Fungi Flashcards

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1
Q

Which bacteria are able to produce penicillin?

A

Penicillum Chrysogenum

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2
Q

How do fungi reproduce?

A

Sexually and asexually

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3
Q

How do moulds reproduce?

A

by producing spores

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4
Q

which domain of life do fungi belong to?

A

Eukaryotic

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5
Q

what are the benefits of fungi/yeast

A
  • alcohol beverage production
  • antibiotic production
  • bread
  • recombinant proteins
  • enzymes
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6
Q

how do fungi grow?

A

they grow as single cells

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7
Q

how do moulds grow?

A

overlapping and interlinking hyphal filaments

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8
Q

what is the asexual mode of reproduction used by fungi?

A

budding / fission

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9
Q

define mycoses

A

infection caused by any fungus that invades the tissues

or

diseases caused by fungal infections

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10
Q

what are the different types of mycoses?

A

1- superficial: white Piedra/ pityriasis versicolor
2- cutaneous: tinea pedis/ onychomycosis/ tinea capitis
3- subcutaneous: chromoblastomycosis/ mycetoma
4- systemic: blastomycosis/ histoplasmosis/ coccidiomycosis

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11
Q

list 3 oppotunistic fungal infections

A

1- candidiasis
2- aspergillosis
4- pneumonia

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12
Q

describe the structure of a yeast cell

A

oval with a rigid cell wall

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13
Q

what are the components of a yeast cell wall?

A

50-60% glucan
(beta-1,6-glucan/beta-1,3-glucan/beta-1,6 complexed with chitin)
25% polysaccharides
15-23% mannan
1-9% chitin

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14
Q

what are the three types of glucan in a yeast cell wall

A

beta-1,6-glucan
beta-1,3-glucan
beta-1,6 complexed with chitin

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15
Q

what is the role of mannoproteins in the cell wall?

A

they form a fibrillar layer that radiates from an internal skeletal layer that is formed by polysaccharides of the cell wall which limits wall permeability to solutes by covalent bonds

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16
Q

what would happen if the cell wall of fungi was removed?

A

it would leave an osmotically fragile protoplast which will burst if not maintained in an osmotically stable environment

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17
Q

what is a protoplast?

A

a cell with a removed cell wall

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18
Q

what is the role of beta-1,3-glucan in the cell wall of fungi?

A

1- provides physical protection
2- maintains osmotic stability
3- it is a scaffold for proteins
4- it mediated cellular communication
5- it is the site of enzymatic reactions

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19
Q

what is the periplasmic space?

A

thing region that lies below the cell wall

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20
Q

what is the plasmalemma?

A

phospholipid region located directly below the periplasmic space

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21
Q

what is the composition of plasmalemma?

A
  • phospholipids
  • lipids
  • proteins
  • sterols
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22
Q

why does the nuclear membrane of the fungal cell contain pores?

A

to allow communication between the nucleus and the rest of the cell

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23
Q

what are the mitochondrial enzymes and where are they located within the mitochondria?

A
  • Matrix: Krebs cycle enzymes
  • inner membrane: electron transport & oxidative phosphorylation enzymes
  • outer membrane: lipid biosynthesis enzymes
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24
Q

TRUE OR FALSE:
the mitochondria has its own DNA and is capable of synthesizing its own proteins, known as mitoribosomes

A

طبعا صح يعني -.-

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25
Q

what are polysomes?

A

ribosomes of the fungal cell which are strung together by mRNA

they are also the site of protein biosynthesis

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26
Q

Draw a fungal cell

A

you should’ve drawn it cheater

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27
Q

what are the classes of antifungal drugs?

A
  • Polyene antifungals
  • Azole antifungals
  • Echinochandins
  • Synthetic antifungals
28
Q

1- what is the mechanism of action of polyene antifungals?

2- name two polyene antifungal drugs

A

1- binds ergosterol, the dominant sterol in fungal cells, thus increasing membrane permeability by formation of pores and allowing intracellular components to escape

2- amphoterecin b / nyastatin

29
Q

1- what is the mechanism of action of azole antifungals?

2- what are the subclasses of azole antifungals?

3- name two azole antifungal drugs

A

1- interfere with ergosterol biosynthesis by binding to cytochrome P450mediated enzyme (14 alpha demethylase), this prevents lanosterol methylation which prevents lanosterol from becoming ergosterol. thus, lessening the amount of ergosterol in cell wall leading to membrane instability, growth inhibition and cell death

2- imidazoles / triazoles

3- ketoconazole / itraconazole

30
Q

1- what is the difference between imidazole antifungals and triazole antifungals?

2- give an example of an imidazole and a triazole

A

1- imidazoles have two nitrogen atoms in the 5 membered sugar whereas triazoles have 3 nitrogens

2- imidazole: ketoconazole
triazole: itraconazole/ voriconazole

31
Q

1- what is the mechanism of action of echinocandins?

A

target the synthesis of b-1,3-glucan which is the major polymer of the cell wall as it provides physical protection, maintains osmotic stability, regulates cell shape..etc therefore inhibition of its synthesis disrupts the structure of the growing cell wall resulting in osmotic instability and intracellular components would leave the cell leading to cell lysis

32
Q

what are the subclasses of echinocandins?

A
  • caspofungin
  • micafungin
  • anidulafungin
33
Q

1- what is the mechanism of action of synthetic antifungal agents?

2- what is one example of a synthetic antifungal?

A

1- synthetic antifungals can work in either of two mechanisms

  • disruption of protein synthesis by inhibiting DNA synthesis
  • Depletion in the amino acid pools within the cell as a result of protein synthesis inhibition

2- flucytosine

34
Q

List six fungal pathogens

A

1- candida albicans
2- aspergillis fumigatus
3- histoplasma capsulatum
4- dermatophytes
5- cryptococcos neoformans
6- saccharomyces cervisae

35
Q

What morphological forms can candida albicans exist as?

A
  • blastospores
  • hyphae
36
Q

what patients are at risk of candida albicans?

A

diabetics
burns/wounds
indwelling urinary catheter
cystitis
trauma
underlying disease
organ transplant

37
Q

how does candida albicans cause disease?

A

candida albicans is an opportunistic fungal pathogen, which means it is present in the normal microflora, however it only manifests as a disease when the microflora is disrupted

38
Q

what is thigmotropism?

A

the ability to sense and respond to changes in surface contours, which aids in finding the line of least resistance in the host tissues

39
Q

how does candida albicans bind to platelets?

A

via fibrinogen binding ligands resulting in fungal cell being surrounded by a cluster of platelets

40
Q

what are the extracellular enzymes of candida albicans? and what is their function?

A

1- phospholipase A
2- phospholipase B
3- phospholipase C
4- lysophospholipase

their function is to aid adherence and degredation of IgG/IgA immunoglobulins

41
Q

what are the most clinically common candida species?

A
candida albicans
candida glabrata (resistant)
42
Q

who is at risk of candida parapsillosis?

A

neutropenic patients
patients on broad spectrum antibiotics
ICU patients
Patients on parenteral nutrition
catheter associated

43
Q

What can disrupt the normal flora?

A
  • *1- antimicrobial agents:** allows candida proliferation on mucosa and maceration of skin
  • *2- decreased t cell immunity**: allow candida proliferation on mucosa
  • *3- neutropenia:** allows candida to escape from gut to bloodstream
  • *4- central venous catheter:** allows entry to blood stream
44
Q

what is the main host defense against candida albicans?

A

t cell mediated immunity

and neutrophils in mucosa

45
Q

why is it that HIV patients have frequent oropharyngeal and vaginal candidiasis?

A

because HIV patients have low counts of CD4 lymphocytes making them susceptible to candidal infections

46
Q

in a neutropenic patient, where does candida occur?

A

eyes/kidneys/heart/brain/liver/spleen

47
Q

how is candida diagnosed?

A

scrapings/ blood culture/ germ tubes for differentiation

48
Q

what is candidemia?

A

A Candida bloodstream infection

49
Q

what are the symptoms of candidemia?

A

candidemia symptoms depend on the end organ and can manifest as meningitis or chorioretinitis abscess

50
Q

who is at risk of cryptococcus neoformans

A

AIDS

Hematologoic malignancies

transplant

corticosteroids

immunosuppressant drugs

51
Q

what is the virulence factor of cryptococcosis?

A

polysaccharide capsule, which inhibits phagocytosis of immune responses thus downregulating Th1 mediators development

52
Q

how is cryptococcosis diagnosed?

A

lumbar puncture where fluid will show lymphocytes/ high proteins/ decreased glucose

53
Q

how is cryptococcosis treated?

A

amphoterecin B + flucytosine for two weeks

after that, fluconazole for a few months

54
Q

how does cryptococcus neoformans protect its cell wall?

A

by producing melanin that resist enzyme degradation of the host immune response

55
Q

what are the most common aspergillus causing pathogens?

A

Aspergillus fumigatus + aspergillus flavus

56
Q

who is at risk of aspergillus?

A

neutropenic

corticosteroids

transplant

immunosuppressant drugs

57
Q

how do aspergillus species cause disease?

A

after entry to the body, they germinate and turn into hyphae which invade tissues thus causing disease

58
Q

main host defenses against aspergillus

A
  • neutrophils

macrophages

59
Q

how do neutrophils defend against aspergillus

A

they line up along their surfaces & secrete reactive oxygen intermediates that kill the organism

60
Q

how do macrophages defend against aspergillus?

A

pulmonary macrophages phagocytose and kill conidia but unable to kill hyphal forms

61
Q

what damage does aspergillus cause?

A

tissue infarction/ haemorrhage/ necrosis

62
Q

how is aspergillus diagnosed?

A

chest radiograph

computed tomography scan

tissue biopsy

63
Q

how is aspergillus treated?

A

amphoterecin b

echinocandin

64
Q

define dermatophytes

A

they are keratinophilic fungi that metabolize keratin, which is abundant in the skin

65
Q

what fungal pathogens cause tinea pedis (athlete’s foot)?

A
  • epidermophyton floccosum
  • trichophyton rubrum
66
Q

are tinea infections contagious?

A

yes