RT5 Flashcards
major contributors to pathogenesis of influenza virus
T cell response, interferon induction, desquamation of mucus secreting and ciliated cells
what is antigenic shift
sudden rearrangement of the 8 genetic subunits which results in major changes of HA and NA genes and is responsible for pandemics/epidemics
what is antigenic drift
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)
antigenic shift and drift is seen in which influenza
antigenic drift is seen in all 3 (with C being less frequent)
antigenic shift is only seen in A
how do you diagnose influenza
clinical diagnosis based on symptoms and laboratory diagnosis
anti flu drugs
amantadine, rimantadine, zanamivir, oseltamvir (tamiflu)
how does amantadine and rimantadine work
by inhibiting the uncoating of type A only since its target is the M2 protein
B and C do not have the M2 protein
how does zanamivir and oseltamvir work
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
what happens with constant use of antimicrobials to treat the flu
we start to build drug resistance
do we build acquired immunity to the flu and is it effective
we do but it is weak because the antigen changes constantly
which influenza has an animal reservoir
just A
another name for subacute LRT infection
walking pneumonia, atypical pneumonia
prokaryotes for subacute LRT infection
mycoplasma spp, chlamydia spp, legionella sp, miscellaneous viruses
eukaryotes for subacute LRT infection
usually fungi: histoplasma sp, blastomyces sp, coccoididiodes sp, candida sp
findings in primary atypical pneumonia
low grade lung infection that resolves around 18 days, a little fever but it only lasts a few days
common cause of walking pneumonia/atypical pneumonia/subacute LRT infection
mycoplasma
walking pneumonia with mycoplasma is common in what population
children greater than 5 years old - young adults
clinical syndrome of streptococcus pneumonia
pneumonia, sinusitis, and otitis media
describe strep pneumonia on a blood agar
- 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
commonest cause of community acquired pneumonia
strep pneumonia
what type of infection is strep pneumonia
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
pathogenesis of strep pneumonia
capsule, IgA protease, pneumolysin, autolysin, transformation
TAPIC
properties of pneumolysin
inhibits ciliated epithelial cell activity, cytotoxic for alveolar and endothelial cells, causes inflammation, decreases PMN effectiveness
prevention of strep pneumonia
polyvalent capsular polysaccharide vaccine , 7-valent conjugated vaccine
clinical syndrome of klebsiella pneumonia
bronchopneumonia and lung abscesses
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
pathogenesis of klebsiella pneumonia
it is gram neg so –> release of endotoxin –> necrotizing of lung tissue
diagnosis of klebsiella pneumonia
sputum will have red currant jelly appearance
clinical syndrome of legionella pneumophila and transmission
legionnaires disease (pneumonia) pontiac fever
inhalation of contaminated aerosols (Rare)
general features of legionella pneumophila
gram neg, motile, non spore forming, facultative intracellular (alveolar macs)
pathogenesis of legionella
endotoxin release, proteases, but most important damage is due to host inflammatory response
stain for legionella
its a gram neg bacteria but cannot be picked up by gram stains so must use methylamine
common infection of pseudomonas
otitis externa: swimmer’s ear
pseudomonas is dangerous in what population
persons with structural defects in body defenses like burn victims, cystic fibrosis
pseudomonas on blood agar
it is non hemolytic but produces mucoid colonies
clinical syndrome of pseudomonas and cystic fibrosis
necrotizing bronchial pneumonia
just know permanent highly drug resistant infections are the rule for pseudomonas and cystic fibrosis
OK
clinical syndrome of mycobacterium tuberculosis
tuberculosis
general features of mycobacterium tuberculosis
aerobic, acid fast, bacillus which grows in long, parallel chain called cords
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
transmission of tuberculosis
inhalation of aerosols
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
