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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
what are pilin genes required for
attachment to host cells and biofilms intracellular growth
26
what is type IV secretion icm/dot complex and what is required for it
membrane spanning translocates effector molecules into host cells requires ATPase DotB
27
what do DotA/B mutants still infect
A. castellani
28
name the virulence determinants for invasion and growth
flagella expression type IV secretion pilin genes macrophage infectivity protein (Mip) KatA/KatB
29
where are KatA/B located
KatA - periplasm KaB - cytosol
30
what happens when L. pneumophila converts to replicative form
it is acid tolerant stops expressing virulent traits
31
what happens once L. pneumophila is ingested by a phagocyte
is converted to a replicative form merges with the lysosome and replicates in there because it is a nutrient rich environment
32
what happens once the amino acids in the lysosome are depleted by L. pneumophila
secondary messenger - ppGpp coordinates entry into stationary phase
33
what does entry into stationary phase for L. pneumonia lead to
transmission traits to exit and invade new phagocyte host cell implodes
34
features of TB
weakly gram negative strongly acid fast aerobic rod multi-lobate colony morphology 24-30 hour doubling time
35
what is unusual about the mycobacterium (i.e. TB) cell wall
unusual cell wall lipids thick layer of mycolic acids
36
what is mycolic acid composed of
polymer sugars N-acetylglucosamine amino acids
37
what is the function of the mycolic acid layer
gives resistance to: biocides detergents antibiotics
38
name some infections caused by mycobacterium
TB leprosy BCG
39
where do tubercle bacili implant themselves upon inhalation
bronchioles alveoli
40
what occur to the bacili after attachment in the lungs
they are engulfed by neutrophils/macrophages
41
what happens to bacili after they are engulfed by phagocytes
multiply intracellularly spread to lymph nodes, blood and distant organs
42
what happens 2 weeks after tubercle bacili multiple and spread
forms ghon tubercle: epithelial cells merge with macrophages forming a granuloma
43
what surrounds Ghon tubercle
lymphocytes
44
what happens to the central portion of the ghon tubercle
undergoes necrosis gets a cheesy appearance
45
what is the effect of the necrosis that the ghon tubercle undergoes
liquefies and spills into connecting bronchus forms a cavitvy
46
what are the sites of primary/secondary biofilm infections
mouth subvenous cathether artificial hip implant
47
what does plaque flora affect and what does it cause
teeth: malodour tooth decay gum disease loss of teeth
48
what are the similarities/differences between H. pylori and E. coli/C. difficile
similarities - effect stomach intestine colon differences: H. pylori - causes gastric ulcers others - cause gastroenteritis
49
what does P. aeruginosa affect and what does it cause
upper respiratory tract: cystic fibrosis - death
50
what does streptococci/yeasts/fungi affect and what does it cause
heart valves: endocarditis - death
51
what does gonococci/candida/treponema affect and what does it cause
urethral/cervical epithelium: gonorrhoea thrush syphilis death
52
what does staphylococci/streptococci/baciluss/proteus affect and what does it cause
bone: deep seated abscess osteomyelitis septicaemia death
53
what does dental plaque inflammation lead to
gingivitis periodontal disease
54
what are the physical barriers for dental health
keratinized epithelium mucin production salivary flow
55
what are the chemical barriers for oral health
salivary enzymes antibacterials gingival fluid secretions
56
what is a non-chemical/physical oral defence system
inflammatory reaction
57
what is caries
its a dental disease associated with poor hygiene and high sugar diet results in holes in teeth
58
what are periodontal diseases
it is a non-destructive gingivitis caused by poor hygiene leads to inflamed and bleeding gums
59
what is destructive periodontitis
usually occurs as people get older leads to gum and bone loss
60
what are saccharolytics
metabolise sucrose and other sugars
61
what are the difference between acidogenic and aciduric
acidogenic - ferments to produce lactic/acetic/formic acids to lower pH aciduric - metabolise and grow at low pH
62
what are the differences between gluco/fructotransferase as a streptococcal virulence factor
gluco - EPS glucan/mutan to form biofilm fructo - EPS frucatn/insulin to form plaque biofilm
63
what are the virulence factors of streptococcal in carious plaque
saccharolytics glucosyltranferase fructosyltransferase acidogenics acidurics
64
features of veillonella
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
features of lactobacillus
gram-positive, anaerobic normally a part of the gut flora some strains cause carious lesions its a ''microbial indicator of disease state''
66
normally spirochetes and fusiform bacilli live in the mouth flora, what happens in the case of fusospicrochetes
when there is bleeding in the oral cavity the bacteria can cause infections and diseases to the oral cavity
67
what are the big 3 responsible for periodontisis
T. denticola P. gingivalis A. actino...mitans
68
features of treponema denticola
gram negative anaerobic motlie highly proteolytic contributes to tissue degradation
69
features of porphyromonas gingivalis
gram-negative anaerobic big factor for periodontitis in adults produces alot of well known virulence factors
70
features of aggregatibacter actino...mitans
gram-negative facultative non-motile big factor in adolescent aggressive periodontitis and bone loss
71
outline the virulence factors of A. actino...mitans
leukotoxins - kills PNMs and monocytes cytolethal distending toxin immunosuppression factors - inhibit blastogenesis, antibody production and activates T-suppressors
72
what is interspecies bacterial cell-cell communication mediated by
dihydroxypentaedione (DPD) autoinducer-2 (AI-2)
73
outline baterial intraspecies cell-cell communication and what does it lead to
gram positive bacteria produce small peptides such as: competence stimulating proteins help promote single species biofilm formation
74
how can periodontal pathogens be prevented from joining the biofilm
attachment blockers detachment signals
75
how does helicobacter pylori colonise the gut and what does it cause
penetrates mucin lining then produces urease to neutralise stomach pH causes - stomach ulcer and cancers
76
outline attachment of helicobacter pylori to the mucin lining and how it survives
survives in the very acidic environment by producing urease - converts urea into basics and buffers cannot be killed by the immune system
77
outline the effect of toxin production of H. pylori
VacA kills cells in the lining of the stomach decreases competition for nutrients for the bacteria
78
how does H. pylori protect itself from the host immune system
invade inner layer of the stomach lining to nest there kills the cells they invade - creates holes leads to formation of ulcers
79
functions of TlpA/D
TlpA/D - independent acid sensors TlpD only - meditates attraction towards basic pH
80
function of omeprazole
blocks acid production increases colonisation of glands
81
what can ureolytic activity cause
production of ammonia when close to the gastric epithelium it causes cell damage and inflammation
82
difference between breast-fed and formular-fed babies in terms of gut flora
breast-fed - becomes dominated by bifidobacteria formula - more diverse flora
83
what are the 3 types of enterotypes
type 1 - high levels of bacteriodes type 2 - low levels of bacteriodes but prevotella are common type 3 - high level of ruminococcus
84
what are the symbiotic benefits of the gut flora
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
function of pattern recognition receptors (PRR)
allow the intestine to distinguish between pathogenic and commensal bacteria
86
what are the 3 main immunosensory cells in the gut
surface enterocytes M cells dendritic cells
87
function of toll-like receptors (TLR) in the gut
help repair damage due to injury (via radiation)
88
what is nucleotide-binding oligomerisation domain/caspase recruitment domain isoform (NOD/CARD)
cytoplasmic proteins that respond to endogenous/microbial molecules or stress forms oligomers that activate inflammatory caspase
89
what is the result of NOD/CARD performing their funtion
inflammatory caspase results in cleavage and subsequent activation of important cytokines and NF-kB signalling pathways induces inflammatory response
90
what are capsular polysaccharides
polysaccharides that provide a mucous-like barrier for the bacteria on its surface
91
what do 2 of the 8 polysaccharides of capsular polysaccharides exhibit
a zwitterionic structure (positive and negative charge on each sugar)
92
difference between T helper 1/2 cells
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
outline how the balance between Th1/2 cells can be achieved in germ-free mice
introduction of B. fragilis or PSA increased IFNγ to normal levels reduced Th2 cytokine levels
94
what do Th17 cells produce
IL-17 potent inflammatory cytokine implicated with every known autoimmune disease

Biomed 2 - Season finale (24 decks)

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