viral infections Flashcards
(35 cards)
Difference between meningitis and encephalitis
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
Viral causes of meningitis and encephalitis
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
What are the characteristics of viral CNS infections ?
- Can be part of a generalised infection (e.g.
polio) - May solely affect the CNS
- May present some time after the initial
presenting infection (e.g. measles - SSPE)
Explain route of infection of virus
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)
How does viral meningitis present?
• 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
Diagnosis of viral meningitis
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
Treatment and prevention of viral meningitis
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)
Causes of Viral encephalitis
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
Route of infection for HSV
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
Which is more benign and self limiting -viral encephalitis / meningitis?
viral meningitis
Clinical features of HSV encephalitis
Acute neurological syndrome
- hemiparesis
- aphasia
- behavioral changes
- focal seizures
Diagnosis of HSV encephalitis
MRI- temporal lobe change
EEG
CSF - HSV PCR
Tx of HSV encephalitis
If suspected- treat w IV aciclovir (even in neonatal encepha)
Characteristics of West Nile Virus
• 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
How does WNV present?
• 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
Diagnosis and Management of WNV
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
rabies characteristics
• 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
clinical presentation of rabies
• Prodrome – Fever, pain at bite site, salivation (autonomic nervous system) • CNS – Restless / irritable/ aggressive (may also be disorientated and have seizures) then – Encephalitis / paralysis
tx for rabies
• 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
prevention of rabies
• Vaccination, including post-exposure
• Preventive veterinary measures include vaccination
of cats and dogs, as well as oral vaccination of wild
animal populations
JE characteristics
• 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
clinical presentation of JE
• 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
diagnosis and tx for je
• 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
Prevention of je
• 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
