- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
PLAY BUTTON
PLAY BUTTON
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 |
