Viral Meningitis Et Al

Front 1

Exceptions to hematogenous spread of viruses
(virus & method of spread)

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Herpes (HSV & Zoster): encephalitis from reactivation in trigem nerve (or de novo infxn)
Rabies: CNS via retrograde movement in neurons

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Aseptic meningitis definition

Back 2

inflamm of meninges w/o an identifiable etiological agent from gram stain or culture (misnomer)

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fatal viral encephalitis

Back 3

inflamm rxn in meninges & brain (moncytes & PMN)
neural cells degen, macrophages engulf neurons, can have giant cells w/ viral antigens

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Leading cause of aseptic meningitis

Back 4

enteroviruses (85-90%) - picornavirus family

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Enteroviruses family, structure
spread, seasonality, pathogenicity

Back 5

Picornavirus family (+ssRNA), Summer/Fall seasonality
Fecal-oral spread, Patho: resists stomach acid/disinfection

Front 6

Picornaviruses

Back 6

Echo, polio, Hep A, coxackie A, B

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Poliomyelitis family?
targets in body?
replicates in?

Back 7

Enterovirus, acute infxn of meninges & motor neurons of anterior horn of spinal cord (flaccid paralysis)
replicates in neurons, mostly elim from vaccine

Front 8

VAPP

Back 8

(VAPP - vaccine associated paralytic polio = when vaccine causes polio)

Front 9

Polio Vaccines
Advantages/problems

Back 9

eIPV (enhanced Inactivated Vaccine, aka Salk) - no VAPP, not good mucosal immunity (can be infected and excrete but be protected)
OPV (Live attenuated, aka Sabin) - can revert and cause polio (VAPP)

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Post-polio syndrome

Back 10

25-30 yrs after recovery - gradual progression of muscle weakness
thought c/o small pool surviving in motor neurons

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Mumps virus family & structure

Back 11

paramyxovirus - large neg ssRNA, enveloped
spread via respiratory (Winter & spring)
"flu floor of helix - cough, big cheek, dots faced man w/ parachute)

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Mumps virus neuro complications

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3x more common in males
encephalitis 1/6000 mumps cases
meningitis (w/ symptoms) in 4-6% of cases, (but clear CSF in 50%)

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Most common cause of aseptic meningitis/encephalitis in unimmunized population

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Mumps virus

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Mumps virus spread in body

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Inhale (respiratory) -> local replication -> viremia -> systemic infxn ->
Pancreas, Parotid gland, CNS, (Tests/Ovaries, Ear, Eye, periph nerves)

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Arboviruses highest incidence

Back 15

late summer/fall (arthropod vector active

Front 16

Arboviruses

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togaviruses, Equine Encepha (EEE, WEE, VEE)
"guy wearing toga w/ ruby in front of crazy horse"

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togavirus structure

Back 17

small, enveloped + ssRNA

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Equine Encephalitis types & seriousness

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EEE, WEE, VEE
VEE = serious encephalitis (esp. children - 60% mortality) w/ serious neuro sequelae if survive

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Equine encephalitis transmission & frequency

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uncommon (0-20 cases/year)
mosquito vector btwn birds & horses/humans (dead end hosts)

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Flavivirus structure
most common neuro disease caused

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small enveloped + ssRNA
St. Louis Encephalitis = #1 for EPIDEMIC encephalitis in US (urban & rural)
less severe than EEE, WEE, VEE

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Flaviviurs transmission

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Bird reservoir
mosquito vector (human = dead end host)

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Flavivirus members

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"Welcome to FLA where people are C NILE"
Hep C, West Nile Virus

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Bunyavirus structure

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ssRNA w/ segmented RNA

Front 24

Bunyavirus transmission
disease

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mosquito
benign aseptic meningitis to severe encephalitis (rarely fatal, some sequelae)

Front 25

Colorado Tick Fever virus structure

Back 25

Reo virus (dsRNA, double capsid, no envelope)
"REO de janeiro sign w/ dbl border & ds below"

Front 26

Colorado Tick Fever virus disease
infects what cells?

Back 26

infects erythroid precursor cells
neonatal infxn -> meningitis & encephalitis
usually benign but may get nuchal rigidity & pleocytosis

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Herpesvirus structure

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large dsDNA w/ envelope from nuclear membrane
"alpha gamma beta picture
alpha = chicken (12 eggs = type 1 & 2)
gamma = BAR w/ 8 ball
beta = giant 6 (CMV)

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Most important Herpes in neuro disorders

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Encephalitis: HSV 1 (95% type 1, 5% type 2)
HSV1 very common - #1 for NONepidemic fatal encephalitis

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HSV1 spread
initial signs of infection

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Spread via infected secretions (usually oral)
Primary infection asymptomatic or gingivostomatitis or pharyngitis

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HSV1 vs. HSV2 disease

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HSV1 = encephalitis (95% type 1, 5% type 2)
HSV2 = meningitis

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HSV pathogenesis

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Primary infxn (asymptomatic, gingivostomatitis or pharyngitis) -> tranport up nerve fibers -> latency in sensory ganglia (usually trigem) -> encephalitis (can be primary, re-infection, or reactivation)

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Rabies structure/disease

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rhabdovirus: neg. ssRNA bulletshaped lipoprotein membrane (bullet w/ bunny in it ontop of helix)
fatal ecephalomyelitis

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Rabies transmission

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infected carnivores (fox, raccoon, skunk, dog)
Rare: respiratory route (inhale bat urine)

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Rabies pathogenesis

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1) bite implants infected saliva in muscle near nerve
2) virus replicates in muscle near bite (10-240 day incubation)
3) virus travels through axon to CNS
4) replication in neurons of gray matter -> negri bodies (cytoplasmic inclusion bodies)
5) migration to other organs

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Rabies manifestations

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1) padromal (nonspecific - abnormal sensations at bite site)
2) excitation phase (anxiety, eye problems, hydrophobia)
3) paralytic phase (flaccid paralysis, apathy, stupor, coma, vascular collapse -> death)

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Rabies Diagnosis

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History (bite by known rabid animal), Symptoms (classic lab findings show nothing)
ID of virus via fluorescent Ab

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Postinfectious encephalomyelitis onset, hallmark/symptoms

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short lag occurs btwn virus and disease
symptoms: inflammation & demyelination (probably from immune response) in brain, spinal cord, optic nerve
SECOND most important complication (#1 is disseminated infxn, pneumonitis, gastroenteritis, 2nd bacterial infxn)

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Postinfectious encephalomyelitis causes
sequelae

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Varicella, measles, mumps, Vaccinia (vaccine), measles (paramyxovirus), unknown URI
50% have blindness, paraplegia, ataxia (10% seizure disorder)

Front 39

Postinfectious encephalomyelitis CSF

Back 39

virus rarely recovered - usually CSF antibody, inclusion antibodies in brain

Front 40

Measles pathogenesis

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1) respiratory tract -> local replication
2) lymphatic spread -> viremia (wide dissemination)
3) infxn of endothelial cells & T-cells -> Rash
4) Sequelae

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Measles Sequelae

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Postinfectious encephalitis, Subacute Sclerosing Panencephalitis, or no recovery

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Experimental Autoimmune Encephalomyelitis

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Experimental: immu w/ Ag in CNS (e.g. myelin) + adjuvant
1-2 wks later: encephalomyelitis (perivascular infiltrates of lymphocytes, macrophages) -> demyelination

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SSPE
cause, frequency, most common in population

Back 43

Subacute Sclerosing Panencephalitis (measles sequelae)
1/1x10^6/year before vaccine (most common in children who had measles before 2yo)

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SSPE onset, relative frequency

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onset 7-8 yo (6 yrs after measles infxn (males:female 3:1)

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SSPE symptoms

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Insidious (slow) onset w/ behavior problems, early dementia
Later: disturbed motor function, seizures, rigid state
death 1-3 years

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SSPE pathogenesis

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Measles Ag AND Ab in CNS
Variant Measles virus (reduced/absent matrix protein, fusion protein, hemmagglutinin) -> restricted reproduction -> few mature viruses, lots of nucleocapsids in many cells

Front 47

Guillain-Barre Syndrome definition

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Acute inflammatory demyelinating polyradiculopathy
#1 cause of severe general paralytic disease in US (c/o poliomyelitis decline)

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Guillain-Barre Syndrome pathogenesis
onset
mortality

Back 48

associated w/ prior virus-like respiratory or GI infxn
onset 1-4 wks after infxn
may be c/o sensitization to PERIPHERAL nerve myelin -> ascending motor weakness
85% recover (may take 4-6 months)