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Microbiology > Chapter 46-50 Fungi 2 > Flashcards

Chapter 46-50 Fungi 2 Flashcards

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1
Q

why are there fewer effective agents for antifungal drugs

A

because of similarity of fungal cells and human cells

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2
Q

easier to treat superficial mycoses than ____

A

systemic infections

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3
Q

where is ergosterol found

A

in fungal cell membranes

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4
Q

what do human cells have instead of ergosterol

A

cholesterol

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5
Q

what do polyene compounds do

A

-bind ergosterol in fungal membranes
- leakage of cell constituents and cell death
- bind cholesterol in mammalian cells but less strongly than ergosterol

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6
Q

what are the polyene compounds and what are they used for

A

-amphotericin B: systemic disease
- nystatin: topical disease

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7
Q

what is the basis for polyene toxicity

A

polyenes bind cholesterol in mammalian cells but less strongly than ergosterol

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8
Q

why is filipin toxic

A

binding of cholesterol

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9
Q

what does terbinafine target

A

squalene epoxidase

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10
Q

what does itraconzole target

A

C14 demethylase

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11
Q

what do allylamines do

A

block ergosterol synthesis by inhibiting squalene epoxidase activity
- mainly effective on the dermatophytes
- topical or tablet

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12
Q

what do azoles do

A

block ergosterol synthesis by inhibitins cytochrome P450 dependent 14alpha lanosterol demethylation

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13
Q

what does azoles supplant

A

ketoconazole

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14
Q

what are azoles active against

A

-candida
- crytococcus
- aspergillus
- endemic fungi
- dermatophytes

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15
Q

what do echinocandins do

A

-inhibit synthesis of Beta 1-3 D glucan - an essential component of fungal cell walls

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16
Q

what are echinocandins active against

A

aspergillus and candida

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17
Q

describe caspofungin and what category it falls under

A
  • echinocandins
  • intravenous use
  • minimal toxicity
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18
Q

what does pyrimidine inhibition do

A

interferes with fungal protein and DNA synthesis

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19
Q

what are pyrimidine inhibitors active against

A

candida species and crytpococcus neoformans

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20
Q

why are pyrimidine inhibitors always used in combination with another antifungal

A

resistance develops quickly if used alone

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21
Q

what are the opportunistic mycoses

A

-candiasis: candida albicans
- aspergillosis: aspergillus funigatus
- crytococcosis: cryptococcus neoformans
- zygomycosis: zygomycetes
- pneumocystits pneumonia: pneumocystis jiroveci

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22
Q

what are the high risk categories for opportunistic mycoses

A
  • immunocompromised individuals
  • blood and marrow transplant
  • organ transplant
  • major surgery
  • AIDS
  • neutropenia
  • neoplastic disease
  • immunosuppressive therapy
  • advanced age
  • premature birth
  • burn victims
  • long term IV catheter users
  • broad spectrum antibiotic therapy
  • DM
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23
Q

what are the candidiasis organisms

A
  • candida albicans
  • candida glabrata
  • candida parapsilosis
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24
Q

what is the common cause of catheter related infections

A

candida parapsilosis

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25
Q

what protects against mucosal candidiasis

A

local factors and T cell mediated defense system

26
Q

what protects against candidiasis invasive infection

A

adequate neutrophil function

27
Q

what are other host factors associated with protection against candida infections

A
  • salivary flow and constituents
  • blood group and secretor status
  • epithelial barrier
    -presence of normal bacterial flora
28
Q

what are the virulence factors of candida

A
  • adherence capability proportional to virulence rnaking of species - candida cell surface glycosylation affects adherence
  • secreted enzymes
  • phenotype switching: yeast to psuedohypha transformation, cell wall glycoprotein expression, proteolytic enzyme secretion
29
Q

what is the clinical presentation of chronic pseudomembranous candidiasis

A

multiple removable white plaques

30
Q

what is the clinical presentation of candida associated angular chelitis

A

bilateral cracks, angles of mouth

31
Q

what is the clinical presentation of median rhomboid glossitis

A

fixed red/white lesion, dorsum of tongue

32
Q

what is pseudomembranous candidiasis on palate also called

A

thrush

33
Q

what is plaquelike/nodular candidiasis also called

A

chronic hyperplastic candidiasis or candidal leukoplakia

34
Q

what percentage of lesions of plquelike/nodular candidiasis turn into cancer

A

40%

35
Q

what other component often accompanies angular chelitis

A

bacteria

36
Q

how do you diagnose mucosal candidiasis

A

scrape and look under the microscope culture

37
Q

how do you diagnose invasive candidiasis

A

-blood culture not sensitive
- biopsy of involved tissue
- microscopy
- culture

38
Q

what are the staining methods to visualize fungi in clinical samples

A
  • periodic acid schiff (PAS): surface carbohydrate
  • potassium hydroxide (KOH): tissue dissolves, fungi do not
  • grocott-gomori methenamine silver: surface carbohydrate
  • Gridley’s method: modificaion of PAS
  • Calcofluor white: fluorescent probe for chitin
39
Q

what drug is used to treat pseudomembranous candidiasis

A

amphotericin B lozenges

40
Q

what drug is used to treat erythematous candidiasis

A

amphotericin B lozenges

41
Q

what drug is used to treat plaquelike/nodular candidiasis

A

amphotericin B lozenges

42
Q

what drug is used to treat denture associated candia lesions

A

miconazole oral gel

43
Q

what drug is used to treat angular chelitis

A

miconazole oral gel

44
Q

what drug is used to treat median rhomboid glossitis

A

amphotericin B lozenges

45
Q

why is candida auris a problem

A
  • causes serious infections
  • resistant to medicines
  • its becoming more common
  • difficult to identify
  • can spread in hospitals and nursing homes
46
Q

where is cryptococcus neoformans found

A

in soil contaminated with bird excreta

47
Q

what percentage of patients with cryptococcosis appear to be immunocompetent

A

20%

48
Q

how does cryptococcus neoformans infect in the body

A
  • yeast cells are inhaled in the alveoli and begin to produce a polysaccharide capsule
  • capsule inhibits phagocytosis and intracellular killing
  • T cell immunity crucial to infection control
  • melanin production in cell wall enhances virulence
  • resists free radicals and enzyme degradation
49
Q

describe how patients with cryptococcus neoformans present

A
  • usually asymptomatic
  • has a striking neurotropism
  • minimal inflammatory response with CNS infection
  • patient often presents with meningitis which worsens
50
Q

how is C. neoformans diagnosed

A

cryptococcal meningtis- examine CSF for encapsulated budding yeast
- latex agglutination test for capsular polysaccharide antigen

51
Q

what is the treatment for C. neoformans

A
  • cryptococcal meningitis
  • drug therapy for several months
  • lifelong therapy required for patients with T cell defects
52
Q

how is aspergillosis acquired and how does it grow

A
  • acquired from environment by inhalation of conidia
  • grow as hyphae in immunosuppressed individuals usually as pulmonary or sinus infection
  • angioinvasive: growth through blood vessel walls, cause tissue infarction, hemorrhage, necrosis
53
Q

how is aspergillosis diagnosed

A

culture on Sabouraud’s agar

54
Q

how is aspergillosis treated

A
  • high mortality
  • expanded spectrum azole voraconazole
  • decreased exposure- filtered air
55
Q

what are the main genera in zygomycosis

A

rhizopus and mucor

56
Q

describe zygomycosis and risk groups

A

-aseptate, broad hyphae
- angioinvasive
- risk groups include DM with ketoacidosis

57
Q

what is rhinocerebral zygomycosis

A

spread from nares/ sinuses to palate, orbit, face and to the brain

58
Q

what is the treatment for zygomycosis

A

amphotericin B and aggressive surgical debridement

59
Q

when are people infected with pneumocystis jiroveci

A

early in life in immunosuppressed patients

60
Q

what is the most common opportunistic infection in AIDS patients

A

pneumocystic pneumonia

61
Q

what is the treatment for pneumocystis jiroveci and what does it target

A

trimethoprim-sulfamethoxazole
- targets folic acid synthesis and utilization

62
Q

P. Jiroveci lacks ____

A

ergosterol

Microbiology (39 decks)

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