Candida Albicans Flashcards

(55 cards)

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
is CA adherence to the host specific? | how does adherence occur
not initially but then becomes specific | adhesions bind to amino acids and sugars on the surface of cells
26
how does CA colonise cells after adhering? think hyphe
hyphe penetrate through the layers of cells
27
what is vascular dissemination?
the CA gets into the blood after hyphe penetration
28
when are biofilms most commonly associated with CA
on biomaterials implants and catheters
29
what is necessary to get through the cells and gain nutrients?
proteases/ phospholipidases | related tissue damage, lipase, lysing competing microflora
30
how many types of pathogens need iron?
most of them
31
why are human good at preventing pathogens reaching iron
locked up in RBC
32
what are Siderophores
small high affinity iron- chelating compounds which are secreted by bacteria to get iron across cell membranes
33
what does CA secrete to get iron
haemolysin
34
why does CA need iron?
essential for the establishment of the infection
35
does haemolysin damage RBCs?
yes it breaks them down
36
allylamines taget?
ergosterol synthesis
37
antimetabolites such as?
flucytosine
38
flucytosine (antimetabolite) targets?
fungal nucleic acid
39
azaleas (fluconazole) targets?
ergosterol synthesis
40
example of a echinocandin drug
caspofungin
41
what does echinocandin (caspofungin) target
cell wall | b1-3- gluten synthesis
42
example of a polyene? what does it target
amphotericin B | ergosterol
43
griseofulin targets?
fungal mitotic apparatus
44
how do fungistatic help the host
allows the immune response to overcome it
45
how long do fungistatic agents need to be taken
long time- usually 6 months
46
amphotericin B is most commonly used in which types of infections?
systemic
47
mechanisms of fungal resistance?
mutations biofilms efflux on membrane persister cells which withstand treatment and can start proliferating over time
48
which drugs have been successful against biofilms? but what is the problem?
amphotericin B and echinocandins | but have bad side effects so only used as last line
49
most available anti fungal drugs are fungi____
static
50
4 new anti fungal approaches which are being thought about?
plant sources- natural silver nanoparticals- inhibit DNA synthesis anti-candida antibodies photodynamic therapy using light
51
how would silver nanoparticals target fungi
inhibit DNA synthesis
52
are there any vaccines against fungi
2 in trial but not available yet
53
what would a vaccine be useful against?
recurrent infections
54
what is a univalent vaccine and why is this a problem (as both the vaccines in development as univalent)
only contain 1 antigen | fungi have lots of different antigens
55
what is the main limitation of fungi vaccines
univalent