 Introduction
 Pathophysiology
 Epidemiology
 Clinical Features
 Differential Diagnosis
 Complications
 Management
 Prognosis
 Prevention

 Meningitis is a potentially life-threatening
infection of the meninges-the tough layer of
tissue that surrounds the brain and the spinal
cord.
 If not treated, meningitis can lead to brain
swelling and cause permanent disability, coma,
and even death.
 Meningitis can be life-threatening because of
the inflammation's proximity to the brain and
spinal cord; therefore the condition is
classified as a medical emergency.

 Meningitis can be caused by a variety of
things, including bacteria (the most serious),
viruses, fungi, reactions to medications, and
environmental toxins such as heavy metals.
 Although bacterial and fungal meningitis
require extended hospitalization, meningitis
caused by viruses can often be treated at
home and has a much better outcome.

 Although meningitis is a notifiable disease in
many countries, the exact incidence rate is
unknown.
 In sub-SaharanAfrica, large epidemics of
meningococcal meningitis occur in the dry
season, leading to it being labeled the
"meningitis belt"; annual rates of 500 cases
per 100,000 are encountered in this area,
which is poorly served by medical care.

A. Bacterial
 Bacterial meningitis is usually part of a
bacteraemic illness, although direct spread
from an adjacent focus of infection in the ear,
skull fracture or sinus can be causative.
 The types of bacteria that cause bacterial
meningitis vary by age group;

In premature babies and newborns up to
three months old, common causes are group
B streptococci ,Escherichia coli & Listeria
monocytogenes.
Older children are more commonly affected
by Neisseria meningitidis (meningococcus),
Streptococcus pneumoniae (serotypes 6, 9, 14,
18 and 23) .

Under five by Haemophilus influenzae type B

In adults, N. meningitidis and S. pneumoniae
together cause 80% of all cases of meningitis,
with increased risk of L. monocytogenes in
those over 50 years old.
Recent trauma to the skull gives bacteria in
the nasal cavity the potential to enter the
meningeal space i.e staphylococcus,

 Immune deficiencies such as complement
deficiency, which predisposes especially to
recurrent meningococcal meningitis
 Tuberculous meningitis, meningitis due to
infection with Mycobacterium tuberculosis

 Viruses are the most common cause of
meningitis, usually resulting in a benign and
self-limiting illness requiring no specific
therapy.
 Occurs mainly in children or young adults,
with acute onset of headache, irritability and
the rapid development of meningism.
 Headache is usually the most severe feature.

 There may be a high pyrexia but focal
neurological signs are rare
 Viruses that can cause meningitis include;
Enteroviruses- most common
 Herpes simplex virus type 2- mollarets
meningitis (and less commonly type 1)

 Varicella zoster virus (known for causing
chickenpox and shingles)
 Mumps virus- where there is no
immunization program
 HIV
CMV

 The term aseptic meningitis refers to all cases
of meningitis in which infection can be
demonstrated.

 Meningitis may occur as the result of several non-
infectious causes:
Spread of cancer to the meninges (malignant
meningitis)
 Certain drugs (mainly non-steroidal anti-
inflammatory drugs, antibiotics and intravenous
immunoglobulins).
 Inflammatory conditions such as sarcoidosis
 Connective tissue disorders such as systemic lupus
erythematosus and certain forms of vasculitis
(inflammatory conditions of the blood vessel wall)

 Chronic meningococcaemia is a rare
condition in which the patient can be unwell
for weeks or even months with recurrent
fever, sweating, joint pains and transient
rash.
 Usually occurs in the middle-aged and
elderly, and in those who have previously had
a splenectomy

 A number of factors influence the development
of bacterial meningitis, including virulence of the
strain, host defenses, and bacteria-host
interactions.
 Bacterial seeding usually occurs by
hematogenous spread. In those without an
identifiable source of infection, local tissue and
bloodstream invasion by bacteria colonized in
the nasopharynx may be a common source.
 Meningeal seeding also may occur with a direct
bacterial inoculate during trauma, neurosurgery,
or instrumentation

 Once in the CSF, the paucity of antibodies,
complement components, and white blood cells
(WBCs) allows the bacterial infection to flourish.
 Bacterial cell wall components initiate a cascade of
complement- and cytokine-mediated events that
result in at least 3 critical events: increased
permeability of the blood-brain barrier, cerebral
edema, and presence of toxic mediators in the CSF.
 Replicating bacteria, increasing numbers of
inflammatory cells, cytokine-induced disruptions in
membrane transport, and increased vascular and
membrane permeability perpetuate the infectious
process and account for the characteristic changes in
CSF cell count, pH, lactate, protein, and glucose.

 Exudates extend throughout the CSF, particularly to the
basal cisterns, damaging cranial nerves (eg, cranial nerve
VIII, with resultant hearing loss), obliterating CSF pathways
(causing obstructive hydrocephalus), and inducing vasculitis
and thrombophlebitis (causing local brain ischemia.
 As intracranial pressure (ICP) continues to rise and brain
edema progresses, CNS autoregulatory processes begin to
fail.This pivotal event may occur when the transient
increase in cerebral blood flow (CBF) reverses and begins to
decrease.
 CBF reduction correlates with the patient's decreasing
alertness and changes in mental status.

 Without medical intervention, the cycle of decreasing
CBF, worsening cerebral edema, and increasing ICP
proceeds unchecked.
 Ongoing endothelial injury may result in vasospasm
and thrombosis, further compromising CBF, and may
lead to stenosis of large and small vessels.
 Systemic hypotension (septic shock) also may impair
CBF, and the patient soon dies from systemic
complications or from diffuse CNS ischemic injury.

 Approximately 25% of patients with bacterial
meningitis present acutely within 24 hours of onset of
symptoms.
 Other patients with bacterial meningitis and most
patients with viral meningitis present with subacute
neurologic symptoms developing over 1-7 days.
 Chronic symptoms lasting longer than 1 week
suggest meningitis caused by some viruses as well as
tuberculosis, syphilis, fungi (especially cryptococci),
and carcinomatous meningitis

 Classic symptoms include :
 Headache
 Nuchal rigidity (generally not present in children
<1 y or in patients with altered mental status)
 Fever and chills, Photophobia
 Phonophobia,Vomiting
 Prodromal upper respiratory infection (URI)
symptoms (viral and bacterial)
 Seizures (30-40% in children, 20-30% in adults)
 Focal neurologic symptoms (including focal
seizures)
 Altered sensorium (confusion may be sole
presenting complaint, especially in elderly)

 Signs of meningeal irritation
Nuchal rigidity or discomfort on neck flexion
Kernig sign: Positive
Brudzinski sign: Positive
 Papilledema is present in only one third of
meningitis patients with increased ICP.
 Focal neurologic signs: Isolated cranial nerve
abnormalities (principally III, IV,VI,VII) in 10-
20% of patients

 Systemic findings:
 Extracranial infection (eg, sinusitis, otitis media,
mastoiditis, pneumonia, urinary tract infection)
may be noted.
 Arthritis is seen with N meningitidis, less
commonly with other bacteria.
 Nonblanching petechiae and cutaneous
hemorrhages are seen classically with N
meningitidis; however, these also can occur with
other bacterial and viral infections.
 Endotoxic shock with vascular collapse is
characteristic of severe N meningitidis infection.

 Risk factors:
Aged 60 years or older
Aged 5 years or younger
Immunosuppressed patients
Splenectomy and sickle cell disease
Alcoholism and cirrhosis
Dural defect (eg, traumatic, surgical,
congenital)
Ventriculoperitoneal shunt

 Brain Abscess
 Neoplasms, Brain
 DeliriumTremens
 Pediatrics, Febrile Seizures
 Encephalitis
 Herpes Simplex
 Subarachnoid Hemorrhage

 Sepsis
 Disseminated intravascular coagulation
 Gangrene
 Focal seizures
 Abnormalities of the cranial nerves:Visual
symptoms and hearing loss
 Encephalitis or cerebral vasculitis
 Severe meningococcal and pneumococcal
infections may result in hemorrhaging of the
adrenal glands, leading to Waterhouse-
Friderichsen syndrome, which is often lethal.

A. Investigations
 Complete blood count
 Serum glucose
 BUN and/or creatinine and liver profile to
assess organ functioning and adjust antibiotic
dosing
 Coagulation profile and platelets
 Cultures : blood, nasopharynx, respiratory
secretions, urine, and skin lesions

 Head CT scan with contrast or MRI with
gadolinium
Imaging is indicated in patients with evidence
of head trauma, altered mental status, or
focal findings.
Rule out brain abscess, sinus or mastoid
infection, skull fracture, and congenital
anomalies.
Presence of papilledema in raised ICP

 Chest x-ray
As many as 50% of patients with
pneumococcal meningitis also have evidence
of pneumonia on initial chest x-ray
 Lumbar puncture
General patterns in CSF pressure
measurement and analysis in bacterial, viral,
and fungal (cryptococcal) meningitis may
support a diagnosis.

Types of meningitis Glucose Protein Cells
Acute bacterial low high PMNs,
often >300/mm³
Acute viral normal Normal/high Mononuclear,
<300/mm³
TB low high Mononuclear &
PMNs,
<300/mm³
Fungal low high <300/mm³
Malignant low high Usually
mononuclear

 PCR- uses enzymes to enhance the presence
of bacterial or viral DNA in CSF.
 Serology -may be useful in viral meningitis
 Diagnosis of cryptococcal meningitis can be
made using an India ink stain of the CSF.

 There is an untreated mortality rate of
around 80%, so action must be swift.
 In meningococcal disease, mortality is
doubled if the patient presents with features
of septicaemia rather than meningitis.

 Initial treatment
Intravenous fluids should be administered if
hypotension or shock are present
Mechanical ventilation may be needed if the
level of consciousness is very low, or if there
is evidence of respiratory failure

Treatments to decrease the intracranial
pressure with medication (e.g.
Dexamethasone).
Seizures are treated with anticonvulsants.

 Empiric antibiotics must be started immediately,
even before the results of the lumbar puncture and
CSF analysis are known.
 Third-generation cefalosporin such as cefotaxime
or ceftriaxone
 In young children and those > 50 years of age,
immunocompromised, addition of ampicillin is
recommended to cover Listeria monocytogenes

 Adjuvant treatment with corticosteroids (usually
dexamethasone) reduces rates of severe hearing
loss and neurological damage in adults but have no
effect on overall mortality.
 Alternatively;
 Vancomycin
 Chloramphenicol
 Clindamycin

 Viral meningitis typically requires supportive
therapy only, such as fluid, bedrest, and
analgesics.
 Fungal meningitis, such as cryptococcal
meningitis, is treated with long courses of
highly dosed antifungals, such as
amphotericin B and fluconazole.

 Untreated, bacterial meningitis is almost
always fatal.
 Viral meningitis, in contrast, tends to resolve
spontaneously and is rarely fatal.
 With treatment, mortality -newborn
patients (20–30%), older children (about 2%)
but rises again to about 19–37% in adults.

 Meningitis caused by H. influenza and
meningococci has a better prognosis
compared to cases caused by group B
streptococci, coliforms and S. pneumoniae.
 In adults, 66% of all cases emerge without
disability.The main problems are deafness (in
14%) and cognitive impairment (in 10%).

 For some causes of meningitis, prophylaxis can be
provided in the long term with vaccine, or in the short
term with antibiotics
 Meningococcus vaccines exist against groups A, C,
W135 andY but not group B serogroup
 Routine vaccination against Streptococcus pneumoniae
with the pneumococcal conjugate vaccine (PCV).
 Childhood vaccination with BCG significantly reduce
the rate of tuberculous meningitis.

Adults who can benefit from Haemophilus
influenza type B (Hib) vaccine-
 Sickle cell anaemia,
 Leukemia,
 HIV/AIDS,
 post splenectomy,
 bone marrow transplantation
 those receiving chemotherapy for cancer.

 Antibiotic prophylaxis, particularly for
meningococcal meningitis- (2Days oral
rifampicin or single dose of ciprofloxacin/
ceftriaxone)