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Erica's ID 3 > Mycology I: Opportunistic fungi > Flashcards

Mycology I: Opportunistic fungi Flashcards

1
Q

5 groups of medically important fungi

A
  1. Yeast
  2. Black molds (Dematiaceous)
  3. Hyaline molds
  4. Mucorales
  5. Dimorphs
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2
Q

Cryptococcous

A

HIV = neoformans (avian excrement)

Normal immune systems = gattii (eucalyptus trees)

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3
Q

Complications of cryptococcous neoformans

A

Meningoencephalitis (non-inflammatory, almost no white/phagocytic cells).

Pulmonary nodules
Disseminated disease: skin, brain abscess, etc. Not a pustule like staph.

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4
Q

Treat cryptococcous with ___?

A

Amphotericin B is the KEY!!

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5
Q

Test for cryptococcous?

A

Direct cryptococcal antigen test - can get from CSF and use a dipstick

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6
Q

White halo with india ink

A

Yeast capsule prevents dye - Cryptococcous

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7
Q

How to differentiate neoformans from the other kinds of cryptococcous

A

Neoformans = grows on birdseed agar (melanin production by phenol oxidase)

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8
Q

Do you need to treat candida in a urine sample?

A

If it’s just colonization, nope.If it’s invasive it will usually be with some other ascending infection related to obstruction.

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9
Q

Do you need a special media to grow candida?

A

Nope, grows on everything

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10
Q

Cryptococcous virulence

A

Capsule inhibits phagocytosis

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11
Q

What explains the neurotropism of cryptococcous?

A

The high levels of dopamine - a substrate to make melanin

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12
Q

Route of entry of cryptococcous

A

Inhalation

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13
Q

CRAG

A

Cryptococcal antigen test - detects the capsular polysaccharide; cheap and fast

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14
Q

CGB agar

A

differentiate gattii from neoformans because gattii will turn blue on CGB agar

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15
Q

3 species of candida associated with majority of invasive infections

A

Candida albicans
Candida parapsilosis
Candida glabrata

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16
Q

What is Candida krusei notable for?

A

Fluconazole resistance

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17
Q

Invasive candidiasis is a disease of _____ _____

A

medical progress

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18
Q

Key feature of C. albicans

A

Germ-tube positive

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19
Q

Virulence of Candida

A

Normal flora… so they overgrow when the host immune system sucks.

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20
Q

Host risks associated with candida

A
  • Intensive medical care (indwelling catheters)

- Immunocompromised hosts (premature infants, neutropenia)

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21
Q

Symptoms of clinical candidiasis

A

Fever +/- leukocytosis; skin papules indicate disseminated infection

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22
Q

3 syndromes of invasive candidiasis

A
  1. Isolated candidemia = easiest to recognize. Indwelling catheters
  2. Candidemia + visceral disease = eye** (endophthalmitis), kidney, brain, lung, etc
  3. Isolated visceral disease = no detectable bloodstream infection
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23
Q

Diagnosis of candida

A
  • Direct microscopy
  • Culture takes 1-5 days
  • Histo but granulomatous reaction is not typical
  • B-D-glucan antigen test! Present in most fungal cell walls
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24
Q

Is the B-D-glucan antigen test specific to candida?

A

Nope, but it is sensitive. Use it in high risk patients

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25
Q

What is 1st line tx of candida?

A

Echinocandins

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26
Q

What treats endophthalmitis?

A

Fluconazole

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27
Q

4 species of aspergillum

A
  1. Aspergillus fumigatus - majority
  2. A. flavus
  3. A. terreus
  4. A. niger
28
Q

What kind of environment does aspergillus enjoy?

A
  • moist such as hay or water-damaged dwellings and old buildings
29
Q

Mycology of aspergillus

A

Septate hypae

30
Q

Rapid growing, fuzzy/velvety

A

Aspergillus

31
Q

Pigmented center with white apron

A

Aspergillus

32
Q

Colors for the different species

A 
Blue-green = Fumigatus
Brown = Terreus
Black = niger
Yellow = Flavus
33
Q

What must the hyphae do to be identified on microscopic examination?

A

Sporulate

34
Q

how do you get aspergillus?

A

Inhalation - usually grow and survive in an abnormal lung (like old TB cavities)

35
Q

Pathogenesis of aspergillus in immunocompromised hosts?

A
  • Angioinvasive –> ischemic necrosis –> clot formation –> infarction
36
Q

Host risk factors for aspergillus

A
  • Neutropenia (such as with AML)

- Old cavitary lung lesions

37
Q

Chronic aspergillosis

A
  • normal hosts

- may have wt loss, hemoptysis, and may look like malignancy

38
Q

Acute invasive aspergillosis

A
  • Fever + abnormal CXR/CT
  • Wedge shaped infarction
  • Rapidly expanding nodules
  • Disseminated aspergillosis from hematogenous spread
39
Q

Cutaneous aspergillosis

A
  • Seen with inoculation sites
40
Q

Sino-orbital aspergillosis

A
  • Identical in presentation to mucormycosis but happens in neutropenic hosts.
41
Q

Diagnosis of aspergillosis

A

Direct microscopy (won’t stain well)

  • Narrow hyphae (10-15 micrometers)
  • Septate, branching at 45 degree angles

Serologic:

  • Aspergillus galactomannan antigen
  • B-D glucan antigen test
42
Q

Tx for aspergillus

A
  • Combo med surg&raquo_space; med treatment alone

- Voriconazole, posaconazole, isavuconazole, amphotericin B, echinocandins

43
Q

Disease producing species of mucormycosis

A
  • Rhizopus arrhizus
  • Mucor
  • Rhizomucor
44
Q

Substance that is 100% on glycemic index produces this fungus…

A

White bread - produces mucorales

45
Q

Mycology of mucormycosis

A
  • Rapid growing, wooly, white colony

- Hyphae are broad, ribbon-like, nonseptate, with 90 degree branching

46
Q

What makes rhizopus grow in the presence of glucose and acid?

A

ketone reductase & free iron

47
Q

Pathogenesis of mucorales

A
  • Angioinvasive

- Spores can be inhaled

48
Q

Host risk factors

A
  • DKA

- Iron overload treatment with deferoxamine (iron chelator). Fungi can use the free iron… wheeee!

49
Q

Rhinocerebral mucormycosis

A

Necrotic ulcer on plate followed by orbital invasion and extension into cavernous sinus and brain

50
Q

Diabetic patient with facial swelling and black thing on the roof of their mouth

A

Rhinocerebral mucormycosis. They be dead soon bro.

51
Q

Cutaneous mucormycosis

A

Seen with contaminated wounds

52
Q

Diagnosis of mucormycosis

A
  • Clinical presentation
  • Culture
  • Biopsy to see the broad hyphae that are non-septate and right angle branching
53
Q

Tx of mucormycosis

A
  • Combined med/surg (debridement + liposomal ampho B)

- Rhinocerebral is an EMERGENCY

54
Q

PCP

A

Looks like protozoan because it is a fungus that lacks ergosterol

55
Q

3 stages of PCP

A
  1. Trophozoite
  2. Pre-cyst
  3. Thick-walled cyst (up to 8 intracystic bodies)
56
Q

Perihilar reticulonodular infiltrates

A

PCP

57
Q

What does a PCP culture show?

A

Nothing, you can’t do it

58
Q

When you use a GMS stain on PCP what do yousee?

A

Small non-budding yeasts that look like candida

59
Q

Tx for PCP

A

TMP/SMX
OR
TMP + dapsone
Clinda + primaquine, atovaquone, pentamidine, and trimetrexate

60
Q

Black moulds

A

Dematiaceous fungi

61
Q

What causes the “black” in black moulds?

A

Melanin within the cell walls and spores

62
Q

What does black mould look like?

A

Narrow septate hyphae that branch at 45 degree angles

Indistinguishable from aspergillus in tissue biopsies

63
Q

How do colonies of black mould differ from any other colonies?

A

The brown-black color is on both the front and back

64
Q

How do you get black moulds?

A

Direct inoculation events in normal hosts - soil or decayed vegetation

65
Q

Clinical features of black moulds

A

Subcutaneous nodules that are slowly progressive and non-painful.

Cerebral abscess - fever + HA + seizure

66
Q

Diagnosis of black moulds

A
  • Culture

- May have positive B-D-glucan antigen test

67
Q

Tx of black moulds

A
  • Surgical debridement

- Ampho B

Erica's ID 3 (13 decks)

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