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Nervous System > M- Viral Infections of CNS > Flashcards

M- Viral Infections of CNS Flashcards

1
Q

What are the clinical symptoms of meningitis?

A
  1. headache
  2. fever
  3. stiff neck

All caused by inflammation of the meninges

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2
Q

When the brain parenchyma is infected, it can be diffuse or focal-space occupying.
What are the 2 types of focal lesions?
How do they tend to present?

A
  1. Abscesses - bacterial, cerebral toxoplasmosis
  2. Cystic- neurocystecircosis

Presentation depends on the brain structures involved but usually has seizures and focal neurological deficits.

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3
Q

What is diffuse infection of the brain parenchyma called?

How does it present clinically?

A

Encephalitis - impaired cognitive function

  1. confusion
  2. disorientation
  3. acute changes in ideation or thought

[depending on brain area, it can result in respiratory failure and death]

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4
Q

Although all categories of microorganisms can infect the brain, _______ cause most infectious encephalitis syndromes. They also cause most infections of the parenchyma of the spinal cord [not CSF].

A

Viruses

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5
Q

How do spinal parenchymal viral infections present?

A
  1. neuritis - sensory neuropathy
  2. radiculitis- radiculopathies [nerve roots–dermatomes]
  3. myelitis syndromes
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6
Q

What are the causes of aseptic meningitis?

What is the most common?

A
  1. virus= most common
  2. rheumatologic
  3. malignancies
  4. toxic/chemical/drugs
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7
Q

What viruses cause meningitis?

A
  1. enterovirus - polio, coxackie, echovirus, entero 71
  2. arbovirus [WNV, east/west equine, st. louis]
  3. herpes [EBV, CMV, HSV1, HSV2]
  4. HIV
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8
Q

What are the clinical characteristics of viral meningitis?

What would the CSF show?

A

headache, fever, photophobia, neck pain/stiffness

CSF shows:

  • elevated WBC could with mononuclear pleocytosis
  • normal to elevated CSF protein
  • normal CSF glucose
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9
Q

What is the most common cause of viral meningitis?

What is the only truly treatable viral meningitis?

A
  1. enterovirus is the most common

2. herpes is the only treatable [acyclovir]

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10
Q

What family of virus does enterovirus belong to?

What is the structure?

A

It is a picornavirus [71 strains are known to affect humans] and is non-enveloped RNA virus.
The viral capsid is what attaches and elicits the host response

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11
Q

Coxsackie B virus causes what?

Coxsackie A 16 and enterovirus 71 cause what?

A

B = cardiomyopathy and myocarditis

A16, entero 71 = hand, foot and mouth disease

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12
Q

How are enteroviruses spread?

A

Person-to-person via fecal oral spread [in contaminated food/water supply]

They are able to resist acid pH, detergents and disinfectants because they are non-enveloped

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13
Q

What is the geographic and seasonal distribution of enterovirus?

A 
Geographic= worldwide 
Seasonal = June to October [summer months] especially in pediatrics
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14
Q

How do you diagnose enterovirus meningitis?

A

PCR - sensitivity/specificity 100%

There is really no treatment for enteroviral meningitis but PCR can help you avoid unnecessary antibiotics

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15
Q

Which herpetic strain is more likely to cause meningitis? Encephalitis?

What is the geographical and seasonal preference of HSV?

A

Meningitis- HSV2 [especially in babies who get it during birth]. They present with fever, stiff neck, headache

There is no seasonal or geographic preference

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16
Q

What is Mollaret’s meningitis?
What are the clinical characterisitics?
Who is the disease most likely to affect?

A

“benign recurrent aseptic meningitis” because it rarely results in death and can resolve w/out therapy and then recur.

Clinical : headache, fever, photophobia, stiff neck. symptoms resolve in 5 days and there will be no sequelae.
The patient will present at intervals every few weeks, months, years

Affects young adults w/ equal prevalence in men and women

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17
Q

What does the CSF show for Mollaret’s meningitis?

How do you diagnose? What could give you a false negative?

A

CSF shows : elevated protein, elevated WBC, normal glucose, sterile bacterial culture

Diagnosed by PCR – may get a false negative if Hb or inhibitors are present. Repeat PCR after 1-3 days

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18
Q

What virus causes most [if not all] cases of Mollaret’s meningitis?
What do a minority of patients have at the time of the meningitis?
What is treatment?

A

HSV2 causes most if not all cases of Mollaret’s meningitis.
Only a minority of patients have recurrent genital herpes or an outbreak of herpes at the same time as the meningitis.

Treatment is acyclovir

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19
Q

What 3 things delineate a poor outcome for Mollaret’s meningitis?

A
  1. under the age of 30
  2. decreased level of consciousness [a sign that it may involve encephalitis too]
  3. symptoms that last >4 days before getting acyclovir
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20
Q

HSVI encephalitis has a predilection for what lobes of the brain?
What will the MRI show?

A

It has a predilection for the frontal and temporal lobes [specifically temporal].

On MRI, there will be a focal contrast-enhancing lesion

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21
Q

What are the known hosts of poliovirus?

A

Only humans

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22
Q

What are the 4 clinical syndromes associated with poliovirus?
Which do 97% of infected people present with?

A
  1. Asymptomatic illness - viral replication in the gut and oropharynx
  2. minor illness- febrile, fever, headache, malaise sore throat

[97% of people present with type 1 or 2]

  1. nonparalytic aseptic meningitis- resolves w/o sequelae [occurs in 2% of people]
  2. Secondary spread to nervous system after apparent 3-4 days of recovery from stage 2 –> infect anterior horn cells –> flaccid paralysis
    * if it affects the bulbar spine –> lose diaphragm
23
Q

What is treatment for poliovirus?

How can it be prevented?

A

There is no specific antiviral therapy for polio so treatment is based on improving fuction of affected patients [physical and occupational therapy]

It can be prevented by vaccination

24
Q

How many types of polio are there?
How many types of polio vaccines are there?
Describe the benefits and drawbacks of each.

A

There are 3 types of poliovirus and 2 types of vaccine.

  1. Live attenuated virus [Sabin]
    pros:
    -mimics natural route of infection so induces secretory IgA and mucosal immunity via GALT
    - secondary spread via herd immunity
    cons:
    -virus could revert to wildtype and cause paralytic disease in nonimmune individuals
2. killed virus 
Pros:
- can't revert to wildtype 
Cons:
- only induces IgG
25
Q

What is the most important cause of SPORADIC encephalitis in the US?
What strain specifically?
How does it cause disease?
What is the presentation?

A

HSV, specifically type 1 is the most important cause of sporadic encephalitis in the US.

  1. infects during childhood
  2. establishes latency in the trigeminal ganglion
  3. reactivates and replicates
  4. some fibers from trigenimal innervate the meninges adjacent to the temporal lobe

It can cause fever, focal/lateralizing neuro signs, seizures, personality changes

26
Q

How can you make a presumptive diagnosis of HSV1 encephalitis?
What can help confirm?

A

Presumptive–>CT or MRI

Confirmation –> PCR assay for HSV in CSF

27
Q

What arboviruses have been reported in Texas?

What are the natural reservoirs for arbovirus?

A
  1. eastern equine, western equine
  2. california, st. louis encephalitis
  3. West Nile Virus

They are all zoonoses meaning that they primarily infect non-humans and have mosquito-bird or mosquito-mammal life cycles

28
Q

What family of virus do St. Louis encephalitis and WNV belong to?
Are they DNA or RNA viruses?
Describe the structure.
Where do most of the viruses of this family originate?

A

They are flaviviruses and are RNA viruses

  • Icosahedral nucleocapsid
  • envelope
  • E glycoproteins, prM protein [if immature]

Most flaviviruses are arthropod-borne [specifically mosquito borne]

29
Q

What is the seasonal/geographical propensity of St. Louis encephalitis?
What conditions lend to epidemics?
Who is most likely to be infected?

A

It is most common in late summer and early fall and is seen nationally as well as in Canada/Mexico

Epidemics occur where there is polluted waste water, ground pools, irrigation ditches, etc [water is where mosquitos habitat]

Older persons are more likely to be infected [incidence increases with advancing age]

30
Q

How would a patient with St. Louis encephalitis present?

How is the diagnosis made?

A

The person would have coarse tremors [related to substantia nigra involvement].
Muscle weakness is rare [a distinction from WNV]

Diagnosis is made serologically by blood and CSF IgM

31
Q

What 2 findings are found at autopsy in people who have died of WNV?

A
  1. meningoencephalitis

2. myocarditis

32
Q

A patient in Dallas presents with a fever, headache, malaise, backache, and pain in the back of the eyes that is made worse with eye movement.

He has a flushed face, rash, and generalized lymphadenopathy.

What is the likely diagnosis?
What is the reservoir and vector for it?

A

WNV

Reservoir= birds 
Vector = mosquitos
33
Q

What are the 2 most common syndromes associated with infections by WNV?

A
  1. West Nile Fever

2. West Nile Neuroinvasive Disease

34
Q

West Nile Neuroinvasive Disease can present in what 4 ways?

Which of these are likely to recover?

A
  1. meningitis–> recover fully w/o complications
  2. encephalitis–>residual neuro defects
  3. meningoencephalitis–>residual neuro defects
  4. poliomyelitis-like syndrome –> permanent deficits
35
Q

What are the 2 highest risk groups for getting WNV?

What is the seasonal/geographical preference?

A
  1. homeless
  2. elderly

Summer/fall nationwide/worldwide

36
Q

What 2 facts distinguish WNV from st. louis encephalitis?

A

WNV can:

  1. tremor due to basal ganglia involvement in 10%
  2. muscular weakness is profound and the characteristic manifestation
37
Q

What is diagnosis and treatment for WNV?

A 
Diagnosis = IgM via serology of serum or CSF
Treatment= rehab b/c there is no specific therapy
38
Q

What viral family does rabies virus belong to?
Is this virus RNA or DNA?
Where is the natural environment for the virus?

A

It is a rhabdovirus.
It is RNA and bullet-shaped.
It is found in the saliva of infected animals

39
Q

Describe how rabies causes disease in the host.

What primary lesion location will present with more rapid appearance of symptoms?

A
  1. infects tissue and stays at the site of the infection [soft tissue] for a variable amount of time
  2. binds to peripheral nerves
  3. retrograde transport up the axon into the DRG->spinal cord–> brain
  4. disseminates down nerves to the salivary glands to potentiate the cycle

Bites closer to the head with have a more rapid appearance of symptoms

40
Q

What areas of the brain are most affected by rabies virus?

A
  1. hippocampus
  2. brain stem
  3. pons
  4. purkinje cells of the cerebellum
41
Q

What clinical presentation is seen in the stages of rabies infection?
How long does each phase last?

A
  1. incubation- asymptomatic [variable]
  2. prodromal - fever, lethargy, nausea/vomiting, anorexia, headache, pain at the bite [2-10days]
  3. Loss of coordination, paralysis, delerium, confusion. They have hypersalivation, hydrophobia
  4. coma & death
42
Q

How is rabies diagnosed?

How can it be prevented?

A

Diagnosis:

  1. Viral antigen detection in the CNS [occurs late]
  2. Brain biopsy –> intracytoplasmic inclusion [Negri bodies]

Prevention:

  1. pre-exposure prophylaxis for high risk individuals [vets, lab personnel]
  2. killed-virus vaccine is given on the day of exposure and 3, 7, 14, 28 days after WITH Hyper-Rabies IG [HRIG]
43
Q

To what family does the JC virus belong?
Is it DNA or RNA?
What is it a known cause of?
Who is most likely to be infected?

A

It is a polyoma virus [like BK and SV40] and is a small DNA virus.

JC –> progressive multifocal leukoencephalopathy [PML] in patients with advanced AIDS

44
Q

Describe the course of infection in the body for JC virus cause of PML.

A
  1. JC virus is ubiquitous and infects almost all individuals.
  2. remains latent in kidneys, b-cells and monocytes
  3. when a patient is immunocompromised, the virus causes a demyelinating disorder of cerebral white matter
45
Q

PML typically presents in what fashion? What feature distinguishes it from other encephalitic processes?

A

It presents as rapidly progressive dementia with motor and cognitive defects.

It is distinguished from other encephalopathies by the fact that it is NOT febrile and the CSF findings will be normal

46
Q

What provides a presumptive and confirmed diagnosis of PML?

A
  1. MRI findings are presumptive

2. PCR of the CSF can confirm

47
Q

A 16 year old presents with gradual progressive neurological deterioration including:
-personality changes
- seizures
-myoclonus
- ataxia/spasicity
His only past medical history is that at age 2 he had uneventful measles that recovered. He has been asymptomatic since then.
You detect viral particles lacking M protein for the nucleocapsid and viral nucleic acid.

What is it likely that this patient has?
What regions of the brain are affected?

A

Subacute sclerosing panencephalitis [SSPE]

Affects white matter of the cerebral hemispheres and brainstem [although grey can be affected]

48
Q

In general for post-infectious encephalitis, what are the morphological features seen in the brain?

A
  1. viral particles are absent
  2. demyelination
  3. perivascular inflammatory infiltrate [predominantly CD8 targeting myelin]
49
Q

How can you differentiate primary infectious encephalitis from post-infectious?

A
  1. in primary, virus is present in the brain and CSF but in post-infectious it is absent
  2. Primary is an immune response directly against the virus [increased virus Ab index and specific T cells] where in post-infectious the T-cells attack myelin
  3. in primary there is perivascular inflammation with microglial nodules where in post-infectious there is perivenous demyelination
50
Q

What is Reye’s syndrome?
What are the 2 most commonly implicated viruses?
How does it present?
What is found at autopsy?

A

It is an encephalopathy associated with viral infectious illness and the use of aspirin [O-acetylsalicyclic acid] in children

  • influenza B
  • varicella

It causes vomiting, lethargy, confusion–>stupor and death. At autopsy acute fatty liver is discovered

51
Q

What are the characteristic pathological lesions involved with CJD?

A
  1. plaque formation

2. neuronal loss–> large vacuolated areas in the brain –> sponge appearance

52
Q

A 65 year old presents with extremely rapid onset progressive dementia. He has been having memory loss, personality changes, hallucinations, myoclonus, gait disturbances and seizures.
It has come one within the past 2 months.

What is the likely cause of this presentation?

A

CJD - prion disease

53
Q

How does new variant CJD [from mad cow] differ from sporadic disease?

A
  1. occurs at a younger age [28 vs 65]
  2. shorter incubation, but longer duration of disease
  3. painful paresthesias are present
54
Q

What is diagnosis for nvCJD?

A
  1. Brain biopsy is definitive

2. LP can show 14-3-3 protein

Nervous System (32 decks)

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