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microbiology > Candida Albicans > Flashcards

Candida Albicans Flashcards

1
Q

why is yeast hard to kill

A

eukaryotic cells like us

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2
Q

is CA part of the human microbiota?

A 
yes
oral
GIT 
vagina 
skin
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3
Q

when does transmission of yeast occur

A

at birth

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4
Q

what can make someones CA carriage increase

A

pregnancy- hormone changes

change in vaginal pH

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5
Q

yeast like which pH

A

acidic

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6
Q

TF yeast can form biofilms

A

yes

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7
Q

TF yeast cannot produce proteases, phospholipidases and haemolytsin

A

false

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8
Q

when can candida become life threatening

A

if it gets into the blood or other organs

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9
Q

people who get yeast infections the most are

A

AIDS- immunocompromised

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10
Q

TF: yeast needs oxygen to survive

A

false, can survive with or without

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11
Q

TF yeast is an opportunistic pathogen

A

true

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12
Q

hospitalised patients carry _____ Candida

more or less

A

more

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13
Q

why do babes commonly get CA

A

lower pH than adults mouth, also exposed to the mothers vagina

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14
Q

how does oral candidiasis present

A

white plaque on the tongue and in the corners of the mouth - cheilitis

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15
Q

what is it called when you have white plaques on the corners of your mouth

A

cheilitis

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16
Q

other things CA causes

A 
solar colitis 
between fingers if get hands wet alot or work with flour 
athletes foot 
groin rash 
onychomycosis 
scalp infection
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17
Q

how does oral candidiasis effect solar colitis

A

wounded lips from sunburn0 mouth candida migrates and colonises the wound

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18
Q

wear us onychomycosis? symptom

A

fungal infection on the nail, fungi destroy the tissue and enter the nail bed
thickening of the nail tissue

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19
Q

what is a common phenotypic presentation of CA when you screen for it

A

germ tube formation IN SERUM OR PLASMA

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20
Q

how do you screen for CA

A

2-3 hours incubation at 37 degrees C

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21
Q

what is the most common site of infection of CA in hospital patients?

A

Urinary tract

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22
Q

what increases the risk of developing a CA infection in the respiratory tract

A

mechanical ventilation

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23
Q

what dimorphism causes CA virulence

A

Transmission between yeast growth and filamentous growth

24
Q

besides dimorphism, what other virulence factors must CA acquire

A

biofilm formation for protection
adherence
hydrolytic enzymes for nutrients

25
Q

is CA adherence to the host specific?

how does adherence occur

A

not initially but then becomes specific

adhesions bind to amino acids and sugars on the surface of cells

26
Q

how does CA colonise cells after adhering? think hyphe

A

hyphe penetrate through the layers of cells

27
Q

what is vascular dissemination?

A

the CA gets into the blood after hyphe penetration

28
Q

when are biofilms most commonly associated with CA

A

on biomaterials implants and catheters

29
Q

what is necessary to get through the cells and gain nutrients?

A

proteases/ phospholipidases

related tissue damage, lipase, lysing competing microflora

30
Q

how many types of pathogens need iron?

A

most of them

31
Q

why are human good at preventing pathogens reaching iron

A

locked up in RBC

32
Q

what are Siderophores

A

small high affinity iron- chelating compounds which are secreted by bacteria to get iron across cell membranes

33
Q

what does CA secrete to get iron

A

haemolysin

34
Q

why does CA need iron?

A

essential for the establishment of the infection

35
Q

does haemolysin damage RBCs?

A

yes it breaks them down

36
Q

allylamines taget?

A

ergosterol synthesis

37
Q

antimetabolites such as?

A

flucytosine

38
Q

flucytosine (antimetabolite) targets?

A

fungal nucleic acid

39
Q

azaleas (fluconazole) targets?

A

ergosterol synthesis

40
Q

example of a echinocandin drug

A

caspofungin

41
Q

what does echinocandin (caspofungin) target

A

cell wall

b1-3- gluten synthesis

42
Q

example of a polyene? what does it target

A

amphotericin B

ergosterol

43
Q

griseofulin targets?

A

fungal mitotic apparatus

44
Q

how do fungistatic help the host

A

allows the immune response to overcome it

45
Q

how long do fungistatic agents need to be taken

A

long time- usually 6 months

46
Q

amphotericin B is most commonly used in which types of infections?

A

systemic

47
Q

mechanisms of fungal resistance?

A

mutations
biofilms
efflux on membrane
persister cells which withstand treatment and can start proliferating over time

48
Q

which drugs have been successful against biofilms? but what is the problem?

A

amphotericin B and echinocandins

but have bad side effects so only used as last line

49
Q

most available anti fungal drugs are fungi____

A

static

50
Q

4 new anti fungal approaches which are being thought about?

A

plant sources- natural
silver nanoparticals- inhibit DNA synthesis
anti-candida antibodies
photodynamic therapy using light

51
Q

how would silver nanoparticals target fungi

A

inhibit DNA synthesis

52
Q

are there any vaccines against fungi

A

2 in trial but not available yet

53
Q

what would a vaccine be useful against?

A

recurrent infections

54
Q

what is a univalent vaccine and why is this a problem (as both the vaccines in development as univalent)

A

only contain 1 antigen

fungi have lots of different antigens

55
Q

what is the main limitation of fungi vaccines

A

univalent

microbiology (19 decks)

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