RT5 Flashcards

1
Q

major contributors to pathogenesis of influenza virus

A

T cell response, interferon induction, desquamation of mucus secreting and ciliated cells

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2
Q

what is antigenic shift

A

sudden rearrangement of the 8 genetic subunits which results in major changes of HA and NA genes and is responsible for pandemics/epidemics

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3
Q

what is antigenic drift

A

gradual accumulation of point mutations in genes encoding HA and NA leading to gradual loss of stereospecificity of the Ag-Ab bond (most impo in HA because effect of neutralizing Ab is lost)

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4
Q

antigenic shift and drift is seen in which influenza

A

antigenic drift is seen in all 3 (with C being less frequent)

antigenic shift is only seen in A

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5
Q

how do you diagnose influenza

A

clinical diagnosis based on symptoms and laboratory diagnosis

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6
Q

anti flu drugs

A

amantadine, rimantadine, zanamivir, oseltamvir (tamiflu)

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7
Q

how does amantadine and rimantadine work

A

by inhibiting the uncoating of type A only since its target is the M2 protein

B and C do not have the M2 protein

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8
Q

how does zanamivir and oseltamvir work

A

inhibits neuraminidase – hence forcing virus to bind to its own sialic acid and form useless clump

essentially virus will not be released from the cell in Type A and B only since C does not have NA

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9
Q

what happens with constant use of antimicrobials to treat the flu

A

we start to build drug resistance

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10
Q

do we build acquired immunity to the flu and is it effective

A

we do but it is weak because the antigen changes constantly

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11
Q

which influenza has an animal reservoir

A

just A

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12
Q

another name for subacute LRT infection

A

walking pneumonia, atypical pneumonia

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13
Q

prokaryotes for subacute LRT infection

A

mycoplasma spp, chlamydia spp, legionella sp, miscellaneous viruses

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14
Q

eukaryotes for subacute LRT infection

A

usually fungi: histoplasma sp, blastomyces sp, coccoididiodes sp, candida sp

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15
Q

findings in primary atypical pneumonia

A

low grade lung infection that resolves around 18 days, a little fever but it only lasts a few days

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16
Q

common cause of walking pneumonia/atypical pneumonia/subacute LRT infection

A

mycoplasma

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17
Q

walking pneumonia with mycoplasma is common in what population

A

children greater than 5 years old - young adults

18
Q

clinical syndrome of streptococcus pneumonia

A

pneumonia, sinusitis, and otitis media

19
Q

describe strep pneumonia on a blood agar

A
  • sensitive to optochin (P disk)
  • does alpha hemolysis which involves a change in the redox potential of RBCs making it less red which is not as transparent as s. pyogenes that does beta hemolysis
20
Q

commonest cause of community acquired pneumonia

A

strep pneumonia

21
Q

what type of infection is strep pneumonia

A

it is both exogenous and endogenous
endogenous - it is within us to start with already
exogenous - if we pass ours to another human it becomes exogenous

22
Q

pathogenesis of strep pneumonia

A

capsule, IgA protease, pneumolysin, autolysin, transformation

TAPIC

23
Q

properties of pneumolysin

A

inhibits ciliated epithelial cell activity, cytotoxic for alveolar and endothelial cells, causes inflammation, decreases PMN effectiveness

24
Q

prevention of strep pneumonia

A

polyvalent capsular polysaccharide vaccine , 7-valent conjugated vaccine

25
clinical syndrome of klebsiella pneumonia
bronchopneumonia and lung abscesses
26
general features of klebsiella pneumonia
- non motile, gram neg bacillus with a large capsule that has smooth/mucoid appearance - part of normal flora - uses aerobactin and enterochelin to uptake iron from host
27
pathogenesis of klebsiella pneumonia
it is gram neg so --> release of endotoxin --> necrotizing of lung tissue
28
diagnosis of klebsiella pneumonia
sputum will have red currant jelly appearance
29
clinical syndrome of legionella pneumophila and transmission
``` legionnaires disease (pneumonia) pontiac fever ``` inhalation of contaminated aerosols (Rare)
30
general features of legionella pneumophila
gram neg, motile, non spore forming, facultative intracellular (alveolar macs)
31
pathogenesis of legionella
endotoxin release, proteases, but most important damage is due to host inflammatory response
32
stain for legionella
its a gram neg bacteria but cannot be picked up by gram stains so must use methylamine
33
common infection of pseudomonas
otitis externa: swimmer's ear
34
pseudomonas is dangerous in what population
persons with structural defects in body defenses like burn victims, cystic fibrosis
35
pseudomonas on blood agar
it is non hemolytic but produces mucoid colonies
36
clinical syndrome of pseudomonas and cystic fibrosis
necrotizing bronchial pneumonia
37
just know permanent highly drug resistant infections are the rule for pseudomonas and cystic fibrosis
OK
38
clinical syndrome of mycobacterium tuberculosis
tuberculosis
39
general features of mycobacterium tuberculosis
aerobic, acid fast, bacillus which grows in long, parallel chain called cords
40
structure of mycobacterium tuberculosis
PG which is rich in mycolic acid which makes bacteria grow slowly, resist detergent, and is hydrophobic LAM (lipoarabinomannan) is equivalent to O antigen on LPS in that it induces cytokine release, suppresses T cell proliferation, and inhibits activation of macrophages by IFNgamma
41
transmission of tuberculosis
inhalation of aerosols
42
resistance to TB is dependent on
subset of CD4+ helper T cells that produce α- interferon | so people with AIDs are more susceptible because they have a low CD4+ T cells