MENINGITIS

Dr F . E Odiase
• Inflammation of the leptomeninges (pia and
arachnoid mater) is known as meningitis.

• A variety of organisms/agents may cause

meningitis including
– viral
– bacterial
– fungal
– parasitic
– chemical
– neoplastic
• Meningitis is classified clinically as either
acute or chronic .

• Acute meningitis occurs within hours or

days while chronic evolves over weeks.

• Acute meningitis due to viral and bacterial

agents while chronic due to tuberculosis,
cryptococcal infection and syphilis.
• Acute bacterial meningitis (ABM) refers to
infections caused mainly by three agents,
streptococcus pneumoniae, neisseria
meningitidis and haemophillus influenza.

• ABM causes over 250,000 deaths globally

annually, with a large proportion occurring in
Africa.

• ABM affects all age groups especially children.

• Risk factors for ABM in Africa includes,
– crowded living conditions
– extremes of age
– virulence of the organisms
– antibiotics resistance
– HIV infection
– malnutrition
– sickle cell disease
– splenectomy
– recent head injury with fracture
– Postneurosurgery
– middle ear infection and pneumonia
• Sreptococcus pneumoniae is a gram positive
cocci with many subtypes.
• The main source of meningeal infection is
haematogenous spread arising from the
reparatory tract (pneumonia) and from otitis
media.
• Mainly presents as sporadic cases.
• Nesseria meningitidis is a gram negative
diplococcus. It is classified into serogroups A,B,
C, Y, W-135 and X.
• Nesseria meningitidis infection are mainly
sporadic but epidemic do occur in Africa
• Large scale epidemics occurs in sub-Saharan
Africa during the dry season in approximately
8 to 10 year cycles.
• These epidemics occurs in a large meningitis
belt which stretches from the Gambia and
Senegal in the west to Sudan and Ethiopia in
the north and as far south as Kenya and
Tanzania in the east and Nigeria and Ghana in
the west.
• During meningococcal epidemics, outbreaks
occurs in areas of overcrowding such as
towns, schools, barracks, prisons etc
• Haemophilus influenzae type b is a small gram
negative coccobacillus. It primarily affects
children and rarely occurs in adults.

• Other less common causes of ABM, includes

group B streptococcus, salmonella,
staphylococci, Escherichia coli, listeria
monocytogens and gram negative bacilli.
• Meningitis, and especially bacterial meningitis
is a medical emergency requiring rapid
evaluation and appropriate treatment.

• PATHOGENESIS AND PATHOLOGY

– Infectious agents reach the meninges by

direct extension from contiguous foci or
through the bloodstream
• In the absence of treatment, the infectious
process is divided into four stages.

• In the first stage there is

– marked inflammation of the meninges with
resultant headaches, fever and neck stiffness .

• In the second stage

– the subpial surfaces and the brain cortex
show microglial proliferation
– and astrocytic reaction that may lead to
seizures.
• In the third stage
– a purulent exudate collects around the base
of the brain
– obstructing the flow of the CSF
– and trapping cranial nerves.
– In this stage vasculitis also develops with
thrombosis of meningeal/cerabral vessels
causing focal neurologic signs.
• In the fourth stage
– a basilar exudate organizes and becomes
fibrotic, with resultant sever hydrocephalus.
– Organisms also invades the brain parenchyma
and produces encephalitis.
 Clinical diagnosis
• Triad of headache, fever and meningism.
• Alteration of consciousness, sezures

• Photophobia, nausea, vomiting, backache

lethargy.

• Haemorrhagic rash suggestive of

meningococcal infection
• Physical signs include

• nuchal rigidity

• positive kernig sign(i.e pain or resistance when

the examiner attempts to extend the patient’s
knee while the hip is flexed).

• Brudzinski’s sign positive(i.e hip flexion when the

examiner bends the patient’s neck forward).

• GCS, depressed consciousness. Papilledema,

cranial nerve palsies
• LABORATORY FINDINGS.

• Lumbar puncture for CSF study.

– Cranial computerized tomography before LP is
indicated when focal findings or clinical evidence
of raised intracranial pressure is present.

• Typical CSF findings in bacterial meningitis.

– Opening pressure– Usually elevated(>18o)
– CSF Fluid– Turbid
– Cell type—Polymorphonuclear leucocytes.
• Additional findings include.
– WBC Cells-->100/mm, often
>1000cells/mm3

– Protein—Elevated, usually >100mg/dl

– Glucose—Depressed, usually < 50% of

blood glucose.(< 40mg )

– Gram stain– Positive in 60 to 80% of cases

• CSF should also be cultured and sensitivity
determined,
– especially with emergence of resistant strains of
common organism.

• Polymerase chain reaction analysis is now

available for
– bacteria as well as viruses and mycobacteria.

• Culture of
– blood, sputum, or fluid from
– potential origins of infection such as the
nasopharynx, ear, skin rash
• FBC reveals leucocytosis.

• X-rays of the chest, sinuses, or mastoid bones may indicate a

primary site of infection.

• E/U/cr

• Typical findings in TB meningitis

– Opening pressure is elevated
– fluid turbid
– protein is elevated >200mg/dl
– predominantly lymphocytes >200cells
– glucose is reduced <30mg/dl
– smears positive in less than 25%
– culture and sensitivity could take 2-8weeks, PCR
recommended.
• DRUG TREATMENT FOR BACTERIA meningitis.

• NEISSERIA MENINGITIDES.
– Penicillin G, 4million units every 4hrs.
– Ampicillin 3g every 4hrs.
– Ceftriaxone 2g every 12hrs
• STREPTOCCUS PNEUMONIA. H. INFLUENZAE
– Penicillin G,or Cefriaxone at same doses as above
• RESISTANT STRAINS
– Meropenem.
• TUBERCULOSIS.

– Isoniazid,300mg daily
– Rifampicin 600mg daily

– etambutol,1.2g/day
– pyrazinamide 2g daily

– steriod also useful

 PREVENTION
• All three main causes of acute bacterial
meningitis are now largely prevented by
vaccination

• Close contacts with patient should have;

– RIFAMPICIN 600mg every 12hrs for 2days or
– CIPROFLOXACIN 500mg as single dose or
– AZITHROMYCIN 500mg as single dose