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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
what protects against mucosal candidiasis
local factors and T cell mediated defense system
26
what protects against candidiasis invasive infection
adequate neutrophil function
27
what are other host factors associated with protection against candida infections
- salivary flow and constituents - blood group and secretor status - epithelial barrier -presence of normal bacterial flora
28
what are the virulence factors of candida
- 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
what is the clinical presentation of chronic pseudomembranous candidiasis
multiple removable white plaques
30
what is the clinical presentation of candida associated angular chelitis
bilateral cracks, angles of mouth
31
what is the clinical presentation of median rhomboid glossitis
fixed red/white lesion, dorsum of tongue
32
what is pseudomembranous candidiasis on palate also called
thrush
33
what is plaquelike/nodular candidiasis also called
chronic hyperplastic candidiasis or candidal leukoplakia
34
what percentage of lesions of plquelike/nodular candidiasis turn into cancer
40%
35
what other component often accompanies angular chelitis
bacteria
36
how do you diagnose mucosal candidiasis
scrape and look under the microscope culture
37
how do you diagnose invasive candidiasis
-blood culture not sensitive - biopsy of involved tissue - microscopy - culture
38
what are the staining methods to visualize fungi in clinical samples
- 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
what drug is used to treat pseudomembranous candidiasis
amphotericin B lozenges
40
what drug is used to treat erythematous candidiasis
amphotericin B lozenges
41
what drug is used to treat plaquelike/nodular candidiasis
amphotericin B lozenges
42
what drug is used to treat denture associated candia lesions
miconazole oral gel
43
what drug is used to treat angular chelitis
miconazole oral gel
44
what drug is used to treat median rhomboid glossitis
amphotericin B lozenges
45
why is candida auris a problem
- causes serious infections - resistant to medicines - its becoming more common - difficult to identify - can spread in hospitals and nursing homes
46
where is cryptococcus neoformans found
in soil contaminated with bird excreta
47
what percentage of patients with cryptococcosis appear to be immunocompetent
20%
48
how does cryptococcus neoformans infect in the body
- 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
describe how patients with cryptococcus neoformans present
- usually asymptomatic - has a striking neurotropism - minimal inflammatory response with CNS infection - patient often presents with meningitis which worsens
50
how is C. neoformans diagnosed
cryptococcal meningtis- examine CSF for encapsulated budding yeast - latex agglutination test for capsular polysaccharide antigen
51
what is the treatment for C. neoformans
- cryptococcal meningitis - drug therapy for several months - lifelong therapy required for patients with T cell defects
52
how is aspergillosis acquired and how does it grow
- 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
how is aspergillosis diagnosed
culture on Sabouraud's agar
54
how is aspergillosis treated
- high mortality - expanded spectrum azole voraconazole - decreased exposure- filtered air
55
what are the main genera in zygomycosis
rhizopus and mucor
56
describe zygomycosis and risk groups
-aseptate, broad hyphae - angioinvasive - risk groups include DM with ketoacidosis
57
what is rhinocerebral zygomycosis
spread from nares/ sinuses to palate, orbit, face and to the brain
58
what is the treatment for zygomycosis
amphotericin B and aggressive surgical debridement
59
when are people infected with pneumocystis jiroveci
early in life in immunosuppressed patients
60
what is the most common opportunistic infection in AIDS patients
pneumocystic pneumonia
61
what is the treatment for pneumocystis jiroveci and what does it target
trimethoprim-sulfamethoxazole - targets folic acid synthesis and utilization
62
P. Jiroveci lacks ____
ergosterol

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