Fungal Infections and it's types
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FUNGAL
INFECTIONSAND IT’S TYPES
ARGAO COMMUNITY HOSPITAL
BY: ZICHRI KEREN O. PEROCHO
MHAM INTERN
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OUTLINE
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SIMPLE RECALL
Fungi- Greek “mykos” – mushroom
widely distributed and are found where
“moisture” is present
Epidemiology:
children
warm, moist climate
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Fungal infections
(Dermatomycosis)1. Superficial- stratum corneum, hair and nails
a. “ Dermatophytosis”
b. “Onychomycosis”
c. Tinea Nigra, Tinea Piedra
2. Deepa. Subcutaneous
i. Sporotrichosis
ii. Chromomycosis (chromoblastomycosis)
iii. Mycetoma (Madura foot )
b. Systemic Respiratory Fungal infections
i. Blastomycosis
ii. Histoplasmosisiii. Coccidioidomycosis
iv. Paracoccidioidomycosis
c. Opportunistic Fungal Infections
i. Cryptococcosis
ii. Aspergillosis
iii. Mucormycosis
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SUPERFICIAL FUNGAL
INFECTIONS
I. Dermatophytosis
“ Dermatophyte- fungus that has
developed the ability to live on theKERATIN (hair, nails or skin scale) ofanimals
3 Genera1. Microsporum
2. Trichophyton
3. Epidermophyton
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Clinical Presentations of
Dermatophyte Infections
Tinea capitis Scalp
Tinea faciei Face
Tinea barbae Beard
Tinea corporis Trunk, Extremities
Tinea cruris Groin
Tinea manuum (manus) Hands
Tinea pedis Feet
Tinea unguum Nails
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Tinea capitis
“SCALP”
Etiologic agents: * Microsporum audounii (Griseofulvin)
Trichophyton tonsurans
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Tinea Capitis
4 Clinical Patterns 1. Seborrheic- dandruff-like scaling: D/Dx;
Seborrheic Dermatitis (prepubertal) 2. Black Dot Pattern- hairs are broken off at the
skin line, black dots are seen within the areas ifalopecia. “Trichophyton tonsurans”
3. Kerion- an inflammatory fungal infecton thatmay mimic bacterial folliculitis or an abscess ofthe scalp; patients usually has posterior cervical
lymphadenopathy 4. Favus- presents with sites of alopecia that
have cup-shaped, honey-colored crusts(scutula) that are composed of fungal mats.
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Tinea capitisTypes of Hair invasion Dermatophyte
1. Endothrix- inside the hairshaft
Trichophyton tonsurans Trichophyton violaceum
Trichophyton soudanense
(TV’s in the house)
2. Ectothrix- outside hairshaft
M. canisM. audouinii
M. distortum
M. ferrugineum
(fluoresce under Wood’s light)3. Favus- presence oflinear air spaces., invasionof hair by hyphae that donot produce conidia
T. schoenleinii
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Tinea capitis
Diagnosis:
Wood’s light (See Cats and Dogs Fight )
Culture (Sabouraud’s Dextrose agar;Mycosel or Mycobiotic agar; DermatophyteTest Media/ DTM)
Treatment;Griseofulvin (with meals) for 4-6 weeksOral Azole
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TINEA PEDIS
Types Dermatophyte
1. Interdigital- presents as scaling,maceration, fissuring,or erythema of
the webspaces between the toes
T. rubrum
T. mentagrophytes
2. Moccasin type- generalizedscaling and hyperkeratosis of thePLANTAR surface of the foot,associated with nail involvement.
T. Rubrum
3. Inflammatory or Vesiculobulloustype- vesicular eruption on the arch
of the foot
T. mentagrophytes
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Tinea Pedis
FYI;
DERMATOPHYTID REACTION- inflammatoryreaction at sites DISTANT from the site of the associateddermatophyte infection secondary to strong host
immunologic response against fungal antigens.
Types of dermatophytid reaction from Tinea pedisincludes:
urticaria Hand dermatitis Erythema nodosum
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Tinea unguium/
Onchomycosis
Tinea unguium/ Onchomycosis- follows
prolonged T. pedis (nail becomes yellow,brittle)
T. mentagrophytes
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Tinea unguium
Clinical Presentation ofonchomycosis
Dermatophyte
1. Distal subungal- oncholysis, subungal
debris, and discoloration beginning at the
hyponychium that spreads proximally.
Trichophyton rubrum
2. Proximal Subungal- begins underneath
the proximal nailfold , strongly associated withimmunosuppressed conditions
T. rubrum
3. Superficial White – white, crumbly nail
surface due to invasion of the top of nailplate.
T. mentagrophytes
Fusarium,Acremonium
Aspergillus
4. Candidal- seen in patients with chronic
mucocutabeous candidiasis
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TINEA CORPORIS/ TINEA
CRURIS-
TINEA CORPORIS/ TINEA CRURIS- jock
itch- dermatophyte of the non-hairy skinof the body giving rise to commonly
annular lesions
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TINEA VERSICOLOR/
PITYRIASIS VERSICOLORPresentation- hypopigmented (Dicarboxylic acid
that inhibits tyrosinase activity)/ hyperpigmented,or erythematous macular eruption that coalesceto form large patches with adherent fine skin
Etiologic agent; Pityrosporum orbiculare
Malassezia furfur
Dx:1. Scraping of the scale- microscopically
seen “meatball and spaghetti appearance
2. Wood’s light- yellow fluorescence
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Tinea Nigra
Etiologic agent : Phaeoanellomyces(Exophiala) wernickii- a dematiaceous(pigment-producing) fungus causingasymptomatic tan. Brown, or black patchon the palms/ soles.
D/Dx: Acral lentiginous melanosis
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FYI
MAJOCCHI’s granuloma- follicular abscessproduced when a dermatophyte infectionpenetrates the follicular wall into the surroundingdermis. Patients usually presents with one ormore tender, boggy, plaques on the legs, or thearms.
Etiologic agent: T. rubrum, T. mentagrophytes
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PIEDRA
PIEDRA- adherent deposits in the hair shaftcaused by superficial fungal infections.
BLACK PIEDRA- caused by Piedraia hortae;
presents as firm black nodules in hair shaft.
WHITE PEIDRA- caused by Trichosporon
beigelii , a white concretion on hair shaft.
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Cutaneous CandidiasisDisease CLINICAL DESCRIPTION
Intertrigo Superficial pustules, erythema, edema,creamy exudates within skin folds
Thrush White, adherent, cottage cheese-like plaqueson oral mucosa
Perleche Erythema, fissuring, creamy exudates at theangles of the mouth
Paronychia Tender, erythematous, indurated proximal
nailfold, with or without a purulent discharge
Erosiointerdigitalisblastomycetica
Erythema, fissuring, maceration of thewebspaces between the fingers
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CANDIDIASIS
Diagnosis:
Wood’s light (See Cats and Dogs Fight )
Culture (Sabouraud’s Dextrose agar;Mycosel or Mycobiotic agar;Dermatophyte Test Media/ DTM)
TREATMENT: ORAL ANTIFUNGALAGENTS
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ORAL ANTIFUNGAL AGENTS
CLASS EXAMPLE MECHANISM OF ACTIONAntibiotic Griseofulvin Arrest of cellular division,
dysfunction of spindlemicrotubules
Polyenes Nystatin Binds irreversibly withergosterol, altering membranepermeability
Azoles Fluconazole
ItraconazoleKetoconazole
Inhibits ergosterol production by
inhibiting the cytochrome P-450lanosterol-14 demethylase
Allylamines Terbinafine Blocks ergosterol production byinhibiting squalene epoxidase
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DEEP FUNGAL INFECTIONS
SUBCUTANEOUS
SYSTEMICRESPIRATORY
OPPORTUNISTIC
Sporotrichosis Blastomycosis Cryptococcosis
Chromomycosis Histoplasmosis Aspergillosis
Mycetoma
(Madura foot)
Coccidioidomycosis
Paracoccidioidomycosis
Mucormycosis
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Subcutaneous infections
SPOROTRICHOSIS
Etiologic agent: Sporothrix schenckii (dimorphic
fungus)
Epidemiology; Most common in Subtropical and
Tropical climates. Occupation at risk forcutaneous inoculation include farmers,gardeners, florists and animal handlers.
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SPOROTRICHOSISClinical Presentations:
Cutaneous Sporotrichosis Lymphocutaneous form – (80%) begins at the site of
inoculation m.c. the upper extremity as a painlesspink papule, pustule, or nodule and rapidly enlargesand ulcerates. Without treatment, infection ascends
along the lymphatics producing secondary nodulesand regional lymphadenopathy. Cutaneous variant (15-20%)- is confined to the site
of inoculation.
Extracutaneous/ Disseminated disease- most common in immunosuppressed patientsand alcoholics. Pulmonary disease is usuallydue to inhalation and generally occurs inalcoholics or debilitated patients.
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SPOROTRICHOSIS
Treatment
SSKI (Saturated Solution of PotassiumIodide)- Cutaneous
Amphotericin B or Itraconazole-
extracutaneous
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CHROMOBLASTOMYCOSISEtiologic agent: Fonsecaea pedrosoi
Epidemiology: 95% occur in males, barefooted, ruralagricultural worker in the tropics.
Clinical Presentations: It is a chronic cutaneous andsubcutaneous infection that usually presents foryears with minimal discomfort. At the site ofinoculation, red papules develop that eventuallycoalesce into a plaque. The plaque slowly enlargesand acquires a verrucous or warty surface. If the
lesion is not treated, it can evolve into a cauliflower-like mass, leading to to lymphatic obstruction andelephantiasis-like edema of the lower extremity
Treatment: disappointing; itraconazole is helpful
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MYCETOMA
Etiologic agents: Actinomycetoma (filamentous bacteria);Eumycetoma (true fungi)
Epidemiology: Rural tropicalClinical Presentations: It is a localized, destructive
infection of the skin and subcutaneous tissue that
eventually involves deeper structures such as muscleand bone.
3 CARDINAL FEATURES1. Formation of nodules in the skin at the site ofinoculation.
2. Purulent drainage and fistula formation.3. Presence of grains or granules that are visiblein the purulent drainage
Treatment: Generally unsatisfactory
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S t i F l
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Systemic Fungal
Infections
Causative organism are found in the soil andinfection occurs with inhalation of the organisminto the lung. The primary infection is pulmonary.Dissemination occurs via thelymphohematigenous route, and each fungushas a predilection for particular organ systems.
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BLASTOMYCOSISBLASTOMYCOSIS/ North American Blastomycosis
Etiologic agent: Blastomyces dermatitidis Epidemiology: endemic in North America. Typical patient is
a middle-aged man with outdoor occupational orrecreational exposure to the soil.
Clinical Presentation:Cutaneous: single/ multiple, crusted, verrucous plaqueon exposed skin (face, hands, arm) with color variationfrom gray to violet.flu-like symptoms which may progress to chronicpneumonia
Treatment: 1. Azoles, Ketoconazole and Itraconazole-immunocompetent patient without CNS disease
2. Amphotericin B – DOC in theimmunocom romised and atients with CNS
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HISTOPLASMOSIS
Etiologic agent: Histoplasma capsulatumEpidemiology: endemic in Midwestern and South Central US.MOT: inhalation of soil infected with excreta from chicken,
pigeons, blackbirds, and bats leading to pulmonary
infection, rarely contracted from traumatic inoculation.
Clinical Presentation: The number of organism inhaled andthe immune status of the host is important forproduction of symptomatic histoplasmosis. Most
patients develop a flu-like, acute pulmonary illnesscharacterized by fever, chills, headache, myalgias,chest pain and non-productive cough.
Cutaneous manifestations: Erythema nodosum, lesscommonly erythema multiforme.
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COCCIDIOIDOMYCOSIS
COCCIDIOIDOMYCOSIS/ SAN JOAQUIN VALLEYFEVER
Etiologic agent; Coccidioides immitis
Clinical Presentation:40% presents with mild flu-like illness orpneumonia50% is asymptomatic; 5% with erythema nodosumCutaneous lesions: warty papules, plaques, or nodules
At risk for disseminated coccidioidomycosis: male, pregnancy,immunocompromised and race (Filipinos>blacks>whites)
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PARACOCCIDIOIDOMYCOS
ISPARACOCCIDIOIDOMYCOSIS/ SOUTH
AMERICAN BLASTOMYCOSIS
Etiologic agent: Paracoccidioides brasiliensis
Clinical presentation: most common in adult men(30-60y.o.) due to inhibitory action of estrogenson mycelium-to-yeast transformation. Lung is
the primary site of infection. Painful mucosalulcerations involving the mouth and nose arethe most common finding. Patients may haveenlarged cervical lymph nodes andverrucuous, crusted edematous facial lesions
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OPPORTUNISTIC FUNGAL
INFECTIONSCRYPTOCOCCOSIS
Etiologic agent: Cryptococcus neoformans, encapsulatedyeast found in the soil contaminated with pigeonexcreta. It is the 4th leading cause of opportunistic
infection in AIDS patients and is the leading cause offungal meningitis.
MOT: inhalation
Clinical presentation: mild subclinical pulmonary infection;great stimulator of molluscum contagiosum, Kaposi’ssarcoma, pyoderma gangrenosum, herpetiformlesions, cellulites, ulcers, subcutaneous nodules, andpalpable purpura.
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Aspergillosis
Increased risk: Neutropenia and Corticosteroidtherapy; solid organ transplant recipients, bonemarrow transplant recipients and leukemicpatients are at high risk.
Lungs and sinuses- major site of infection.
Cutaneous lesions: single/multiple that begins asa well circumscribed papule that enlarges intoan ulcer with a necrotic base and surroundingerythematous halo.
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MUCORMYCOSIS
Etiologic agents: Mucor, Rhizopus, Absidia, andRhizomucor
At risk: patients with DM and DKAClinical presentation: Rhinocerebral
mucormycosis: patient presents with fever,headache, facial pain, orbital cellulites, andcranial nerve dysfunction.
Treatment: Correction of underlying disease,administration of Amphotericin B andaggressive debridement of necrotic tissue.
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