Flashcards in Cutaneous Fungal Infections Deck (30):
Characteristics of Fungi
Yeast, Molds, Rusts, and Mushrooms
Eukaryotic, aerobes or facultative anaerobes
Unique rigid cell walls (e.g.,glucan, chitin) and ergosterol in cell membrane are targets for anti-fungal antibiotics
Heterotrophic and absorptive nutrition
Pathogenic fungi grow best at 25-30ºC and at acid pH
Morphology of Molds
Hyphae (the mold form of growth)
Tubular, branching filaments (2–10 μm in width) of fungal cells, with or without cross walls (septate or non-septate hyphae)
mycelium- Mass or mat of hyphae, mold colony
Spore (reproductive structure)
Sexually or asexually (conidia) generated structures resist adverse conditions and promote dispersion. Spores disperse, germinate and grow by apical elongation into hyphae.
Vegetative hyphae penetrate the substrate for absorptive nutrition
Fungal mycelium: loose network of hyphae
Aerial hyphae differentiate into spore-producing or conidia- producing structures.
Morphology of Yeast
Unicellular, spherical to ellipsoid (3–15 μm) fungal cells that usually reproduce by budding.
Elongated chain of budding yeast may form (pseudohyphae)
If in nutritional environment, they will send out a germ tube so that the bud will elongate and mimic a hyphal structure and create pseudohyphae
Types of Fungal Disease
Superficial - Noninvasive, noninflammatory infection of hair, outermost dead skin; cosmetic symptoms only
Systemic (true fungal pathogens)
Fungal Virulence vs. Host Defenses
Most fungi are poorly virulent and noninvasive in immunocompetent people
Phagocytes (neutrophils) readily ingest and kill most fungi. Strong cell-mediated immunity (Th1 and Th17) is induced by fungal agents of cutaneous infection and systemic infection.
Neutrophil and CMI deficiency predisposes to systemic fungal infection.
Fungal pathogens lack toxins but can cause tissue necrosis (via infarction) and inflammatory injury (DTH reactions) by absorbing nutrients via digestion of tissues; hyphal elements will penetration blood vessels and damage them and get local necrosis or ischemia; also local inflammatory processes in sites of infection
Superficial Fungal Infections
Tinea Versicolor: chronic mild, usually noninflammatory infection of stratum corneum; hypo and hyperpigmented macules with scales; lesions fluoresce under UV light
Tinea Nigra: brown black non-scaly macules on palmar surface and soles
Black Piedra: infection of scalp hair shaft with black hard nodules
White Piedra: infection of external scalp hairshafts forming soft irregular whitish nodules on shaft
Mycotic Keratitis: trauma induced infection of cornea or ear
Malassezia, a lipophilic yeast that may be normal flora, is associated with seborrheic dermatitis (dandruff)
Scraping of the skin and look for fungal morphology, put KOH on it and examine with light microscope; normal skin cells with lose the architecture with KOH, but the fungal walls resist KOH
Spaghetti and meatballs - causes tinea versicolor
Cutaneous Fungal Infections: Dermatophyte Infections
Dermatophytes: fungal agents (in soil, on animals and humans) that degrade and grow on keratin
Dermatophytoses: fungal infections of the keratinized tissues (hair, skin, nails).
Contagious by direct contact
Restricted to outer layers due to temperature tolerance of fungi
Strong cell-mediated immune response explains the inflamed skin lesions of ringworm
etiologic agents: Trichophyton, Microsporum, Epidermophyton
Dermaphyte Infections Association with Body Sites
Trichophyton species: infect hair, skin, or nails.
Epidermophyton species: infect the skin and nails but not hair.
Microsporum species: infect only hair and skin
Common agents = T. rubrum, T. mentagrophytes, E. floccosum
Dry flaky and minimal inflammatory, but can become boggy and highly inflammatory = depends on amount of keratin present and environmental conditions; love highly keratinized areas that are moist and warm
Have in groin, armpits, feet, under breasts
Use of lotions and creams, sweat a lot = risk
Tinea unguium (onychomycosis)
Common agents= T rubrum, T mentagrophytes, E floccosum)
Nail becomes brittle, yellow
Any fungal infections, dermaphytes = scrap + KOH = see fungal structures because KOH won’t change them
Tinea capitis- ringworm of scalp and hair
A Wood’s lamp can be used diagnostically to detect fluorescence of some agents of tinea capitis.
See inflammation and hair loss
Can grow outside hair shaft or penetrate hair shaft
Cell mediated immune response = more inflammation
Kerion formation: high inflammation areas with hair loss; moist keratinized areas
Agents of Tinea Capitis
T. mentagrophytes: fungal growth PENETRATES hairshaft = endothrix spores, non-florescent
M. canis: fungal growth forms sheath on OUTSIDE of hairshaft = ectothrix spores, fluorescent
animal acquired, nodular clusters of fungus
Used to cause epidemic tinea capitis
Tinea corporis (“ringworm”) caused by Trichophyton mentagrophytes contracted from a dog; hair areas
On hairless areas, common agents = T rubrum, E floccosum
Tinea cruris (jock itch)
Common agents = T rubrum, T mentagrophytes, E floccosum
Dx of Dermaphyte Infections
Direct microscopic exam for fungal morphologies in skin/hair/nail scrapings (KOH prep or fluorescent stains for chitinous cell walls).
Lab culture of dermatophyte from sample (dermatophyte test medium) and morphological identification.
Therapy of Dermaphyte Infections
Topical anti-fungal agents, keratolytics
Systemic antifungals for nail infections
Good hygiene, keep areas dry
Subcutaneous Fungal Infections
Acquired from soil or plant material by traumatic implantation in patients with mild immunosuppression
Spread along lymphatic channels in subcutaneous layer
Strong cell-mediated immune response plus suppuration
Example: sporotrichosis caused by Sporothrix schenckii
S. schenckii, a dimorphic fungus, appears as yeast in tissues (37ºC) and a mold at 20ºC.
*Unicellular yeast form in the skin, or if culture it will grow as a mold in the lab = grows in two different forms in two different temperatures
Chromomycosis and Actinomycetoma
Chromomycosis: traumatic implantation of dematiaceous (pigmented) soil fungi.
See in tropical areas with farming and people aren’t wearing shoes and get from soil
Verrucous / cauliflower lesions on skin
Soil fungi are pigmented (can be colored but usually dark)
Actinomycetoma is caused by implantation of filamentous soil bacteria, not fungi
Mycetoma and Phaeohyphomycosis
Mycetoma: can be pigmented with yellow or red and get granulomatous lesions (supportive) and will drain and have tracts; same kind of lesion can be caused by a bacteria, so differentiate in lab
Candida albicans (also Candida tropicalis, Torulopsis glabrata)
Yeast in laboratory culture but forms pseudohyphae (germ tubes) when grown in serum or in tissues
Normal flora in humans (oropharynx, gastrointestinal tract, vagina). Most infections are of endogenous origin but may be contagious
Opportunistic: grows best in immunocompromised host (depressed cell-mediated immunity) or in host with altered normal bacterial flora
Predisposing factors: breaks in skin, low neutrophils, decreased lymphocyte function, corticosteroids, diabetes, antibiotic therapy, pregnancy, use of contraceptive pills
Cutaneous Fungal Infection:Non-dermatophyte agent
Candida Infections (Candidiasis)
Oral Thrush- common in elderly homes because immunosuppressed
Nonesophageal Mucous Membrane
Onychomycosis (nail infection)
Paronchyia (candida of hands & fingers in "wet workers")
Diaper rash, Perianal
Cutaneous Lesions Associated with Systemic Fungal Infections
Systemic Fungal Pathogens cause a primary self-resolving respiratory infection in immunocompetent patients but systemic agents disseminate to disease-specific target organs in immunocompromised patients
Infection occurs via inhalation of a large inoculum of spores generated by disturbance of soil with high filamentous mold growth due to enrichment with bird or bat droppings in chicken coops, bat caves, parks with pigeon populations, natural bird roost areas
Geographic localization of fungi: disease association with certain occupations and geographic areas
Diagnosis must be consistent with probable exposure
Strong cell-mediated immune response with granulomatous inflammatory response
Cutaneous Lesions Associated with Systemic Fungal Infections: Histoplasmosis, Blastomycosis, and Paracoccidiomycosis
True fungal pathogens = all acquired from inhalation and can happen in perfectly healthy
Dissemination to the skin as a target organ occurs in:
Disseminated Histoplasmosis: mucocutaneous ulcers of the nose, mouth, tongue
Disseminated Blastomycosis: skin lesions on exposed surfaces; may evolve to ulcerated verrucous granulomas
Disseminated Paracoccidiomycosis: mucocutaneous lesions (often oral: granulomas with central caseation or microabscesses )
Cutaneous Lesions Associated with Systemic Fungal Infections: Coccidioidomycosis
Pulmonary Coccidioidomycosis: 15% of patients develop hypersensitivity reactions, which present as a rash, erythema nodosum, or erythema multiforme.
Disseminated Coccidioidomycosis: extrapulmonary skin lesions occur after 1 year in
Diagnosis and Lab ID of Systemic Fungal Pathogens
Dimorphism (temperature dependent):
True fungal pathogens grow as filamentous molds at room temperature but as unicellular yeasts in infected tissues at body temperature.
Mold & yeast form morphologies
Fungal-specific immune responses:
DTH skin test reactivity
Rising antibody levels
Presence of fungal antigen in tissues or blood
Dimorphic Growth of Systemic Fungi
Systemic fungi are “dimorphic”, growing as yeast at 37ºC but growing as filamentous molds at room temperature
Blastomyces dermatitidis yeast cell undergo broad-base budding (37°C), but mold with microconidia at 20°C.