Encephalitis

Dr/ Asmaa Nasr El-DIN Thabet

• Encephalitis is inflammation of the brain. The
severity can be variable with symptoms
including headache, fever, confusion, a stiff
neck, and vomiting.

• Complications may include seizures,

hallucinations, trouble speaking, memory
problems, and problems with hearing.
• Causes of encephalitis include: viruses such as
herpes simplex virus and rabies as well as
bacteria, fungi, or parasites. Other causes include
autoimmune diseases and certain medications.
In many cases the cause remains unknown.

• Diagnosis is typically based on symptoms and

supported by blood tests, medical imaging, and
analysis of cerebrospinal fluid.
• Treatment may include antiviral medications
(such as acyclovir), anticonvulsants, and
corticosteroids. Treatment generally takes
place in hospital. Some people require
artificial respiration. Once the immediate
problem is under control, rehabilitation may
be required. In 2015, encephalitis was
estimated to have affected 4.3 million people
and resulted in 150,000 deaths worldwide.
 Signs and symptoms
• Adults with encephalitis present with acute onset
of fever, headache, confusion, and sometimes
seizures. Younger children or infants may present
with irritability, poor appetite and fever.
• Neurological examinations usually reveal a
drowsy or confused person. Stiff neck, due to the
irritation of the meninges covering the brain,
indicates that the patient has either meningitis or
meningoencephalitis.
 Causes of Encephalitis
(I) VIRAL ENCEPHALITIS

• Viral encephalitis can occur either as a direct

effect of an acute infection, or as one of the
sequelae of a latent infection. The majority of viral
cases of encephalitis have an unknown cause,
however the most common identifiable cause of
viral encephalitis is from herpes simplex infection.
Other causes of acute viral encephalitis are rabies
virus, poliovirus, and measles virus.
• Additional possible viral causes are:
• Arboviral flavivirus (St. Louis encephalitis,
West Nile virus),
• Bunyavirus (La Crosse strain),
• Arenavirus (lymphocytic choriomeningitis
virus), reovirus (Colorado tick virus.
• Henipavirus infections.
• Powassan virus is a rare cause of encephalitis
 Bacterial Encephallitis

• It can be caused by a bacterial infection, such as bacterial

meningitis. or may be a complication of a current
infectious disease syphilis (secondary encephalitis).

• Other bacterial pathogens, like Mycoplasma and those

causing rickettsial disease, cause inflammation of the
meninges and consequently encephalitis.

• Lyme disease or Bartonella henselae may also cause

encephalitis.[citation needed]
 Protozoal Encephalitis
• Certain parasitic or protozoal infestations,
such as toxoplasmosis, malaria, or primary
amoebic meningoencephalitis, can also cause
encephalitis in people with compromised
immune systems.
 Autoimmune encephalitis

• Autoimmune encephalitis signs can include catatonia,

psychosis, abnormal movements, and autonomic
dysregulation. Antibody-mediated anti-N-methyl-D-
aspartate-receptor encephalitis and Rasmussen encephalitis
are examples of autoimmune encephalitis.

• Anti-NMDA receptor encephalitis is the most common

autoimmune form, and is accompanied by ovarian teratoma
in 58 percent of affected women 18–45 years of age.
 Encephalitis lethargica

• Encephalitis lethargica is identified by high

fever, headache, delayed physical response,
and lethargy. Individuals can exhibit upper
body weakness, muscular pains, and tremors,
though the cause of encephalitis lethargica is
not currently known.
 Diagnosis of Encephalitis
• People should only be diagnosed with encephalitis if
they have a decreased or altered level of
consciousness, lethargy, or personality change for at
least twenty-four hours without any other explainable
cause.

• Brain scan, done by MRI, can determine inflammation

and differentiate from other possible causes.
• EEG, in monitoring brain activity, encephalitis will
produce abnormal signal.

• Lumbar puncture (spinal tap), this helps determine via

a test using the cerebral-spinal fluid, obtained from the
lumbar region.

• Polymerase chain reaction (PCR) testing of the

cerebrospinal fluid, to detect the presence of viral DNA
which is a sign of viral encephalitis
 Prevention

• Vaccination is available against tick-borne and Japanese

encephalitis and should be considered for at-risk individuals.

• Post-infectious encephalomyelitis complicating smallpox

vaccination is avoidable, for all intents and purposes, as
smallpox is nearly eradicated.

• Contraindication to Pertussis immunization should be

observed in patients with encephalitis.
 Treatment
• Antiviral medications (if virus is cause)
• Antibiotics, (if bacteria is cause)
• Steroids are used to reduce brain swelling
• Sedatives for restlessness
• Acetaminophen for fever
• Occupational and physical therapy (if brain
is affected post-infection)
 HERPES SIMPLEX VIRUSES
• There are two herpes simplex virusus, that
cross-react serologically but some unique
epitopes exist for each type.
• Mood of transmission:
HSV-1 spread by contact with infected saliva.
HSV-2 transimitted sexually or to newborns
through transvaginal delivery.
The infections that occurs by these routes are
primary infections.
 Primary infection
• Commonly occur in children 2-4 years of
ages in case of herpes simplex 1 after
droplet infection, and in case of HSV 2
Primary infection occur after sexual
contact In adults or after vaginl delivery in
newborns.
 PATHOGENESIS
• HSV multiply locally in the mucous
membranes or abraded skin causing
cytolysis, necrosis, ballooning, and
multinucleated giant cell formation with
intranuclear inclusion bodies.
• Giant cell formation occurs due cell fusion
that provide cell-to-cell spread even in the
presence of neutralizing antibodies.
 Clinical manifestations

HSV-1:
Primary infection is either asymptomatic or
in the form of tonsillopharyngitis.
Reactivation:
After disappearance of the primary lesions
the virus persist in a latent focus
( trigeminal ganglia), where the persists
life long.
• Reactivation takes the form of vesicular
eruption that changes to shallow ulcers
and scab forms that heals without
scarring.
• In HSV-1 reactivation may take one of the
following forms:
1- herpes labialis: crops of vesicles at the
mucocutaneous junctions of the lips or the
nose that recurred at the same site.
2- keratoconjunctivitis: corneal ulcers that
may leave opacities after healing and
leads to blindness.
3- encephalitis: that has a fatal outcome.
4- disseminated infections: such as
pneumoniae in immunocompromized
patients e.g. AIDS or transplant patients
.
Rabies virus
 BULLET-SHAPED
(1 flat end and 1 round end)

 ss RNA

 NON SEGMENTED

 ENVELOPED

 1 serotype & 2 biotypes

(street & Fixed)
Rabies Virus
 Moods of transmission
 Bite of rabid animal (Zoonotic)

through infected saliva. Virus migrates up

peripheral nerves to the spinal cord and ends
in the brain with no viraemia <<<< the
salivary glands(Saliva) & the cornea

 Non bite transmission

1. Aerosol transmission from bats.
2. Organ donations: in 2004, 4 cases in USA
documented from corneal transplantation.
3. Contamination of an open wound or a
mucous membrane
 Incubation of Rabies
 Averages 2 - 16 weeks

 Can be as short as 1 week or up to

1 year

 The two most important factors in

incubation of the virus are
1. Bite location & severity &
2. amount of the viruses
 In Humans
 fever, headache, and general
weakness or discomfort.
 insomnia, anxiety, confusion, slight
or partial paralysis, excitation,
hallucinations, hypersalivation
difficulty in swallowing, and
hydrophopia (fear of water).
 Convulsions, paralysis, coma, Death.
  In unvaccinated humans,
rabies is almost always fatal after
neurological symptoms have
developed,

But ?????
rapid post-exposure vaccination may
prevent the virus from progressing
 LABORATORY DIAGNOSIS
(1)Diagnosis in humans(antemortum)
Saliva, CSF, serum ,skin biopsy, corneal smear

1. Antigen detection by direct immunofluorescence

in skin, cornea (99% accurate)

2. the isolation of virus from saliva or CSF

3. viral RNA by RT-PCR (except serum)

4. Serological diagnosis(antibodies in serum &

 LABORATORY DIAGNOSIS
(2)Diagnosis in animals

 Animal<< observation for 10 days

 Signs appear <<< brain tissue smears

 Antigen detection by direct immunofluorescence

 Intracytoplasmic inclusion bodies (Negri
bodies).
 the isolation of virus from saliva or brain
 viral RNA by RT-PCR
Fluorescent Antibodies
 Management of rabies
Impending rabies
A. Immediately wash wounds vigorously
with soap and apply iodine solution, no
sutures

B. Tetanus toxoid & antibiotics

C. Post exposure prophylaxis

(passive-active immunization)
 ACTIVE IMMUNIZATION (Vaccines)
(inactivated vaccines)

1. Human diploid cell vaccine (HDCV)

2. Rabies vaccine adsorbed (RVA)

3. Purified chich embryo cell vaccine

(PCEC)
 Immunity within 7 days & lasts for 2
years
 5 IM doses(1 ml) on days 0,3,7,14,28.
 PASSIVE IMMUNIZATION

 Human rabies immuno globulins(HRIG)

 20 IU/kg IM at the bite site

 Prevention of rabies
 High risk occupations:
 Veterinarians
 Animal Control Employees
 Diagnostic Laboratory Workers
 Workers in Wildlife Fields
(1) Pre-exposure prophylaxis:
HDCV : 3 doses on days 0,7,21 or 28
Booster doses / 2 years
(2) Killing of stray dogs
(3) Quarantine of imported dogs
(4) Animal vaccination (Recombinant vaccine)
Thank you