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Block 8 Week 2 Colt > Viral Encephalitis - AuCoin > Flashcards

Viral Encephalitis - AuCoin Flashcards

1
Q

T/f: helminths may invade the CNS

A

true

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2
Q

CNS infections occur within which two areas?

A

cranium and spinal column

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3
Q

What are the common features of CNS infections?

A

fever
headache
altered mental status
focal neurologic deficits

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4
Q

Clinical presentation of a CNS infection may be acute, subacute, or chronic depending on the (blank) factors of the innfecting agent and its location

A

virulence factors and locations

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5
Q

Viremia and CNS invasion begins via the colonization of…

A

mucosal surfaces

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6
Q

Which Ig neutralizes viruses and prevents attachment tot he mucosal surface and cell penetration

A

IgA

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7
Q

Most CNS viruses replicate at (neuronal/non-neuronal) sites

A

non-neuronal sites

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8
Q

Is viremia established before or after invasion of the CNS via the BBB?

A

before moving through the BBB

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9
Q

Even if the cililary action of the respiratory system is passed, what cells kill viruses in the lower respiratory tract?

A

alveolar macs

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10
Q

Gastric acidity inactivates most (viruses/viral capsules)

A

viruses

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11
Q

Gastric enzymes inactivate most (viruses/viral capsules)

A

viral capsules

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12
Q

Bile disrupts what part of the virus?

A

viral envelope; its a lipid!

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13
Q

what are the acid resistant viruses that can survive in the GI tract?

A

enterovirus
adenovirus
reovirus
parvovirus

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14
Q

Where does enterovirus have its primary replication/

A

peritonsillar lymphatics
Peyer’s patches
lamina propria of intestine
vascular and endothelial cells

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15
Q

(blank) cells mediate viral penetration from the gut lumen to the lymphoid cells

A

M cells

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16
Q

What sites does the virus spread to to cause viremia?

A

liver
spleen
muscle

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17
Q

After viremia, particles are cleared by what cell class?

A

phagocytic cells

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18
Q

Viruses like measles, mumps, and herpes grow and are transported in what cell type?

A

phagocytic cells

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19
Q

What is the advantage for a virus to replicate in the immune cells?

A

prevents phagocytosis and neutralization via circulating Ab

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20
Q

What are the four mechanisms of viral invasion of the CNS?

A
  1. invasion directly across cerebral capillary endothelial cells of the BBB
  2. infection of glial w/o endo infection
  3. transport via immune cells
  4. via olfactory or peripheral nerves
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21
Q

endo cells of the BBB secrete what type of basement membrane?

A

laminin basement membrane

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22
Q

Perivascular (blanks) lies close to the BBB vessel wall

A

perivascular macrophages and pericytes

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23
Q

What are pericytes responsible for in the BBB?

A

tight junction formation

vesicle trafficking amongst endo cells

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24
Q

How do infected monocytes gain access to the CNS?

A

via normal turnover perivascular macrophages or as a result of proinflammatory mediators like CCL2

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25
Q

HTLV1 gains access to the BBB via which transport protein?

A

GLUT1

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26
Q

Passage of virus through endo cells of the BB can release which two inflammatory cytokines?

A

IL6

IFNg

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27
Q

HSV1 enters peripheral neurons via which transport protein?

A

nectin 1

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28
Q

Nectin 1 is expressed on the cell (soma/axon)

A

axon

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29
Q

Spread of HSV1 from axon to soma is facilitated by hijacking of the (blank)

A

axonal retrograde transport system

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30
Q

Which two viruses are released at a synapse and use a retrograde trans-synaptic pathway to infect neighboring cells/

A

HSV1

rabies virus

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31
Q

Measles virus dissemination between neighboring neurons occurs via (blanks) between neighboring cells

A

microfusions (two termini that are actually touching vs. crossing the synaptic cleft)

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32
Q

Reactivation of HSV1 uses (retrograde/anterograde) transport to infect neighboring neurons

A

anterograde; from soma to axon termini exits via axonal varicosities then reinfects epithelial cells

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33
Q

Which two proteins does HSV1 use to reinfect epithelial cells during reactivation/

A

nectin 1

herpesvirus entry medator (HVEM)

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34
Q

Production of CNS dz requires viral (blank) and penetration of susceptible cells

A

attachment

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35
Q

viral entry into the (blank) leads to dispersion of virus within the CSF in contact with meningeal cells

A

subarachnoid space

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36
Q

virus in the CSF can spread to which cell types?

A

glia and neurons

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37
Q

T/F: the INITIAL inflamm response to virus int the CNS is immunologically specific to the virus

A

true; consists of lympho’s sensitized to the virus

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38
Q

Blood vessles that carry viral load lie in the (blank) space above the (blank) covering of the brain

A

in the subarachnoid space above the pia mater

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39
Q

Monocytes respond to virus-specific (protein/glycolipid) that diffuses or is transported to the luminal surface of the endothelium

A

protein

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40
Q

After the dev of a CNS inflamm response, alterations in the BB permit what to pass?

A

CSF serum proteins INCLUDING IG

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41
Q

Intracerebral accumulation of Ig is seen as an increase of CSF-serum ratios that persist for how long after infection?

A

several weeks

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42
Q

Are T or B cell responses more important for viral clearance from the CNS?

A

T cell

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43
Q

chronic viral infx happen in what type of patients/

A

pts with depressed CELL MEDIATED immunity

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44
Q

HSV causes hemorrhage in which lobe the brain/

A

temporal

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45
Q

viral infections produce what type of inflammatory infiltrate?

A

mononuclear

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46
Q

Viral meningitis is ID’d by a high (blank) count in the CSF

A

WBC

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47
Q

what is the most common cause of meningitis?

A

viral meningitis

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48
Q

Which bacteria may also cause meningitis?

A

strep pneumo
N. meningitidis
Listeria monocytogenes

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49
Q

Acute meningitis has its Sx onset over what period of time/

A

hours to days

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50
Q

what does aseptic meningitis mean?

A

its viral

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51
Q

T/F: pyogenic bacteria are the cause of aseptic meningitis

A

false

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52
Q

The cause of aseptic meningitis is not apparent after initial eval of (blank)

A

stains and cultures of CSF

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53
Q

Is viral meningitis more or less severe than bacterial meningitis?

A

less severe

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54
Q

T/F: viral meningitis, while less severe, still needs aggressive Tx

A

false; resolves on its own

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55
Q

Most viral meningitis cases in the US happen during the summer and are caused by….

A

enterovirus

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56
Q

What are the three most common causes of aseptic meningitis?

A

non-polio enterovirus
mumps
herpesvirus

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57
Q

What are the less common causes of aseptic meningitis?

A 
Arboviruses
Lymphocytic choriomeningitis virus (LCMV)
Human immunodeficiency virus
Adenovirus
Influenza virus
Measles virus
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58
Q

viral meningitis occurs in what age group?

A

younger than 5

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59
Q

What is one of the most common ways of kids getting enteroviral meningitis?

A

Changing a diaper/going to the bathroom and not washing your hands

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60
Q

What is the triad of symptoms in meningitis

/

A

sudden onset fever
headache
stiff neck

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61
Q

What are the additional symptoms of meningitis?

A

Nausea
Vomiting
Photophobia (sensitivity to light)
Altered mental status

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62
Q

How long do the symptoms of meningitis last?

A

7-10 days

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63
Q

T/F: people with normal immune systems recover completely from aseptic meningitis

A

true

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64
Q

What types of samples are taking for testing for aseptic meningitis/

A

blood or CSF

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65
Q

what is the leading cause of ID’d aseptic meningitis?

A

enterovirus

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66
Q

what is the route of transmission of enterovirus/

A

fecal-oral spread

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67
Q

Swimming in (blank) contaminated water can lead to enterovirus infx

A

sewage contaminated :( fucking yuck

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68
Q

in order, what are the most common enteroviruses that cause meningitis?

A

echovirus

coxsackie virus B2 and A9

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69
Q

T/F: Enterovirus D68 does not cause meningitis

A

true

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70
Q

which coxsackie causes hand foot mouth syndrome/

A

coxsackie a

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71
Q

what is another word for hand foot mouth ?

A

herpangia; ulcers in oropharynx w/ sore throat

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72
Q

what type of coxsackie causes pleurodynia and myocarditis?

A

coxsackie b

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73
Q

T/F: both coxsackie A and B can cause meningitis

A

true

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74
Q

T/F: both coxsackie a and b can cause mild paralysis

A

true

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75
Q

How do you Dx coxsackie virus meningitis?

A

PCR of enterovirla RNA in CSF

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76
Q

Is there a Tx for Coxsackie virus

A

nope

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77
Q

Which type of virus may be transmitted via pool water?

A

echovirus

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78
Q

Besides meningitis, what other Sx may echovirus have?

A

URI, fever, infantile diahrrea, hemorrhagic conjunctivitis

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79
Q

T/F: echovirus may also cause hand foot mouth disease

A

true

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80
Q

how do you Dx echovirus?

A

PCR

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81
Q

is there a Tx for echovirus?

A

nope

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82
Q

Are serologic tests useful for echoviral infx?

A

nope; multiple serotypes and no common Ag

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83
Q

What fluids can transmit coxsackie and echo viruses?

A

feces, ENT secretions, blister fluid

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84
Q

Mumps is the most common cause of aseptic meningitis and encephalitis in which population group?

A

unvaccinated

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85
Q

meningitis occurs in what percent of mumps patients?

A

10-30%

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86
Q

T/F: mumps meningitis can occur without parotitis

A

true

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87
Q

T/F: mumps meningitis is self limiting

A

true

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88
Q

What age group and gender is most likely to get mumps?

A

males 5-9 years old

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89
Q

how many serotypes of mumps are there?

A

only one

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90
Q

how is mumps transmitted?

A

respiratory droplets

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91
Q

Mumps spreads via the blood to which organs?

A

testes
ovaries
pancreas
meninges

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92
Q

what is in the mumps vaccine?

A

live, attenuated vaccine

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93
Q

Which virus is transmitted via aerosol inhalation of the secretions and excretions of house mice and hamsters?

A

lymphocytic choriomeningitis

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94
Q

T/F: most cases of LCM are asymptomatic

A

true

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95
Q

What are the symptoms of LCM?

A

flu like, fever, headache, myalgia, and malaisde

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96
Q

is there a treatment for LCM?

A

nope

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97
Q

How do you test for LCM?

A

serologic testing for IgM or IgG

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98
Q

what percent of encephalitis cases remain unknown to the etiology
?

A

1/2

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99
Q

Of the ID’d cases of encephalitis, what percent were due to viruses?

A

2/3

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100
Q

What are the criteria for encephalitis?

A

altered consciousness for 24 hours or more
fever
seizures
focal neurologic findings
cerebrospinal fluid (CSF) pleocytosis or
electroencephalogram (EEG) or neuroimaging findings

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101
Q

Which six members of the herpes virus family can cause neurologic disease?

A 
herpes simplex virus-1 (HSV-1)
herpes simplex virus-2 (HSV-2)
varicella-zoster (VZV)
Epstein-Barr (EBV)
cytomegalovirus (CMV)
human herpes virus-6 (HHV-6)
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102
Q

T/F: when herpesvirus infects the CNS, the presentation is nonspecific

A

true; makes it hard to know what is going on

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103
Q

Prompt Dx of HSV based CNS infection requires what?

A

neuroimaging

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104
Q

Why is it important to get an early Dx of HSV CNS infx?

A

progressive neurologic deficits, seizures, and death may happen

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105
Q

T2 weighted images will show increased signal where with an HSV infection?

A

temporal lobes

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106
Q

T2 weighted images will show increased signal where with a VZV infection?

A

multiple areas of infarction in both hemispheres

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107
Q

what is the geographic limit of the inflammation in HSV1 infx of the CNS?

A

insular cortex; BUT DOES INVOLVE THE CINGULATE GYRUS

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108
Q

HSV1 and HSV2 cause encephalitis via (anterograde/retrograde) transmission

A

retrograde from a peripheral site on the face along a nerve axon and to the brain

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109
Q

The HSV virus lies dorman in the ganglion of the (blank) nerve

A

trigeminal

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110
Q

Does HSV use the trigeminal to gain access to the brain?

A

not necessarily; pathway unclear

111
Q

what other cranial nerve besides 5 may be involved in HSV infections?

A

olfactory nerve; explains temporal lobe involvement

112
Q

What causes tissue injury in HSV encephalitis?

A

viral killing of neurons

113
Q

What is the most common cause of viral encephalitis, causing 10% of all cases?

A

HSV

114
Q

in immunocompetent adults, HSV1 accounts for what percent of HSV encephalitis?

A

90%

115
Q

What must you do to Dx HSV encephalitis?

A

MRI and PCR of HSV DNA from teh CSF

116
Q

Most pts with HSV encephalitis have a CSF (blank)cytosis

A

pleocytosis >5WBC/mm3 with lymphocytic predominance

117
Q

What are the protein and glucose levels like in HSV enceph?

A

elevated protein (80-85) and normal glucose

118
Q

What is the drug of choice for HSV enceph?

A

Acyclovir

119
Q

VZV goes latent in the (blank)

A

dorsal root ganglia

120
Q

VZV CNS infections can result in what two dz?

A

enceph or vasculopathy

121
Q

T/F VZV CNS infx can occur during primary infx or during reactivation

A

true

122
Q

During primary VZV infx, acute (blank) happens to 1 in 400 children younger than 15

A

acute cerebellar ataxia

123
Q

acute disseminated encephalomyelitis occurs in 1 in 2500 cases of (blank)

A

VZV

124
Q

Describe the CSF profile of ADEM?

A

standard for encephalitis:

pleocytosis with lympho predominance, normal glucose, elevated protein

125
Q

T/F; VZV encephalitis is caused by VZV vasculopathy

A

true

126
Q

Dx of (enceph/vasculopathy) can be made using VZV -specific Ab or PCR of VZV DNA in the CSF

A

vasculopathy

127
Q

For fucks sake like it wasn’t bad enough, what ELSE can VZV do in the CNS?

A

cause meningitis

128
Q

What is the tx for VZV CNS infx?

A

acyclovir

129
Q

How is HCMV transmitted?

A

via blody fluids

130
Q

T/F: HCMV only causes acute dz

A

false; acute and reactivates

131
Q

What Sx can HCMV mimic acutely?

A

mono

132
Q

What are the major neuro complications of HCMV

A

retinitis
enceph
neuropathy

133
Q

in what group of pts do you get neuro complications from HCMV?

A

immunocompromised

134
Q

T/F: HCMV can cause congenital malformations

A

true

135
Q

Infected neurons and glial cells develop cytoplasmic and intranuclear (blanks) of HCMV

A

inclusions

136
Q

At what T cell level does HCMV enceph occur?

A

lower than 50

137
Q

What’s the CSF look like in HCMV enceph?

A

nonspecific…..
mild lympho pleocytosis
mild elevation in protein

138
Q

What’s the really bad form of HIV-associated HCMV eneph that kills you in a month?

A

ventriculoencephalitis

139
Q

How do you Dx HCMV enceph?

A

CMV DNA from CSF via PCR

140
Q

What two drugs are given in CNS invasive HCMV?

A

gancyclovir and foscarnet

141
Q

If you see the ventricles outlined in a T2 MRI and they have encephalitis, what virus is causing it?

A

HCMV; ventriculoencephalitis

142
Q

Primary EBV infx has what symptom profile?

A

mono like; cervical LAD, exudative pharyngitis, splenomegaly

143
Q

What are the complications of CNS infx of EBV?

A

meningitis
encephalitis
transverse myelitis
Guillain-Barre syndrome

144
Q

HHV-6 infects what type of cell?

A

T cells

145
Q

HHV causes what exanthem in infants?

A

exanthem subitum (roseola)

146
Q

What particular group of pts gets enceph from HHV-6

A

allogenic BMTs

147
Q

Describe the CSF profile in HHV-6 enceph?

A

lymphocytic pleocytosis
elevated protein
normal glucose

148
Q

Describe the general onset for roseola?

A

sudden high fever
after a few days the rash subsides
just as the child is getting better a red rash appears, BEGINS ON TRUNK AND SPREADS TO LEGS AND NECK
does not itch, lasts 1-2 days

149
Q

How do you Dx HHV-6 enceph?

A

CSF PCR or serum serology

150
Q

How do you treat HHV-6 enceph?

A

gancyclovir and foscarnet

151
Q

What are the vector borne viral enephalitis family?

A

Arboviruses

152
Q

WHich arboviruses may cause enceph?

A 
California encephalitis virus (La Crosse virus)
West Nile virus
St. Louis encephalitis
Eastern equine encephalitis
Western equine encephalitis
Venezuelan equine encephalitis
153
Q

California encephalitis virus is transmitted by what fucking bug?

A

god damn mosquitoes

154
Q

What CE subtype most often causes encephalitis?

A

La Crosse Virus–californians like to play LaX!

155
Q

IN what age group and in what season do we see the most cases of CE?

A

<16y, during the summer

156
Q

Half the patients with CE develop (blanks)

A

seizures

157
Q

T/F: most patients with CE suffer long term brain damage from the seizures

A

false; most recover completely. 1% mortality is due to asceptic meningitis

158
Q

T/F: people seropositive for CE are protected against reinfection

A

true

159
Q

What part of the US do we normally see CE?

A

Eastern US, WTF!

160
Q

What type of mosquito is the vector for West Nile virus?

A

Aedes albopticus; female Asian tiger mosquito

161
Q

Birds, especially CROWS, are susceptible to this virus

A

West Nile virus

162
Q

What two age groups are at higher risk of getting west nile?

A

children and elderly

163
Q

How does west nile travel in the body and what is its target organ?

A

spreads via monocytes and macrophages, targets the brain

164
Q

What percent of people with WNV are symptomatic?

A

only 1%

165
Q

What is the range of symptoms of WNV?

A

flu like to encephalitis; Headache, nausea, high fever, malaise, myalgia, backache, neck stiffness

166
Q

Is there a vaccine and/or treatment for WNV?

A

nope

167
Q

What are the two ways to diagnose WNV?

A

virus specific IgM in the serum or CSF!

168
Q

what is the vector for St. Louis virus

A

mosquitoes, of course

169
Q

T/F: St. louis encephalitis has outbreaks in the US

A

true

170
Q

when are SLE outbreaks common?

A

late summer and early fall

171
Q

Serious SLE (blank) infections cause headache, nausea, high fever, malaise, myalgia, backache, and neck stiffness

A

neuroinvasive

172
Q

What is the mortality of SLE? What group is most susceptible?

A

3-30%; elderly

173
Q

How do you diagnose SLE?

A

serodiagnosis of IgM in serum OR CSF!

174
Q

What are some clinical pearls that point you towards SLE?

A

Onset in early fall
working outside/landscaping
CSF negative for WNV

175
Q

EEE has what type of vector?

A

it is an arbovirus

176
Q

What is the reservoir of EEE?

A

wild birds!

177
Q

What is the mortality rate of EEE?

A

33%

178
Q

(blank) type infections of EEE can hapen in horses in the US

A

epizootic

179
Q

Severe headaches, nausea, vomiting, fever; changes in mental status, seizures and coma are suggestive of?

A

EEE

180
Q

T/F: survivors of EEE are left with permanent brain damage

A

true; think about getting kicked in the head by a horse

181
Q

How is EEE diagnosed?

A

isolating virus or detecting rise in Ab titer

182
Q

Is there a vaccine or antiviral for human infection of EEE? Horses?

A

No for humans, yes for horses

183
Q

What region of the US is infected with EEE?

A

East coast, south east

184
Q

EEE may have similar symptoms at onset to (blank)

A

meningitis

185
Q

Is Western equine encephalitis more or less severe than EEE?

A

less severe

186
Q

Where is WEE found?

A

West of Mississippi and South America

187
Q

What is the mortality rate of WEE?

A

2%

188
Q

T/F: WEE has a vaccine for horses but not for humans

A

true

189
Q

Is the reservoir horses or birds in Venezuelan equine encephalitis?

A

horses

190
Q

Where is VEE found?

A

South and Central America

191
Q

What are the symptoms of VEE? Is it fatal?

A

flu like symptoms, only fatal to those with weak immune systems

192
Q

T/F: VEE has a vaccine for both horses AND people

A

true

193
Q

What types of people are vaccinated against VEE?

A

laboratory and military

194
Q

what is the most common form of polio?

A

abortive poliomyelitis

195
Q

What are the Sx of abortive polio?

A

mild, febrile illness characterized by headache, sore throat, nausea, and vomiting

196
Q

T/F: nonparalytic polio presents as meningitis

A

true

197
Q

In (blank) polio, the major finding is FLACCID paralysis

A

paralytic polio

198
Q

In paralytic polio, involvment of which brain structure can lead to respiratory failure?

A

brainstem

199
Q

What specific type of meningitis is involved in paralytic polio?

A

meningoencephalitis

200
Q

Which two types of polio have spontaneous recovery?

A

abortive and nonparalytic

201
Q

Is the motor nerve damage permanent following polio muscle spasms?

A

yes, that’s why they are in wheel chairs

202
Q

If the spinal cord is involved in polio, what type of meningitis is it?

A

meningomyeloencephalitis

203
Q

Poliomyelitis is an acute infection of the (blank) and the motor neurons of the spinal cord and brain stem

A

meninges

204
Q

The Salk and Sabin vaccines are used for(blank)

A

polio

205
Q

Where is polio still ENDEMIC?

A

Nigeria, Pakistan, and Afghanistan

206
Q

How do you Dx polio?

A

Acute onset of flaccid paralysis, or recovery of poliovirus from stool sample or swab of pharynx

207
Q

How many polio serotypes are there?

A

three

208
Q

T/F: protection from one polio serotype will protect against them all

A

FALSE; little immune cross reactivity, therefore you need unique Abs to all three

209
Q

Which polio vaccine is the killed vaccine?

A

Salk (inactivated vaccine)

210
Q

Which polio vaccine is the live attenuated vaccine?

A

Sabin, ORAL vaccine

211
Q

After the polio virus is ingested, where does it first establish infection?

A

GALT, tonsils, peyer’s patches, invades the M cells and replicates in the monoctyes

212
Q

From the initial site of infection, where does polio travel?

A

regional lymph nodes, virus rep’s in the monocytes

213
Q

After establishing in regional lymph nodes, where does polio go?

A

into the blood to cause plasma viremia

214
Q

Once plasma viremia of polio is established, how does it cross the BBB?

A

via the endothelium

215
Q

Polio replicates in the (blank) cells of the spinal cord

A

anterior horn cells

216
Q

Replication of polio in the spinal cord leads to cell destruction and (blank)

A

paralysis

217
Q

How is polio shed from the body?

A

via the feces

218
Q

Weakness in one leg seen in polio is known as…

A

Equinus foot

219
Q

AIDS dementia results from infection of what two cell types in the brain?

A

macrophages and microglial cells

220
Q

What are the Sx of AIDS dementia?

A

slow deterioration of intellectual abilities

221
Q

AIDS dementia is similar to what other degenerative dz?

A

Alzheimer’s

222
Q

What are the other reasons that someone with AIDS could have neurologic deterioration?

A

from an opportunistic infection

223
Q

What are some of the opportunistic infections that can cause neuro symptoms in AIDS pts?

A

CMV
HSV encephalitis
cryptococcal meningitis

224
Q

what is the most common neuro complication of late stage HIV infection?

A

subacute or chronic HIV enceph presenting as dementia

225
Q

What percent of AIDS pts progress to dementia?

A

3%

226
Q

Once the constitutional symptoms of AIDS have been established, what is the frequency of dementia?

A

2/3

227
Q

in what age group is AIDS dementia most common?

A

kids; more than 60% :(

228
Q

what are specific cognitive losses in AIDS dementia?

A

(loss of retentive memory, inattentiveness, language disorder, and apathy) abnormalities of motor function

229
Q

What is the survival after AIDS dementia onset?

A

3-6 months, may be longer if treated

230
Q

What changes in the CSF do we see in pts with AIDS dementia?

A

normal, maybe a slight elevatoin in protein

231
Q

T/F: HIV can be isolated from the CSF

A

true

232
Q

Can the AIDS dementia complex be caused by a CMV infection?

A

no, it is a direct result of HIV

233
Q

T/F: rabies can infect all animals

A

true

234
Q

How is rabies transmitted?

A

animal bites

235
Q

How long is the incubation period of rabies virus?

A

2 weeks to a year

236
Q

What phase of rabies is this: Fever, nausea, headache, spread to CNS from muscle

A

prodrome phase

237
Q

What phase of rabies is this: Hydrophobia, anxiety, paralysis, coma, death (~100%)

A

neurologic phase

238
Q

After being bitten, what is the treatment protocol?

A

Administration of BOTH the vaccine AND human rabies IgG

239
Q

What speical type of inclusion bodies does rabies show that is diagnostic?

A

Negri bodies

240
Q

What are the two methods of rabies Dx?

A

cytologic detection of Negri bodies or immunochemical detection of viral antigen in brain tissue

241
Q

Rabies is spread through what animal secretion?

A

saliva

242
Q

Rabies virus remains in the site of infection, (aka blank), for days to months before moving to the CNS

A

muscle

243
Q

Rabies virus initially infects the CNS how?

A

infects nerve endings by binding to receptors

244
Q

T/F: rabies in humans also spreads to the salivary glands

A

true; via afferent nerves

245
Q

After rabies invades the CNS, what happens to the brain?

A

ecephalitis and neuronal degeneration

246
Q

Rabies travels via (antero/retro)grade axoplasmic transmission to the DRG and spinal cord

A

retrograde

247
Q

What are the first symptoms of rabies after the initial incubation period?

A 
fever
malaise
headache
fatigue
GI
248
Q

How long is the incubation period of rabies?

A

60-365 days

249
Q

What is hydrophobia in rabies?

A

pain associated with swallowing water, the desire to not drink

250
Q

T/F: hallucinations and seizures are common in rabies

A

true

251
Q

Seizures in rabies can lead to what serious complication?

A

paralysis leading to respiratory failure

252
Q

What is the cause of death from rabies?

A

Coma then death via pulmonary complications

253
Q

In the incubation phase of rabies, pts are asymptomatic

A

true

254
Q

What is the viral load like in the incubation phase of rabies/

A

low titer, virus still in muscle

255
Q

At what point are Abs to rabies formed/

A

once it reaches the neurologic phase; can be found in serum and CNS

256
Q

the symptoms of fever, vomiting, nausea, headache are part of the (blank) phase of rabies

A

prodrome

257
Q

In the prodrome phase of rabies, the virus titer is (low/high) and is present in the CNS and brain

A

LOW titer, but present in the brain!

258
Q

In the neurologic phase of rabies, the virus titer is (high/low) and in the brain and other sites

A

high titer and now the virus is everywhere

259
Q

Prion diseases are disorders of protein….

A

conformation

260
Q

What is the most common prion disease?

A

Creutzfeldt-Jakob disease (CJD)

261
Q

What are the symptoms of CJD?

A

dementia, ataxia, and myoclonus

262
Q

What is the prognosis of CJD?

A

death within 1 year of onseet

263
Q

What is the most common age group for CJD?

A

60-65

264
Q

what is the incubation period of CJD?

A

5-20 years

265
Q

Prions reproduce by bindning the normal cellular isoform of the prion protein (PrPc/PrPsc) and making it the disease causing form

A

normal: PrPc
dz: PrPsc

266
Q

T/F: prions don’t have nucleic acids

A

true

267
Q

Da fuck is scrapie?

A

prion dz of sheeps and goats

268
Q

what are the three ways of getting CJD?

A
  1. sporadic
  2. familial
  3. acquired
269
Q

What are the ways of acquiring CJD?

A

eating contaminated meat

transplant of tissues with prions or use of contaminated surgical instruments

270
Q

Da fuck is Kuru?

A

form of CJD involving only tremors and ataxia seen only in the Fore tribes of new Guinea

271
Q

What are the histologic characteristics of CJD?

A

spongiform degeneration of the grey matter

272
Q

What region of the brain undergoes the greatest change in CJD?

A

cerebral cortex

273
Q

CJD is characterized by the presence of many (blanks) from 1-50um in diameter

A

round vacuoles

274
Q

T/F: CSF analysis is the gold standard for Dx of CJD

A

false; rarely helpful!

Block 8 Week 2 Colt (6 decks)

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