unrecognized
chronic osteoarticular sporotrichosis.
• Disseminated sporotrichosis: Most patients respond to initial amphotericin
B therapy. In patients with AIDS, life-long suppressive itraconazole therapy
following induction therapy with amphotericin B appears to be necessary to
control infection.
 Mycetoma
Madura foot, Maduromycosis, Tumor produced by fungi
1842 ,Dr. John Gill description in Madura (india).
1.Localized chronic granulomatous swelling with sever S.c. tissue and
bones of hands &feet affection, may extend to muscle or bone.
2.Formation of draining sinuses
3.Granules of different coloures are discharged
Two types : EUMYCOTIC & ACTINOMYCOTIC
Risk factors : Lack of protective footwear , Malnutrition,exposed cuts,
abrasions, more in agricultural workers who walk barefoot
Epidemiology : Rural tropical & subtropical
Eumycotic : Africa .
Actinomycotic : Central & south America
Age & Sex : Men , 20—50 years .
A.Eumycetoma(fungi) :- Caused by true fungi -I.P. 20 Years,
Madurella mycetomatis→→→→→Black grains
M.Grisea→→→→→→→→→→→→→Black grains
Leptosphaeria senegalensis→→Black grains
Pseudallescheria boydii→→→→→→White grains
Acremonium →→→→→→→→→→White grains
Fusarium→→→→→→→→→→→→Yellow grains
2.Actinomycetoma(actinomycetes)
Caused by filamentous aerobic & anaerobic G+ve bacteria
IP 5 years
Nocardia brasiliensis→→→→→→ white or No grains
N.asteroides→→→→→→→→→→→White or No grains
Streptomyces somaliensis→→→→→yellow grains or brown
Actinomadura madurae→→→→→→→Yellow grains
Actinomadura pelletierii→→→→→→Red grains.

Organisms are saprophytes in soil →penetrating injury→skin

Organism survive in S.C. Because they develop thick cell wall,
extracellular melanin deposition which allow them to resist
neutrophil attack.
In tropical & subtropical ,adults ,barefoot,agricultural workers,
malnutrition,exposed cuts, abrasions
MYCETOMA- causative agents
FUNGI ACTINOMYCETES
Madurella mycetomatis
Actinomadura madurae
Madurella grisea
Actinomadura pelletieri
Leptosphaeria senegalensis
Nocardia brasiliensis
Neotestudina rosatii
Nocardia asteroides
Fusarium moniliforme
Streptomyces somaliensis
Fusarium solani
 Summary of Clinical Difference
Actinomycotic
1. Multiple tumour masses
with ill defined margins
2. Sinuses Appear early,
numerous ,Raised
inflammed opening
3. Discharge Purulent Granules
White, Red,Yellow
4. Bone Osteolytic lesions
5. Filament < 2um (bacilli)
6. Gram : positive
7. H&E : homogenous
eosinophilic
8. Giemsa: blue center &pink
filaments periphery
Eumycotic
1. Tumor Single, well defined
margins
2. Appear late, few in No.
3. Serous Discharge
Black/white/brown
4. Bone Osteosclerotic
lesions
5. >2um (fungal hyphae)
6. Gram : negative
7. H&E : brownish
8. Giemsa: black with green
tinge
Clinical:-
On foot or LL.slow progressive firm painless nodules,irregular lumpy appearance
,breakdown and discharge pus contain grains through multiple sinus
tract.Extension to underlying bones or joints lead to periostitis
,oesteomyelitits,arthritis.
Diagnosis:-
1.KOH of Pus:- color of granules.
2.Culture:- A.Fungi + chloramph. At room tempert..growth occurs within 5-10 days
B. Actinomycets:-+ cyclohexamide at room temp..Growth occur within 2-3 d.
3.PCR .
4.Biopsy:- Chronic granulomatous reaction with abscess contain granules and dense
fibrosis.
Ø Differentiation is accomplished by microscopic examination of exudate from the
draining sinuses.
Ø Actinomycetes: have granules of about 100 µm in diameter, with delicate,
branched filaments measuring about 1 µm in diameter.
Ø Fungal grains : are observed as a mass of hyphae embedded in intercellular
cement, and the filaments are wider than 1 µm.
5. Radiologic tests : X-ray , CT scans & MRI should be performed if underlying bony
involvement & soft tissues is suspected
Madura foot. Note the soft tissue swelling of the foot as
well as multiple nodules with pustular discharge.
 Madura foot
A 45 year old man with slowly progressive
deformity since 13 years.
Diagrammatic sketch of mycetoma of the foot showing the
formation of suppurating abscesses and draining sinuses
 Actinomycotic mycetoma showing numerous draining
sinuses. There is destruction of bone, distortion of the foot,
and hyperplasia at the openings of the sinus tracts.
 Eumycetoma Treatment
• Generally less successful than for actinomycetoma. In adults
weighing 70 kg, ketoconazole 400 mg daily,or itraconazole
300 mg-400mg daily, or intravenous amphotericin B 1-1.5
mg/kg iv slowly over 8-10 hr for 8-10 weeks(total dose 2
gram) or liposomal amphotericine B 5mg/kg.
• Isolated cases of successful treatment with voriconazole and
Posaconazole (NOXAFIL) 400mg BD orally over many weeks
have been reported.
• Therapy is suggested for 1-2 years (or greater) for complete
eradication, unless adverse effects warrant cessation of
medication.
• In two cases, the authors have used a combination of
itraconazole and terbinafine resulting in remission of the
disease.
• Combined medical and surgical treatment is a viable therapy
for mycetoma caused by fungi.
 Actinomycetoma Treatment
• Current treatment is trimethoprim-sulfamethoxazole 7.5-40 mg/kg daily divided
in 2 oral doses for several months or years. In certain anatomical sites (eg,
thorax,
head), extensive lesions, or cases recalcitrant to the above therapy, amikacin 15
mg/kg intramuscularly daily should be added.Every three weeks, a periodic
audiometric and creatinine clearance analysis must be performed. This treatment
is
maintained for 5-20 weeks and in rare cases, for a longer period, depending on
the
clinical response and renal and auditory adverse effects.
• Netilmicin can be used in cases resistant to amikacin. Other antimicrobials, such
as
minocycline, amoxicillin-clavulanic acid, streptomycin, imipenem, meropenem, and
rifampin, have also been used with variable success.
• Actinomycetoma may respond to prolonged combination chemotherapy—e.g.,
with streptomycin (14mg/kg daily IM for 3 months) and either dapsone (1.5mg/kg
12 hourly orally) or trimethoprim-sulfamethoxazole. Rifampicin or amikacin can
be used in stead of streptomycin
• An oxazolidinone, linezolid, has been proven to be active in vitro, in vivo, and
in
clinical nocardial infections. Other experimental oxazolidinone drugs such as DA-
7867 and DA-7218 are active in vitro and in experimental models of N brasiliensis
infection, although they have not been used in humans.
• Fluoroquinolones such as gatifloxacin and moxifloxacin have been observed to be
active in vitro and in a murine model of actinomycetoma by N brasiliensis.
However, clinical assays are necessary to determine its usefulness in human cases
 Surgical Care
• In eumycetoma, surgical therapy is an option if the
patient's disease has not responded to antifungal
medical treatment, in local lesions, and in patients
with massive disease. In these cases, wide local and
debulking excisions and even amputation are used
together with medical fungal treatment.
• In actinomycetoma surgical treatment, including
amputation, is infrequently indicated.
 Prognosis
qActinomycetomas generally respond well to
trimethoprim-sulfamethoxazole/amikacin in 90% of
cases. In those cases in which bacteria have become
resistant to this treatment, antibiotic susceptibility
testing should be performed to select the best
antimicrobial agent or agents to be used.
qEumycetoma tends to be a more chronic disease, and
success with medical therapy is observed in only about
40% of cases. If the response is partial or negative to
medical treatment, surgery of the affected area should
be performed, and antifungal drugs continued until
complete remission of the disease