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FUNGAL INFECTIONS AND ITS 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. Deep a. Subcutaneous i. Sporotrichosis ii. Chromomycosis (chromoblastomycosis) iii. Mycetoma (Madura foot ) b. Systemic Respiratory Fungal infections i. Blastomycosis ii. Histoplasmosis iii. 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 the KERATIN (hair, nails or skin scale) of animals 3 Genera 1. Microsporum 2. Trichophyton 3. Epidermophyton

Clinical Presentations of Dermatophyte Infections


Tinea capitis Tinea faciei Tinea barbae Tinea corporis Tinea cruris Tinea manuum (manus) Tinea pedis Tinea unguum Scalp Face Beard Trunk, Extremities Groin Hands Feet 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 if alopecia. Trichophyton tonsurans 3. Kerion- an inflammatory fungal infecton that may mimic bacterial folliculitis or an abscess of the 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 capitis
Types of Hair invasion Dermatophyte 1. Endothrix- inside the hair Trichophyton tonsurans shaft Trichophyton violaceum Trichophyton soudanense (TVs in the house) 2. Ectothrix- outside hair shaft M. canis M. audouinii M. distortum M. ferrugineum (fluoresce under Woods light) T. schoenleinii

3. Favus- presence of linear air spaces., invasion of hair by hyphae that do not produce conidia

Tinea capitis
Diagnosis:
Woods light (See Cats and Dogs Fight) Culture (Sabourauds Dextrose agar; Mycosel or Mycobiotic agar; Dermatophyte Test Media/ DTM)

Treatment; Griseofulvin (with meals) for 4-6 weeks Oral Azole

TINEA PEDIS
Types Dermatophyte

1. Interdigital- presents as scaling, maceration, fissuring,or erythema of the webspaces between the toes 2. Moccasin type- generalized scaling and hyperkeratosis of the PLANTAR surface of the foot, associated with nail involvement. 3. Inflammatory or Vesiculobullous type- vesicular eruption on the arch of the foot

T. rubrum T. mentagrophytes T. Rubrum

T. mentagrophytes

Tinea Pedis
FYI;

DERMATOPHYTID REACTIONinflammatory reaction at sites DISTANT from the site of the associated dermatophyte infection secondary to strong host immunologic response against fungal antigens. Types of dermatophytid reaction from Tinea pedis includes: 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 of onchomycosis
1. Distal subungal- oncholysis, subungal debris, and discoloration beginning at the hyponychium that spreads proximally. 2. Proximal Subungal- begins underneath the proximal nailfold , strongly associated with immunosuppressed conditions 3. Superficial White white, crumbly nail surface due to invasion of the top of nailplate. Dermatophyte Trichophyton rubrum

T. rubrum

T. mentagrophytes Fusarium, Acremonium Aspergillus

4. Candidal- seen in patients with chronic mucocutabeous candidiasis

TINEA CORPORIS/ TINEA CRURISTINEA CORPORIS/ TINEA CRURIS- jock itch - dermatophyte of the non-hairy skin of the body giving rise to commonly annular lesions

TINEA VERSICOLOR/ PITYRIASIS VERSICOLOR


Presentation- hypopigmented (Dicarboxylic acid that inhibits tyrosinase activity)/ hyperpigmented, or erythematous macular eruption that coalesce to 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. Woods light- yellow fluorescence

Tinea Nigra

Etiologic agent : Phaeoanellomyces (Exophiala) wernickii- a dematiaceous (pigment-producing) fungus causing asymptomatic tan. Brown, or black patch on the palms/ soles.
D/Dx: Acral lentiginous melanosis

FYI
MAJOCCHIs granuloma- follicular abscess produced when a dermatophyte infection penetrates the follicular wall into the surrounding dermis. Patients usually presents with one or more tender, boggy, plaques on the legs, or the arms.

Etiologic agent: T. rubrum, T. mentagrophytes

PIEDRA
PIEDRA- adherent deposits in the hair shaft caused 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 Candidiasis
Disease Intertrigo Thrush Perleche Paronychia CLINICAL DESCRIPTION Superficial pustules, erythema, edema, creamy exudates within skin folds White, adherent, cottage cheese-like plaques on oral mucosa Erythema, fissuring, creamy exudates at the angles of the mouth Tender, erythematous, indurated proximal nailfold, with or without a purulent discharge

Erosio Erythema, fissuring, maceration of the interdigitalis webspaces between the fingers blastomycetica

CANDIDIASIS
Diagnosis: Woods light (See Cats and Dogs Fight) Culture (Sabourauds Dextrose agar; Mycosel or Mycobiotic agar; Dermatophyte Test Media/ DTM) TREATMENT: ORAL ANTIFUNGAL AGENTS

ORAL ANTIFUNGAL AGENTS


CLASS EXAMPLE MECHANISM OF ACTION

Antibiotic

Griseofulvin

Polyenes

Nystatin

Azoles

Fluconazole Itraconazole Ketoconazole Allylamines Terbinafine

Arrest of cellular division, dysfunction of spindle microtubules Binds irreversibly with ergosterol, altering membrane permeability Inhibits ergosterol production by inhibiting the cytochrome P-450 lanosterol-14 demethylase
Blocks ergosterol production by inhibiting squalene epoxidase

DEEP FUNGAL INFECTIONS


SUBCUTANEO US
Sporotrichosis

SYSTEMIC RESPIRATORY
Blastomycosis

OPPORTUNISTIC

Cryptococcosis Aspergillosis Mucormycosis

Chromomycosis Histoplasmosis Mycetoma (Madura foot) Coccidioidomycosis Paracoccidioidomyco sis

Subcutaneous infections
SPOROTRICHOSIS Etiologic agent: Sporothrix schenckii (dimorphic fungus) Epidemiology; Most common in Subtropical and Tropical climates. Occupation at risk for cutaneous inoculation include farmers, gardeners, florists and animal handlers.

SPOROTRICHOSIS
Clinical Presentations: Cutaneous Sporotrichosis
Lymphocutaneous form (80%) begins at the site of inoculation m.c. the upper extremity as a painless pink papule, pustule, or nodule and rapidly enlarges and ulcerates. Without treatment, infection ascends along the lymphatics producing secondary nodules and regional lymphadenopathy. Cutaneous variant (15-20%)- is confined to the site of inoculation.

Extracutaneous/ Disseminated diseasemost common in immunosuppressed patients and alcoholics. Pulmonary disease is usually due to inhalation and generally occurs in alcoholics or debilitated patients.

SPOROTRICHOSIS
Treatment
SSKI (Saturated Solution of Potassium Iodide)- Cutaneous Amphotericin B or Itraconazoleextracutaneous

CHROMOBLASTOMYCOSIS
Etiologic agent: Fonsecaea pedrosoi Epidemiology: 95% occur in males, barefooted, rural agricultural worker in the tropics. Clinical Presentations: It is a chronic cutaneous and subcutaneous infection that usually presents for years with minimal discomfort. At the site of inoculation, red papules develop that eventually coalesce into a plaque. The plaque slowly enlarges and acquires a verrucous or warty surface. If the lesion is not treated, it can evolve into a cauliflowerlike mass, leading to to lymphatic obstruction and elephantiasis-like edema of the lower extremity Treatment: disappointing; itraconazole is helpful

MYCETOMA
Etiologic agents: Actinomycetoma (filamentous bacteria); Eumycetoma (true fungi) Epidemiology: Rural tropical Clinical Presentations: It is a localized, destructive infection of the skin and subcutaneous tissue that eventually involves deeper structures such as muscle and bone. 3 CARDINAL FEATURES 1. Formation of nodules in the skin at the site of inoculation. 2. Purulent drainage and fistula formation. 3. Presence of grains or granules that are visible in the purulent drainage Treatment: Generally unsatisfactory

Systemic Fungal Infections


Causative organism are found in the soil and infection occurs with inhalation of the organism into the lung. The primary infection is pulmonary. Dissemination occurs via the lymphohematigenous route, and each fungus has a predilection for particular organ systems.

BLASTOMYCOSIS
BLASTOMYCOSIS/ North American Blastomycosis Etiologic agent: Blastomyces dermatitidis Epidemiology: endemic in North America. Typical patient is a middle-aged man with outdoor occupational or recreational exposure to the soil. Clinical Presentation: Cutaneous: single/ multiple, crusted, verrucous plaque on exposed skin (face, hands, arm) with color variation from gray to violet. flu-like symptoms which may progress to chronic pneumonia Treatment: 1. Azoles, Ketoconazole and Itraconazoleimmunocompetent patient without CNS disease 2. Amphotericin B DOC in the immunocompromised and patients with CNS

HISTOPLASMOSIS
Etiologic agent: Histoplasma capsulatum Epidemiology: 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 and the immune status of the host is important for production of symptomatic histoplasmosis. Most patients develop a flu-like, acute pulmonary illness characterized by fever, chills, headache, myalgias, chest pain and non-productive cough. Cutaneous manifestations: Erythema nodosum, less commonly erythema multiforme.

COCCIDIOIDOMYCOSIS
COCCIDIOIDOMYCOSIS/ SAN JOAQUIN VALLEY FEVER
Etiologic agent; Coccidioides immitis

Clinical Presentation:40% presents with mild flu-like illness or pneumonia 50% is asymptomatic; 5% with erythema nodosum Cutaneous lesions: warty papules, plaques, or nodules At risk for disseminated coccidioidomycosis: male, pregnancy, immunocompromised and race (Filipinos>blacks>whites)

PARACOCCIDIOIDOMYCOS IS
PARACOCCIDIOIDOMYCOSIS/ SOUTH AMERICAN BLASTOMYCOSIS Etiologic agent: Paracoccidioides brasiliensis Clinical presentation: most common in adult men (30-60y.o.) due to inhibitory action of estrogens on mycelium-to-yeast transformation. Lung is the primary site of infection. Painful mucosal ulcerations involving the mouth and nose are the most common finding. Patients may have enlarged cervical lymph nodes and verrucuous, crusted edematous facial lesions

OPPORTUNISTIC FUNGAL INFECTIONS


CRYPTOCOCCOSIS Etiologic agent: Cryptococcus neoformans, encapsulated yeast found in the soil contaminated with pigeon excreta. It is the 4th leading cause of opportunistic infection in AIDS patients and is the leading cause of fungal meningitis. MOT: inhalation

Clinical presentation: mild subclinical pulmonary infection; great stimulator of molluscum contagiosum, Kaposis sarcoma, pyoderma gangrenosum, herpetiform lesions, cellulites, ulcers, subcutaneous nodules, and palpable purpura.

Aspergillosis
Increased risk: Neutropenia and Corticosteroid therapy; solid organ transplant recipients, bone marrow transplant recipients and leukemic patients are at high risk.
Lungs and sinuses- major site of infection. Cutaneous lesions: single/multiple that begins as a well circumscribed papule that enlarges into an ulcer with a necrotic base and surrounding erythematous halo.

MUCORMYCOSIS
Etiologic agents: Mucor, Rhizopus, Absidia, and Rhizomucor At risk: patients with DM and DKA Clinical presentation: Rhinocerebral mucormycosis: patient presents with fever, headache, facial pain, orbital cellulites, and cranial nerve dysfunction. Treatment: Correction of underlying disease, administration of Amphotericin B and aggressive debridement of necrotic tissue.