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173 Cards in this Set
- Front
- Back
name some common disease manifestations of paramyxoviridae
|
measles
mumps |
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how do paramyxoviridae and orthomyxoviruses differ
|
nature of their genome
stratgey of replication |
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what do paramyxoviruses resemble
|
rhabdoviridae
filoviridae |
|
paramyxoviridae is encased by a fragile -- ----
|
lipid envelope
|
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paramyxoviridae is segmented/nonsegmented w/ ss/ds RNA genome
|
nonsegmented
ss |
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what's para genome separated by
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noncoding termination
polyadenylation initiation signals |
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where does viral replication occur in para
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cytoplasm
|
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para virus attaches to sialoglycoprotein or glycolipid receptor by the ---- ---
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envelope glycoprotein
|
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key to pathogenicity to para
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two membrance glycoproteins
1. H, HN or G 2. F (fusion protein) |
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what allow virus to fuse cells to form the characteristic synctia
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F protein
|
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what enables viral penetration by fusion fo viral envelope w/ plasm membrane
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F protein
|
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what allows intracellular spread by cell-to-cell fusion
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F protein
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the f protein allsw transfer of infectious ------ to adjacent cells while evading the body's circulating antibodies
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nucleocapsids
|
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what inhibits the para infection
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neutralizing antibody that inhibits adsorption of virus to cell receptors
|
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how do F proteins become biologically active
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by cleavage
|
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what immunity does the body have against para virus
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neutralizing antibodies
nonperssive cells to prevent cleavage |
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what always results in clincal manifestations
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measles
|
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measles infection occur via the ---- system to local lymph nodes adn other lymph nodes and ----
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resp
spleen |
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after 6 days what occurs in measles
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viremia
|
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after viremia occurs in measles what occurs
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spread to epithelial surfaces from local blood vessels
|
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what contributes to resp damage, fever, and early symptoms in measles
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the immune systems
|
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s/s of measles
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cough
runny nose inflammed conjunctiva koplik's spots |
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measles infection decreases resistance fo resp epithelium to ---- ------ infections
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secondary bacterial
ex: pneumonia and otitis media |
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types of immunity in measles
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natural
passive live vaccines |
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what's necessary for young adults after receiving the measles during childhood
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booster shot
|
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severity of measles influenced by
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young age
low socioeconomical status malnutrition |
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what should be given w/ the measles vaccine
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vit A
|
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cna diseases in measles
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subacute sclerosing panencephalitis
subacute measles encephalitis acute postinfectious measles encephalitis |
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what occurs years after the disease and is fatal
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subacute sclerosing panencephalitis
|
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what cns occurs in immunocompromised kids
this occurs cuz the body fails to eliminate the virus infected cells cuz lack of cytotoxic T cells |
subacute measles encephalitis
|
|
most dangerous cns disease of measles; 15% case fatality
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acute postinfectious measles encephalitis
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how is mumps transmitted
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saliva
other resp fluids |
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clincal features of mumps
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distorted face
enlargement of salivary glands |
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how is mumps presented in kids
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asymptomatic
resp infection |
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mumps encephalitis may result in unilateral ----
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deafness
|
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----- provides protective levels of antibody by a single injection for at least 90% injected over a --- year period
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MMR
20 |
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due to vaccine the incidence of mumps has dropped ---%
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98
|
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genus of rhabdoviridae
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lyssavirus rabies
|
|
vesiculovirus complication
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vesicular stomatitis indiana virus
|
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what's transmissible to humans from vesicular fluids and tissue of infected animals
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vesicular stomatits indiana virus
|
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how long does it take to resolve the vesicular stomatitis indiana virus
what type of complications? |
7-10 days
no complications; resembles flu |
|
mononegavirales
nonsegmented/segmented negative/positive sense single/double stranded infectious/noninfectious rna genomne |
non-segmented
negative sense single stranded noninfectious rna genome |
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what type of nuclecapsid does the mononegavirales have
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helical
|
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significance of having negative sense
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can't go inside cells and act directly as mRNA
it need to make it's own machinery |
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monomegavirales has what type of polymerase
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virion-associated rna-dependent rna
|
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what type of promoter does monomegavirales have
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single 3' promoter
|
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what order is rabies, measles, mumps
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monomegavirales
|
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what typeof lipids do mononegavirues have
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glycoprotein G
|
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t/f
rabies can infect all animals |
f
all warm blooded animals |
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rabies causes ----, contagious infection of the ----- system
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acute
nervous |
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how fatal is rabies
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100% once commence
|
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where doesn't rabies occur
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hawaii
japan great britain smaller islands |
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principles rabies host are
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wild carnivores
bats |
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transmission from animals occurs how
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bite or scratch
thru skin or mucous membranes |
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------ transmission a bat
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aerosol
|
|
rare way to transmit rabies
|
tissue transplant
|
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when the rabies virus enters the body it travels w/in the ----
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neurons to the CNS
|
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what can be causes inside the brain due to rabies
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encephalitis
|
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once the virus is in the brain what occurs
|
it travels to multiple organs
|
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what glands are the most importaant in the spread of rabies from animal to human
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salivary glands
|
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what's the incubation period once infected
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14-90 days
|
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early symptoms are
|
nonspecific
fever HaA general malaise |
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as rabies disease progresses s/s include
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insomnia
anxiety confusion paralysis hallucinations hypersalivation difficulty swallowing hydrophobia |
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what come last in rabies
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delirium
coma death |
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dx of rabies
|
direct flurorescent antibody test using brain tissue
|
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rabies test for humans
where do you test |
RT-PCR immunofluorescence assays
serum skin biopsy spinal fluid saliva |
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what does the PT-PCR detect
|
rabies antigen
antibody |
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most definative means of dx of rabies
|
virus cultivation
|
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once innoculation of saliva, ---- gland, and ---- tissue death is w/in --- days.
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salivary
brain |
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the only disease that can be prevented by postexposure vaccination
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rabies
|
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the incubation period of rabies is long and the incubation period for rabies is accessible to -----
|
antibody
|
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what should be done after bitten
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cleansing of wound
|
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how many doses of HDCV is given
on which days |
5 doses
0, 3, 7, 14, 28 days |
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tx for rabies should be before ------- to reduce mortalitiy to 100% to 0
|
onset of symptoms
|
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shape of rotavirus
|
wheel shaped
|
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what type of capsids surround the inner core of the rotavirus
|
concentric icosahedral
|
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rotavirus is double/single stranded RNA
|
double
|
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how many segments in the RNA
|
11
|
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does the rotavirus have an envelope
|
no
|
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what serotype of rotavirus most common
|
Group A
|
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where does the rotavirus replicate
|
cytoplasm
|
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where receptors does the rotavirus bind to
|
sialic acid recpetors on cell via VP4
|
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after rotavirus enters the cells what occurs
|
cell lysis
|
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what occurs w/ the rotavirus between species w/ each genus
|
gene reassortment
|
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what cells do rotavirus infect and what does it do to them
|
intestinal cells
kills them |
|
which is mose severe initial infection or subsequent
|
1st
|
|
what causes diarrhea in rota
|
absorptive surface of intestine reduced
fluid accumulation in the lumen |
|
is the disease self limiting
|
yes
|
|
what type of probs occur due to rota
|
dehydration
|
|
t/f
maternal protection of rotavirus possible |
f
no protection w/ maternal IgG |
|
what from the mom is protective
|
IgA in colostrum
so breastfeed! |
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what Ig's does rota stimulate
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IgA
neutralizing IgG |
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is there significant immunity againt reinfection
|
no
|
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what route is rota transmitted
|
fecal-oral route
daycare! |
|
rota can survive for ---- to --- on toys, countertops
|
hours
days |
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what from the mom is protective
|
IgA in colostrum
so breastfeed! |
|
what Ig's does rota stimulate
|
IgA
neutralizing IgG |
|
is there significant immunity againt reinfection
|
no
|
|
what route is rota transmitted
|
fecal-oral route
daycare! |
|
rota can survive for ---- to --- on toys, countertops
|
hours
days |
|
other areas of outbreaks of rota
|
nosocomial
hospitals nurseries |
|
incubation period of rota
|
1-3 days
it's very fast |
|
s/s of rota
|
may be asymptomatic
fever vomiting non-bloody watery diarrhea |
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fatalites of rota due to
|
dehydration
electrolyte imbalance |
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dx of rota
|
immunolgoical assay
ELISA ELFA detect viral capsid protein |
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how do you see shape of rota
|
microscopy
|
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tx of rota
|
oral rehydration: glucose, water, electrolyes
IV replacement |
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most common cause of gastroenteritis in young kids
|
group A rotavirus
|
|
ages for rota
|
6 months to 24 months
|
|
where is rota a year round disease
|
tropics
|
|
in temperate countries when is the peak for rota
|
winter
|
|
t/f
almost all children infected w/ rota by the age of 4 |
t
|
|
prevention of rota
|
good hygene
chemical disinfectant: bleach breast feeding vaccination |
|
t/f
alchol sanitizer should be used for rota |
f
doesn't work uses soap and water |
|
vaccine for rota
|
rotashield
give at 2, 4, 6 months in develping countries |
|
new rota vaccine
|
rota teq
different serotypes: g1. 2, 3, 4, P |
|
problem of rotashiled
|
blockage of intestine: intussusception
|
|
3 syndromes of flu virus
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1. uncomplicated rhinotracheitis: URI
2. respiratory viral infection follwoed by bact pneumonia 3. viral pneumonia |
|
t/f
more people die of flu than hiv in the us |
t
|
|
w/ the flu the --- is damaged so mucous can't get out
|
cilia
|
|
what essential for prevention of URI
|
secretory IgA
|
|
what essential to prevent lung infection
|
systemic antibody
|
|
what's essential for recovery in the URI and Lung
|
cell mediated immunity
|
|
amantadine adn rimantadine are ----- channel blockers which inhibit replication of the flu virus by targeting -- protein which destablizes --
|
ion
M2 HA |
|
amantadine block the acidifiction of ---- whcih inhibits the fusion of HA w/ the endosome
|
endosome
|
|
w/ amantadiene and rimantadine -- is also blocked from proper conformational insertion in the cell membrane
|
HA
|
|
what activates the M2 channels
|
low pH
|
|
what allow the protein to change conformation
|
acid
|
|
tamiflu is a ----- inhibitor
|
neuraminidase
|
|
tamiflu is designed to attack to structure of the flu viruses -- and -- preventing spread of the virus w/in the body
|
A
B |
|
how does flu get out of the cell
|
using neuramidase
|
|
good way to prevent spread to virus from cell
|
tamiflu
|
|
antibody + virus =
|
neutralization
|
|
what type of icosahedral does picornaviruses have
|
naked
|
|
piconarviruses
single/double stranded what type of sense RNA? |
single
plus sense |
|
where does teh piconavirus replicate
|
cytoplasm
|
|
how many capsid proteins does poliovirus have
|
4:
VP1: pentamers VP2 and 3: hexamer VP4: maturation protein associated w/ attachment |
|
which polio capsid protein has a maturation protein associated w/ attachment
|
VP4
|
|
which polio capsid has hexamer
|
VP2
VP 3 |
|
name some picornaviruses
|
enteroviruses: polio
rhinoviruses |
|
polio is internalized in certain ----
|
vesicles
|
|
polio is adsorbed to specific/nonspecific receptors
|
specific
|
|
how are the hydrophobic groups on the polio virus exposed
|
by lowering the pH
|
|
comlications of polio
|
meningitis
encephalitis myocarditis |
|
what type of polio vaccine should be given
|
inactivated
|
|
problems w/ polio vaccines
|
reversion of serotype 3 to virulence
virus not killed |
|
three serotypes of polio vaccine
|
P1
P2 P3 |
|
how many polio vaccines recommened
|
3 immunizations
|
|
s/s of people who survived polio
|
muslce weakness
paralysis fatigue |
|
what occured due to polio
|
degeneration of nerves
|
|
t/f
no virus has been isolated in post polio |
t
|
|
condition that can strike polio survivors 10-40 yrs after their recovery.
|
post polio syndrome (pps)
|
|
s/s of PPS
|
muscle weakness
muscle and joint pain muscular atrophy |
|
cause of pps
|
death of individual nerve terminals in the motor units that remain after the initial polio attack
|
|
what's the cure for pps
|
no cure
symptoms tx |
|
pps occurs cuz denegeneration of nerves as you ---
|
age
|
|
why is zinc beneficial agaist viruses
|
blocks pore so they can't get in
|
|
more common viral or bacterial meningitis
|
viral
|
|
t/f
aseptic meningitis is bacterial |
F
it's viral |
|
t/f
clear CSF is bacterial meningitis |
f
viral |
|
some causes of viral meningitis
|
mumps
measles enteroviruses: coxsackie B, coxsackie A7 and A9, poliovirus herpes simplex virus |
|
how is viral meningitis spread
|
coughing
sneezing poor hygiene |
|
viral menin can be found in ---- polluted water
|
sewage
|
|
incubation of viral menin
|
up to 3 weeks
|
|
t/f
viral menin needs an md |
no, not in all cases
|
|
t/f
antibiotics are best tx for viral menin |
f
|
|
severe cases can cause permanent neuro defects such as
|
seizures
motor abnormalities mental retardation |
|
name some enteroviruses
|
poliovirus
coxsackie A coxsackie B ECHO enterovirus |
|
which replicates in the heart
|
coxsackie B
adenovirus |
|
pH in which enteroviruses are stable
|
pH 3
so can survive passage thru the stomach, spread thru fecal oral route (bad hygiene!) |
|
where do enteroviruses multiply
|
cytoplasm
|
|
enteroviruses produce a large precursor protein that undergoes ---- ---- cleavage
|
post translational
|
|
drugs that may be beneficial against viruses
|
amantidine
rimantadine relenza GS 4104 |