viral infections Flashcards

1
Q

Difference between meningitis and encephalitis

A

Meningitis is the inflam of meninges
Encephalitis is the inflam of brain parenchyma
Present differently

Meningitis presentation :
fever, vomiting, headache, photophobia, neck stiffness, rash , irritability, confusion/reduced consciousness(partially awake and aware) , seizures

Encephalitis presentation (Affects functioning of brain)

  • motor or sensory deficits
  • behavior/personality changes
  • altered mental state
  • speech or movement disorders
  • seizures
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2
Q

Viral causes of meningitis and encephalitis

A

Meningitis (self limiting causing viruses)
Mumps
Enteroviruses eg cox sackie B, echovirus– most common
Herpes simplex

Encephalitis 
Japanese encephalitis 
Rabies
Enteroviruses 
Herpes Simplex 
WNV
Varicella Zoster 

Paralysis
enteroviruses esp polio , JE, Zika, WNV - flaccid paralysis (lower motor neurone with or w/o meninigitis)

Post infectious encephalitis
VZV, measles - present w acute illness and neuro symptoms

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3
Q

What are the characteristics of viral CNS infections ?

A
  1. Can be part of a generalised infection (e.g.
    polio)
  2. May solely affect the CNS
  3. May present some time after the initial
    presenting infection (e.g. measles - SSPE)
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4
Q

Explain route of infection of virus

A

Multiplies in primary site then spreads to CNS via

1) blood - most common
2) nerves- HSV, rabies
3) olfactory mucosa

Causes damage to CNS via
multiplication and resulting damage and or host immune response (Cellular immune mediated and cytokine)

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5
Q

How does viral meningitis present?

A
• Classic symptoms
– Fever
– Headache
– Neck stiffness
– Vomiting
– Photophobia
• Not usually as sick as patients with bacterial
meningitis
• Symptoms usually evolve more slowly than bacterial
meningitis (several days)
• But may be indistinguishable from bacterial
meningitis
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6
Q

Diagnosis of viral meningitis

A

CSF findings : • CSF typically clear and colourless
• CSF white cell count elevated (lymphocytes) and
protein elevated but glucose normal
• Sometimes called “aseptic” meningitis
• PCR: Enterovirus RNA/ HSV DNA/ VZV DNA
Differential diagnosis: A similar CSF picture is seen in
a number of other conditions e.g.
– Other infection: Leptospirosis, Syphilis, Lyme,
Cryptococcosis, Toxoplasmosis, occasionally TB
– Malignant infiltration of the meninges
– Connective tissue diseases

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7
Q

Treatment and prevention of viral meningitis

A

VIRAL MENINGITIS: TREATMENT
• Excluding the neonatal period, usually mild, selflimiting
• Supportive: Rest, hydration, anti-pyretics
• Seizure management
• Unclear whether aciclovir is of benefit in HSV
meningitis (N.B. differentiate from HSV encephalitis,
which must be treated with aciclovir)
VIRAL MENINGITIS: PREVENTION
• Mumps meningitis is preventable by vaccination
(MMR)

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8
Q

Causes of Viral encephalitis

A

HSV, rabies, JE and West Nile

Herpes simplex; HSV 1>2 in adults and >3months ; most common cause in NE countries

For adults: HSV1

  • usually confined to CNS
  • primary infection/reactivation
  • temporal lobe mainly affected
  • mortality at 70% w/o treatment

For neonates- HSV2

  • usually involves dissemination
  • acquire infection at birth
  • global brain involvement ; brain is almost liquefied
  • mortality 100% if untreated
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9
Q

Route of infection for HSV

A

The virus spreads from sites of primary infection,
or from latent infection in cranial nerve trigeminal ganglia or olfactory nerve, to
the frontal or temporal lobes of the brain
causes haemorragic necrosis and inflam infiltrates

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10
Q

Which is more benign and self limiting -viral encephalitis / meningitis?

A

viral meningitis

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11
Q

Clinical features of HSV encephalitis

A

Acute neurological syndrome

  • hemiparesis
  • aphasia
  • behavioral changes
  • focal seizures
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12
Q

Diagnosis of HSV encephalitis

A

MRI- temporal lobe change
EEG
CSF - HSV PCR

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13
Q

Tx of HSV encephalitis

A

If suspected- treat w IV aciclovir (even in neonatal encepha)

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14
Q

Characteristics of West Nile Virus

A
• Belongs to a group of viruses known as
'arboviruses’ (= “arthropod-borne” viruses; viruses
transmitted by insects, ticks etc.)
• Birds = usual host
• Transmitted by the bite of
an infected mosquito
• Can infect humans, birds,
horses and some other
mammals
• Temperate countries (e.g., Northern North America)
– Late summer or early autumn
• Tropical climates (temperatures are higher and
mosquitoes active throughout the year)
– Can be transmitted year-round
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15
Q

How does WNV present?

A

• No Symptoms: (80%)
• Mild Symptoms: mild influenza-like illness, with
fever, headache and generalised aches and pains –
usually make full recovery
• Severe Symptoms: (less than 1%)
– Encephalitis
– Meningoencephalitis
Risk increases with age + immunosuppression

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16
Q

Diagnosis and Management of WNV

A

Diagnosis
• West Nile Virus IgM (blood or CSF)
– Since IgM antibody does not cross the bloodbrain
barrier, IgM antibody in CSF strongly
suggests central nervous system infection
Management
• Usually self limiting illness
• Supportive if severe infection
– Hospitalisation, intravenous fluids, respiratory
support, prevention of secondary infections

17
Q

rabies characteristics

A

• Acute encephalitis
• Bite or direct contact with the saliva of infected
animal
– The main reservoir = wild and domestic dogs,
wolves, foxes, coyotes, dingoes, bats
• Virus travels to brain by following peripheral nerves
• Incubation period depends on the distance the virus
has to travel to reach the CNS
– Once it does, symptoms appear
– Untreatable
– Fatal then within day

18
Q

clinical presentation of rabies

A
• Prodrome
– Fever, pain at bite site, salivation (autonomic
nervous system)
• CNS
– Restless / irritable/ aggressive (may also be
disorientated and have seizures)
then
– Encephalitis / paralysis
19
Q

tx for rabies

A

• Wash the wound as soon as possible
• Post-exposure prophylaxis as soon as possible
(within 10 days of exposure)
– Rabies immunoglobulin (around the bite site and
also IM)
– Rabies vaccine

20
Q

prevention of rabies

A

• Vaccination, including post-exposure
• Preventive veterinary measures include vaccination
of cats and dogs, as well as oral vaccination of wild
animal populations

21
Q

JE characteristics

A
• Major cause of encephalitis in Asia
• JE virus closely related to West Nile virus
• Transmitted to humans: infected mosquito,
primarily Culex species
– Humans =incidental host
– JEV is maintained in an enzootic cycle
between mosquitoes and vertebrate hosts,
primarily pigs and wading birds
• Rural agricultural areas
– Rice paddy fields
– Flood irrigation
22
Q

clinical presentation of JE

A

• In endemic areas, adults have acquired immunity from
infection or immunisation, and the infection is primarily
seen in children
• Clinical presentation
– Most human infections are asymptomatic
– <1% of infected individuals develop clinical disease
• Acute encephalitis (most common)
• Meningitis and acute flaccid paralysis, or febrile
illness are other less common manifestations
• Case fatality rate: 20-30%. Some 30-50% of survivors
have serious CNS sequelae

23
Q

diagnosis and tx for je

A

• Clinical:
• Neurological infection in an individual who
resides/recently travelled to an endemic area
• Laboratory:
• JE virus specific IgM detection on blood or CSF

no antiviral tx

24
Q

Prevention of je

A

• Minimise exposure
– Avoidance of outdoor or night-time exposure in areas with
active transmission; clothing/insecticides/ insecticide treated
bed nets
– Insecticide spraying and fogging
– Improved agricultural practices (centralised pig production)
• Immunisation =most important preventive measure:
– WHO recommend JE vaccine as part of routine immunisation
programmes in all areas where JE infection is a public health
problem
– Included in the routine childhood immunisation schedule in
Sarawak, Malaysia

25
Q

Polio transmission

A

faecal oral , human only reservoir

26
Q

How does polio present

A

90% asymptomatic/ mild illness OR 1-2%: biphasic illness: 2-3 days (fever and GIT symptoms) -
appear to recover then develop fever, severe headache and other
symptoms.
• Meningitis (1-5%)- usually recover
• Paralytic poliomyelitis (1 in 1,000)

27
Q

Define paralytic polio

A

• Spinal polio (80%)
– Asymmetric paralysis, usually legs
– Paralysis of muscles innervated by efferent
nerves from infected anterior horn cells
(asymmetric flaccid paralysis with no sensory
loss – destruction of lower motor neurons)
• Bulbar polio
– Replication in motor nuclei of lower cranial nerves
– Weakness of tongue & pharyngeal muscles
• Bulbospinal (combination of the above)

28
Q

Define post polio syndrome

A
  • 30-40 years after paralytic polio
  • Patients note increased weakness + muscle pain,
  • Due to loss of neurons in initially affected nerves
29
Q

Diagnosis and Treatment of polio

A

Diagnosis
• Clinical presentation
• CSF – PCR
• Early in illness – Viral culture for poliovirus (throat
secretions + faeces)
Treatment
• Supportive - pain relief and physical therapy.
• If respiratory failure may need mechanical
ventilation.
• Bulbar involvement = monitor closely CVS
(association with blood pressure fluctuations,
circulatory collapse, and autonomic dysfunction)

30
Q

Causes of chronic viral CNS infections

A
Subacute sclerosing
panencephalitis (SSPE)
• Persistent measles virus
infection in the CNS,
develops years after original
infection
• Rare: 1 in 1 million who had
measles in the first 2 years
of life
• Behavioural+ intellectual
deterioration+ seizures
• Fatal outcome

Immunosuppressed Host

HIV encephalopathy
• Convulsions
• Dementia
• Motor disorders

Progressive multifocal
leukoencephalopathy (PML)
• Uncommon opportunistic
infection caused by
reactivation of JC virus
resulting in demyelination
• No treatment – reduce
immunosuppression
31
Q

Cause of TSE

A

TSE= TRANSMISSIBLE SPONGIFORM
ENCEPHALOPATHY
• Fatal degenerative brain diseases
– E.g. Creutzfeldt- Jakob disease (CJD)
• Occur in humans and some animal species
• Causative agent is a protease‐resistant protein
which accumulates in the brain
– An altered form of naturally occurring prion
protein (PrP) present in human and animal
brain tissue
The altered prion proteins are resistant to
inactivation by standard chemical, thermal and
other means of inactivating microorganisms

32
Q

Two types of CJD

A
Variant CJD (vCJD)
CAN be prevented
Ingestion of BSE (bovine
spongiform
encephalopathy)-
contaminated animal
products + potentially,
receipt of contaminated
blood products
Iatrogenic CJD
CAN be prevented
Transmission of altered
prion protein via a
medical procedure
33
Q

Characteristics of TSE

A
  • Incubation period of months to years
  • Gradual increase in severity leading to death
  • They don’t evoke an immune response
34
Q

Diagnosis of CJD

A
• MRI brain changes may be helpful in diagnosis
• CSF 14-3-3 protein: non-specific
• Diagnosed conclusively by histological
examination at post-mortem
– Spongiform changes
– Amyloid plaques
– Prion proteins
35
Q

Prevention of CJD

A

• No proven effective therapy
• Prevention is focused on
– Protecting the blood supply by excluding those at risk from
donation (COMMUNITY)
– Protecting the food supply from BSE e.g. ban on feeding
bonemeal to cattle (COMMUNITY)
– Measures to protect staff from inoculation injuries (HOSPITAL)
– Appropriate management of surgical instruments that have
been used on patients with or at risk of CJD (HOSPITAL)
CJD PREVENTION: SURGICAL
INSTRUMENTS i.e
• Autoclaving (steam sterilisation) is highly effective at killing
micro-organisms BUT even autoclaving is not completely
effective against prion proteins
• Surgical instruments used on brain, spinal cord, posterior eye
of a patient with CJD should not be reused and should be
destroyed by incineration
• If used in other, low-risk surgical procedures
– After thorough cleaning, autoclave using standard protocol