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MID II > Viral Encephalitis > Flashcards

Viral Encephalitis Flashcards

1
Q

What is on your differential for fever/HA/confusion?

Works for any pathological process

A

Vitamin D

Vascular/ischemic

Infectious

Trauma

Autoimmune/inflammatory

Metabolic/systemic

Inherited/congenital

Neoplasm

Drug/toxic

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2
Q

What is the difference between viral meningitis and viral encephalitis?

A

Viral meningitis: viral infection of subarachnoid space
Symptoms = fever, HA, n/v, malaise, stiff neck, photophobia
Self-limited illness
Causes = enteroviruses, arboviruses, herpesviruses, acute HIV infecition, mumps

Viral encephalitis: viral infection of brain parenchyma
Symptoms = fever, HA, altered mental status, decreased consciousness, focal neurological findings
Causes = HSV-1, Arboviruses, enteroviruses

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3
Q

How do you distinguish the cause of meningitis?

A

CSF findings:

Bacterial = high protein (>100), low glucose (<40), neutrophilic pleocytosis

Viral = normal glucose, slightly elevated proteins, lymphocytic pleocytosis

Harder to distinguish viral/TB/cryptococcal meningitis

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4
Q

What is meninvoencephalitis?

A

When meningitis and encephalitis occur simultaneously

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5
Q

What is myelitis?

A

Inflammation of the spinal cord

Polio can cause poliomyelitis

West Nile Virus can also cause myelitis

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6
Q

Who is susceptible to viral encephalitis?

A

Very young, very elderly, immunocompromised

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7
Q

What viruses are more common in the summer?

A

Arboviruses, bc mosquito vector

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8
Q

How do neurotropic viruses enter the body/spread to nervous system?

A
  1. Enter host (respiratory trat, GI, GU, skin/subcutaneous tissue, ocular conjunctiva, direct inoculation to blood, transplant)
  2. Then adhere to M cells & transport to undelrying lymphoid tissue
  3. Hematogenous spread through BBB (where tight junctions aren’t so tight i.e. chorid plexus or through diapedesis

OR

  1. Neural spread i.e. Herpes 1/2, rabies, polio: retrograde transport
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9
Q

How do viruses cause neurovirulence?

A

Mostly direct effect of viral DNA: on cellular functions, cell death via apoptosis or necrosis

Some (JC virus) can infect oligodendroglial cells –> demyelination –> progressive multifocal leukoencephalopathy (PML)

Pathology is alsu due to host response to infection

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10
Q

How do you diagnose viral encephalitis?

A

Complete history including travel/exposures/sex/ immunization status

Signs: rash, lymphadenopathy, stiff neck,

Lab: PCR, serology, culture

  • CSF profile: normal glucose, slightly elevated protein
  • Rule out other causes: bacterial, fungal, parasitic, syphilis

Neuroimaging- MRI

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11
Q

How do you treat viral encephalitis?

A

Supportive care only

EXCEPT for HSV – treat with acycolvir

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12
Q

What features are indicative of HSV-1 viral encephalitis?

A

Reactivation from latency

Personality changes/bizarre behavior

Temporal lobe involvement: edema, enhancement, hemorrhage, mass effect

Hemorrhagic: find RBC in CSF

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13
Q

What strain of herpes virus is responsible for most herpes viral encephalitis?

A

HSV-1, 96%

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14
Q

What is the treatment for HSV-1 viral encephalitis?

A

Acyclovir- IV

Treat asap!! Even before you confirm diagnosis

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15
Q

What are common examples of arboviruses?

A

Togaviridae:
Eastern equine encephalitis- EEE
Western equine encephalitis

Flaviviridae:
Japanese encephalitis
St. Louis encephalitis
West Nile encephalitis

Bunyaviridae:
California serogroup – LaCrosse virus

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16
Q

What’s unique about the mode of transmission/life cycle of arboviruses?

A

Mosquito vector
Bite –> replicatoin in local tissue –> viremia/ hematogenous dissemination

Nonhuman animal host

Humans are dead end hosts

This means they are more common during the summer!

17
Q

How do you diagnose arbovirus encephalitis?

A

CSF serology or PCR

Note that West Nile Virus is diagnosed with serology, not PCR, bc viral load is usually too low

18
Q
A
19
Q

What’s unique about the clinical presentation of West Nile virus?

A

Incubation period of 2-15 days

3-5 day flu-like fever, lymphadenopathy, maculopapular rash

1/150 develop encephalitis + myelitis (acute flaccid paralysis syndrome, asymetric weakness, decreased tendon reflexes, localized damage to anterior horn cells of spinal cord

Seizures, CN abnormalities, ataxia (lack of voluntary control of muscles), movement disorders

20
Q

What does rabies virus look like?

A

Bullet shaped

Nonsegmented -RNA

21
Q

How is rabies transmitted?

A

Saliva of infected animals - bite/break in skin –> virus replication in muslce cells –> infects a nerve, spreads throughout CNS

BATS, dogs in developing countries

22
Q

What is indicative of rabies in histology?

A

Negri bodies: cytoplasmic inclusions containing lots of viral antigen

23
Q

What are the 5 proteins important in rabies & what do they do?

A

GLMNP

G=Glycoprotein, target for antibodies

L/P = RNA polymerase (“Lumbar Puncture” of polymerase)

N= wraps RNA (Nests the RNA)

M = viral assembly (Makes the virus)

24
Q

Why can you give postexposure prophylaxis for a long time with rabies?

A

Bc the incubation period is long (up to 1 year) and it can help, as long as the patient has not yet developed symptoms

25
Q

What is the fatality rate for patients who have symptoms due to rabies?

A

100%s

Except one girl from Wisconsin

26
Q

What’s the clinical presentation of rabies?

A

Asymptomatic incubation period

Flu-like prodrome of up to 2 weeks

Then you get anxiety, agitation, delerium, hypersalivation, hydrophobia (spasm of pharyngeal muscles at sound, sight, or taste of water), paralysis, seizures, coma

27
Q

How do you diagnose rabies?

A

RTPCR of saliva

Viral antigen (i.e. biopsy of hairline of neck, CSF, cornea)

28
Q

How can you prevent rabies?

A

Preexposure prophylaxis: 3 doses or rabies vaccine for high risk individuals

Postexposure prophylaxis: clean the bite with iodine, passive vaccination with immune globulin injected at the bite, and rabies vaccine

MID II (22 decks)

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