7 - fungi and parasites Flashcards

1
Q

why are chronic infections common caused by fungi and parasites

A

they have many adaptions

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2
Q

features of fungi

A

can be uni or mulitcellular
often commensal
contribute to nutrient recycling
can be dispersed by airborne spores

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3
Q

unicellular fungi

A

yeasts

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4
Q

multicellular fungi

A

filamentous

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5
Q

endemic mycoses

A

groups of fungi that occupy ecological niches

geographically located due to climate
often thermally dimorphic

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6
Q

example of commensal fungi

A

microbial flora

e.g.candida albicans

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7
Q

example of fungi dispersed by airborne spores

A

aspergillus fumigatus

reaches terminal air spaces of lungs

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8
Q

types of mycoses

A

endemic mycoses
environmental saprophytes
human commensal fungi

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9
Q

examples of endemic mycoses

A

histoplasma
coccidiodes
blastomyces
paracoccidiodes

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10
Q

where are histoplasma found

A

often mississipi/ohio

bird/bat poo (guano) in soil

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11
Q

where are coccidiodes found

A

arid desert areas (south west USA)

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12
Q

where are blastomyces found

A

near lakes/river valleys

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13
Q

where are paracoccidiodes found

A

tropical and sub forests in South america

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14
Q

examples of environmental saprophytes

A
aspergillus
rhizopus
absidia
mucor
cryptococcus
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15
Q

features of environmental saprophytes

A

often opportunistic and invasive

dangerous

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16
Q

where is aspergillus often found

A

decaying veg matter

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17
Q

where is cryptococcus found

A

soil with pigeon poo (guano) and eucalyptus trees

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18
Q

examples of human commensal fungi

A

candida albicans

dermatophytes

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19
Q

where is candida albicans often found

A

bowel

pharyngeal flora

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20
Q

where are dermatophytes found

A

keratinized tissue

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21
Q

fungi mortality rate?

A

high in infected populations

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22
Q

example of high mortality rate of fungi

A

Aspergillus fumigatus causes more than 200,000 life threatening infections per year

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23
Q

persistant superficial infection of candida albicans

A

causes disription of mucosal barriers

e..g thrush

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24
Q

candida albicans in immunocompromised

A

disseminates to life-threatening diseases

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25
Q

prevalence of candida albicans

A

most common human infection

4th most common nosocomial bloodstream infection in USA –> very expensive for government

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26
Q

candida albicans virulence

A
reproduces asexually (budding)
dimorphic in repsonse to microenvironmental signals
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27
Q

dimorphic

A

transition from yeast to filamentous

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28
Q

role of yeast form candida albicans in infection

A

disseminates easily in bloodstream

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29
Q

role of filamentous c. albicans in infection

A

facilitates invasion and evasion of phagocytosis

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30
Q

if c albicans has no dimporphic switch

A

it is non pathogenic

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31
Q

innate host recognition of fungi

A

interactions with cell wall components

PAMPs

32
Q

examples of fungi PAMPs

A

glucans
mannans
galactans

33
Q

dectin-1

A

c-type lectin
highly conserved on surface of dendritic cells
important in anti-fungal immunity

34
Q

role of c-type lectin carbphydrate recognition domain

A

mediates recognition of B1,3-glucans and B1,6-glucans and zymosan

35
Q

dectin-1 interacts with ITAM in cytoplams

A

tyrosine phosphorylation

then acts together with TLRs to induce inflammatory cytokines and ROS

36
Q

ITAM

A

immunoreceptor Tyrosine-based Activation Motif

important in signal transduction
found in T cells, B cells and Fc domains

37
Q

4 examples of PRR that recognise fungi/parasites/viruses

A

Dectin-1
Dectin-2
Mincle
CLEC5a

38
Q

knock out dectin-1 genes in mice
infect with candida albicans
what happens

A

mice susceptible and die

evidence that dectin-1 is important in anti-fungal immunity

39
Q

importance of TLRs

A

distinguish between pathogenic molecules and normal apoptotic particles

40
Q

what to TLRs stimulate

A

cytokine production and secretion –> inflammatory response

initiation of adaptive immune response

41
Q

what do most TLRs signal through

A

MyD88

42
Q

what is MyD88

A

myeloid differentiation factor 88

adaptor protein

43
Q

role of MyD88

A

binds to TLR after activation by fungal component (PAMP) and CD14
initiates signalling cascade

44
Q

Syk

A

enzyme
(spleen tyrosine kinase)
important in signal transduction

45
Q

MBL

A

mannose-binding lectin

46
Q

mannose binding lectin

A

collectin protein
opsonin
coupled to complement pathway via MASPS
bind to MASPS to cause conformational chage

47
Q

oxidative burst killing mech

A

kill by rapidly producing and releasing ROS

48
Q

what is chromoblastomycosis

A

a chronic but non-fatal fungal infection of the skin and subcutaneous tissue
usually caused by F. Pedrosi

49
Q

helminth

A

class of parasite that can cause disease in humans

50
Q

why do helminths require an intermediate host

A

they do not replicate within the host

51
Q

examples of helminth intermediate host

A

soil

water

52
Q

3 larval stags of sexual reproduction of helminths

A

nematodes
trematodes
cestodes

53
Q

what is schistosoma

A

the most important trematode (fluke) infection of humans

54
Q

vector of schistosoma

A

water snail

55
Q

vector of schistosoma

A

water snails

become infected by eggs in fresh water
miracidia mature and multiply to release more cercariae

56
Q

which stage is dangerous for causing infection of schistosoma

A

motile

fork-tailed cercariae

57
Q

what happens when free swimming cercariae come in contact with host skin

A

use proteases and muscular action of oral sucker to penetrate host skin
head enters body
shed tails

58
Q

what do cercariae transition into

A

schistosoma and then into a schistosome

59
Q

where do immature schistosomula migrate to

A

the liver microcirculation to mature

60
Q

male/female interaction of schistosomula

A

females reside in a canal within the male
pairs then migrate against the venous flow from the GI tract to the liver
eggs are released into the veins

61
Q

impact of schistosome eggs being released into liver veins

A

elicit granulomatous inflammatory response

62
Q

T helper cell response to schistosome eggs

A

early stage - Th1 profile directed at schistosomula

Th2 response then takes over against egg antigens

63
Q

granulomatous response to schistosome eggs

A

granulomas surround eggs
recruit eosinophils, IgE, Th2
characteristics of schistomiasis shown
granulomas then translocated to the intestinal lumen and then excreted

64
Q

what happens when granulomas dissipate

A

collagenous scars coalesce and cirrhosis develops

blood bypass channels (varices) form and bleed to cause death

65
Q

what are protozoa

A
class of parasite 
unicellular
66
Q

why are protozoa good at chronic infections

A

they have lots of evolutionary adaptations

67
Q

why is antigenic variation important

A

underlies capacity of organisms to survive in a host

68
Q

how are the two groups of protozoal infections introduced

A
  1. by bites or tissue injury

2. by ingestion of contaminated water

69
Q

trypanosoma cruzi

A

protozoa that causes mega colon

kissing beetles penetrate skin and take blood meal to infect body

70
Q

what causes african sleeping sickeness

A

protozoa parasite

trypansoma brusei

71
Q

VATs

A

variable antigen type

72
Q

how does antigenic variation allow escape from host defences

A

successive dominance of each series of a variable antigen type (VAT) over time

73
Q

VATs cause appearance of remission in trypansosomes

A

antibodies destroy homologous trypanosomes
almost successful clearance
parasites then express new VSG thus becoming a new VAT and multiply

74
Q

VSG

A

variant-specific surface glycoprotein

75
Q

VSG release

A

VSG is released through flagellar resevoir and covers parasite as a surface coat

76
Q

where are VSG expression sites

A

at the ends of chromosomes

77
Q

role of syk

A

adaptor protein for dectin-1 (PRR)

enhances signalling