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
Q

clinical syndrome of klebsiella pneumonia

A

bronchopneumonia and lung abscesses

26
Q

general features of klebsiella pneumonia

A
  • 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
Q

pathogenesis of klebsiella pneumonia

A

it is gram neg so –> release of endotoxin –> necrotizing of lung tissue

28
Q

diagnosis of klebsiella pneumonia

A

sputum will have red currant jelly appearance

29
Q

clinical syndrome of legionella pneumophila and transmission

A
legionnaires disease (pneumonia)
pontiac fever

inhalation of contaminated aerosols (Rare)

30
Q

general features of legionella pneumophila

A

gram neg, motile, non spore forming, facultative intracellular (alveolar macs)

31
Q

pathogenesis of legionella

A

endotoxin release, proteases, but most important damage is due to host inflammatory response

32
Q

stain for legionella

A

its a gram neg bacteria but cannot be picked up by gram stains so must use methylamine

33
Q

common infection of pseudomonas

A

otitis externa: swimmer’s ear

34
Q

pseudomonas is dangerous in what population

A

persons with structural defects in body defenses like burn victims, cystic fibrosis

35
Q

pseudomonas on blood agar

A

it is non hemolytic but produces mucoid colonies

36
Q

clinical syndrome of pseudomonas and cystic fibrosis

A

necrotizing bronchial pneumonia

37
Q

just know permanent highly drug resistant infections are the rule for pseudomonas and cystic fibrosis

A

OK

38
Q

clinical syndrome of mycobacterium tuberculosis

A

tuberculosis

39
Q

general features of mycobacterium tuberculosis

A

aerobic, acid fast, bacillus which grows in long, parallel chain called cords

40
Q

structure of mycobacterium tuberculosis

A

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
Q

transmission of tuberculosis

A

inhalation of aerosols

42
Q

resistance to TB is dependent on

A

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