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ANSC 375 mt 2 > TSE pt 1 > Flashcards

TSE pt 1 Flashcards

1
Q

TSE definition

A

transmissible spongiform encephalopathies
-family of human and animal diseases characterized by spongy deterioration of the brain w sever and fatal neurological signs and symptoms
-no cure

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2
Q

TSE theories

A
  1. virus
    2.prion
    3.virin
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3
Q

TSE virus theory

A

-virus w unusual biochemical and biophysical characteristics

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4
Q

prion theories

A

-exclusively produce host protein which is protease resistant
- prion catalyze further modifications in other PrPc
-no non host involved components of the agent

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5
Q

virino theory

A

-host derived protein coat (PrPc) and small non coding regulatory nucleic acid

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6
Q

Prions definition

A

-defined by transmission and involvement of neurodegeneration by abnormal form of prion protein
-most accepted theory- group of diseases caused by same type of infectious agent: prion

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7
Q

prion mechanism

A

-miss folding and cyclic amplification of PrPc –> PrPTSE
-autocatalytic: agragates and difficult to degrade
-forms plaques

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8
Q

what does TSE resemble

A

-alzheimers
-parkinsons
-huntingtons
-glyocosylphosphatidylinositol anchor

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9
Q

PrP^TSE survivability

A

-resistant to all but the strongest solvents
-highly resistant: proteases, sunlight, heat, normal sterilization process
-survives: in tissue preserved w formalin
-no readily available detectable immune responses

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10
Q

PrP^c fxns on organs

A

1.neurons
2.neural and hematopoetic stem cells
3.T cells: activation
4. other leukocytes

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11
Q

PrP^c neuron fxns

A

adhesion and signalling (intracell)
-growth facotrs of synapses
-survival: pro and anti apoptosis
-copper binding: presynaptic membrane and during oxidative stress

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12
Q

PrP^c neural/hematopoetic

A

-increases cell proliferation in neuron rich regions
-targets stem cells to appropriate area for differentiation (co-receptor)

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13
Q

PrP^c T cell function

A

copper binding in thymus

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14
Q

PrP^c other leukocyte functions

A

-expressed on monocyte/lymphocyte lineages
-enhances leukocyte homing to inflammation (possibly bad)
-modulates phagocytosis

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15
Q

Theories for neurotoxicity of PrP^TSE

A
  1. if PrP^TSE anchored= neurotoxic
  2. a metabolite of PrP^c to PrP^TSE has negative effect on neuronal membranes
  3. loss of normal PrP^c fxn: induce neuron injury wo presence of PrP^TSE (disproven)
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16
Q

tissue tropism

A

-nervous tissue: peripheral and central
-lymphoid tissue: primary and secondary

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17
Q

TSE transmission

A

-oral uptake
-increase in ileum and other lyphoid tissue replicates prions and other increased infectivity = antigen presenting cells and tissue stromal cells in lymph nodes and spleen
-compliment receptors: on dendritic cells help uptake prions
-B and T cells: uptake help transport to other areas of the body (lymphoid)
-B cells: cytokine profiles to help mature and increase activity of antigen presenting
-ANS innervates lymphoid tissue = location for transport from lymphoid system to nervous system

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18
Q

tse inflammation

A

-inflammatory disease model
-rheumatoid arthritis
-type 1 diabetes
-hashimotos disease
-mastitis sheep: scrapies
-mice nephritis: urine

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19
Q

tse injury

A

-cns spongiform vacuolation and neuronal cell, microglial activation, and astrocyte proliferation

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20
Q

tse type of pathogen

A

-primary pathogen can have less or more virulence (based on strain and host susceptibility)

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21
Q

tse hallmark

A

-prolonged incubation: months-yrs
-progressive neurological illness: 100% mortality

22
Q

tse symptoms

A

-presence of scrapie assoc fibrils: nerual PcP^TSE plaques
-brain: vacuolation, astrocytosis
-rare to no inflammatory and immune response in the brain

23
Q

human TSE diseases

A

-kuru
-creutzfeldt-jakob disease
-variant of CJD (vCJD)
-gerstmann-straussler-scheinker syndrome
-fatal familial insomnia
-tse: spongiform vacuolation and neruonal cell, microglial activation and astrocyte proliferation

24
Q

Kuru

A

-new guinnea
-over 10 yrs process
-1.1k ppl dead
-long incubation period(10.3- 13.2 yr) some students siuggested 50+ yrs

25
kuru cause
-theorized: ritual eating of body parts: in particular brain: seen in women, children and elderly (primary consumer of nervous tissue)
26
CJD
-uncommon disease: sporadic
27
CJD onset
-older than 65yrs -1-2/10^6 ppl per year or 1000-2000/10^9 ppl per year -death: 3-12months gollowing onset of symptoms -dementia and myoclonus "jerky motion"
28
CJD types
1. spontaneous: 85% 2. genetic: 10-15% 3.iatrogenic: <1%
29
nvCJD effects
-vacuolation of neurons and large plaque like aggragates of prion protein -new neuropathologican epidemiology
30
nvCJD onset
-death: 28yr old -duration: 13-14 months -occured in UK and france
31
nvCJD cause
-ppl exposed to offal and meat infected by BSE
32
animal tse
-bovine: BSE (mad cow) -sheep: scrapie -wild ruminants: chronic wasting disease -mink: mink spongiform encephalopathy -cats: feline spongiform encephalopathy- same strain as BSE -others given experimentally: feeding PrP^TSE to animals
33
BSE causes
-improper rendering of cattle prodcuts to reduce costs (removal of solvent extraction that included steam-heat treatment
34
BSEtimeline
-UK:1986 -1988: UK bans meant and bone meal from ruminants in cattle feed -1989: USDA bans importation from countries w BSE -1993: peak of BSE in UK: 1k new cases reported weekly and new cases steadily deacreased 2002: 1144 -until 1998: 170k cases since first discovered in UK
35
BSE transmission
-cattle fed rendered sheep products -an animal (cow) underwent spontaneous PrPc mutation and was rendered and then fed back to cattle -maternal transmission: uncommon but unsure if its transmission or genetic effects
36
BSE control countries
-1997: US and Canada ban ruminant products fed back to ruminants -EU: proactive/ reactive- all animals over 30 months tested for BSE
37
BSE alberta
-may 2003: 6yr old angus diagnosed w BSE = 2700 cattle slaughtered -recent case: AB feb 2015
38
BSE alberta costs
-may 2003-2005: $4/06b -from extra processing costs, reduced live animal export, reduced beef and veal products, reduced byproducts export and reduced imports
39
Scrapie
-domestic and wild sheep disease -higher in black faced sheep -recognized 250 years ago in great britain and west europe -reportable disease
40
scrapie occurence
-1938 canada -more than 1k flocks - suffolk sheep -most susceptible: sheep w gluatmine of histidine at codon 171 or valine at codon 136 -resistant: arginine present at codon 171 or alanine at codon 136
41
scrapie causes
- glutamine change -transmitted from mother to fetus: placenta and amniotic fluids
42
transmissible mink encephalopathy
-rre: northern usa 1947 then canada, finland, russia, and east germany
43
TME cause
-feedingof BSE infected parts in diet
44
TME clinical signs
-aggressive behaviour, ataxia, tremors, difficulty eating, rapid cycling -incubation: 7-12 months -death imminent= somnolent (depressed) -lesions: mainly cerebrum and thalamus
45
classical scrapie transmission
1.mainsource= natural transmission 2. horizontal transmission: expelled placenta from infected ewes 3. vertical transmission: inter uterine trasnfer or milk and colostrum 4. experimental: skin and aerosolization REPORTABLE DISEASE
46
Classical Scrapie mechanism
-PrP^Sc uptake by peyers pathces in gut and palatine tonsils
47
classical scrapie clinical signs
-flock separation, bruxism, lip licking -ataxia, hypermetria (exagerrated mvmnts), head tremors -loss of body condition pruritis: alopecia and skin wounds, classical scrapies only
48
atypical scrapie
-norway 1998 but worldwide now -
49
atypical scrapie diagnostic
-PrP^sc decposits in cerebellum - first area to detect PrPSC preclinically but may be in cerebellum -not in obex (brain stem) -non infectious: spontaneous mutation -non reportable
50
atypical scrapie clinical signs
-similar to classical scrapie but not pruritis -onset: >5yrs
51
atypical scrapie antemorten
biopsy: third eyelid, rectal mucosa, tonsil

ANSC 375 mt 2 (10 decks)

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