Meningitis

and
Encephalitis

Dr. Sugandha Shrestha

Meningitis
It is aninflammationof the protective
membranes covering thebrainandspinal cord,
known collectively as themeninges.

The inflammation is usually caused by an

infection of the fluid surrounding the brain and
spinal cord.

It can be life-threatening condition and is

classified as amedical emergency.
Etiology
Infectious causes of meningitis include :
Bacteria ,Viruses ,Fungi

environmental and exposure history,

recent travel or immunocompromised
state (such as HIV, diabetes, steroids,
chemotherapy) are important elements.
Meningitis
Conditions most common
pathogen
Neonatal period -------- Group B beta hemolytic
streptococci
Under age of 5 --------- Haemophilus
influenzaetype B
Adolescent -------- Neisseria Meningitidis
(meningococcal meningitis)
(Epidemic meningitis)
Adult -------- Strept. Pneumoniae
AIDS -------- cryptococcus neoformans
Neurosurgical pt. ------- Staph. Aureus
 Symptoms and sign
Sudden high fever
Severe headache
Nausea or vomiting
Confusion or difficulty concentrating
Seizures
Sleepiness or difficulty waking
Sensitivity to light
No appetite or thirst
Skin rash (sometimes, such as in meningococcal
meningitis)
 Nuchal rigidity
Photophobia

Meningism : its a sign of irritation of

meninges. Its triad of nuchal rigidity,
photophobia and headache.
 Nuchal rigidity is a condition in which the neck is
extremely stiff or inflexible .A key indicator of
meningeal irritation.

Clinical tests for it, from least to most sensitive are

Kernig sign (resistance to passive knee extension)
Brudzinski sign (full or partial flexion of the hips and
knees when the neck is flexed).
Bacterial meningitis


Bacterial meningitis
Bacterial meningitis is an acute purulent
infection within the subarachnoid space.
It is most common form of suppurative CNS
infection.
But it can also occur when bacteria directly
invades the meninges.
This may be caused by an ear or sinus
infection, URTI ,skull fracture or rarely after
some surgeries.


Etiology
The bacteria can spread person to person through
coughing and sneezing, sharing utensils and hand
to hand contact.

It is an extremely serious illness that requires

immediate medical care. if not can lead to
permanent brain damage and other parts of body
or death.

Average Incubation period is 4 days but can range

from 2-10 days.
 Bacterial cause
Several strains of bacteria can cause acute bacterial
meningitis, most commonly :
Streptococcus pneumoniae (pneumococcus): most
common and commonly causes pneumonia or ear or
sinus infections .
Neisseria meningitidis (meningococcus): This
bacterium is another leading cause of bacterial
meningitis and commonly cause an upper respiratory
infection .
Haemophilus influenzae (haemophilus)
Listeria monocytogenes (listeria) :These bacteria can
be found in unpasteurized cheeses, hot dogs and
luncheon meats.
Pathophysiology
symptoms
Common symptoms of bacterial meningitis
include:
Difficulty thinking clearly
Fever
Generalized aches and pains
Headache
Increased sensitivity to light (photophobia)
Irritability in children
Loss of appetite or poor feeding in children and
infants
Malaise or lethargy
Neck stiffness
Rash
 Serious symptoms of bacterial meningitis include:
Change in level of consciousness or alertness, e.g
unresponsiveness
Change in mental status or sudden behavior
change, such as confusion, delirium, lethargy,
hallucinations and delusions
High fever
Tachycardia
Seizure
Severe dizziness or sudden loss of balance
Severe headache
Unusual irritability or poor feeding in children and
infants
Unusual neck stiffness or pain
Risk factor
Skipping vaccinations
Age: viral meningitis <5yrs and bacterial
meningitis is common in those under age 20 .

Living in a community setting

Pregnancy :caused by listeria monocytogenes.
increases the risk of miscarriage, stillbirth and
premature delivery.

Compromised immune system: AIDS,

alcoholism, diabetes, use of
immunosuppressant drugs and other factors
that affect immune system e.g h/o splenectomy.
Examinations
Laboratory screening of blood, urine,
and body secretions : throat culture
Analysis of the cerebrospinal fluid
Brain imaging : CT and MRI
can reveal signs of brain inflammation, internal
bleeding or hemorrhage, or other brain
abnormalities .
CSF findings
CSF is turbid.
Glucose (mg/dL): Normal to marked decrease
<40 mg/dL.
Protein (mg/dL) Marked increase > 250 mg/dL.
WBCs (cells/L)>500 (usually > 1000). Early:
May be < 100.
Cell differential: Predominance of Neutrophils
(PMNs)
Culture: Positive Opening Pressure Elevated
Treatment
Antibiotics : ceftriaxone & vancomycin
Anticonvulsant : phenytoin or
phenobarbitol
(if seizures in severe case)
Antiemetics : ondensetron
Steroids : reduce inflammation and
swelling
Sedatives
IV fluids
complication
Long term complications of bacteria meningitis
may include permanent neurological deficits
such as
Mental retardation
Deafness
Brain damage
Cranial nerve palsies
Gait problems
Viral meningitis
Viral meningitis is usually caused by
enteroviruses.
Viral meningitis is more common than the
bacterial form.
Viruses such as herpes simplex virus, HIV,
mumps, West Nile virus and others also can
cause viral meningitis.
Much less likely to cause permanent brain
damage after infection is resolved. most will
recover completely.
CSF findings
Glucose: Normal (> 40 mg/dL.)
Protein :<100 mg/dL (moderate increase)

WBCs (cells/L)< 100 cells/L.

Cell differential :Early: neutrophils. Late:

lymphocytes.
Culture: Negative Opening Pressure

Usually normal
DNA-based test known as a polymerase
chain reaction (PCR) amplification.
 Meningitis of lyme disease may have:
History of tick bite (20%)
Migratory type of joint involvement
Rash bulls eye rash / Target / red
outside pink inside rash
Meningitis of RMSF: (rocky mountain spotted
fever)
Camping / hiking history
History of tick bite (60%)
Rashes start peripherally and moves
centrally (centripetal)
 RMSF
Treatment
Lyme disease meningitis :
Ceftriaxone
RMSF :
Doxycycline
Nisseria meningitis:
Ciprofloxacin and rifampicin.
Rifampicin is given to all in close contacts
Fungal meningitis
Fungal meningitis
Fungal meningitis is relatively uncommon . It
may mimic acute bacterial meningitis .
Fungal meningitis isn't contagious from person
to person .
Cryptococcal meningitis is a common fungal
form of the disease that affects people with
immune deficiencies, such as AIDS.
It's life-threatening if not treated with an
antifungal medication .
Pathogenesis
Fungi reach the CNS by hematogenous spread
from:
Lungs
Heart
GI or genitourinary tract
Skin
by direct extension from para-meningeal sites:
Orbit
Paranasal sinus
 symptoms
Common symptoms include:
Headache
Lethargy or confused
Nausea and vomiting
Photophobia
Seizure
Nuchal rigidity
Careful examination of the skin, orbits, sinuses,
and chest may reveal evidence of systemic
fungal infection.
 Neurologic examination may show signs:
Meningeal irritation
Papilledema
Ptosis
Visual loss
Focal neurological abnormalities e.g
hemiparesis
exopthalamus
Investigations
Lab: blood culture, CBC, RBS, Electrolytes,
LFT, RFT, urinalysis (candida).
Chest X-Ray: may show hilar
lymphadenopathy, or miliary infiltrates,
cavitation, or pleural effusion.
CT or MRI: may demonstrate intracerebral
mass lesions associated with cryptococcus or
other organisms, a contiguous infectious
source in the orbit or paranasal sinuses, or
hydrocephalus.
Lumbar Puncture (LP): CSF pressure is
usually elevated, and the fluid is usually clear.
 Hilar lymphadenopathy lung cavitation
 CSF findings:
Glucose :<40 mg/dL (Low)
Protein :(moderate to marked increase) 25 -500
mg/dL
WBCs (cells/L) :Variable (10 -1000 cells/L)
<500cells/L.
Cell differential: Predominance of Lymphocytes
Culture: Positive (fungal)
Opening Pressure : Variable
Gram stain and india ink preparation may
reveal the infective organism.
 Treatment
Amphotericin B :
1 mg intra-venous as a test dose given over 20-
30 minutes.
followed the next day by 0.3 mg/kg
intravenously in 5% dextrose, given over 2-3
hours. The dose is then increased daily in 5- to
10-mg increments until a maxi-mal dose of 0.5-
1.5 mg/kg/d is reached.

Treatment is usually continued for 12 weeks.

Nephrotoxicity is common.
 Flucystocin :
Cryptococcus meningitis.
100mg/kg/d orally, added to amphotericin B
and given in four divided dose.
reduces the duration of therapy from 12wks to
6 weeks.
Side effects :bone marrow suppression
(reversible).
Dose should be adjusted in case of renal
failure.
Not used in patients with AIDS.
 Fluconazole :
Not responding to amphotericin B alone.
initial dose of 400mg, followed by 200 mg/d,
orally or intravenously, for at least 10-12
weeks after CSF cultures are negative.
Long-term maintenance therapy with
fluconazole, 100-200 mg/d orally,
may also reduce the likelihood of recurrence
following successful treatment of cryptococcus
meningitis in patients with AIDS.
Tubercular meningitis
 Tubercular meningitis is mycobaterium
tuberculosis infection of meninges.
It is the most common form of central nervous
system tuberculosis (TB).
has very high morbidity and mortality.

Individuals with increased risk for TBM include

young children with primary TB and patients
with immunodeficiency caused by aging,
malnutrition, or disorders such as HIV and
cancer .
Pathogenesis
TBM usually results from reactivation of latent
infection with Mycobacterium tuberculosis.
Primary infection may be associated with
metastatic dissemination of blood-borne bacilli
from the lungs to the meninges and the
surface of the brain.
Here the organisms remain in a dormant state
in tubercles that can rupture into the
subarachnoid space at a later time, resulting in
tuberculous meningitis.
Clinical manifestations
Symptoms have usually been present for less
than 4 weeks at the time of presentation.
low-grade fever, malaise, headache, dizziness,
vomiting, and/or personality changes may
persist for a few weeks .
after which patients can then develop :
severe headache
altered mental status,
stroke, hydrocephalus, and cranial
neuropathies.
Seizure is absent .
Examinations
Lab:
Only 1/2 - 2/3 of patients show a positive skin
test for tuberculosis .
Chest X-Ray:
2/3 of pt. shows evidence of active or healed
tubercular infection on chest x-ray.
Lumbar puncture:
The diagnosis is established by CSF analysis.
 CSF findings:
CSF pressure is usually increased, and the fluid
is clear, colorless or yellow. The fluid may form
a clot upon standing.
Glucose :<40 mg/dL (Low)
Protein: (moderate to marked increase) 50
-500 mg/dL
WBCs (cells/L) :Variable (10 -1000 cells/L)
<500cells/L.
Cell differential: Predominance of Lymphocytes
Culture: Positive for AFB
Opening Pressure :Variable
 Acid-fast smears of CSF should be performed
in all cases of suspected tuberculous
meningitis, but they are positive in only a
minority of cases.
Definitive diagnosis is most often made by CSF
culture.
The PCR has also been used for diagnosis.
CT Head : may show contrast enhancement of
the basal cisterns and cortical meninges, or
hydrocephalus.
Treatment
Four drugs are used for initial therapy,
until culture and susceptibility test
results are known.
These are isoniazid 300 mg; rifampin
600 mg, pyrazinamide 25 mg/kg and
ethambutol 15 mg/kg, each given orally
once daily for 2 months, followed by 4-
10 months of treatment with isoniazid
and rifampin alone.
 Corticosteroids (eg, prednisolone, 60 mg/d
orally in adults or 1-3mg/kg/d orally in children,
tapered gradually over 3-4 weeks) are indicated
as adjunctive therapy in patients with spinal
subarachnoid block.
They may also be indicated in seriously ill
patients with focal neurologic signs or with
increased intracranial pressure from cerebral
edema.
Pyridoxime (vitamin B6) along with the drug.
 Complications of therapy include :
Hepatic dysfunction: isoniazide,
rifampicin and pyrazinamide.
Polyneuropathy: isoniazide
Optic neuritis: ethambutol
Seizure : isoniazide
Ototoxicity : streptomycin
Prognosis
Even with appropriate treatment, about
one-third of patients with tuberculous
meningitis will die.
Coma at the time of presentation is the
most significant predictor of a poor
prognosis.
Encephalitis
 Encephalitis is inflammation of brain parenchyma.

Enkephalous brain, and the medical suffix-

itisinflammation .

Encephalitis withmeningitis is known

asmeningoencephalitis.

If both the brain and the spinal cord are involved,

the condition is called encephalomyelitis.
Epidemiology
Theincidenceof acute encephalitis is 7.4
cases per 100,000 population per year.

In tropical countries, the incidence is 6.34 per

100,000 per year.

Herpes simplex encephalitis has an incidence

of 24 million population per year.
Etiology
The common causes of acute viral encephalitis are:
Herpes simplex CMV virus
Rabies virus Epstein-Barr virus
Poliovirus mumps
Measles virus

Other causes include infection byflavivirusessuch as:

Japanese encephalitis virus

St. Louis encephalitis virus

West Nile virus

By Togaviridae such as:

Eastern equine encephalitis virus(EEE virus)

Western equine encephalitis virus (WEE virus)

Venezuelan equine encephalitis virus (VEE virus)

There are 2 main types of encephalitis:
1. Primary encephalitis
2. Secondary (post infection) encephalitis:
e.g syphilis, malaria.

Lyme disease also cause encephalitis.

Cryptococcus neoformansis notorious for
causing fungal encephalitis in the
immunocompromised.
Risk factors
The groups most at risk of encephalitis are:
older adults
children under the age of 1
people with weak immune systems

higher risk of getting encephalitis where

mosquitoes or ticks are common esp. in
summer and fall.
symptoms
Mild symptoms include:
Fever
Headache
Vomiting
Neck stiffness
lethargy
 Severe symptoms :

very high fever (103F or higher)

Confusion, drowsiness , hallucinations
Seizure
Irritability
Photophobia
Coma
Herpes simplex virus (HSV)
encephalitis
HSV is the most common cause of sporadic
fatal encephalitis.

Primary herpes infections most often present

as stomatitis (HSV type 1) or a venerably
transmitted genital eruption ( HSV type 2).

The virus migrates along nerve axons to

sensory ganglia, where it persists in a latent
form and may be subsequently reactivated.
 HSV type 1 encephalitis is an acute, necrotizing,
asymmetric, hemorrhagic process with
lymphocytic and plasma cell reaction.

usually involves the medial, temporal and

inferior frontal lobes.

Patients who recover may show cystic necrosis

of the involved regions. But it also has potential
to cause significant brain damage or death.
Clinical manifestation
The clinical syndrome may include headache,
stiff neck, vomiting, behavioral disorders,
memory loss, anosmia, aphasia, hemiparesis,
and focal or generalized seizures.

It usually progress rapidly over several days

and may result in coma or death.

The most common sequel in patients who

survive are memory and behavior
disturbances.
Examinations
CSF findings:
CSF most often shows increased pressure.

lymphocytic or mixed lymphocytic and

polymorphonuclear pleocytosis ( 50-100 white

cells/ml).
mild protein elevation

normal glucose. Red blood cells and decreased

glucose are seen in some severe cases.

Most accurate test for Herpes is polymerase
chain reaction (PCR).
 The EEG may show periodic slow-wave
complexes arising from one or both temporal
lobes.

CT scans and MRI may show abnormalities in

one or both temporal lobes. However, imaging
studies may also be normal.

Brain biopsy: it may be indicated for patients

who are worsening, responding poorly to
treatment with or another antimicrobial, or
who have a lesion that is still undiagnosed.
 Patients with following conditions, CT is
considered before LP:-
Focal neurological deficit

Severe confusion

Papilledema

Seizure
Treatment
Acyclovir : most effective drug.
10-15 mg/kg every 8 hours, with each dose
given over 1 hour (to prevent nephro toxicity).
Treatment is continued for 14-21 days.
Acyclovir is relatively nontoxic but can cause :
liver function abnormalities

bone marrow suppression

transient renal failure

 bacterial CNS infection is often difficult to
exclude when patients appears seriously ill so
empiric antibiotics are often given until
bacterial meningitis is excluded.

Antibiotics : vancomycin & ceftriaxone

Steroids
Anticonvulsants
IV fluids
Complications
Most people who are diagnosed with severe
encephalitis will experience complications:
loss of memory
behavioral/personality changes
intellectual disability
lack of muscle coordination
vision problems or hearing problems
epilepsy

speaking issues


Follow up therapy
Physiotherapy : to improve strength, flexibility,
balance, motor co-ordination and mobility.
Occupational therapy: to develop everyday
skill and to use adaptive products that help
with everyday life.
Speech therapy: to relearn muscle control and
co-ordination to produce speech.
Psychotherapy : to learn coping strategies and
new behavioral skills to improve mood
disorders or address personality change- with
medication management if necessary.
Prognosis
Recovery from viral encephalitis may take a
very long time.

Mortality rate varies with cause, but severity of

epidemics due to the same virus varies during
different years.

Permanent neurologic deficits are common

among patients who survives severe infection.
The end.