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Biomed 2 - Season finale > Medical Micro - Lung/gut > Flashcards

Medical Micro - Lung/gut Flashcards

1
Q

what are mechanical factors in the lung that act as a barrier to disease

A

epithelial surfaces
movement of cilia
trapping effect of mucus

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2
Q

what are chemical factors in the lung that act as a barrier to infections

A

fatty acids
lysozyme and phospholipase
low pH
surfactants in the lungs act as opsonins

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3
Q

what are the biological factors that prevent infections

A

normal flora in the skin/GI tract

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4
Q

what are the clearance mechanisms in the lungs

A

mucociliary escalator
coughing
phagocytosis via alveolar macrophages

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5
Q

particle clearance in the lungs is biphasic - what does this mean

A

fast (half life of minutes - hours) - tracheobronchial mucociliary clearance
slow (half life of days - years) - alveolar clearance

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6
Q

what is the rate and mechanism of particle clearance in the lung in part determined by

A

the site of particle deposition

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7
Q

what is the difference in mucus in a non-CF vs CF lung

A

non-CF - depth of periciliary fluid is normal, mucus floats to the top and is co-ordinated towards the mouth via cilia
CF - mucus is poorly hydrated and hypoxic, compacted mucus inhibits cilia beating

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8
Q

what happens shortly after birth to those born with CF

A

mucus in the bronchial tree stagnates in the smaller bronchioles

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9
Q

what are the early infections that CF leads to

A

staphylococcus aureus
haemophilus influenzae

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10
Q

what are the later on infections that CF leads to

A

pseudomonas aeruginosa
burkholderia cepacia

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11
Q

what is the main reason of death due to CF

A

progression of pulmonary diseases via bacterial infection

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12
Q

what are the main features of pseudomonas aeruginosa

A

motile
aerobic
gram-negative

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13
Q

where does P. aeruginosa live

A

almost any environment
primarily in water, soil and vegetation

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14
Q

what type of pathogen is P. aeruginosa

A

opportunistic pathogen
infects individuals with immune system deficiencies
common for cancer/burn patients

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15
Q

what are the P. aeruginosa virulence factors

A

produces toxins that kill host cells
extensive tissue damage via degrative enzymes
alginate production causes thick biofilms which causes chronic inflammation response

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16
Q

where do intracellular bacteria live and replicate

A

either in endosomal compartments
or in cytosol of diverse amount of host cells

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17
Q

what are classified as intracellular pathogens

A

all viruses
many bacterial pathogens
certain protozoa and fungi

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18
Q

how are particles cleared from the alveoli

A

cleared by phagocytic cells
including alveolar macrophages

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19
Q

what are the features of legionnaires disease

A

acute fulminating pneumonia
low attack rate (>12% fatalities)

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20
Q

features of pontiac fever

A

mild
non-pneumonic
febrile infection
high attack rate

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21
Q

how is legionella contracted

A

by breathing water droplets containing legionella bacteria

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22
Q

what is the main thing legionella infects

A

lung macrophages

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23
Q

after phagocytosis into the macrophage, what are the survival strategies used by L. pneumophila inside the macrophage

A

establishes a replication-permissive vacuole
during/shortly after initial contact
inhibits lysosome/phagosome fusion - no enzyme/free radical release

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24
Q

what is formation of the vacuole in macrophages by L. pneumophila dependant on

A

bacterial icm/dot (intracellular multiplication/defective organelle trafficking) genes

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25
Q

what are pilin genes required for

A

attachment to host cells and biofilms
intracellular growth

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26
Q

what is type IV secretion icm/dot complex and what is required for it

A

membrane spanning
translocates effector molecules into host cells
requires ATPase DotB

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27
Q

what do DotA/B mutants still infect

A

A. castellani

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28
Q

name the virulence determinants for invasion and growth

A

flagella expression
type IV secretion
pilin genes
macrophage infectivity protein (Mip)
KatA/KatB

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29
Q

where are KatA/B located

A

KatA - periplasm
KaB - cytosol

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30
Q

what happens when L. pneumophila converts to replicative form

A

it is acid tolerant
stops expressing virulent traits

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31
Q

what happens once L. pneumophila is ingested by a phagocyte

A

is converted to a replicative form
merges with the lysosome and replicates in there because it is a nutrient rich environment

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32
Q

what happens once the amino acids in the lysosome are depleted by L. pneumophila

A

secondary messenger - ppGpp coordinates entry into stationary phase

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33
Q

what does entry into stationary phase for L. pneumonia lead to

A

transmission traits to exit and invade new phagocyte
host cell implodes

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34
Q

features of TB

A

weakly gram negative
strongly acid fast aerobic rod
multi-lobate colony morphology
24-30 hour doubling time

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35
Q

what is unusual about the mycobacterium (i.e. TB) cell wall

A

unusual cell wall lipids
thick layer of mycolic acids

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36
Q

what is mycolic acid composed of

A

polymer sugars
N-acetylglucosamine
amino acids

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37
Q

what is the function of the mycolic acid layer

A

gives resistance to:
biocides
detergents
antibiotics

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38
Q

name some infections caused by mycobacterium

A

TB
leprosy
BCG

39
Q

where do tubercle bacili implant themselves upon inhalation

A

bronchioles
alveoli

40
Q

what occur to the bacili after attachment in the lungs

A

they are engulfed by neutrophils/macrophages

41
Q

what happens to bacili after they are engulfed by phagocytes

A

multiply intracellularly
spread to lymph nodes, blood and distant organs

42
Q

what happens 2 weeks after tubercle bacili multiple and spread

A

forms ghon tubercle:
epithelial cells merge with macrophages forming a granuloma

43
Q

what surrounds Ghon tubercle

A

lymphocytes

44
Q

what happens to the central portion of the ghon tubercle

A

undergoes necrosis
gets a cheesy appearance

45
Q

what is the effect of the necrosis that the ghon tubercle undergoes

A

liquefies and spills into connecting bronchus
forms a cavitvy

46
Q

what are the sites of primary/secondary biofilm infections

A

mouth
subvenous cathether
artificial hip implant

47
Q

what does plaque flora affect and what does it cause

A

teeth:
malodour
tooth decay
gum disease
loss of teeth

48
Q

what are the similarities/differences between H. pylori and E. coli/C. difficile

A

similarities - effect stomach intestine colon
differences:
H. pylori - causes gastric ulcers
others - cause gastroenteritis

49
Q

what does P. aeruginosa affect and what does it cause

A

upper respiratory tract:
cystic fibrosis - death

50
Q

what does streptococci/yeasts/fungi affect and what does it cause

A

heart valves:
endocarditis - death

51
Q

what does gonococci/candida/treponema affect and what does it cause

A

urethral/cervical epithelium:
gonorrhoea
thrush
syphilis
death

52
Q

what does staphylococci/streptococci/baciluss/proteus affect and what does it cause

A

bone:
deep seated abscess
osteomyelitis
septicaemia
death

53
Q

what does dental plaque inflammation lead to

A

gingivitis
periodontal disease

54
Q

what are the physical barriers for dental health

A

keratinized epithelium
mucin production
salivary flow

55
Q

what are the chemical barriers for oral health

A

salivary enzymes
antibacterials
gingival fluid secretions

56
Q

what is a non-chemical/physical oral defence system

A

inflammatory reaction

57
Q

what is caries

A

its a dental disease associated with poor hygiene and high sugar diet
results in holes in teeth

58
Q

what are periodontal diseases

A

it is a non-destructive gingivitis
caused by poor hygiene
leads to inflamed and bleeding gums

59
Q

what is destructive periodontitis

A

usually occurs as people get older
leads to gum and bone loss

60
Q

what are saccharolytics

A

metabolise sucrose and other sugars

61
Q

what are the difference between acidogenic and aciduric

A

acidogenic - ferments to produce lactic/acetic/formic acids to lower pH
aciduric - metabolise and grow at low pH

62
Q

what are the differences between gluco/fructotransferase as a streptococcal virulence factor

A

gluco - EPS glucan/mutan to form biofilm
fructo - EPS frucatn/insulin to form plaque biofilm

63
Q

what are the virulence factors of streptococcal in carious plaque

A

saccharolytics
glucosyltranferase
fructosyltransferase
acidogenics
acidurics

64
Q

features of veillonella

A

gram-negative anaerobic cocci
thrives in the acidic environment of caries
slows down the formation of caries
converts lactic acid to less acidic products

65
Q

features of lactobacillus

A

gram-positive, anaerobic
normally a part of the gut flora
some strains cause carious lesions
its a ‘‘microbial indicator of disease state’’

66
Q

normally spirochetes and fusiform bacilli live in the mouth flora, what happens in the case of fusospicrochetes

A

when there is bleeding in the oral cavity
the bacteria can cause infections and diseases to the oral cavity

67
Q

what are the big 3 responsible for periodontisis

A

T. denticola
P. gingivalis
A. actino…mitans

68
Q

features of treponema denticola

A

gram negative anaerobic
motlie
highly proteolytic
contributes to tissue degradation

69
Q

features of porphyromonas gingivalis

A

gram-negative anaerobic
big factor for periodontitis in adults
produces alot of well known virulence factors

70
Q

features of aggregatibacter actino…mitans

A

gram-negative facultative
non-motile
big factor in adolescent aggressive periodontitis and bone loss

71
Q

outline the virulence factors of A. actino…mitans

A

leukotoxins - kills PNMs and monocytes
cytolethal distending toxin
immunosuppression factors - inhibit blastogenesis, antibody production and activates T-suppressors

72
Q

what is interspecies bacterial cell-cell communication mediated by

A

dihydroxypentaedione (DPD)
autoinducer-2 (AI-2)

73
Q

outline baterial intraspecies cell-cell communication and what does it lead to

A

gram positive bacteria produce small peptides such as: competence stimulating proteins
help promote single species biofilm formation

74
Q

how can periodontal pathogens be prevented from joining the biofilm

A

attachment blockers
detachment signals

75
Q

how does helicobacter pylori colonise the gut and what does it cause

A

penetrates mucin lining
then produces urease to neutralise stomach pH
causes - stomach ulcer and cancers

76
Q

outline attachment of helicobacter pylori to the mucin lining and how it survives

A

survives in the very acidic environment by producing urease - converts urea into basics and buffers
cannot be killed by the immune system

77
Q

outline the effect of toxin production of H. pylori

A

VacA kills cells in the lining of the stomach
decreases competition for nutrients for the bacteria

78
Q

how does H. pylori protect itself from the host immune system

A

invade inner layer of the stomach lining to nest there
kills the cells they invade - creates holes
leads to formation of ulcers

79
Q

functions of TlpA/D

A

TlpA/D - independent acid sensors
TlpD only - meditates attraction towards basic pH

80
Q

function of omeprazole

A

blocks acid production
increases colonisation of glands

81
Q

what can ureolytic activity cause

A

production of ammonia
when close to the gastric epithelium it causes cell damage and inflammation

82
Q

difference between breast-fed and formular-fed babies in terms of gut flora

A

breast-fed - becomes dominated by bifidobacteria
formula - more diverse flora

83
Q

what are the 3 types of enterotypes

A

type 1 - high levels of bacteriodes
type 2 - low levels of bacteriodes but prevotella are common
type 3 - high level of ruminococcus

84
Q

what are the symbiotic benefits of the gut flora

A

ferment unused energy substrates
train immune system
prevent growth of pathogenic bacteria
regulate gut development
produce vitamins - biotin/vitamin K
produce hormones to store fats

85
Q

function of pattern recognition receptors (PRR)

A

allow the intestine to distinguish between pathogenic and commensal bacteria

86
Q

what are the 3 main immunosensory cells in the gut

A

surface enterocytes
M cells
dendritic cells

87
Q

function of toll-like receptors (TLR) in the gut

A

help repair damage due to injury (via radiation)

88
Q

what is nucleotide-binding oligomerisation domain/caspase recruitment domain isoform (NOD/CARD)

A

cytoplasmic proteins that respond to endogenous/microbial molecules or stress
forms oligomers that activate inflammatory caspase

89
Q

what is the result of NOD/CARD performing their funtion

A

inflammatory caspase results in cleavage and subsequent activation of important cytokines and NF-kB signalling pathways
induces inflammatory response

90
Q

what are capsular polysaccharides

A

polysaccharides that provide a mucous-like barrier for the bacteria on its surface

91
Q

what do 2 of the 8 polysaccharides of capsular polysaccharides exhibit

A

a zwitterionic structure
(positive and negative charge on each sugar)

92
Q

difference between T helper 1/2 cells

A

1 - activate cellular arm of the immune system - cytokines, killer T cells, macrophages
2 - activate humoral arm of the immune system - produces B cells

93
Q

outline how the balance between Th1/2 cells can be achieved in germ-free mice

A

introduction of B. fragilis or PSA increased IFNγ to normal levels
reduced Th2 cytokine levels

94
Q

what do Th17 cells produce

A

IL-17
potent inflammatory cytokine
implicated with every known autoimmune disease

Biomed 2 - Season finale (24 decks)

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