Bacterial Meningitis
Dr.T.V.Rao MD
Dr.T.V.Rao MD
What is meningitis?
The brain and spinal cord are covered by connective
tissue layers collectively called the meninges which
form the blood-brain barrier.
1-the pia mater (closest to the CNS)
2-the arachnoid mater
3-the dura mater (farthest from the CNS).
The meninges contain cerebrospinal fluid (CSF).
Meningitis is an inflammation of the meninges, which,
if severe, may become encephalitis, an
inflammation of the brain.
Dr.T.V.Rao MD
In Meningitis Meninges are infected
and Inflamed
Dr.T.V.Rao MD
Causes of Meningitis
-Bacterial Infections
-Viral Infections
-Fungal Infections
(Cryptococcus neoformans
Coccidiodes immitus)
-Inflammatory diseases
(SLE)
Cancer
-Trauma to head or spine.
Dr.T.V.Rao MD
Introduction
Bacterial meningitis is an inflammation of the
leptomeninges, usually causing by bacterial
infection.
Bacterial meningitis may present acutely
(symptoms evolving rapidly over 1-24 hours),
sub acutely (symptoms evolving over 1-7days),
or chronically (symptoms evolving over more
than 1 week).
Dr.T.V.Rao MD
Epidemiology
Annual incidence in the developed countries is
approximately 5-10 per 100000.
30000 infants and children develop bacterial
meningitis in United States each year.
Approximately 90 per cent of cases occur in
children during the first 5 years of life.
Dr.T.V.Rao MD
Epidemiology
Cases under age 2 years account for almost 75%
of all cases and incidence is the highest in early
childhood at age 6-12 months than in any other
period of life.
There are significant difference in the incidence
of bacterial meningitis by season.
Dr.T.V.Rao MD
Bacterial meningitis..
Etiological Agents:
Pneumococcal, Streptococcus pneumoniae
(38%)
Meningococcal, Neisseria meningitides
(14%)
Haemophilus influenza (4%)
Staphylococcal, Staphylococcus aureus
(5%)
Tuberculosis, Mycobacterium
tuberculosis
Dr.T.V.Rao MD
Etiology differs .
Causative organisms vary with patient age,
with three bacteria accounting for over
three-quarters of all cases:
Neisseria meningitidis (meningococcus)
Haemophilus influenza (if very young and
unvaccinated)
Streptococcus pneumoniae ( pneumococcus)
Dr.T.V.Rao MD
Other Bacterial Etiologies
Other organisms
Neonates and infants at age 2-3 months
Escherichia coli
B-hemolytic streptococci
Staphylococcus aureus
Staphylococcus epidermidis
Listeria Monocytogenes
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Etiology in .
Elderly and immunocompromised
Listeria Monocytogenes
Gram negative bacteria
Hospital-acquired infections
Klebsiella
Escherichia coli
Pseudomonas
Staphylococcus aureus
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Etiology
The most common organisms
Neonates and infants under the age of
2months
Escherichia coli
Pseudomonas
Group B Streptococcus
Staphylococcus aureus
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Etiology
Children over 2 months
Haemophilus influenza type b
Neisseria meningitides
Streptococcus pneumoniae
Children over 12 years
Neisseria meningitides
Streptococcus pneumoniae
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Routes of Infection
Major routes of leptomeninges infection
Bacteria are mainly from blood.
Uncommonly, meningitis occurs by direct
extension from nearly focus (mastoiditis, sinusitis)
or by direct invasion (dermoid sinus tract, head
trauma, meningo-myelocele).
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Pathogenesis
Susceptibility of bacterial infection on CNS in
the children
Immaturity of immune systems
Nonspecific immune
Insufficient barrier (Blood-brain barrier)
Insufficient complement activity
Insufficient chemo taxis of neutrophils
Insufficient function of monocyte-macrophage system
Blood levels of diminished interferon (INF) -and
interleukin -8 ( IL-8 )
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Pathogenesis
Susceptibility of bacterial infection on CNS in the
children
Specific immune
Immaturity of both the cellular and Humoral
immune systems
Insufficient antibody-mediated protection
Diminished immunologic response
Bacterial virulence
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Pathogenesis
A offending bacterium from blood invades the
leptomeninges.
Bacterial toxics and Inflammatory mediators are released.
Bacterial toxics
Lipopolysaccharide, LPS
Teichoic acid
Peptidoglycan
Inflammatory mediators
Tumor necrosis factor, TNF
Interleukin-1, IL-1
Prostaglandin E2, PGE2
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Pathogenesis
Bacterial toxics and inflammatory mediators
cause Suppurative inflammation.
Inflammatory infiltration
Vascular permeability alter
Tissue edema
Blood-brain barrier destroy
Thrombosis
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Pathology
Diffuse bacterial infections involve the leptomeninges,
arachnoid membrane and superficial cortical structures,
and brain parenchyma is also inflamed.
Meningeal exudate of varying thickness is found.
There is purulent material around veins and venous
sinuses, over the convexity of the brain, in the depths of
the sulci, within the basal cisterns, and around the
cerebellum, and spinal cord may be encased in pus.
Ventriculitis (purulent material within the ventricles) has
been observed repeatedly in children who have died of
their disease.
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Pathology
Invasion of the ventricular wall with perivascular
collections of purulent material, loss of ependymal
lining, and subependymal gliosis may be noted.
Subdural empyema may occur.
Hydrocephalus is an common complication of
meningitis.
Obstructive hydrocephalus
Communicating hydrocephalus
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Pathology
Blood vessel walls may infiltrated by inflammatory cells.
Endothelial cell injury
Vessel stenosis
Secondary ischemia and infarction
Ventricle dilatation which ensues may be associated with
necrosis of cerebral tissue due to the inflammatory
process itself or to occlusion of cerebral veins or arteries.
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Pathology
Inflammatory process may result in cerebral edema
and damage of the cerebral cortex.
Conscious disturbance
Convulsion
Motor disturbance
Sensory disturbance
Meningeal irritation sign is found because the
spinal nerve root is irritated.
Cranial nerve may be damaged
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Symptoms of Meningitis and Septicemia
Meningitis and meningococcal septicemia may
not always be easy to detect, in early stages
the symptoms can be similar to flu. They may
develop over one or two days, but sometimes
develop in a matter of hours
It is important to remember that symptoms
do not appear in any particular order and
some may not appear at all.
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Clinical manifestation
Bacterial meningitis may present acutely (symptoms
evolving rapidly over 1-24 hours) in most cases.
Symptoms and signs of upper respiratory or
gastrointestinal infection are found before several days
when the clinical manifestations of bacterial meningitis
happen.
Some patients may access suddenly with shock and DIC.
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Clinical manifestation
Toxic symptom all over the body
Hyperpyrexia
Headache
Photophobia
Painful eye movement
Fatigued and weak
Malaise, myalgia, anorexia,
Vomiting, diarrhea and abdominal pain
Cutaneous rash
Petechiae, purpura
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Clinical manifestation
Clinical manifestation of CNS
Increased intracranial pressure
Headache
Projectile vomiting
Hypertension
Bradycardia
Bulging fontanel
Cranial sutures diastasis
Coma
DE cerebrate rigidity
Cerebral hernia
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Clinical manifestation
Clinical manifestation of CNS
Meningeal irritation sign
Neck stiffness
Positive Kernigs sign
Positive Brudzinskis sign
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Kernig's sign.
One of the physically
demonstrable
symptoms of
meningitis is Kernig's
sign. Severe stiffness
of the hamstrings
causes an inability to
straighten the leg
when the hip is
flexed to 90 degrees.
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Brudzinski's sign
Dr.T.V.Rao MD
Another physically
demonstrable
symptoms of
meningitis is
Brudzinski's sign.
Severe neck stiffness
causes a patient's
hips and knees to
flex when the neck is
flexed.
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Clinical manifestation
Clinical manifestation of CNS
Seizures
Seizures occur in about 20%-30% of children with
bacterial meningitis.
Seizures is often found in Haemophilus influenza
and pneumococcal infection.
Seizures is correlative with the inflammation of brain
parenchyma, cerebral infarction and electrolyte
disturbances.
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Clinical manifestation
Clinical manifestation of CNS
Conscious disturbance
Drowsiness
Clouding of consciousness
Coma
Psychiatric symptom
Irritation
Dysphoria
dullness
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Clinical manifestation
Clinical manifestation of CNS
Meningeal irritation sign
Neck stiffness
Positive Kernigs sign
Positive Brudzinskis sign
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Clinical manifestation
Clinical manifestation of CNS
Transient or permanent paralysis of cranial nerves
and limbs may be noted.
Deafness or disturbances in vestibular function are
relatively common.
Involvement of the optic nerve, with blindness, is
rare.
Paralysis of the 6th cranial nerve, usually transient,
is noted frequently early in the course.
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Clinical manifestation
Symptom and signs of the infant under the age of 3
months
In some children, particularly young infants under the age of
3 months, symptom and signs of meningeal inflammation
may be minimal.
Fever is generally present, but its absence or hypothermia in a
infant with meningeal inflammation is common.
Only irritability, restlessness, dullness, vomiting, poor
feeding, cyanosis, dyspnea, jaundice, seizures, shock and
coma may be noted.
Bulging fontanel may be found, but there is not meningeal
irritation sign.
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Skin rashes
Is due to small skin bleed
All parts of the body are affected
The rashes do not fade under pressure
Pathogenesis:
a. Septicemia
b. wide spread endothelial damage
c. activation of coagulation
d. thrombosis and platelets aggregation
e. reduction of platelets (consumption )
f. BLEEDING 1.skin rashes
2.adrenal hemorrhage
Adrenal hemorrhage is called Waterhouse-Friderichsen
Syndrome.It cause acute adrenal insufficiency and is uaually
fatal
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Skin rashes
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Glass Test
A rash that does not fade
under pressure will still
be visible when the side
of a clear drinking glass is
pressed firmly against the
skin.
If someone is ill or obviously
getting worse, do not wait
for a rash. It may appear
late or not at all.
A fever with a rash that does
not fade under pressure is
a medical emergency.
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Complications
Subdural effusion
Subdural effusions occur in about 10%-30% of children with
bacterial meningitis.
Subdural effusions appear to be more frequent in the
children under the age of 1 year and in Haemophilus
influenza and pneumococcal infection.
Clinical manifestations are enlargement in head
circumference, bulging fontanel, cranial sutures
diastasis and abnormal trans illumination of the skull.
Subdural effusions may be diagnosed by the examination of
CT or MRI and subdural pricking.
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Complication
Ependymitis
Neonate or infant with meningitis
Gram-negative bacterial infection
Clinical manifestation
Persistent hyperpyrexia,
Frequent convulsion
Acute respiratory failure
Bulging fontanel
Ventriculomegaly (CT)
Cerebrospinal fluid by ventricular puncture
WBC>50109/L
Glucose<1.6mmol/L
Protein>o.4g/L
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Complications
Cerebellar hyponatremia
Syndrem of inappropriate secretion of
antidiuretic hormone (SIADH)
Hyponatremia
Degrade of blood osmotic pressure
Aggravated cerebral edema
Frequent convulsion
Aggravated conscious disturbance
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Complication
Hydrocephalus
Increased intracranial pressure
Bulging fontanel
Augmentation of head circumference
Brain function disorder
Other complication
Deafness or blindness
Epilepsy
Paralysis
Mental retardation
Behavior disorder
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Meningococcal Meningitis
Less common bacterial causes of Meningitis, such as
Staphylococci, enteric bacteria, group B streptococci
and Listeria, occur in sub-populations like the
immunocompromised, neonates, or head trauma
patients.
Patients with Meningococcal Meningitis present with
sudden onset of fever, intense headache, nausea,
vomiting, stiff neck and, frequently, a petechial rash
with pink macules or, very rarely, vesicles. Delirium
and coma often appear.
Case fatality rate is between 5% and 15%.
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Laboratory Findings
Peripheral hemogram
Total WBC count
20109/L 40109/L WBC
Decreased WBC count at severe infection
Leukocyte differential count
80%90% Neutrophils
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Diagnosis
Isolation of the organism
from CSF or blood.
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Characteristics of CSF on common disease in CNS
PM
TM
VW
FM
TE
Pressure
Cloudiness
or
Pandy T
or
or or
WBC
Protein
Glucos
Chloridate
or
Cultivation Bacterium
or
TB
or
Viral
Dr.T.V.Rao MD
or
orL
or
Fungus
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Laboratory Findings
Rout examination of cerebrospinal fluid (CSF)
Increased pressure of cerebrospinal fluid
Cloudiness
Evident Increased total WBC count (>1000109/L)
Evident Increased neutrophils in leukocyte differential count
Evident Decreased glucose (<1.1mmol/l)
Evident Increased protein level
Decreased or normal chlorinate
CSF film preparation or cultivation : positive result
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Laboratory Findings
Especial examination of CSF
Specific bacterial antigen test
Countercurrent immuno-electrophoresis
Latex agglutination
Immunoflorescent test
Neisseria meningitides (meningococcus)
Haemophilus influenza
Streptococcus pneumoniae ( pneumococcus)
Group B streptococcus
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Laboratory Findings
Especial examination of CSF
Other test of CSF
LDH
Lactic acid
CRP
TNF and Ig
Neuron specific enolase (NSE)
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Laboratory Findings
Other bacterial
test
Blood cultivation
Film preparation
of skin petechiae
and purpura
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Diagnosis
Diagnostic methods
A careful evaluation of history
A careful evaluation of infants signs and
symptoms
A careful evaluation of information on
longitudinal changes in vital signs and
laboratory indicators
Rout examination of cerebrospinal fluid (CSF)
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Differential diagnosis
Clinical manifestation of bacterial meningitis is similar to
clinical manifestation of viral, tuberculosis , fungal and
aseptic meningitis.
Differentiation of these disorders depends upon careful
examination of cerebrospinal fluid obtained by lumbar
puncture and additional immunologic, roentgenographic,
and isotope studies.
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Treatment
Antibiotic Therapy
Therapeutic principle
Good permeability for Blood-brain barrier
Drug combination
Intravenous drip
Full dosage
Full course of treatment
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Antibiotic Therapy
Selection of antibiotic
No Certainly Bacterium
Community-acquired bacterial infection
Nosocomial infection acquired in a hospital
Broad-spectrum antibiotic coverage as noted below
Children under age 3 months
Cefotaxime and ampicillin
Ceftriaxone and ampicillin (children over age 1months)
Children over 3 months
Cefotaxime or Ceftriaxone or ampicillin and chloramphenicol
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Antibiotic Therapy
Certainly Bacterium
Once the pathogen has been identified and the
antibiotic sensitivities determined, the most
appropriate drugs should selected.
N meningitides : penicillin, - cephalosporin
S pneumoniae: penicillin, - cephalosporin, Vancomycin
H influenza: ampicillin, cephalosporin
S aureus: penicillin, nefcillin, Vancomycin
E coli: ampicillin, chloramphenicol, - cephalosporin
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Antibiotic Therapy
Course of treatment
7 days for meningococcal infection
1014 days for H influenza or S pneumoniae
infection
More than 21 days for S aureus or E coli infection
1421 days for other organisms
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Treatment
General and Supportive Measures
Monitor of vital sign
Correcting metabolic imbalances
Supplying sufficient heat quantity
Correcting hypoglycemia
Correcting metabolic academia
Correcting fluids and electrolytes disorder
Application of cortical hormone
Lessening inflammatory reaction
Lessening toxic symptom
lessening cerebral edema
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General and Supportive Measures
Treatment of hyperpyrexia and seizures
Pyretolysis by physiotherapy and/or drug
Convulsive management
Diazepam
Phenobarbital
Subhibernation therapy
Treatment of increased intracranial pressure
Dehydration therapy
20%Mannitol 5ml/kg vi q6h
Lasix 1-2mg/kg vi
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General and Supportive Measures
Treatment of septic shock and DIC
Volume expansion
Dopamine
Corticosteroids
Heparin
Fresh frozen plasma
Platelet transfusions
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Treatment
Complication Measures
Subdural effusions
Subdural pricking
Draw-off effusions on one side is 20-30ml/time.
Once daily or every other day is requested.
Time cell of pricking may be prolonged after 2 weeks.
Ependymitis
Ventricular puncture drainage
Pressure in ventricle be depressed.
Ventricular puncture may give ventricle an injection of antibiotic.
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Complication Measures
Hydrocephalus
Operative treatment
Adhesiolysis
By-pass operation of cerebrospinal fluid
Dilatation of aqueduct
SIADH (Cerebral hyponatremia)
Restriction of fluid
supplement of serum sodium
diuretic
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Prognosis
Appropriate antibiotic therapy reduces the
mortality rate for bacterial meningitis in
children, but mortality remain high.
Overall mortality in the developed countries
ranges between 5% and 30%.
50 percent of the survivors have some sequelae
of the disease.
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Prognosis
Prognosis depends upon many factors:
Age
Causative organism
Number of organisms and bacterial virulence
Duration of illness prior to effective antibiotic
therapy
Presence of disorders that may compromise
host response to infection
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Aseptic Meningitis
Definition: A syndrome characterized by acute onset of
meningeal symptoms, fever, and cerebrospinal fluid
pleocytosis, with bacteriologically sterile cultures.
Laboratory criteria for diagnosis:
CSF showing 5 WBC/cu mm
No evidence of bacterial or fungal meningitis.
Case classification
Confirmed: a clinically compatible illness diagnosed by a
physician as aseptic meningitis, with no laboratory
evidence of bacterial or fungal meningitis
Comment
Aseptic meningitis is a syndrome of multiple etiologies, but
most cases are caused by a viral agent
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Viral Meningitis
Etiological Agents:
Enteroviruses (Coxsackie's and echovirus): most common.
-Adenovirus
-Arbovirus
-Measles virus
-Herpes Simplex Virus
-Varicella
Reservoirs:
-Humans for Enteroviruses, Adenovirus, Measles, Herpes Simplex, and Varicella
-Natural reservoir for arbovirus birds, rodents etc.
Modes of transmission:
-Primarily person to person and arthopod vectors for Arboviruses
Incubation Period:
-Variable. For enteroviruses 3-6 days, for arboviruses 2-15 days
Treatment: No specific treatment available.
Most patients recover completely on their own.
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Non Polio Enteroviruses
Types:62 different types known:
-23 Coxsackie A viruses,
-6 Coxsackie B viruses,
-28 echoviruses, and 5 other
How common?
-90% of all viral meningitis is caused by Enteroviruses
-Second only to "common cold" viruses, the rhinoviruses.
-Estimated 10-15 million/ more symptomatic infections/yr in US
Who is at risk? Everyone.
How does infection spread?
Virus present in the respiratory secretions & stool of a patient.
Direct contact with secretions from an infected person.
Parents, teachers, and child care center workers may also become infected
by contamination of the hands with stool.
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Public Health Importance
Challenges:
-Educating public
-Timely reporting and records keeping
-Updating information daily.
-Alleviating public anxiety and concerns
-Collaborating with health partners
Opportunities:
-Educating public
-Communication
-Strengthening partnerships
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