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40 Cards in this Set

  • Front
  • Back
how many people are given prophylaxis for poss rabies infections in the US each year
16,000 to 40,000
structure and genome of Rabies
bullet shaped Rhabdovirus
ssRNA
clinical manifestations of rabies
fatal once symptoms are overt
2 week to 2 year incubation
Prodrome- fever, pharyngitis, sensations referred to bite site
excititory phase- anxiety, apprehension, hydrophobia
paralytic phase- coma, hypertension, death
what is a diagnostic feature of a rabies infection
Negri bodies
how does rabies get to the CNS
replication at the bite site
enters peripheral nerves
retrograde xport to limbic region of brain
what is the host range for rabies
all mammals
what are the typical reservoirs for rabies in the US
Bats
raccoons
skunks
foxes
coyote
is rabies transmitted via bite only
no,
aerosolized xmission doccumented in bat caves

only req exposure of mucous membrane to saliva of infected animals

8 cases of corneal xplants documented
how do you control rabies
vaccinate your animals
vaccine baiting programs
pre-exposure prophylaxis
rabies diagnosis
regard all wild animals as rabid unless proven otherwise
direct flourescent Ab test
RT-PCR
cytoplasmic inclusions- Negri body
animal innoculation
what is the post-exposure prophylaxis for rabies
Human Rabies ImmunoGlobulin (HRIG)
-half in the wound, half in the butt
AND
Human Diploid Cell vaccine (HDCV)
-deltoid, 5 shots over 3-4 weeks
what is the most common cause of sporadic, fatal encephalitis in the US
HSV 1 & 2

mostly type 1
who is predominantly effected by HSV 2 encephalitis
neonates

passed on from the mother who has an active infection during birth
who is most likely to get HSV encephalitis
<18
>50
what area of the brain is effected by HSE
frontal and temporal lobes
what is the result of an HSE
High fatality
those treated early still suffer neurological deficits
very small percentage recover completely
diagnosis of HSE
EEG or MRI
followed by brain biopsy
- Tzanck smear (FA)
- PCR
Treatment of HSE
Acyclovir
what are the 4 known human prion diseases
Kuru
CJD
Gerstmann-Straussler-Scheinker
fatal familial insomnia
what are the clinical symptoms of Kuru
ataxia
dimentia
choreiform movements
fatal in 3 to 15 months
what is Kuru named for
a tribe in papua New Guinea where it was discovered
kuru means trembling from fear
what is the incubation period of kuru
4 to 30 years
who does CJD effect
people in their 60s and 70s
what does CJD present as?
dimentia
ataxia
seizures

just like kuru
what is the incubation period for CJD
15 to 20 months
what are the inherited prion diseases
G,S,S disease
fatal familial insomnia
what is the only known component of infectious prion particles
PrPsc
what are prions resistant to
UV
EtOH
formalin
boiling
what inactivates proins
Na hypochlorite
NaOH
extended autoclaving
what conformational change do infectious prion particles induce
switching a-helices to B-sheets
what happens in the CNS with prion diseases
spongiform encephalopathy
astrocyte gliosis (brain scar tissue)

sometimes amyloid plaques
what are the 3 forms of prion disease
inherited
sporadic (most cases. usually elderly)
infectious (direct innoculation of PrPsc)
how do you get the infectious form of a prion disease
ingestion of infected neuronal tissue
corneal xplants
human pituitary growth hormone
improperly sterilized neurological equipment
what is different about vCJD
substantially younger population affected
core amyloid deposits with a halo of spongiform deposits surrounding

hypothesized to have arisen from BSE
how are we working on preventing vCJD
attempting to detect and quantify BSE in cattle before they enter the food chain
restrictions on blood donations for likely suspects
banning MBM feeding
prohibition of human consumption of neurologic material
tonsilar screening in the UK
what is the estimated incubation period of vCJD
up to 50 yrs
what is subacute sclerosing panencephalitis (SSPE)
a rare, slowly progressing demyelinating disease (lymphocytic infiltration and destruction of neuronal cells)

occurs 2 to 10- years after a measles infection
what is progressive multifocal leukoencephalopathy
subacute, progressive, demyelinating disease
undelying immune disorder that allows for the activation of latent JC virus
causes the lysis of oligodendricytes
increased with the advent of AIDS
MS
demyelinating disease that produces patchy white lesions

sugested viral etiology
HIV mediated neurologic infection
40 - 60% of AIDS pts are symptomatic for CNS disease
similar to alzheimers disease progression
destruction of neural cells is probably an indirect effect of abnormal viral V1&2 proteins and gp120, macrophage and microglial cytokine secretions all neurotoxic