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30 Cards in this Set

  • Front
  • Back
What causes pityriasis versicolor (tinea versicolor)?
How does it present?
Dx?
How do you treat it?
Malassezia furfur - lipophilic spherical yeast, hyphae
Discoloration (hypo/hyper-pigmentation) on skin, affected areas do not tan
KOH prep, fluoresces golden green-yellow, spaghetti & meatballs
Tx with keratolytic agents, topical ketoconazole
What causes tinea nigra?
How does it present?
Dx?
Tx?
Exophiala (hortaea) werneckii, branched septate hyphae, budding yeast
pdx melanin --> hyperpigmentation
Microscopic view of fungi
Tx: keratolytics, salicylic acid, azoles
What causes black piedra?
How does it present?
Dx?
Tx?
Piedraia hortai (tropical, underdevo countries)
Hard nodules along infected hair shaft
Dx N/A
Tx: hair removal, topical antifungals
What causes white piedra?
How does it present?
Dx?
Tx?
Genus trichosporon
Px: larger, softer, yellowish nodules on hairs
Dx: N/A
Tx: hair removal, topical antifungals
What are the dermatophytes?
How does it reproduce?
How does it infect?
Skin, hair, nail fungal infections
Microsporum, trichophyton, epidermophyton
Sexual reproduction, ascospores
Infects with keratinase (secreted enzyme) --> digests keratin --> scaling of skin, loss of hair, crumbling of nails
What is tinea pedis?
How does it present?
Dx?
Tx?
Athlete's foot, most common infection, VIA CONTACT
T. rubrum: not viable for long post-shedding from host
E. flocossum: not assoc w chronic infxn, but resistant conidia can stay in host a long time
T. mentagrophytes: rodents in environment
M. canis: c
Athlete's foot, most common infection, VIA CONTACT
T. rubrum: not viable for long post-shedding from host
E. flocossum: not assoc w chronic infxn, but resistant conidia can stay in host a long time
T. mentagrophytes: rodents in environment
M. canis: colonized cat
Px: itching vesicles and pustules, skin cracked, watery discharges, macerated, peeling
Tx: E. flocossum, T. mentagrophytes: topical antifungal
Tx: T. rubrum & other resistant strains: oral antifungals (griseofulvin, terbinafine, itraconazole)
What is tinea cruris?
Px?
Dx?
Tx?
Jock itch, tropics & men
T. rubrum, T. mentagrophytes, E. flocossum
What is tinea corporis?
Px?
Dx?
Tx?
Body/skin, tropics
Microsporum canis, T. rubrum, T. mentagrophytes
Tiny red purple, itching --> spreads peripherally with actively inflamed vesiculo-pustular margin + healing scaly center
TX: Uncomplicated infxns - creams/lotions/powders
TX: T. rubrum
Body/skin, tropics
Microsporum canis, T. rubrum, T. mentagrophytes
Tiny red purple, itching --> spreads peripherally with actively inflamed vesiculo-pustular margin + healing scaly center
TX: Uncomplicated infxns - creams/lotions/powders
TX: T. rubrum & other resistant - griseofulvin, itra-/flu-conazole, terbinafine
What is tinea barbae?
Px?
Dx?
Tx?
Beard infection
T. rubrum (infrequent), T. verrucosum (cows), T. mentagrophytes (cows, dogs, horses)
Via contact with animals in rural environment
Circular margin --> invasion & spread --> nodules & abscesses (bumps)
What is tinea capitis?
Px?
Dx?
Tx?
Scalp
M. canis, T. tonsurans; severe: favus (T. schoenleini); kerion (tumor-like granuloma)
Sx/Px: spreads peripherally, forming patches with broken hair stumps
Ectothrix – outside hair shaft – anthropophilic, geophilic, zoophilic fungi
Endothrix – inside hair shaft – anthropophilic fungi only – more difficult to treat
Dx: microsporum fluoresces BRIGHT green, trichophyton fluoresces DULL green
Tx: oral griseofulvin
What is tinea manuum?
Px?
Dx?
Tx?
Hands, associated with tinea pedis
T. rubrum
Tx: oral antifungal
What is tinea unguium?
Px?
Dx?
Tx?
Nails
T. rubrum (most common), T. mentagrophytes, E. floccosum
Onychomycosis – fungal infection of the nails Paraonychomycosis – fungal infection of nail bed
(Candida can mimic these sx, more yellow)
Tx: Oral systematic anti-fungal drugs – fluconazole, itraconazole, terbinafine
PinPoint laser
Most resistant to treatment
What is fusariosis?
Cutaneous infections caused by Fusarium solani, Fusarium oxysporum
Disseminated in immunocompromised --> death
Tx with voriconazole
What is erythrasma?
~ tinea cruris, due to Corynebacterium minitussimum
Wood's light = coral red
Tx with erythromycin
What are the endemic mycoses?
Describe their structure and morphology.
Dimorphic.
Histoplasma: hyphae/mycelia in environment, budding yeast in host
Blastomyces: hyphae/mycelia in environment, budding yeast in host
Cocci: hyphae/mycelia in environment, large endosporulating spherule in host
What are the routes of infection for endemic mycoses? Who do they affect, typically?
Most common: respiratory
Sites of implantation (e.g., skin prick) --> cutaneous lesions
Dissemination: meningitis, bone lytic granulomas, skin granulomas, other organs
True pathogen of immunocompromised individuals
Histoplasma capsulatum, structure/morphology.
Most common fungal infection in the world
Found in bird/bat droppings
Environment: Multinucleated, branched hyphae; micro & macro conidia
Host: 15-18 hours conversion to uni-nucleated oval budding yeast
Histoplasma capsulatum, infection.
Microconidia inhalation --> bind CD2/CD18 integrins on macrophages --> engulfed into phagolysosome --> microconidia secrete CATALASE to interfere with lysosomal enzyme activation --> converts to yeast form --> replicates --> secretes Ca2+ BINDING PROTEIN --> Cellular immunity develops within 2 weeks to control infection (CD4+ cells) --> Secrete cytokines (IFN-γ) --> macrophages activated to a fungistatic state --> Caseating and/or noncaseating granulomas
Histoplasma capsulatum, most frequent result of infection.
Non-specific flu-like syndrome.
o fever, chest pain, dry/non-productive cough, headache, joint/muscle pain
o Sx occur 10 DAYS after exposure
o Resolution does not indicate eradication --> latent (inactive) infection occurs
Histoplasma capsulatum, severe infections.
Less than 5% of cases
Pulmonary: coin lesions, caseating necrotic granulomas
Acute pericarditis
Dissemination
Ocular histoplasmosis syndrome
Cutaneous
Fibrosing mediastinitis
Severe histoplasmosis = HIV/AIDS
Histoplasma capsulatum, dx & tx.
Dx: biopsy, serological Abs, PAS/GMS staining
Dx: histoplasmin skin-test immunological reactivity > 85%
Tx: Antifungals used as therapeutic adjunct, itraconazole, amphotericin B
Blastomyces dermatitidis aka Chicago Disease, Gilchrist’s Disease
Blastomyces dermatitidis aka Chicago Disease, Gilchrist’s Disease
Environment – uninucleate hyphae, microconidia
Host – multinucleate large budding yeast with broad bud neck
Blastomyces dermatitidis, infection.
Inhalation of microconidia --> Transform at body temperature to yeast --> WI-1 surface protein binds to host macrophage integrins --> 4-6 week incubation after exposure --> BAD1 cell-wall protein – prevents complement C3 deposition onto yeast cells

Clinical infections – lobar or segmented pneumonias
Trauma --> deep cutaneous infection
Blastomyces dermatitidis, clinical syndromes & tx.
Benign and self-limiting infection

Chronic granulomatous and suppurative mycosis
o Primary infection initiated in lungs
o Pulmonary Blasto lesions rarely caseate or calcify

Extra-pulmonary infections
o Cutaneous infections (20-40%) – subcutaneous nodule or papule --> progress to a pustule --> irregular ulcer with wart-like elevations. Painless lesions
o Bone (10-25%); urogenital tract (5-15%); CNS (5%)
o Blastomycosis may occur coincident with bronchogenic carcinoma, Histoplasmosis, Tuberculosis, or other severe pulmonary disease

Latent Infection/Reactivation – seems to be rare

Antifungal Drug Therapy – itraconazole or amphotericin B
Coccidioides immitis (CA San Joaquin Valley)
Coccidioides posadasii (SW, New Mexico)
Most virulent fungal pathogen
Occupational – construction, ranchers, agriculture, archeologists
Ethnic – dark-skinned populations
Pregnant women are at high risk during 3rd trimester
Depresses cellular Immunity – lymphoma, HIV/AIDS, transplants, high-dose corticosteroids --> higher likelihood of disseminated disease
3rd most common Opportunistic pathogen of AIDS (behind Pneumocystis, Cryptococcus)
Cocci, structure.
Cocci, structure.
In host, spherules packed with endospores.
Environment, septate multicellular hyphae & arthroconidia
Cocci, infection.
Acquisition by the respiratory route --> Conversion within 72 hours into large spherules containing numerous small endospores --> Spherule ruptures releasing endospores --> enlarge, internal septation to form new endospores

Immune system:
Humoral immunity – IgM followed by IgG
Cell-mediated immunity – key factor in determining recovery

Pyogenic infection develops --> granulomatous respiratory infection
Caseation without calcification may occur
Cocci, clinical syndromes.
60% asymptomatic
Symptomatic:
- Mild flu-like syndrome – fever, cough, headaches, rash, myalgias (devo 7-21 d post-exposure)
- Acute severe pneumonia – cough, fever, chest pain
- erythema nodosum
- granulomatous inflammation with caseous necrosis
Cocci, dx.
X-ray films: Sharply circumscribed pulmonary nodule – usually non-calcified, Patchy bronchopneumonia, Pleural effusion (hilar adenopathy is common)

Coccidioides Spherical Stains – Periodic Acid-Schiff (PAS); KOH + Calcofluor; Methenamine Silver Stain
X-ray films: Sharply circumscribed pulmonary nodule – usually non-calcified, Patchy bronchopneumonia, Pleural effusion (hilar adenopathy is common)

Coccidioides Spherical Stains – Periodic Acid-Schiff (PAS); KOH + Calcofluor; Methenamine Silver Stain

Coccidiodin hypersensitivity skin test
Cocci, tx.
95% of acute episodes resolve without therapy (treat with bed rest)
Severe pulmonary and disseminated disease – tx Itraconazole or fluconazole