Unit 2 - Superficial, cutaneous, and subcutaneous mycoses Flashcards
what are superficial and cutaneous mycoses?
dermatophytosis
tinea versicolor
tinea nigra
what are subcutaneous mycoses?
sporotrichosis
chromocycosis
mycetoma
what are cutaneous and opportunistic mycosis?
candidiasis
what are the two types of mycoses?
molds - asexual or sexual reproduction with spores
-multicellular (not very mobile in body)
yeasts - asexual by budding
-single-celled, can circulate resistant to phagocytosis
what is dermatophytosis caused by? how is it spread?
cutaneous mycoses (ringworm, tinea) caused by dermatophytes
- 3 major genera:
- -epidermophyton: direct contact
- -Trichophyton: direct contact
- -Microsporum: direct contact and zoonosis from pets
- all allow invasion of cornified cell layer
where does dermatophytoses infect?
only superficial keratinized structures (skin, hair, nails)
- named for affected body parts
- -head: Tinea capitis
- -ringworm: T. corporis
- -jock itch: T. cruris
- -Athlete’s foot: T. pedis
pathology of dermatophytosis?
- form chronic infections in warm, humid areas
- inflamed circular border of papules and/or vesicles
- normal skin inside (skin within borders normal)
- broken hairs, thickened, broken nails
how is dermatophytosis transmitted?
by fomites or by autoinoculation from other sites on body
what is hypersensitive dermatophytin reaction?
“id” reaction on some patients after dermatophytosis infection
- causes vesicles on fingers
- caused by hypersensitivity to circulating fungal Ag
- vesicles don’t contain live fungus or spores
prevalence of Tinea? morbidity?
very common (10-20% of visits to US dermatologists) -no morbidity from primary infection, but prolonged itching may lead to bacterial superinfection
how do you diagnose dermatophytosis?
exam: itching, redness, history of tight/wet clothing
lab: scraping from affected skin or nail
- treat with 10% KOH to break down dead skin, and examine remains for hyphae and spores
- culture on Sabouraud’s agar at room temperature
- PPD w/ trichophytin
- microsporum show fluorescence under Wood’s lamp
treatment and prevention of dermatophytosis
- topical antifungal cream
- Terbinafine, undecylenic acid, miconazole, tolnaftate - oral griseofulvin (Fulvicin)
- keep skin cool and dry
organism of pathogenesis of Tinea versicolor?
Malassezia furfur (dimorophic normal flora, common overgrowth)
- superficial skin infection of only cosmetic importance
- hypopigmented or hyperpigmented areas with slight scaling/itching
- usually on trunk, back, or abdomen
- most frequent in hot, humid weather
- other presentations (face, extremities, folliculitis) may occur, particularly with immunocompromised patients
- family has history of infection, but genetic predisposition not yet characterized
how do you diagnose and treat tinea versicolor?
- take skin scrapings (light in area with scalpel releases lots of keratin)
- treat with 10% KOH and stain (blue ink)
- examine microscopically for mix of budding yeasts and short “cigar butt” hyphae
- examination with Wood lamp may show coppery-orange fluorescence - topical selenium sulfide or azole used daily for 2 weeks
- repeat as needed, as they may recur
- alternative oral azoles
what is the organism and pathogenesis of Tinea nigra?
species: werneckii
- spores in soil enter injury
- germinate in keratinized skin layers (cutaneous)
- generates brown pigment which appears as brown spot resembling melanoma (but benign and curable)
- seen in southern coastal US, mostly pediatrics, and not common
how to diagnose Tinea nigrans?
- patient reports new brown spot on an extremity, may itch slightly, possible travel to Caribbean, Asia, Africa
- take skin scrapings, treat with 10% KOH and examine microscopically for thick septate, branching hyphae with dark pigment in walls
- culture on Sabourad’s agar at room temperature –> yeast-like shiny black colonies grow in 1 week (form mix of yeast and septate hyphae)
treatment of Tinea nigra?
topical keratolytic agent (salicyclic acid + topical azole
how do subcutaneous mycoses occur?
introduced by trauma exposing subcutaneous tissue to soil or vegetation
what is the organism and pathogenesis of sporotrichosis?
Sporothrix schenkii and other species that are theramlly dimorphic
- found on vegetation
- often in gardeners (particularly roses due to thorns)
- yeasts grow at site and form painless pustule or ulcer
- draining lymphatics form suppurating subcutaneous nodules
- symptoms wax and wane over years
- may progress to disseminated disease and meningitis if immunosuppressed
what is the importance of sporotrichosis in COPD, alcoholics, or cortico-steroid using patients? what is difficult to distinguish from? what about AIDS patients?
COPD, alcoholics, or corticosteroids may develop pulmonary symptoms from inhaling spores
-looks like TB or histoplasmosis
AIDS patients will see nodules disseminated over whole body
how to diagnose sporotrichosis?
exam: painless pustule/ulcer on hand/arm
- reddish, necrotic, nodular papules may extend along lymphatics from initial injury site
- history of thorns, and ineffective antibiotic treatment
lab: tissue biopsy shows round/cigar-shaped budding yeasts
- culture at room temp shows oval conidia in clusters at tip of slender conidiophores (resembles daisy)
diagnosis and prevention of sporotrichosis?
big discrepancy
- treatment: 3-6 mo itraconazole (Sporanox) or other oral azoles for normal form of disease
- -for more serious, use Amphotericin B
- prevent with gardening gloves
what is the organism and pathogenesis of chromomycosis?
(also called chromoblastomycosis or dermititis verrucosa)
- caused by dermatiaceous fungi: Fonsecaea, Phialophora, Cladosporium
- found in soil in tropics
- Conidia or hyphae are gray or black
- introduced in legs or feet with injury, gradually progressing into subcutaneous disease
- granulomas form as immune system attempts to contain it
- wartlike lesions gradually spread from initial site over years
diagnosing chromomycosis?
exam: history of farming, travel to tropical locasions
- wartlike, dark-colored lesions
- crusting abscesses extending along lymphatics
- black dots scattered among lesions
- secondary infection with bacteria produces ill odor and elephantitis
lab: tissue specimen with dark brown, round fungal cells inside leukocytes or giant cells
- KOH mount shows dark colored septate hyphae or conidia
- ELISA available for some species
treatment and prevention of chromomycosis?
big discrepancy; hard to treat successfully
- oral flucytosine and/or itraconazole
- combine with local surgery (cryosurgery can be effective)
- topical application of heat from pocket warmers also helps reduce and reverse fungal growth over months
prevention: shoes
what is the organism and pathogenesis of mycetoma? what does it look similar to?
Petriellidium or Madurella
- found in soil and enters through wounds, but rare in US
- replicating fungi form abscesses
- pus containing compact colored granule forms and drains through local sinuses
- looks similar to actinomycosis (forms in foot, lower leg, and hand rather than face)
- granulomatous inflammatory response in deep dermis and subcutaneous itssue may extend to bone
- after years of infection, initial painless nodule swells and bursts, becoming painful
diagnosis of mycetoma?
needle biopsy for culture
- H&E staining reveals grains in pus
- X-ray to determine whether bone is involved
how do differentiate mycetoma from actinomycosis?
staining
- mycetoma has filamentous structures, larger, have fungal stains with Gomori methenamine silver or periodic acid-Schiff stain
- actinomyces is small, G+ branching filaments
treatment of mycetoma?
first attempt: admit for initial IV amphotericin B, add antibiotics for secondary infections, and send home with oral azole
-surgical excision of abscess usually necessary
what is Candidiasis usually attributed to?
Candida albicans
- normal flora, doesn’t cause disease in previously healthy people
- oval yeast w/ single bud, may also appear as pseudohyphae or hyphae when invading tissues
virulence factors of candidiasis?
adhesins - surface attachment
acid proteases and phospholipases - tissue invasion
phenotypic switching/morphogenesis - changes Ag expression and tissue affinity
what is common pathogenesis for candidiasis?
- thrush/esophagitis - overgrowth leading to pseudomembrane formation in mouth
- predisposition by steroid inhalers for asthma
- inevitable in HIV+ not on HAART
- generally not dangerous, but can contribute to wasting cycle in AIDS - diaper rash - dampness predisposes to overgrowth
- vaginitis - overgrowth leading to itching and curdlike discharge
- cervix regular on exam
- predisposition to antibiotics, diabetes
- may spread to male partner, who develops penile vesicles, white spots
what happens in Candidiasis in IV drug users?
right-sided endocarditis
explain a predisposition to candidiasis?
less common (becomes opportunistic)
- chronic mucocutaneous candidiasis arises with impaired CMI
- -genetic predisposition to low IFN-Y, IL-2/17/22
- persistent refractory cutaneous infections, little dissemination
- infection of entire GI may occur w/ leukemia/lymphoma
what are candidiasis pathogenesis that were rare, but now increasing?
sepsis, endophthalmitis, IV/catheter infections; systematic and disseminated infections
-usually due to vulnerable patients
what is the importance of Candida…
- globrata
- krusei
- lusitaniae
- parapsilosis
- tropialis
G: more drug resistant
K: intrinsic resistance to azoles and elss susceptible to all antifungals
L: intrinsic resistance to amphotericin B
P: common in infections of vascular catheters
T: often in leukemia patients
explain systemic dandidiasis?
candidemia; got into bloodstream
- usually nosocomial with underlying major illness
- fever unresponsive to broad-spectrum antibiotics
- history of catheterization
- endocarditis with large septic emboli to major organs
- may see symptoms on skin/mouth
- blood cultures positive
- 30-40% mortality
explain disseminated candidiasis
organ invasion
- one or more deep organs infected (eye, kidney, CNS, joints, muscles, heart/pericardium, peritonium, spleen)
- blood cultures often negative
- fever unresponsive to broad-spectrum antibiotics
- sepsis/septic shock
- extremely high mortality rate
lab diagnoses of candidiasis?
exudates and biopsies: budding yeasts + pseudohyphae that look G+ and visualized by calcofluor-white stain
culture: agar shows yeast colonies similar to bacteria
- at 37C, germ tubes form
- positive culture results from sterile sites are diagnostic
- culture from nonsterile sites may give evidence of increased colonization
- in refractory cases, including AIDS or anything else dangerous: do antifungal susceptibility testing
what should you look for if disseminated candidiasis is suspected?
- persistent leukocytosis
- neutropenia
- other risk factors
- fever remaining despite antibiotic coverage
