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MSII Microbiology > Unit 2 - Superficial, cutaneous, and subcutaneous mycoses > Flashcards

Unit 2 - Superficial, cutaneous, and subcutaneous mycoses Flashcards

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1
Q

what are superficial and cutaneous mycoses?

A

dermatophytosis
tinea versicolor
tinea nigra

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2
Q

what are subcutaneous mycoses?

A

sporotrichosis
chromocycosis
mycetoma

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3
Q

what are cutaneous and opportunistic mycosis?

A

candidiasis

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4
Q

what are the two types of mycoses?

A

molds - asexual or sexual reproduction with spores
-multicellular (not very mobile in body)
yeasts - asexual by budding
-single-celled, can circulate resistant to phagocytosis

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5
Q

what is dermatophytosis caused by? how is it spread?

A

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
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6
Q

where does dermatophytoses infect?

A

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
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7
Q

pathology of dermatophytosis?

A
  • 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
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8
Q

how is dermatophytosis transmitted?

A

by fomites or by autoinoculation from other sites on body

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9
Q

what is hypersensitive dermatophytin reaction?

A

“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
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10
Q

prevalence of Tinea? morbidity?

A 
very common (10-20% of visits to US dermatologists)
-no morbidity from primary infection, but prolonged itching may lead to bacterial superinfection
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11
Q

how do you diagnose dermatophytosis?

A

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

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12
Q

treatment and prevention of dermatophytosis

A
  1. topical antifungal cream
    - Terbinafine, undecylenic acid, miconazole, tolnaftate
  2. oral griseofulvin (Fulvicin)
  3. keep skin cool and dry
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13
Q

organism of pathogenesis of Tinea versicolor?

A

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
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14
Q

how do you diagnose and treat tinea versicolor?

A
  1. 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
  2. topical selenium sulfide or azole used daily for 2 weeks
    - repeat as needed, as they may recur
    - alternative oral azoles
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15
Q

what is the organism and pathogenesis of Tinea nigra?

A

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

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16
Q

how to diagnose Tinea nigrans?

A
  • 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)
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17
Q

treatment of Tinea nigra?

A

topical keratolytic agent (salicyclic acid + topical azole

18
Q

how do subcutaneous mycoses occur?

A

introduced by trauma exposing subcutaneous tissue to soil or vegetation

19
Q

what is the organism and pathogenesis of sporotrichosis?

A

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
20
Q

what is the importance of sporotrichosis in COPD, alcoholics, or cortico-steroid using patients? what is difficult to distinguish from? what about AIDS patients?

A

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

21
Q

how to diagnose sporotrichosis?

A

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)

22
Q

diagnosis and prevention of sporotrichosis?

A

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
23
Q

what is the organism and pathogenesis of chromomycosis?

A

(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
24
Q

diagnosing chromomycosis?

A

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

25
Q

treatment and prevention of chromomycosis?

A

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

26
Q

what is the organism and pathogenesis of mycetoma? what does it look similar to?

A

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
27
Q

diagnosis of mycetoma?

A

needle biopsy for culture

  • H&E staining reveals grains in pus
  • X-ray to determine whether bone is involved
28
Q

how do differentiate mycetoma from actinomycosis?

A

staining

  • mycetoma has filamentous structures, larger, have fungal stains with Gomori methenamine silver or periodic acid-Schiff stain
  • actinomyces is small, G+ branching filaments
29
Q

treatment of mycetoma?

A

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

30
Q

what is Candidiasis usually attributed to?

A

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
31
Q

virulence factors of candidiasis?

A

adhesins - surface attachment
acid proteases and phospholipases - tissue invasion
phenotypic switching/morphogenesis - changes Ag expression and tissue affinity

32
Q

what is common pathogenesis for candidiasis?

A
  1. 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
  2. diaper rash - dampness predisposes to overgrowth
  3. 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
33
Q

what happens in Candidiasis in IV drug users?

A

right-sided endocarditis

34
Q

explain a predisposition to candidiasis?

A

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
35
Q

what are candidiasis pathogenesis that were rare, but now increasing?

A

sepsis, endophthalmitis, IV/catheter infections; systematic and disseminated infections
-usually due to vulnerable patients

36
Q

what is the importance of Candida…

  • globrata
  • krusei
  • lusitaniae
  • parapsilosis
  • tropialis
A

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

37
Q

explain systemic dandidiasis?

A

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
38
Q

explain disseminated candidiasis

A

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
39
Q

lab diagnoses of candidiasis?

A

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

40
Q

what should you look for if disseminated candidiasis is suspected?

A
  1. persistent leukocytosis
  2. neutropenia
  3. other risk factors
  4. fever remaining despite antibiotic coverage

MSII Microbiology (23 decks)

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