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Block 8 Week 2 > Viral Encephalitis- Aucoin > Flashcards

Viral Encephalitis- Aucoin Flashcards

1
Q

What are the viral infections of the CNS?

A
  • aseptic meningitis
  • viral encephalitis
  • paralysis
  • AIDS dementia
  • rabies
  • prions
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2
Q

CNS infections occur within the (blank) or (blank), they may be associated with significant morbidity and mortality.
Who is this especially dangerous in?

A

cranium or spinal cord.

infants and immunocompromised patients

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3
Q

Most patients with CNS infections present with the clinical features of …?

A

fever, headache, altered mental status, or focal neurologic deficits (speech, sight issues, paralysis)

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4
Q

The clinical presentation of a CNS infection may be (blank, blank or blank) depending on the virulence of the infecting agent and the (blank) of the infection.

A

acute, subacute, or chronic

location

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5
Q

Numerous (blank) etiologies may account for syndromes that mimic CNS infections

A

noninfectious

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6
Q

Viruses colonize mucosal surfaces and then the host posseses numerous barriers to prevent (blank)

A

viral entry

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7
Q

If one has previous contact with a virus, the mucosa of the GI and respiratory tracts may be coated with (blank)

A

secretory IgA

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8
Q

What does IgA do?

A

neutralizes the virus and prevents attachment and subsequent cell penetration

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9
Q

what do viruses have to do to get to the CNS?

A

escape host defense mechanisms, replicate and disseminate

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10
Q

The steps of infection of most neurotropic viruses is….

A

1) non neuronal sites (initially at portal of entry)
2) establish viremia
3) cross BBB to invade the CNS

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11
Q

What is the most common route that viruses get into the body? What do viruses have to overcome in the mucosal surfaces to become dangerous?

A

respiratory> GI

-mucus, cilia, IgA

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12
Q

In the GI tract, what kind of viruses can survive in there?

A

naked capsid viruses

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13
Q

(blank) initially multiply in the peritonsillar lymphatics, peyers patches, lamina propria of the intestine, and vascular endotheial cells

A

Enteroviruses

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14
Q

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

A

M cells

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15
Q

After viremia, viral particles are normally cleared by (blank)

A

phagocytic cells

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16
Q

SOme viruses are sneaky and can avoid been cleared by host cells by doing what?

A

associating with certain cells such as growing and being transported with phagocytic cells

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17
Q

What types of viruses grow and are transported in phagocytic cells?

A

measles, mumps, herpes

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18
Q

What are the different mechanisms in which CNS invasion by viruses occurs?

A
  • direct invasion across cerebral capillary endothelial cells
  • infection of glia
  • transport via infected immune cells (monocytes) b/w cerebral capillary and endothelial cells
  • olfactory or peripheral nerves
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19
Q

What do glial cells do?

A
  • surround neurons and hold them in place
  • supply nutrients and oxygen to neurons
  • insulate one neuron from another
  • destroy pathogens and remove dead neurons
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20
Q

Some viruses such as HIV, use a “trojan horse” method of entry into the BBB. explain this.

A

they enter monocytes and during normal turnover of perivascular macrophages or as a result of the production of pro-inflammatory mediators compromising the barrier, monocytes with the infecting virus will pass through the BBB

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21
Q

SOme viruses, like HTLV bind to (blank) such as glucose transport type 1 (GLUT 1), allowing for the infection of endothelial cells and release of pro-inflammatory mediators which will make the BBB leaky.

A

endothelial receptors

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22
Q

Viral CNS entry also occurs through (blank). HSV1 travels like this. What facilitates this?

A 
peripheral neurons
nectin 1 (expressed axons)
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23
Q

How does HSV1 replicate and infect?

A

it utilizes retrograde transport up the axon into the dendrite and then replicates in the nucleus. It will then utilize anterograde transport to cause a flare up

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24
Q

Rabies virus and HSV-1 are released at a synapse and use a (blank) pathway to infect neighboring neurons.

A

retrograde trans-synaptic

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25
Q

Measles virus dissemination between neurons is thought to occur through (blank) between neighboring cells.

A

microfusions

dendrite and axon kiss for a second and pass virus

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26
Q

In the case of HSV-1, anterograde transport (from cell body to axon) can lead to infection of neighboring cells when the virus exits via (blank) before reaching the axon termini. During HSV-1 reactivation, the virus uses the anterograde system (dashed black arrow) to reach axon termini and reinfect epithelial cells by binding to (blank) or herpesvirus entry mediator (HVEM) receptors.

A

axonal varicosities

nectin 1

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27
Q

(blank) are contractile cells that wrap around the endothelial cells of capillaries and venules throughout the body.
What do they do?

A

Pericytes

-regulate capillary blood flow, clearance and phagocytosis of cellular debris and permeability of BBB

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28
Q

Viruses in the CNS (in order to spread) must induce (blank) changes

A

cellular

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29
Q

Viral entry into the (blank) space leads to dispersion of virus within the CSF in contact with meningeal cells. If this happens where can the infection spread?

A

subarachnoid

-glia and neurons

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30
Q

Once viral infection of the CNS occurs, (blank) cells usually accumulate

A

inflammatory

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31
Q

The initial inflammatory response appears immunologically specific and consists of a population of (Blank) sensitized by the virus

A

lymphocytes

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32
Q

(blank) may respond to a virus-specific protein that diffuses or is transported to the luminal surface of the endothelium

A

monocytes

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33
Q

When viruses pass through endothelial cells, this will release (blank)

A

cytokines-> IFNy and IL-6

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34
Q

After development of a CSF inflammatory response, alterations in the (Blank) will permit the traversal into CSF of (blank) including (blank)

A

BBB
serum proteins
Ig

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35
Q

Intracerebral accumulation of Ig is reflected by what?

A

increase in CSF-to-serum ratio of specific Ig that persists for several weeks after infection

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36
Q

Which immune response is more important to get rid of viruses?

A

T-cell responses

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37
Q

What may develop in patients with depressed cell-mediated immunity?

A

Chronic viral infections

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38
Q

Failure of an immune response to develop results in the virus escaping (blank)

A

immune surveillance

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39
Q

If you see a hemorrhage in the temporal lobe, then what is the virus that caused it?

A

herpes simplex virus

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40
Q

(Blank) is the inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges

A

meningitis

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41
Q

How is meningitis identified?

A

pleocytosis -> abnormal number of WBC in CSF

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42
Q

The common etiologic agents of acute meningitis are (blank). But bacteria can too, what are some causes of bacterial meningitis?

A

viruses

-strep pneumoniae, N meningitis, listeria monocytogenes

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43
Q

Acute meningitis is clinically defined as a syndrome characterized by the onset of meningeal symptoms over the course of (blank)

A

hours to up to several days

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44
Q

T or F

pygoenic bacteria are NOT the cause of aseptic meningitis

A

T

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45
Q

What is aseptic meningitis (viral)?

A

when the cause of meningitis is not apparent after initial eval and routine stains and cultures of CSF

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46
Q

Most aseptic viral meningitis are caused by (blank) and are (more/less) severe than bacterial meningitis

A

enterovirus

less

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47
Q

How do you treat aseptic viral meningitis? What tis the season for aseptic viral meningitis?

A

-no specific-> symptoms just usually resolve.

Summer

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48
Q

A (small/large) percentage of people with enterovirus infections develop meningitis

A

small

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49
Q

What are the 3 most common causes of aseptic meningitis?

A
  • nonpolio enteroviruses (coxsackie, echovirus)
  • mumps virus
  • herpesvirus
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50
Q

What are some less common causes of aseptic meningitis?

A
  • arboviruses
  • lymphocytic choriomeningitis virus (LCMV)
  • HIV
  • adenovirus
  • influenza virus
  • measles virus
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51
Q

Viral meningitis occurs mostly in…?

A

children under 5 (can happen from changing a diaper or using a toilet and not properly washing hands afterwards)

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52
Q

Meningitis infection is characterized by what 3 major symptoms?

A

sudden onset of fever
headache
stiff neck

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53
Q

What are other symptoms of viral meningitis?

A
  • nausea
  • vomiting
  • photophobia (sensitivity to light)
  • altered mental status
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54
Q

The symptoms of viral meningitis usually last how many days?

A

7-10 days

people with normal immune systems usually recover completely

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55
Q

If meningitis is suspected, what do you get?

A

blood or CSF fluid samples

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56
Q

(blank) are the leading recognizable cause of aeptic meningitis, accounting for 85% to 95% of all cases in which a pathogen is identified.

A

Enteroviruses

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57
Q

Why does warm weather facilitate the spread of enterovirus?

A

-wearing sparse clothing may facilitate the fecal-oral spread of these viruses

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58
Q

Enteroviruses have been recovered from (blank); and disease has been reported after swimming in (blank) water

A

wastewater and sewage

sewage-contaminated seawater

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59
Q

In the US, the (blank) most commonly occuring enteroviral serotypes account for most all of the isolates

A

14

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60
Q

What were the predominant enteroviruses associated with viral meningitis?

A
  • echoviruses 30,11,9,6 and 7
  • coxsackieviruses B2 and A9
  • echoviruses 18 and 16
  • coxsackieviruses B1 and B3
  • enterovirus 71
  • coxsackievirus B4
  • echovirus 25
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61
Q

What kind of virus is the coxsackie virus?
Who typically gets it?
How does it typically get transmitted?

A

picornaviridae-> enterovirus

  • young people (naive immune system)
  • fecal-oral and respiratory aerosals
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62
Q

What is this:
herpangina (ulcers in the oropharynx, fever, sore throat)
-AKA hand foot mouth disease due ulcer formation

A

Group A coxsackie virus

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63
Q

What is this:

  • pleuodynia (fever and severe pleuritic-type chest pain)
  • myocarditis (fever, chest pain, and signs of CHF)
A

Group B coxsackie virus

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64
Q

Both Coxsackie A and B can cause what?
How do you diagnose it?
How do you treat it?

A

aesptic meningitis and mild paralysis

  • PCR of enteroviral RNA in spinal fluid
  • no treatment
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65
Q

What kind of virus is an echovirus?

  • how many serotypes?
  • How is it transmitted?
A

picornaviridae-> enterovirus
30 serotypes
fecal-oral route and pool water

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66
Q

What does echovirus cause?

How do you diagnose and treat?

A
  • leading cause (along with coxsackie virus) of aseptic (viral) meningitis
  • upper respiratory infection, febrile illness, infantile diarrhea, and hemorrhagic conjunctivitis
  • hand foot and mouth disease

-PCR, you dont treat it (no vaccine, no therapy)

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67
Q

Stiff neck, photophobia, and a campground pool should trigger you to think about what viruses?

A

Coxsackievirus and Echovirus

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68
Q

In an unimmunized population, (blank) is one of the most common causes of aseptic meningitis and encephalitis

A

mumps

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69
Q

Meningitis is estimated to occur in (Blank) percent of mumps patients

A

10-30%

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70
Q

CNS disease caused by mumps virus can occur in patients without evidence of (blank)

A

parotitis

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71
Q

(blank) is the most common neurologic manifestation of ithe mumps virus and is usually benign and is a self-limited process.

A

Meningitis

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72
Q

What age and gender is most often affected with mumps?

A
  • males (2 to 5 times more likely than females)

- ages 5-9

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73
Q

What does the mumps virus cause?
When does it occur?
How is it transmitted?
How many serotypes does it have?

A

swelling of the parotid gland

  • childhood
  • respiratory droplets
  • one
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74
Q

The mumps virus infects the upper respiratory tract and spreads via blood to…..?
How do you diagnose the mumps?

A

parotid glands, testes, ovaries, pancreas and some cases, meninges
-clinically (testing is available though)

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75
Q

Is the incidence of mumps high in the US?

How do you prevent mumps?

A

low

immunization with live, attenuated vaccine

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76
Q

What kind of virus is Lymphocytic choriomeningitis (LCM)?
How is transmitted?
What is a common reservoir for LCM?
What is the distrubtion and fatality of LCM?

A
  • arenavirus
  • aerosal inhalation, ingestion of contaminated food
  • hamster or house mice
  • worldwide distribution w/ low case fatality rate (<1%)
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77
Q

What are the infections of the arenaviridae like?
What are the symptoms?
Whats the treatment?
How do you test for it?

A

most are asymptomatic
-influenza like symptoms, fever, headache, myalgia, malaise
OR
-Aseptic meningitis, fever, headache, and stiff neck in minority of patients
-No treatment or vaccine
-sero testing for IgM or IgG

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78
Q

If you have lab evidence of neurologic dysfunction and inflammation of brain parenchyma, what do you have?

A

encephalitis

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79
Q

(blank) of cases of encephalitis have unknown etiology

A

half

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80
Q

Of cases of encephalitis with identified etiologies, (blank) accounted for almost 2/3rds

A

viruses

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81
Q

What is the defined criteria for encephalitis?

A 
Altered consciouness for 24 hours or more and at least one of the following characteristics:
-fever 
-seizures
-focal neurologic findings
-CSF pleocytosis
or
-EEG or neuroimaging findings
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82
Q

6 members of the herpesvirus family cause well-described neurologic disease…. what are they?

A
  • HSV1
  • HSV2
  • VZV (varicella-zoster)
  • EBV (ebstein-barr)
  • Cytomegalovirus (CMV)
  • Human Herpes virus 6 (HHV-6)
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83
Q

When (blank) infect the CNS, the clinical presentation is non-specific and often confounding.

A

herpesviruses

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84
Q

The clinical urgency of herpes encephalitis is often underscored by progressive (blank, blank or even blank) and prompt diagnosis and tx rely heavily on (blank)

A

neurologic deficits
seizures
death
neuroimaging

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85
Q

How can HSV1 cause encephalitis?

A

through retrograde transmision following HSV-1 reactivation

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86
Q

Where does HSV lie dormant?

A

in the ganglion of the trigeminal cranial nerve

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87
Q

The (blank) nerve may be involved with HSV causing encephalitis which may explain the (blank) lobe involvment, since this nerve has branches there.

A

olfactory

temporal

88
Q

Cell death and tissue injury in HSV encephalitis likely results from direct (blank) of neurons and immune-mediated mechanisms of cell death.

A

viral killing of neurons

89
Q

What is the most common cause of viral encephalitis (but still acounts for only app. 10 % of all cases)?

A

HSV

90
Q

In immunocompetent adults (blank) accounts for more than 90% of all cases of HSV encephalitis with the remainder caused by (blank)

A

HSV-1

HSV-2

91
Q

Patients with HSV encephalitis present with (blank, blank and blank). What are some other features?

A

fever, altered consciousness, and headache

-seizures, behaviors or personality change, memory disturbance, motor deficit, and speech disturbances

92
Q

How do you diagnose HSV?
What are some lab findings of HSV?
What drug do you use to treat HSV encephalitis?

A

MRI and PCR of HSV DNA in CSF
-pleocytosis (>5 white blood cells/mm^3) w/ a lymphocytic predominance
AND
elevated protein in CSF w/ normal glucose

-acyclovir

93
Q

How does acyclovir work?

A

nucleoside analog that stops polymerase

94
Q

In whom does primary VZV infection (chickenpox) occur in? after this the virus becomes latent and hangs out in the (Blank). Reactivation results in (Blank)

A

chidren 1-9
dorsal root ganglion
shingles (herpes zoster)

95
Q

How can you get VZV CNS infection (encephalitis or vasculopathy)?

A

during primary infection or after viral reactivation from latency (shingles)

96
Q

During primary infection with VZV, (blank) develops in 1 in 400 children younger than 15 years old

A

Acute cerebellar ataxia

97
Q

After primary VSV infection, (blank) occurs in 1/2500 cases

A

ADEM (acute disseminated encephalomyelitis)

98
Q

The basic CSF profile in ADEM is typical for infectious encephalitis, including a predominance of (blank), a normal (blank), and a normal or elevated (blank)

A

lymphocytes
glucose
protein

99
Q

VZV encephalitis is caused by (Blank).

How do you treat VSV encephalitis?

A

vasculopathy

acyclovir

100
Q

How do you diagnose VZV vasculopathy?

A

presence of VZV-specific antibody or PCR of VZV DNA in CSF

101
Q

VZV also causes (blank) in about ~8% of cases.

A

meningitis

102
Q

What is caused by VZV and is an autoimmune demyeination disease?

A

Acute disseminated encephalomyelitis (ADEM)

103
Q

(blank) is a ubiquitous human virus, with a 90% to 100% antibody seroprevalence in adults.

A

HCMV

104
Q

How is HCMV transmitted?

A

Via body fluids (saliva, genital secretions, blood transfusions and organ transplants)

105
Q

What will a primary infection with HCMV cause?

A

often clinically silent, but may cause mononucleosis syndrome

106
Q

What are the neurologic complications from HCMV infections in adults?

A

retinitis, encephalitis, and neuropathy-> occuring in immunocompromised hosts

107
Q

HCMV is also an important cause of (blank) infections

A

congenital

108
Q

In HCMV, infected neurons and glial cells enlarge and develop cytoplasmic and intranuclear (blank)

A

inclusions (resemble owl eyes)

109
Q

CMV encephalitis occurs in (blank) patients due to aids or transplant

A

immunocompromised patients

110
Q

In AIDs, CMV encephalitis occurs when the CD4+ cell count is less than (blank)

A

50 cells/mm^3

111
Q

The CSF in patients with CMV encephalitis is nonspecific with mild elevations in (blank)

A

CSF protein

112
Q

HIV-associated CMV (blank) has a median survival of 42 days

A

ventriculoencephalitis

113
Q

How do you diagnose HCMV?

A

by amplication of CMV DNA from CSF by PCR

114
Q

How do you treat viral encephalitis-HCMV?

A

gancyclovir and foscarnet

115
Q

How does foscarnet work?

A

blocks viral DNA polymerase (binds to pyrophosphate binding site)

116
Q

Primary EBV infection can be asymptomatic, or can result in a (blank) syndrome characterized by..?

A

mononucleosis syndrome

-> cervical lymphadenopathy, exudative pharyngitis, and splenomegaly

117
Q

CNS disease occurs in ~1% of EBV infectious mononucleosis cases and can cause (blank X 4)

A

meningitis, encephalitis, transverse myelitis, and Guillain-Barre syndrome

118
Q

THe frequency of EBV as a cause of encephalitis is unknown, although it has been reported to account for approx. 10% of childhood (blank)

A

encephalitis cases

119
Q

Patients with EBV encephalitis present with ….?

A

fever, headache, altered consciousness, seizures and focal neurologic deficits

120
Q

(blank) is a ubiquitous viral infection of T lymphocytes that causes a spectrum of disease on primary infection

A

HHV-6

121
Q

What does HHV-6 cause?

A

exanthem subitum (roseola) in infants, febrile seizures, and lymphadenopathy syndromes

122
Q

Is HHV-6 a one and done infection

A

nah, it can be latent and then reactivate

123
Q

HHV-6 is recognized as a cause of encephalitis in immunocompromised adults, particularly patients with (Blank)

A

allogeneic bone marrow transplants (hematopoietic stem cell transplants)

124
Q

What are the labs like in HHV-6?

A

CSF lymphocytic pleocytosis, elevated protein and normal glucose

125
Q

What is this:
Typically the disease affects a child between six months and two years of age, and begins with a sudden high fever (39–40 °C; 102.2-104 °F). After a few days the fever subsides, and just as the child appears to be recovering, a red rash appears. This usually begins on the trunk, spreading to the legs and neck. The rash is not itchy and may last 1 to 2 days.

A

Viral encephalitis caused by HHV-6

126
Q

How do you diagnose HHV-6 viral encephalitis?

A

CSF-PCR or serum serology

127
Q

How do you treat HHV-6?

A

gancyclovir and foscarnet

128
Q

What are the 6 vector borne viral encephalitis arboviruses?

A
  • california encephalitis virus (La Crosse virus)
  • West Nile virus
  • St. Louis encephalitis
  • Eastern equine encephalitis
  • Western equine encephalitis
  • Venezuelan equine encephalitis
129
Q

What is this:

  • an arbovirus
  • subtype is La Cross virus (causes encephalitis)
  • typically occur in summer in children less than 16 years of age
A

California encephalitis virus

130
Q

What are the symptoms of california encephalitis virus?

A

-severe headache, fever, stiff neck, vomiting, and convulsions
-half the patients develop seizures
-

131
Q

What is the mortality rate of california encephalitis virus? How do you diagnose it? How do you treat it?

A

1% (most recover completely)
sero IgM or IgG
No vaccine or effective drugs but seropositive individuals are protected from re-infection

132
Q

What family does the california encephalitis virus belong?

A

bunyavirus

133
Q

What is this:
arbovirus transmitted by bit of mosquitos, birds (crows) susceptible.
-children and elderly at higher risk
-virus inoculated into blood, spreads via monocytes/macrophages, brain is the target organ.

A

Flaviviridae-> west nile virus

134
Q

Is west nile virus highly symptomatic? what are the symptoms?
whats the treatment?
how do you diagnosis it?

A

No, only 1% symptomatic

  • range from flu-like to encephalitis
  • headache, nausea, high fever, malaise, myalgia, backache, neck stiffness
  • no vaccine, or specific tx
  • detection of IgM in the serum or CSF
135
Q

When you hear the word crow what should you be thinking?

A

West nile virus

136
Q

What is this:

  • arbovirus transmitted by mosquitos that bite infected birds
  • outbreaks happen in late summer and early fall in US
  • mainly affects US
A

St. Louis encephalitis

137
Q

What kind of virus is St. Louis encephalitis?

A

flavi virus

138
Q

What is this:
symptoms range from flu-like febrile illness to encephalitis
More serious neuroinvasive infections headache, nausea, high fever, malaise, myalgia, backache, neck stiffness

A

St. Louis Encephalitis

139
Q

What is the mortality rate of St. Louis encephalitis?

How do you diagnose St. Louis encephalitis?

A

3-30% with elderly at risk

Sero of IgM in serum or CSF

140
Q

What i s this:
Severe headaches, nausea, vomiting, fever; changes in mental status, seizures an coma occurs
Survivors left with brain damage

A

Eastern equine encephalitis virus

141
Q

What is the resevoir for EEE?
What kind of virus is it?
Whats the mortality rate?

A

wild birds to humans
toga virus
33%
super infects horses*

142
Q

How do diagnose EEE and how do you treat it?

A

isolate virus or detect antibody titer

-no antiviral or vaccine available (one available for horses)

143
Q

What is this:
an arbovirus that is primarily seen west of Mississippi and South America.
-wild birds (resevoir) to humans
-less severe than EEE (2% mortality rate)

A

WEE (togavirus)

144
Q

How do you diagnose or treat WEE?

A

Diagnosis by isolating virus or detecting rise in antibody titer

No antivirus or vaccine available (available for horses)

145
Q

What is this:

  • An arbovirus
  • mosquitos transfer virus from equines (horses) to humans
  • found predominantly in South and Central American it has spread to US.
A

VEE (togavirus)

146
Q

What are the symptoms of VEE?

A
  • flu-like symptoms, high fever, headache

- can die if you have a weakened immune system

147
Q

How do you treat VEE?

Who are vaccinated?

A
  • with a vaccine for horses and humans

- at risk military and lab personnel

148
Q

What is the most common form of Poliovirus?

A

abortive poliomyelitis

149
Q

What is abortive poliomyelitis?

A

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

150
Q

(blank) manifests as aseptic meningitis with fever, headache, stiff neck

A

nonparalytic poliomyetlitis

151
Q

How does paralytic poliomyelitis present?

A

flaccid paralysis (predominant finding) but brainstem involvement can lead to life-threatening respiratory paralysis
AND
muscle spasm due to motor nerve damage (its permanent)

152
Q

In (blank), the meninges and brain parenchuma (meningoencephalitis) are involved

A

paralytic polio

153
Q

If paralytic polio involves the spinal cord also, what do you call it?

A

meningomyeloencephalitis

154
Q

What kind of virus is the poliovirus?

A

a picornaviridae-> enterovirus

155
Q

How is the poliovirus transmitted?
Where do you find it?
What percent of polio infections are clinically apparent?

A

fecal-oral route
high in developing countries
1%

156
Q

Where does the poliovirus initially replicate?

A

oropharynx and small intestine (nausea and vomiting)

157
Q

What is the disease range for polio?

A
  • asymptomatic
  • abortive
  • nonparalytic
  • paralytic poliomyelitis
158
Q

Poliomyelitis (polio) is an acute viral infection of the (blank) and the (blank) of the spinal cord and the brainstem

A

meninges

motor neurons

159
Q

Where can you find polio?

A

Nigeria, Pakistan, Afghanistan

160
Q

How do you diagnose polio?

A

stool sample or swab of pharynx

-paralytic can be clinically diagnosed due to the flaccid paralysis

161
Q

How does polio do its thing and become an infectious and stuff?

A
  • ingest the virus
  • encounters GALT where virus invades M cells and replicated in monocytes
  • heads to regional lymph nodes and replicates
  • heads to blood to cause plasma viremia
  • cross BBB
  • Heads to spinal cord
  • > replicated in anterior horn and causes cell destruction and paralysis
  • > goes to gut and gets excreted in feces
162
Q

(blank) related dementia may result from HIV infection of the macrophages and microglial cells of the brain

A

AIDS

163
Q

What is the progression of AIDS dementia?

A

patients undergo slow deterioration of their intellectual abilities and exhibit other neurlogic deficits

164
Q

AIDS dementia looks very similiar to what?

A

Alzheimer disease

165
Q

Neurologic deterioration could also result from infection with one of the many opportunistic infections…Such as?

A

-CMV, herpes encephalitis, cryptococcal meningitis

166
Q

In late stages of HIV infection, the most common neurologic complication is….?

A

subacute or chronic HIV encephalitis presenting as a form of dementia

167
Q

When you get subacute or chronic HIV encephalitis, what do you call this?

A

AIDS dementia complex

168
Q

It is estimated that only (blank) percent of AIDS cases present as AIDS dementia. However this number increases after the (Blank) of AIDS have become established.

A

3%

constitutional symptoms and opportunistic infections

169
Q

In children with AIDS, (blank) is more common than all opportunistic infections, more than 60 percent of children of children eventually being affected

A

dementia

170
Q

(blank) symptoms refers to a group of nonspecific symptoms that can affect many different systems of the body.

Examples include weight loss, fevers, fatigue, and malaise.
Other examples include chills, night sweats, and decreased appetite.

A

Constitutional

171
Q

In children with AIDS, (blank) is more common than all opportunistic infections, more than 60 percent of children eventually being affects

A

dementia

172
Q

What does slow, progressive dementia result in?

A

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

173
Q

In AIDS dementia, the dementia evolves over a period of months; survival after the onset of dementia is generally (blank) but may be longer if treated.

A

3 to 6 months

174
Q

HIV can be isolated from the (blank).

A

CSF

175
Q

The CSF of AIDS dementia patients will look like what?

A

normal or with slightly elevated protein

176
Q

Evidence of CMV infection may occur but evidence indicates that the AIDS dementia complex is a result of direct infection with (blank).

A

HIV

177
Q

What is this:

on an MRI you see large areas of white matter change. You can see cortical atrophy and ventricular enlargment.

A

AIDS dementia

178
Q

What kind of virus is a Rabies virus?

A

Rhabodviris-> lyssavirus

179
Q

(blank) virus is the only medically important Rhabdovirus.

A

Rabies

180
Q

The rabies virus has a (Blank) host rage and infects all mammals. It is transmitted by the (blank) of a rabid animal. (bats, racoons, skunks)

A

broad

bite

181
Q

What are the three phases of rabies? How long does the first phase last?

A

incubation phase (2 weeks to a year)
prodrome phase
neurologic phase

182
Q

What are the symptoms of the prodrome phase of Rabies?

A

fever, nausea, headache, spread to CNS from muscle

183
Q

What are the symptoms of the neurologic phase?

A

hydrophobia, anxiety, paralysis, coma, death

184
Q

Following bite of rabid animal administer (blank) and (blank)

A

vaccine

human rabies IgG

185
Q

How do you diagnose Rabies?

A

-cytologic detection of inclusion bodies (Negri bodies) or immunochemical detection of viral antigen in brain tissue

186
Q

Why do you get hydrophobia in rabies?

A

painful spasm of throat muscles on swallowing, you therefore get an aversion to swallowing water because it is so painful

187
Q

Rabies infection of an animal causes secretion of the virus in the animals (blank), and is spread though biting.
The virus will remain at the site of infection (muscle) for (blank) before CNS involvement

A

saliva

days to months

188
Q

The rabies virus eventually infects (blank) by binding to receptors on neurons

A

nerve endings

189
Q

How does the rabies virus disseminate from the CNS?

A

via afferent nerves to the salivary glands and other tissue

190
Q

After the rabies virus invades the brain and spinal cord (blank) develops and neurons degenerate

A

encephalitis

191
Q

Explain how Rabies can result in CNS involvement

A
  • virus inoculatd
  • viral replication in muscle
  • virion enters PNS
  • passive ascent via sensory fibers
  • replication in DRG
  • rapid ascent in spinal cord
  • infection of spinal cord, brainstem, cerebellum, and other brain structures
  • descending infection via nervous system to eye, salivary glands, skin and other organs
192
Q

What is the incubation period of Rabies?

A

60-365 days

193
Q

What are the symptoms of rabies immediately following the incubation period?

A

fever, malaise, headache, fatigue, and GI symptoms

194
Q

(blank) is common and results from the pain associted with swallowing water (found in rabies)

A

hydrophobia

195
Q

What are some serious symptms of Rabies?

A

seizures, hallucinations, paralysys which may lead to respiratory failure

196
Q

Following the neurologic phase in Rabies, what happens to the patient?

A

become comatose then death occurs due to neurologic and pulmonary complications

197
Q

What are the disease phases of rabies?

A 
incubation period
prodrom phase
neurologic phase
coma
death
198
Q

What stage of rabies is this:
lasts 0-14 days
high titer, virus in brain and other sites
-coma, hypotension, hypoventilation, secondary infections, cardiac arrest

A

Coma

199
Q

What stage of rabies is this:
2-7 days
high titer, virus in brain and other sites
-hydrophobia, pharyngeal spasm, hyperactivity, anxiety, depression
-CNS symptoms: loss of coordination, paralysis, confusion and delirium
-detectable antibody in serum and CNS

A

Neurologic phase

200
Q

What stage of rabies is this:
2-10 days
-fever, nausea, vomiting, loss of appetite, headache, lethargy, pain at site of bite
-low titer, virus in CNS and brain

A

Prodrom phase

201
Q

What is this:
asymptomatic
60-365 days
low titer, virus in muscle

A

incubation phase

202
Q

(blank) are infectious proteins that cause degeneration of the CNS

A

prions

203
Q

Prion diseases are disorders of protein conformation, in humans called (blank) disease

A

creutzfeldt-Jakob disease (CJD)

204
Q

How does CJD typically present?

A

with dementia, ataxia, myoclonus, is relentlessly progressive and generally causes death within a year of onset

205
Q

What age group gets CJD?

A

45-75 year olds.

Most commonly 60-65

206
Q

How long is the incubation period for CJD?

A

5-20 year incubation period

207
Q

Prions are devoid of (blank), all infectious agents possess genomes that direct the synthesis of their progeny

A

nucleic acid

208
Q

(blank) is a brief, involuntary twitching of a muscle or a group of muscles.

A

myoclonus

209
Q

(blank) is a fatal, degenerative disease that affects the nervous systems of sheep and goats. It is one of several transmissible spongiform encephalopathies (TSEs), which are related to bovine spongiform encephalopathy (BSE or “mad cow disease”) and chronic wasting disease of deer.

A

Scrapie

210
Q

(blank) is the most common of the human prion diseases

A

CJD (Creutzfeldt-Jakob disease)

211
Q

What are the three types of CJD?

A
  • sporadic (cause not known)
  • familial (genetic or inherited, defect in prion protein gene)
  • acquired (from contaminated meat or transplant of contaminated tissues or use of contaminated instruments during surgical procedures
212
Q

(blank) is characterized by progressive tremors and ataxia but not dementia. It occurs only among the Fore tribes in New Guinea.

A

Kuru disease

213
Q

What does CJD look like on a histology slide?

A 
spongy appearance (spongiform degeneration)
spongiform change in the gray matter
214
Q

Where do the spongiform changes occur in CJD?

A

in cerebral cortex and many regions of the brain

215
Q

What wil you see lots of round vacuoles form one to 50 um in?

A

CJD

216
Q

What wil the spongiform changes and vacuoles in CJD cause?

A

dementia characterized by memory loss, impaired judgement, decline in intellectual function

217
Q

What does the CSF look like in CJD?

A

pretty much normal (its not helpful to look at)

Block 8 Week 2 (8 decks)

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