MENINGITIS

AND
ENCEPHALITIS
BY DR .. MAGDI ELBALOOLA AHMED PHYSCIAN
& GASTROHEPATOLOGIST
 Definitions
 Meningitis ; Inflammation of the meninges
(brain coverings)
 Encephalitis ; Inflammation of the brain parenchyma

 Meningoencephalitis ; Inflammation of the brain

parenchyma and meninges

 Myelitis ; Inflammation of the spinal cord, causing

paraparesis or tetraparesis
Meningitis
Causes
Bacterial
Viral
Fungal
Parasitic
Bacterial Meningitis -
Pathogenesis
Infection of upper respiratory tract

Invasion of blood stream (bacteraemia)

Seeding & inflammation of meninges

Causative Organisms
3 mths - 3 yrs: Pneumococcus, Meningococcus
H. Influenza

3 yrs+ adult: Pneumococcus, Meningococcus

 Streptococcus pneumoniae

(Diplococci positive gram stain )

Haemophilus influenzae type B
(Rods negative gram stain )
 Neisseria meningitidis
(Diplococci negative gram stain )
Clinical Features
 Typical triad ;
fever , headach and neck stiffness
photophobia and vomiting are often present

 Other features ;
intense malaise , rigors associating
fever , irritability and preference of lying still . Positive
neck stiffness , Kernig´s sign & Brudzinski´s sign .
Acute Vs Chronic B.Meningitis
 Acute B. meningitis ;
Onset is typically sudden with high fever and rigors
this associated with N.meningitidis & streptocccus

 Chronic B. menigitis ;
Onset is incidious with vague headach , lassitude ,
anorexia & vomiting this associated with TB ,
cryptococcal infection , syphilis , sarcoidosis &
Behcets .
 Acute Meningococcaemia
This caused by Neisseria meningitidis: serotype Group
B is the commonest . It secretes endotoxins causing
vasodilatation, vascular damage, third spacing& severe
shock .
Severe complication:
Waterhouse- Friderichsen syndrome: massive
haemorrhage of adrenal glands secondary to sepsis:
adrenal crisis-low B.P, shock, DIC, purpura, adreno-
cortical insufficiency .
 Meningococcaemia - poor prognosis

 Onset of Petechiae within 12 hrs of first symptom

 Absence of meningitis
 Shock (SBP 70 mmhg or less)
Normal or low WCC
  Normal or low ESR
 DIAGNOSIS OF MENINGITIS
History and examination
that suggest meningitis

Investigations:
FBC Blood C/S
CRP Skin scrapings
Coagulation profile PCR
Blood gases CXR+ Mantoux if TB
Glucose level suspected
 DIAGNOSIS

LUMBAR PUNCTURE
CSF PICTURE OPENING WBCs GLUCOSE PROTEIN (mg/
IN DIFFERENT PRESSURE COUNT / (mg/ dl) dl)
FORMS OF (cm-H2O) DIFFERENTIAAL
MENINGITIS

NORMAL
VALUES 5-18 0-5 40-85 15-45

BACTERIAL
MENINGITIS ↑↑↑↑ >1000 <40 >250
↑↑ neut(PMNs) ↑↑↑↑

FUNGAL
MENINGITIS variable 25-500 < 40 25-500
↑↑lymphocytes

TUBERCULAR
MENINGITIS variable 10-1000 < 40 50-500
↑↑lymphocytes

VIRAL < 100

MENINGITIS/ usually normal > 40 < 100
ENCEPHALITIS early; neut
late; lymph
Contraindications to LP
Skin infection near the site of lumbar puncture
 CNS lesion causing ↑ ICP or spinal mass
 PLT c <20.000 is an absolute C/I .
20.000 – 50.00 is a relative C/I .
> 50.000 is safe for LP .
 INR > 1.5
 Administration of LMWH in the 24 hours
Haemophilia , Von Willebrand or other coagulopathy
 Trauma to lumbar vertebrae
 DIAGNOSIS
CT scan of the head ;
- To diagnose secondary hydrocephalus
- To exclude other causes of ↑ ICP
- To exclude SAH
 Bacterial Meningitis
Management
It´s a medical emergency that needs Early diagnosis.
immediate admission and possibly isolation thereafter .

Immediate optimum treatment

Intensive supportive therapy
Rehabilitation
Prophylaxis to family
Notification to GP & Public Health
 Bacterial Meningitis/Meningococcaemia
Management
 ABC
ICU
Fluid management: aggressive resuscitation
Dexamethasone: only in Pneumococcal and HiB,
given before antibiotics
Inotropes : increasing aortic diastolic pressure and
improving myocardial contractility
 Antibiotics
IV Cefotaxime meningitic dose 2 gm /6-8 hours /7-10 days

Others ;
Ceftriaxone Chloramphenicol
Ampicillin Penicillin G
Rifampicine Gentamycin
Vancomycin
 Prophylaxis
Rifampicine:
Children 5mg/kg bd x 2/7
Adults: 600 mg bd x 2/7

Pregnant contact:
Cefuroxime l mg IM single dose .
Complications of Meningitis
Septic shock - DIC
Cerebral oedema
Seizures
Arteritis/venous thrombosis
Subdural effusions
Hydrocephalus . Abscess . Brain damage
Deafness
 ASEPTIC MENINGITIS

ASEPTIC MENINGITIS is the clinical syndrome of

meningeal inflammation with NEGATIVE CULTURE
FOR ROUTINE BACTERIAL PATHOGENS in a patient
who did not receive antibiotics before lumbar
puncture
Causes of Aseptic meningitis
Virus Bacteria
Fungi Parasite
Drugs Malignancy
Autoimmune Others
 Cases of aseptic meningitis have been reported after
immunization with several live attenuated virus vaccine
including:

Oral polio
Combined measles-mumps-rubella (MMR)
Varicella
Yellow fever
Smallpox
Rabies
∆∆ Of aseptic meningitis

 Bacrerial meningitis
 Encephalitis
 Cerebral malaria
Diagnosis Of aseptic meningitis
 Lumbar puncture
 White cell count
 Blood culture
 Cerebral imaging ;
CT & MRI
 Treatment of aseptic meningitis

No antibiotic treatment is required in aseptic

meningitis
Symptomatic treatment ;Rest in a quiet, dimly lit
room Acetaminophen, ibuprofen for headache, pain
and fever (avoid aspirin) .
ENCEPHALITIS
 Encephalitis refers to inflammation of the brain,
that should be distinguished from meningitis ,
which refers to inflammation of the meninges.

 Unlike viral meningitis, which is usually benign and

self-limited, viral encephalitis, depending on the
specific pathogen and the host-pathogen interaction,
is not infrequently associated with substantial
morbidity and mortality.
 causes of acute
encephalitis/encephalomyelitis
Virus family Specific virus
Adenoviridae ; Adenovirus
Arenaviridae ; LCMV (lymphocytic choriomeningitis
virus), Lassa
Bunyaviridae ; La Crosse, Rift Valley
Filoviridae ; Ebola, Marburg
Flaviviridae ; St. Louis, Murray Valley, West Nile,
Japanese B, Tick-borne complex
Herpesviridae ; HSV-1, HSV-2, VZV, HHV-6, EBV,
CMV, Herpes B
 Virus family Specific virus
Paramyxoviridae ;
(Paramyxovirus); Mumps
(Morbillivirus) ; Measles, Hendra,
Nipah
Picornaviridae ; Poliovirus, Coxsackie virus,
Echovirus
Reoviridae ; Colorado tick fever
Retroviridae ; HIV
Rhabdoviridae ; Lyssavirus, Rabies
Togaviridae ; Eastern equine, Western equine,
Venezuelan equine
Epidemiology
 20.000 cases of encephalitis occur annually in USA
 10.000 deaths due to Japanese encephalitis in Asia
occur annually
 60.000 deaths due to rabies worldwide annually

Japanese encephalitis virus is the most common cause of viral

encephalitis worldwide, and HSV-1 is the most common cause of
sporadic viral encephalitis in the U.S. Specific viruses tend to
occur in specific geographic regions. For example, arbovirus
infections which are caused by the bite of a mosquito tend to
occur in the summer in temperate climates .
Terminology
Neurotropism: the
ability of a virus to infect
neural cells
Neuroinvasiveness: the
ability of a virus to enter
the central nervous
system (CNS)
Neurovirulence: the
ability of a virus to cause
disease of nervous tissue
once it enters the CNS
Examples
Rabies virus has high
neuroinvasiveness and high
neurovirulence t
HSV has low neuroinvasiveness but
high neurovirulence (always enters
the peripheral nervous system but
rarely enters the central nervous
system; can lead to severe
consequences when it enters the
CNS).
Mumps virus has high
neuroinvasiveness but low
neurovirulence (often invades the
CNS, but neurological disease is
mild).
Routes of entry
 1- Haematogenous; (mechanisms);
A- Escape between untight junctions of capillary
endothelial cells to CSF then ependymal then
subendymal tissues .
B- Direct invasion of endothelial capillary cells
then spread to surround tissue .
C- The virus may infect and be transported within
circulatory cells (including monocytes, macrophages,
neutrophils, lymphocytes) which subsequently enter
the CNS via diapedesis, bringing virus with them.
2- Neural ;

By this route the virus can travel in retrograde way up

the neuronal axons (axoplasmic transport) .
For example HSV –l can do this after reactivation of
virus latency in the dorsal root ganglia . From which
site & after reactivation the virus can pass in
anteretrograde way to infect the skin causing
vesicular lesions .
Immunopathology
As with many viral infections, a substantial
proportion of the pathology may actually be caused
by the host immune response to the viral infection.
During severe encephalitis, an inflammatory reaction
is usually prominent in the meninges and in a
perivascular distribution within the brain. To what
degree this plays a protective (clearing virus and virally
infected cells) vs. pathologic (release of pro-
inflammatory cytokines which contributes to neuronal
dysfunction and death) role is unclear.
 Acute disseminated
encephalomyelitis
Is an illness of the CNS in which demyelination occurs
after infection with a virus, usually following the
systemic illness by days to weeks. The clinical
manifestations can be difficult to differentiate from
encephalitis caused by direct invasion of the virus. The
pathogenesis of this syndrome is thought to be related
to induction of an immune response to CNS myelin.
Systemic infection with measles, varicella, and
influenza A, to name a few, have been associated with
a postviral encephalomyelitis.
Viral encephalitis is usually an acute illness, with or without a prodrome, but
can also be a slowly progressive disease as in progressive multifocal
leukoencephalopathy (PML) caused by JC virus, subacute sclerosing
panencephalitis (SSPE) occurring after measles, and HIV encephalopathy.

 Clinical picture ;- 9-movement disorders

1-headache 10-accentuated deep tendon
2-fever reflexes, and extensor
3- alterations of consciousness plantar responses
(ranging from lethargy to coma)
4- confusion 11- Increased intracranial
5- cognitive impairment pressure can occur,
6- personality changes manifested by papilledema,
7- motor weakness 12-cranial nerve palsies, and
8- seizures. progression to coma
 DIFFERENCES BETWEEN
MENINGITIS & ENCEPHALITIS
 Diagnosis of encephalitis
1- Careful history & examination .
2- Serology of the commonest viruses .
3- CSF for ; analysis , serology & PCR
4- CT or MRI to look for oedema & exclude other causes
of ↑ ICP .
5- EEG ; Diffuse slowing of waves .
Treatment of Viral Encephalitis
1- Treatment is often supportive, involving
management of increased intracranial pressure,
treatment of seizures, and management of
metabolic derangements.
2- HSV encephalitis responds to treatment with
intravenous acyclovir
 Because this is a relatively well-tolerated treatment,
most patients presenting with a syndrome consistent
with encephalitis are treated empirically with acyclovir
for the possibility of HSV encephalitis, until HSV
encephalitis is ruled out or another etiology is
confirmed .
CHARACT DEFINITION CAUSE COMMON ALTERED DIAGNOSIS MEDICAL
ERISTICS CAUSES MENTAL TREATMENT
STATUS
(AMS)

CEFOTAXIME/
STREP. AMPICILLIN/
INFLMMATION BACTERIA PNEUMONIAE NO FND CBC GENTAMYCINE
MENINGITIS OF THE
MENINGES VIRUS N.
OR AMS CRP
MENINGITIDIS
FUNGI = HiB BLOOD
CULTURE &
STAINING

INFLAMMATION
ENCEPHALITIS
OF THE BRAIN MOSTLY =HSV-l AMS PRESNTATION ACYCLOVIR
=JAPANESE CSF – PCR
PARENCHYMA VIRAL ENCEPHALITIS IMMAGING I.V /7-10
VIRUS DAYS
THANK YOU