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MSII: Microbio Unit 2 > Mycoses (9) > Flashcards

Mycoses (9) Flashcards

1
Q

What are the cutaneous mycoses?

A

Dermatophytoses, Tinea vesicolor, tinea nigara

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2
Q

What causes dermatophytoses?

A

Dermatophytes

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3
Q

What do dermatopytes infect?

A

Superficial keratinized structures only!

skin, hair, nails

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4
Q

What is the virulence factor of dermatophytes?

A

Keritinase–> allows invasion of the cornified cell layer

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5
Q

What are the 3 major genera of dermatophytes? How are each spread?

A

Epidermophyton (direct contact)

Trichophyton (direct contact)

Microsporum (Direct contact, zoonosis from pets)

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6
Q

Describe how dermatophytosis presents?

A

Forms chronic infections in warm, humid areas of body surface

Inflammed circular border of papules and or vesicles (skin w/in can be normal)

Broken hairs, thickened/ broken nails

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7
Q

What can be found in some patietns with dermatophytosis that are hypersensitive?

A

They can form “id” reactions–> vesicles on fingers

They are caused by circulating fungal antigen.

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8
Q

Do “id” vesicles contain live fungus or spores?

A

No

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9
Q

What can happen due to prolonged dermatophytosis?

A

bacterial superinfection

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10
Q

How do you diagnose dermatophytosis?

A

PPD w/ trichophyton

Microskope exam of scraping and KOH mount–> you will see hyphae and spores

Culture on sabouraud’s ager at room temp

Microsporum under wood’s lamp

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11
Q

How is dermatophytosis treated?

A

Topical antifungal cream
(**need to treat all affected areas simultaneously)

Oral griseofulvin

Keep skin dry and cool

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12
Q

What causes tinea versicolor?

A

Malassezia furfur or Malessezia globosa

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13
Q

Importance of Tinea versicolor?

A

Superficial skin infection only of cosmetic importance. It is an overgrowth of normal flora.

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14
Q

How does tinea versicolor present?

A

Hypopigmented areas w/ slightly scaling/ itching

Seen in hot, humid weather

There is also an uncharacterized genetic component (seen in families)

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15
Q

How is tinea versicolor diagnosed?

A

Microscope exam: Skin scraping w/ KOH mount–> you will see yeast and hyphae

Wood lamp will show coppery-orange fluorescence

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16
Q

Treatment of tinea versicolor?

A

Topical selenium sulfide or azole used daily for 2 weeks

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17
Q

What causes tinea nigra?

A

Cladosporium weneckii

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18
Q

What is the pathogenesis of tinea nigra?

A

1- spores in soil enter injury
2- Germinate in the keratinized skin layers
3- Generate a brown pigment which appears as a brown spot

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19
Q

Who is tinea nigra mostly seen in?

A

Soutern coastal US and mostly in children.

Overall, it is not common

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20
Q

Diagnosis of tinea nigra?

A

Microscope: skin scraping and KOH mount will show tick septate branching hyphae with dark pigment on their walls

Culture: sabourd’s agaer–> yeast like shiny black colonies grow in 1 week

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21
Q

Treatment of tinea nigra?

A

Topical keratolytic agen (like salicylic acid)

Topical azole

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22
Q

What are the subcutaenous mycoses? And how are they contracted?

A

Sporotrichosis
Chromocycosis
Mycetoma

Introduced by trauma exposing subcutaenous tissue to soil or vegitation

23
Q

What causes sporotrichosis?

What is special about the organism?

What is another name for this diease?

A

Sporothrix schenckii

It is thermally dimprophic.

“rose picker’s disease”

24
Q

Pathogenesis of sporotrichosis?

A

Introduced into the skin by thorn puncture.

Yeasts grow at sites and form painless pustule or ulcer.

Draiing lymphatics form suppurating subcutaneous nodules

May progress to disseminated disease and meningitis if immunosuppressed

25
Q

What happens in patients with COPD and those on corticosteroids with a sporotrichosis infection?

A

They may develop pulmonary symptoms from inhaling the spores (which is difficut to distiguish from TB or histoplasmosis)

26
Q

How is sporotrichosis diagnosed in exam?

A

Painless pusule/ ulcer (usually on hand or arm)

History of gardening

History of ineffective antibiotic treatment

27
Q

How is sporotrichosis diagnosed in the lab?

A

Tissue biopsy–> shows round or cigar-shaped budding yeasts

Culture of pus/ biopsy at room temp–> shows hyphae “daisy chains”

28
Q

Treatment of sporotrichosis?

A

2- months of intraconazole or oral azoles

More serious need amphotericin B

29
Q

Where is chromomycosis seen?

A

Found in soil of the tropics

30
Q

Pathogenesis of chromomycosis?

A

Introduced into legs or feet with injury by wood splinters or thorns

Gradually progressive dubcutaneous disease

Granulomas from as immune system attempts to contain the infection

Wartlike lesions gradualy spread from initial site

31
Q

What will physical exam show for chromomycosis?

A

History or travel

Wartlike dark colored lesions

Crusting abscesses extending along lymphatics

32
Q

How does lab diagnose chromomycosis?

A

KOH mount shows dark colored septate hyphae or condidia

Biopsy shows dark brown, round fungal cells inside leukocytes or giant cells

ELISA

33
Q

How is chromomycosis treated?

A

Oral flucytosine and or itraconazole

Local surgery

34
Q

Which two mycosis have dark colored hyphae?

A

tinea nigra and chromomycosis

35
Q

What causes mycetoma? Where are the organisms found?

A

Petriellidum or Madurella

Found in soil but rare in the US

36
Q

Pathogenesis of mycetoma?

A

Replicating fungi form abscesses

Pus containing compact colored granules forms and drains through the local sinuses

Granulomatoous inflammatory response in the deep dermis and subcutaenous tissue may extend to the bone

37
Q

What can mycetoma resemble and how can it be differentiated?

A

Resembles actinomyces

Forms in foot, lower leg or hand, rather than the face

actinomyces are smaller and are gram +

mycetoma causing fungi are larger and appear in fugal stains

38
Q

How is mycytoma diagnosed?

A

Needle biopsy for culture

H&E stain will show grains in pus

X ray to determine whether bone is involved

39
Q

How is mycetoma treated?

A

First attempt antifungal/ antibiotic therapy

Surgical excision of abscess is sometime needed

40
Q

Name a cutaenous and opportunistic mycosis?

A

Candisiasis

41
Q

Describe candidia?

A

Yeastlike, oval w/ single bud

May also appear as psuedohyphae or hyphae when invading tissues

42
Q

Virulence factors of candidia?

A

Adhesins for surface attachment

Acid proteases and phospholipases for tissue invasion

Phenotypic switching/ morphogenesis

43
Q

Symptoms of candidiasis? Common conditions caused by candidia?

A

Range from trivial superficial to life-threatening systemic.

Diaper rash, vaginitis, thrush/ esophagitis

44
Q

Pathogenesis of diaper rash?

A

dampness from wet diapers predisposing to overgrowth

45
Q

Pathogenesis of vaginitis?

A

Overgrowth leading to itching and curdlike discharge

46
Q

Pathogenesis of thrush?

A

Overgrowth leading to psuedomembrane formation in the mouth

47
Q

Who is predisposed to thrush?

A

Steroid inhaler users

HIV + patients not on HAART

48
Q

Name some less common presentations of candidasis?

A

Skin–> overgrowth becomes red and wet, may be seen on fingers in dishwasers, butt of infants, nail beds in diabetics

Folliculitis–> forms a boil

Chronic mucocutanous candidiasis–> seen in people with impaired CMI

GI infection–> may occur with leukemia/ lymphoma

49
Q

T/F: systemic and disseminated infections of cancidiasis is rare

A

Once true, but they are now increasing

50
Q

Pathogenesis of systemic candidiasis (candidemia)?

A

Usually nosocomial with underlying major illness

Fever unresponsive to broad-spetrum antibiotics

History of cathetarization

Endocarditis is seen, also symtoms on skin or moth

30-40% mortality

51
Q

Pathogenesis of disseminated candidiasis (w/ organ invasion)?

A

One or more deep organs infected (eye, kidney, CNS, joints, muscles, heart/ pericardium, peritonium, spleen)

Blood cultures are often negative

Fever unresponsive to broad-spectrum antibiotics

Mortality is very high

52
Q

How does the lab make the diagnosis of candidiasis?

A

Exudates and biopsies show: Mix of budding yeasts, psuedohyphae, and hyphae. Gram positive.
Visualized by KOH smear, calcoflour white and methylene blue stain

Cultures show: Colonies are large

Bloodwork: will sometimes be positive for disseminated infection

53
Q

Can candidia develop drug resistance?

A

Yes, antifungal resistance is common

54
Q

How are candida infections treated?

A

Treatment ramps up with severity:

Topical azoles and polyenes for superficial

Oral azoles for more serious but not life threatening

Add amphoteracin B for more life threatening

Add echinocandins and/ or voriconazole for life threatening drug resistant

MSII: Microbio Unit 2 (10 decks)

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