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Neuro > Rabies, Prion disease and Herpes > Flashcards

Rabies, Prion disease and Herpes Flashcards

1
Q

Why is rabies a more common cause of death in the developing world?

A

more exposure to animals

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2
Q

What group of viruses is rabies included in?

A

rhabdovirus, subtype lyssavirus

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3
Q

What are the key proteins in rabies virus?

A

viral glycoprotein/envelope (G)
nucleocapside (N)
matrix (M)
NS and L proteins rarer

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4
Q

What type of genome does rabies have?

A
  • ss RNA
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5
Q

What can envelope (G) bind?

A

nicotinic ACh receptor in muscle, gangioside and CD56 in neurons

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6
Q

How does rabies virus enter cells?

A

is endocytosed and envelope fuses at low pH with endosomal membranes to release nucleoprotein

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7
Q

What switch must occur in order for rabies genome production to occur?

A

viral polymerase switches from mRNA mode to making full length + RNA which will serve as a template for - genome production
due to a buildup of N protein

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8
Q

Does rhabdovirus budding usually kill cells? Does it kill cells in the case of rabies?

A

yes

no

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9
Q

Which rabies molecule eleicits neutralizing antibodies?

A

G glycoprotein
is not protective
allows for vaccine production

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10
Q

How does rabies typically enter the body?

A

through a wound or ski abrasion via a bite and introduction to infected saliva
-also, rarely via infected cornea/organ transplants

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11
Q

Where does virus replicate during the “incubation” period?

A

muscle or connective tissue

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12
Q

How quickly does rabies virus travel in the CNS?

A

8-20mm/day

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13
Q

When is rabies intervention effective?

A

before spread to the nerves/CNS

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14
Q

Where does the rabies virus disseminate to after replicating in high levels in the brain?

A

eye, salivary glands, innervated ski (ie/hair follicles)

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15
Q

How long does the incubation period usually last?

A

3-8wks
patients usually asymptomatic
*the closer a bite is to the brain the shorter this period

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16
Q

What is the prodrome phase of rabies infectioin?

A

early after infection of brain
nervousness, headache, anxiety, pain at bite site, fever, nausea
progresses to myoclonus, slurred speech and tingling
presents to brain at end of this period, patients usually still Ab negative

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17
Q

Describe the acute neurological phase of rabies infection

A

high virus titer in brain and elsewhere
Ab present in serum and CNS
Progression from here can be “furious”/fulminant, or “dumb”/paralytic

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18
Q

Describe furious/fulminant progression of rabies

A

classic rabies
bizarre behavior, hallucinations, seizures, hydrophobia
fury later gives way to paralysis, then either coma or sudden fatal cardiac or respiratory arrest

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19
Q

Descirbe the paralytic or dumb progression of rabies

A

ascending flaccid paralysis, leads to fatal paralysis of respiratory muscles

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20
Q

What is the “hydrophobia” associated with rabies?

A

violent spasms of respiratory muscles triggered by drinking water
sight sound or mention of water can trigger it

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21
Q

What are “negri bodies”?

A

virus vactories, seen in some but not all cases of rabies

22
Q

What is Dr. Wiloughby’s theory on the pathology of rabies?

A

that it is a metabolic disease
(a disease of ‘software’, not ‘hardware)
based on observation that patient’s brains are normal on gross path, there are Abs during final acute phase, and there is often little virus remaining at end stages

23
Q

How is rabies diagnosed?

A

neurologic sx in living person w/suspected exposure

confirmed by detecting virus in CSF, saliva, skin or PCR

24
Q

How are animals tested for rabies?

A

brain tissue tested by dFA

25
Q

How is rabies prevented?

A

immunization of domestic animals and high risk individuals (ie/vets)

26
Q

What is post-exposure prophylaxis protocol?

A

passive immunization-Ig introduced into wound area and IM, keeps virus ‘local’
active immunization-human diploid cell vaccine of killed virus, 4-5 doses
this should be initiated ASAP after exposure

27
Q

Which wild animals most commonly lead to rabies exposure in the US?

A

raccoons, bats, skunks, foxes

28
Q

How are most cases imported into the US?

A

tourest exposure outside the US, often via dog bites

29
Q

List some animal prion diseases

A

Scrapie-sheep/goats
BSE/madcow
CWD

30
Q

What are the human prion diseases?

A 
Kuru (ritualistic cannibalism assoc.)
CJD
variant CJD
Gerstemann-Straussler-Scheinker disease
Fatal Familial insomnia
31
Q

What prions?

A

unconventional virus like agents

a proteinacious infectious particle

32
Q

What are the symptoms of Creutzfeldt Jakob disease?

A

progressive dementia leading to ataxia, paralysis, wasting and death (usually via pneumonia) within 6mo of onset

33
Q

What are the origins of Creutzfeldt Jakob disease?

A

sporadic, in older individuals, thought to be spontaneous change in prion protein to a pathologic form
familial/genetic-dominantly inherited
transmitted via contaminated GH inj, corneal transplant, or electrode implants

34
Q

How is vCHD contracted?

A

via consumption of BSE contaminated beef

35
Q

How is Gerstemann-Straussler-Scheinker disease contracted?

A

familial CJD
inherited PrP mutation
illness evolves more slowly (3-5yr)

36
Q

Describe fatal familial insomnia

A

inherited PrP mutation, causes sleep problems leading to ataxia and death

37
Q

What does histology look like in a prion disease?

A

vacuolization in neurons, gives a spongiform appearance in grey matter
soemtimes amyloid plaques or tangles

38
Q

How long does it take to go from prion infection to symptoms?

A

long incubation, takes months-decades for sx to appear

39
Q

What type of immune response is generated by prion disease?

A

no response of any kind

40
Q

How are prion diseases diagnosed?

A

based on clinical grounds

41
Q

How are prion disease treated?

A

no treatments

careful disinfection of medical instruments important when prion disease suspected

42
Q

What normal cellular gene encodes for prion protein?

A

PRNP, encodes PrPc

43
Q

What change in PrPc occurs in prion disease?

A

alpha helical sturcutre to insoluble beta sheet form (PrPsc)

44
Q

How is PrPsc ‘replicated’?

A

pathologic form recruits or converts normal protein to adupt the PrPsc shape

45
Q

What type of genome do herpes viruses have?

A

linease dsDNA

46
Q

Where does herpes replicate?

A

in the nucleus

47
Q

How are herpes infections maintained in the latent lifecycle?

A

as an episome

48
Q

What happens with herpes infections are reactivated?

A

virion components are transported within a peripheral axon in anterograde manner such that infectious virions are released at or close to the site of original inoculation hwere lesions can again appear
can also lead to retrograde transport to CNS, where serious encephalitis results

49
Q

Where does herpes encephalitis usually occur?

A

one of the temporal lobes

50
Q

What are symptoms of herpes encephalitis?

A

seizures, focal neuro abnormalities, other features of viral encephalitis

51
Q

How is HSV infection treated?

A

acyclovir and derivatives
inhibit viral DNA pol but not cellular DNA pol
viral TK phosphorylates acyclovir and incorporates is like dGTP, resulting in chain termination
cellular kinases convert to triphosphate, VIRAL pol inhibited

Neuro (14 decks)

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