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

OUTLINE

SIMPLE RECALL

Fungi- Greek “mykos” – mushroom

widely distributed and are found where

“moisture” is present

Epidemiology:

children

warm, moist climate

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

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

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

Tinea capitis

“SCALP”

Etiologic agents: * Microsporum audounii (Griseofulvin)

Trichophyton tonsurans

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.

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

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

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

Tinea Pedis

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

Tinea unguium/

Onchomycosis

Tinea unguium/ Onchomycosis- follows

prolonged T. pedis (nail becomes yellow,brittle)

T. mentagrophytes

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

TINEA CORPORIS/ TINEA

CRURIS-

TINEA CORPORIS/ TINEA CRURIS- jock

itch- dermatophyte of the non-hairy skinof the body giving rise to commonly

annular lesions

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

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

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

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.

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

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

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

DEEP FUNGAL INFECTIONS

SUBCUTANEOUS

SYSTEMICRESPIRATORY

OPPORTUNISTIC

Sporotrichosis Blastomycosis Cryptococcosis

Chromomycosis Histoplasmosis Aspergillosis

Mycetoma

(Madura foot)

Coccidioidomycosis

Paracoccidioidomycosis

Mucormycosis

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.

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.

SPOROTRICHOSIS

Treatment

SSKI (Saturated Solution of PotassiumIodide)- Cutaneous

Amphotericin B or Itraconazole-

extracutaneous

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

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

S t i F l

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.

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

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.

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)

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

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.

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.

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.

Fungal Infections and it's types

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