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HNNS > HNS11 Infections Of The CNS II Viral Infection > Flashcards

HNS11 Infections Of The CNS II Viral Infection Flashcards

1
Q

Pathogenesis of viral CNS disease

A
  1. Direct invasion of CNS / Cytopathic / Cytolytic infection
    - Viral replication in CNS —> Neuronal damage —> disease
  2. Post infectious syndromes (e.g. Rubella)
    - Viral replication outside CNS (e.g. respiratory/GI tract)
    —> cross-reacting immune response (Ab/T-cell response) to myelin / dysregulation of immune response
    —> ***Demyelination of CNS
    —> disease
  • Biphasic illness
    —> 1st phase: mild respiratory / GI illness (then recover)
    —> 2nd phase: CNS disease
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2
Q

Infections of nervous system

A
  • Life-threatening with high mortality and morbidity
  • Presentation: Acute / Subacute / Chronic
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3
Q

Definitions of terms

A

Infection of:
- Brain —> Encephalitis
- Meninges —> Meningitis
- Spinal cord —> Myelitis
- Peripheral nerves —> Neuritis / Neuropathy

Many viral infections involve more than one site e.g. Meningo-encephalitis

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4
Q

***Clinical signs and symptoms

A
  1. Meningeal irritation (inflammation and pain sensitive)
    - Neck stiffness (difficulty stretching meninges)
    - Kernig’s sign (flex hip, difficulty extend knee (meninges at sacral spinal cord))
  2. Encephalopathic signs (brain involvement)
    - Alteration of consciousness
    - Fits
  3. Increased ICP (swelling of brain)
    - Headache
    - Vomiting
  4. Focal neurological signs
    - e.g. motor neuron paralysis, hemiplegia, spasticity
  5. Fever
    - systemic signs of infection
  6. Other features
    - mumps —> parotitis (inflammation of parotid gland)
    - enterovirus —> skin rash
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5
Q

Meningitis clinical signs and symptoms

A
  1. Infection —> fever
  2. Meningeal irritation —> neck stiffness, Kernig’s sign
  3. Increased ICP —> headache, vomiting

If progresses to brain parenchymal involvement —> Meningo-encephalitis
4. Alteration of consciousness, fits/seizures
5. Focal neurological signs —> paralysis

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6
Q

CSF findings in CNS infection

A
  1. Appearance
    Pyogenic: Turbid
    Viral: Clear / slightly turbid
    TB/Fungal: Clear / slightly turbid
  2. Total cell (per mm^3)
    Pyogenic: >500
    Viral: <500
    TB/Fungal: <500
  3. WBC
    Pyogenic: PMN (Neutrophil)
    Viral: Lymphocyte
    TB/Fungal: Lymphocyte
  4. Glucose
    Pyogenic: Very low
    Viral: Normal
    TB/Fungal: Low
  5. Protein
    Pyogenic: ++
    Viral: +
    TB/Fungal: ++
  6. Gram stain
    Pyogenic: 65-95%
    Viral: Negative
    TB/Fungal: Negative (but +ve in acid-fast stain for TB)
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7
Q

Distinguish between pyogenic, viral, TB/fungal infection

A

Viral vs Pyogenic:
- Clear CSF
- Low cell count
- Lymphocyte

Viral vs TB/Fungal:
- Normal glucose

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8
Q

Laboratory diagnosis of infection

A
  1. Virus detection
    - CSF (main stay)
    - brain biopsy / autopsy
    - throat swab (mumps, enterovirus)
    - stool (enterovirus)
  2. Serology
    - Serum
    —> Rising antibody titres (paired sample; early vs 14 days): Flu A/B, VZV, HSV, enterovirus, mycoplasma, (mumps, measles)
    —> IgM (single sera): JE, EBV, (CMV)
  • Intra-thecal Ab synthesis in CSF (compared to serum)
    —> detectable only later in illness (>10 days)
    —> paired serum / CSF specimens —> Ab index
  • Serology for enterovirus: problem: many serotypes and no common antigen
  1. Virus isolation / culture
    - limitations: isolation rate from CSF in meningitis is good (∵ close contact), but poor in encephalitis (e.g. HSV/enterovirus) —> brain biopsy only reliable specimen in encephalitis to isolate virus
    - unlikely to isolate virus from post-infectious encephalitis (∵ autoimmune attack)
    - isolation rate best early in illness
    - many enterovirus serotypes (most coxsackie A) do not grow on cell culture
  2. Viral nucleic acid (RNA/DNA) (***method of choice for CNS disease)
    - PCR of CSF
    —> herpes simplex encephalitis
    —> CMV encephalitis / myelitis
    —> VZV encephalitis / meningitis / myelitis
    —> more sensitive than culture in diagnosis of enterovirus
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9
Q

Etiology of viral meningitis

A

Common:
1. Enterovirus (ECHO, Coxsackie A/B) (summer months)
2. Herpes simplex type 2 (genital herpes)

Less common:
1. Mumps (∵ immunisation)
2. Lymphocytic choriomeningitis (LCM) (associated with rodents)
3. HIV seroconversion illness (very early phase)

Rare:
Other viruses

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10
Q

Enterovirus

A
  • One genus within family Picornaviruses
  • single +ve stranded RNA
  • non-enveloped
  • ***summer seasonality
  • > 100 human types (original classification: coxsackie A, B, ECHO, polio; current classification: enterovirus A, B, C, D; recent identification: numerically e.g. EV68-71)
  • EV types share a few common antigens, but protective immunity is type specific
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11
Q

Clinical syndromes associated with enterovirus (Polio, Cox A, Cox B, ECHO, EV70, EV71)

A
  1. Asymptomatic:
    ALL enterovirus
  2. ***Meningitis:
    ALL enterovirus
  3. ***Flaccid paralysis (anterior horn of spinal cord infected):
    ALL enterovirus (Polio, EV71, EVD68 ++)
  4. **Hand foot and mouth disease
    - Cox A (A16) +
    - **    EV71 ++
    - Cox B -
    - ECHO -
  5. Carditis
    - Cox A +
    - Cox B ++
    - ECHO +
  6. Conjunctivitis
    - Cox A (A24) +
    - EV70 ++
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12
Q

Hand foot and mouth disease (HFMD)

A
  • Usually only skin / mucosal lesions —> mild
  • but occasionally (esp. EV71) causes:
    1. Lower motor neuron —> Flaccid paralysis
    2. Brainstem encephalitis
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13
Q

Herpes simplex virus meningitis

A
  • Usually Herpes simplex type 2
  • > 30% of female, 11% of male with primary (1st time) genital HSV have meningitic involvement
  • Self-limited (unlike HSV encephalitis)
  • Acyclovir role/need unclear
  • Latent in ganglion, can recur from time to time
  • young adults with ***aseptic meningitis —> think of HSV2 possibility esp. during winter months
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14
Q

Etiology of viral encephalitis

A

Common:
- Herpes simplex type 1 (antiviral available) (HSV2 in neonates)
- Enterovirus
- VZV

Less common:
- Febrile exanthems (measles, rubella, HHV-6)
- Arboviruses (e.g. Japanese encephalitis) (travel in last 3 weeks)
- Other: EBV, influenza, mumps, adenovirus, HIV, LCM etc.
- Rabies

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15
Q

How does herpes simplex virus get into brain

A
  • Follow primary infection / reactivation
  • Entry into CNS via:
    1. Spread along **olfactory nerve (from nasopharynx) —> through cribriform bone —> affects frontal lobe
    2. Reactivation from **    trigeminal ganglion (innervates ***pia mater) —> infection of brain
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16
Q

Herpes simplex encephalitis (HSE) lesions

A
  • Usually Temporal lobe / Orbital surface of frontal lobe
  • but adjacent frontal, parietal, occipital lobe, cingulate gyri may also be involved
17
Q

HSE clinical features

A
  1. History
    - altered consciousness
    - headache
    - seizures
    - vomiting
    - memory loss
  2. Clinical findings
    - fever
    - personality change
    - dysphasia
    - autonomic dysfunction
    - ataxia
    - hemiparesis
    - seizures
    - cranial nerve deficits
18
Q

HSE CSF findings

A
  1. Protein >40 mg/dL
  2. Lymphocyte pleocytosis > 5/mm^3: 96% (median 130)
  3. RBC >50: 42% (not diagnostic of HSE) (necrosis of brain —> bleeding into CSF)
  4. Normal CSF: blood glucose ratio 95%
19
Q

HSE Lab diagnosis

A
  1. ***HSV DNA detection by PCR in CSF (method of choice)
    —> HSV DNA may still be detectable up to 7 days after start of ACV therapy
    - intrathecal CSF Ab may confirm, but usually later in illness
  2. Virus rarely cultured from CSF
  3. Isolating HSV in throat / mouth is of little significance
    —> may be reactivation of latent virus unconnected with CNS
    —> ~1% of healthy persons have HSV isolated from mouth
  4. Serology in blood little use, not conclusive
20
Q

HSE treatment

A
  • Life threatening, medical emergency
  • if untreated, 70% mortality, many survivors have permanent brain damage
  • Start treatment on clinical suspicion while waiting for CSF PCR results
  • ***IV acyclovir is life and function saving
  • Relapse of HSE is being recognised with early stopping of acyclovir —> ***14-21 day acyclovir therapy
21
Q

Japanese encephalitis

A
  • Arbovirus (arthropod borne)
  • common in South China and SE Asia, present but rare in HK
  • Mosquito-borne
    —> present in water bird
    —> transmitted by mosquitoes
    —> pigs bitten by mosquitoes
    —> peri-domestic amplifier host (pigs have a lot of virus)
    —> bitten by mosquitoes again
    —> mosquitoes bite human
  • transmission between animals is by a mosquito typically associated with rice fields
  • considered as Zoonosis (maintained in an animal reservoir (water birds and pigs))
  • human infection is “dead end” —> NO human-to-human transmission (very rare case via blood transfusion)

Clinical features:
- Asymptomatic (90-95%)
- Symptomatic —> 10-30% mortality, many survivors have permanent brain damage

Vaccine:
- Available for prevention in endemic areas

22
Q

Myelitis / Neuropathy etiology

A
  • Enterovirus (EV71, Polio, others)
  • VZV
  • EBV
  • CMV
  • Exanthems
  • Mumps
  • HSV2
  • Japanese encephalitis
  • Zika (Guillain Barre syndrome)
23
Q

Varicella-zoster virus

A

Primary infection: Chicken pox —> virus latent in dorsal root ganglion
Recurrence: activation of virus by trigger factors —> transmit down peripheral nerves / spinal cord —> Shingles —> restricted to dermatome (unilateral)

Skin lesions may precede / follow CNS disease
—> may be absent: Zoster sine herpete: only dermatomal pain with absence of rash

Zoster causes:
- Encephalitis
- Myelitis

Reactivation in AIDS (40% no rash):
- Myelo-radiculitis
- Chronic progressive encephalitis
- Ventriculitis

24
Q

Etiology of CNS infection in immunocompromised patients

A
  1. Cytomegalovirus
    - encephalitis
    - cranial nerve palsies
    - poly-radiculopathy
  2. VZV
    - myelitis
    - encephalitis (acute/progressive)
    - radiculitis
    - ventriculitis
  3. JC virus
    - progressive multifocal leukoencephalopathy
  4. HIV
  5. Chronic enteroviral meningo-encephalitis in agammaglobulinaemics
25
Q

Rabies

A
  • Rabies virus
  • RNA virus, Rhabdovirus
  • Zoonosis, main reservoir: Dogs
  • In HK: last local human case 1981, last animal rabies 1987
  • common in neighbouring countries
    —> imported cases seen
    —> exposure of dog bites overseas need to be managed
  • animal saliva is infectious if introduced on mucosal surface / broken skin
  • human-to-human transmission very uncommon

Pathogenesis:
Virus replicates at site of bite (e.g. muscles)
—> enter peripheral nervous system via stretch spindles
—> **passive ascend via **sensory fibres (slow axonal transport: long incubation period)
—> **replication in dorsal ganglion
—> **rapid ascend in **spinal cord (axonal transport)
—> infection of spinal cord, brainstem, cerebellum, other brain structures
—> **descending infection via sensory, autonomic nervous system to retina, cornea, salivary glands, skin, nasal mucosa, other organs

26
Q

Clinical features and managment of Rabies

A

Long incubation period: usually 20-90 days, can be >1 year

Prodromal: non-specific, onset of itching at site of healed bite wound

2 presentations:
1. Furious rabies (typical): hydrophobia (spasm of swallowing reflex), aerophobia, meningo-encephalitis
2. Paralytic rabies: paralysis begins in bitten limb and spreads, may be confused with myelitis / encephalitis due to other causes
—> Both invariably fatal

Laboratory diagnosis —> demonstration of virus:
1. Brain (Viral inclusion bodies / Negri bodies)
2. Skin biopsy (after descending infection)
3. Corneal impression smear

Management:
- No treatment once symptoms appear —> fatal
- Prevention only

Prevention:
1. Management of dog bites
- good wound toilet, aggressive washing of bite to physically wash out virus, use local anaesthesia if needed
- avoid suturing
- manage Tetanus risk (Tetanus vaccine)

  1. Assess rabies risk (where, what animal, unprovoked, break in skin / mucosal exposure)
    - rabies only affect ***mammals (no risk from insects, reptile, bird, fish), domestic rats in HK are NOT infected
    - endemic area: no endemic rabies in HK, infection in China / other parts of Asia. is the animal imported? Bite occur overseas?
    - behaviour of animal: unprovoked bite? has animal bitten other human/animal? clinical signs of rabies (paralysis, increased salivation) of the animal?
    - is animal available for observation? If animal is alive after 7 days —> rabies excluded, animal brain submitted for virology examination —> infection can be diagnosed by looking for viral inclusion bodies (Negri bodies) / virus antigens by IF
  2. Post-exposure prophylaxis
    - possible due to long incubation period
    - active / passive immunisation (for risk present / high risk present respectively)
    - Active immunisation: **Human diploid cell vaccine (killed vaccine), 4 doses give IM to deltoid at days 0, 3, 7, 21 —> immunisation course can be aborted if animal later shown to be NOT infected
    - Passive immunisation: **    Human rabies immune globulin (HRIG) —> infiltrate bite wounds thoroughly —> inject any reminder IM to thigh (at a site different to vaccine)
  3. Control of source
    - control stray dogs
    - vaccination of dogs (done in HK)
  4. Pre-exposure prophylaxis
    - vaccine for high risk individuals (e.g. vets, long term travel in endemic areas)

HNNS (58 decks)

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