Meningitis

Introduction

• Meningitis is inflammation of the protective

membranes covering the brain and spinal
cord.
• 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.
Causes

• Most cases are due to infection with viruses, with

bacteria, fungi, and parasites being the next most
common causes.
• It may also result from various non-infectious causes.
Bacterial cause
The types of bacteria that cause bacterial meningitis vary
by age group.
• In premature babies and newborns up to three months
• Escherichia coli
• Listeria monocytogenes .
Older children are more commonly affected by
• Neisseria meningitidis (meningococcus),
• Streptococcus pneumoniae
• Haemophilus influenzae type B
Bacterial cont’d
In adults,
• N. meningitidis and
• S. pneumoniae
 Since the pneumococcal vaccine was introduced,
however, rates of pneumococcal meningitis have
declined in children and adults.
• Recent trauma to the skull gives bacteria in the nasal
cavity the potential to enter the meningeal space
Bacterial cont’d
• Individuals with a cerebral shunt or related device are increased
the risk of infection through those devices. (Istaphylococci)
• In a small proportion of people, an infection in the head and
neck area, such as otitis media or mastoiditis, can lead to
meningitis
• Recipients of cochlear implants for hearing loss are at an
increased risk of pneumococcal meningitis.
• Tuberculous meningitis, meningitis due to infection with
Mycobacterium tuberculosis, is more common in those from
countries where tuberculosis is common, but is also
encountered in those with immune problems, such as AIDS.
Viral & Parasitic
Viruses that can cause meningitis include
• enteroviruses
• herpes simplex virus type 2 (and less commonly type 1),
• varicella zoster virus
• mumps virus
• HIV
• CMV
• A parasitic cause is often assumed when there is a predominance of
eosinophilsn the CSF.
• Schistosoma
• Ameoba
Non-infectious
• Meningitis may occur as the result of several non-infectious causes:
• spread of cancer to the meninges (malignant or neoplastic meningitis)
• certain drugs (mainly non-steroidal anti-inflammatory drugs,
antibiotics and intravenous immunoglobulins).
o It may also be caused by several inflammatory conditions such as
sarcoidosis (which is then called neurosarcoidosis),
o connective tissue disorders such as systemic lupus erythematosus
o certain forms of vasculitis such as Behçet's disease.
 Mechanism
The meninges comprise three membranes that, together with the cerebrospinal
fluid, enclose and protect the brain and spinal cord (the central nervous
system).
• The pia mater is a very delicate impermeable membrane that firmly adheres
to the surface of the brain, following all the minor contours.
• The arachnoid mater (so named because of its spider-web-like appearance) is
a loosely fitting sac on top of the pia mater.
• The subarachnoid space separates the arachnoid and pia mater membranes,
and is filled with cerebrospinal fluid.
• The outermost membrane, the dura mater, is a thick durable membrane,
which is attached to both the arachnoid membrane and the skull.
Mechanism cont’d
• In bacterial meningitis, bacteria reach the meninges by one of two main routes: through
the bloodstream or through direct contact between the meninges and either the nasal
cavity or the skin.
• In most cases, meningitis follows invasion of the bloodstream by organisms that live
upon mucous surfaces such as the nasal cavity.
• This is often in turn preceded by viral infections, which break down the normal barrier
provided by the mucous surfaces.
• Once bacteria have entered the bloodstream, they enter the subarachnoid space in
places where the blood-brain barrier is vulnerable—such as the choroid plexus.
• Direct contamination of the cerebrospinal fluid may arise from indwelling devices,
skull fractures, or infections of the nasopharynx or the nasal sinuses that have formed a
tract with the subarachnoid space ; (occasionally, congenital defects of the dura mater
can be identified.)
Mechanism cont’d
• The large-scale inflammation that occurs in the subarachnoid
space during meningitis is not a direct result of bacterial
infection but can rather largely be attributed to the response of
the immune system to the entrance of bacteria into the central
nervous system.
• When components of the bacterial cell membrane are identified
by the immune cells of the brain (astrocytes and microglia),
they respond by releasing large amounts of cytokines, hormone-
like mediators that recruit other immune cells and stimulate
other tissues to participate in an immune response.
• The blood-brain barrier becomes more permeable, leading to
"vasogenic" cerebral edema
Mechanism cont’d
• Large numbers of white blood cells enter the CSF, causing
inflammation of the meninges, and leading to "interstitial"
edema
• In addition, the walls of the blood vessels themselves become
inflamed (cerebral vasculitis), which leads to a decreased
blood flow and a third type of edema, "cytotoxic" edema.
• The three forms of cerebral edema all lead to an increased
intracranial pressure; together with the lowered blood
pressure often encountered in acute infection, this means
that it is harder for blood to enter the brain, and brain cells
are deprived of oxygen and undergo apoptosis (automated
cell death).
Signs and symptoms
Clinical features
In adults,
• A severe headache is the most common symptom of meningitis,
• Nuchal rigidity
• The classic triad of diagnostic signs consists of nuchal rigidity,
sudden high fever, and altered mental status; however, all three
features are present in only 44–46% of all cases of bacterial
meningitis.
If none of the three signs is present, meningitis is extremely unlikely.
Other signs commonly associated with meningitis include:
• Photophobia
• Phonophobia
Neck stiffness, MENINGITIS
Acute, severe headache with stiff
neck and fever suggests meningitis.
LP is mandatory
Signs and symptoms cont’d
• Nuchal rigidity occurs in 70% of adult cases of bacterial meningitis.
• Other signs of meningism include the presence of positive Kernig's sign or
Brudzinski's sign.
• Kernig's sign is assessed with the patient lying supine, with the hip and knee
flexed to 90 degrees. In a patient with a positive Kernig's sign, pain limits
passive extension of the knee.
• A positive Brudzinski's sign occurs when flexion of the neck causes
involuntary flexion of the knee and hip.
• Although Kernig's sign and Brudzinski’s neck sign are both commonly used
to screen for meningitis, the sensitivity of these tests is limited.
• They have very good specificity for meningitis: the signs rarely occur in other
diseases.
• Another test, known as the "jolt accentuation maneuver" helps determine
whether meningitis is present in patients reporting fever and headache. The
patient is told to rapidly rotate his or her head horizontally; if this make the
headache worse, it shows meningitis.
Kernig's Test
Brudzinski's Sign
Signs and symptoms
cont’d
• Meningitis caused by the bacterium Neisseria
meningitidis (meningococcal meningitis) can be
differentiated from meningitis with other causes by
a rapidly spreading petechial rash which may
precede other symptoms.
• The rash consists of numerous small, irregular
purple or red spots on the trunk, lower extremities,
mucous membranes, conjuctiva, and (occasionally)
the palms of the hands or soles of the feet.
• The rash is typically non-blanching: the redness
does not disappear when pressed with a finger.
Signs and symptoms cont’d
• The inflammation of the meninges may lead to abnormalities of
the cranial nerves.
• Visual symptoms and hearing loss may persist after an episode of
meningitis .
• Inflammation of the brain (encephalitis) or its blood vessels
(cerebral vasculitis), as well as the formation of blood clots in the
veins (cerebral venous thrombosis), may all lead to weakness, loss
of sensation, or abnormal movement or function of the part of the
body supplied by the affected area in the brain.
 Diagnosis
 Analysis of Cerebrospinal Fluid (CSF) Assessment of CSF is critical
for patients with suspected meningitis or encephalitis
 CSF findings in different forms of meningitis

Type of meningitis Glucose Protein Cells

Acute bacterial Low High PMNs, often > 300/mm³

Normal or
Acute viral Normal mononuclear, < 300/mm³
high

mononuclear and
Tuberculous Low High
PMNs, < 300/mm³

Fungal Low High < 300/mm³

Malignant Low High Usually mononuclear

Investigations
• FBC, Uand E, LFT,clotting studies
• Throat swab viral or bacterial
• Cxray (Tb,HIV)
Treatment
Initial treatment
• Meningitis is potentially life-threatening and has a high
mortality rate if untreated.
• delay in treatment has been associated with a poorer outcome.
• Thus treatment with wide-spectrum antibiotics should not be
delayed while confirmatory tests are being conducted.
• If meningococcal disease is suspected in primary care,
guidelines recommend that benzylpenicillin be administered
before transfer to hospital.
• Intravenous fluids should be administered or shock are present
Treatment cont’d
• One of the third-generation cefalosporin antibiotics recommended
for the initial treatment of bacterial meningitis in young children
and those over 50 years of age, as well as those who are
immunocompromised, addition of ampicillin is recommended to
cover Listeria monocytogenes
• Tuberculous meningitis requires prolonged treatment with
antibiotics
• Fungal meningitis, such as cryptococcal meningitis, is treated with
long courses of highly dosed antifungals, such as amphotericin B
and flucytosineb
Treatment cont’d
• Supportive (IV fluids) if there is hypotention or shock
• If there are signs of raised intracranial pressure, measures to
monitor the pressure may be taken; this would allow the
optimization of the cerebral perfusion pressure and various
treatments to decrease the intracranial pressure with medication
(e.g. mannitol). Seizures are treated with anticonvulsants.
• Hydrocephalus (obstructed flow of CSF) may require insertion of
a temporary or long-term drainage device, such as a cerebral
shunt.
Encephalitis
Introduction
• Encephalitis is inflammation of the brain. This leads to brain
dysfunction (encephalopathy) with evidence of inflammation
measured in CSF, or using imaging or EEG.
• is a neurological emergency which can result in severe
disability/death
• Suspect if neurological symptoms or change in behaviour preceded by
an infectious prodrome (T°, rash, lymphadenopathy, cold sore,
conjunctivitis).
• Encephalopathy Altered consciousness >24h including lethargy and change
in
behaviour. Differential: includes encephalitis, but also sepsis, hypoglycaemia,
hepatic encephalopathy, diabetic ketoacidosis, drugs, hypoxic brain injury,
uraemia, SLE, vasculitis, Wernicke’s encephalopathy , metastases.
• Encephalitis Encephalopathy and evidence of CNS inflammation: fever,
seizures,
focal neurology, CSF findings, EEG, neuroimaging.
Signs and symptoms
• • Confusion, change in personality, drowsiness.
• • Seizures
• • Fever.
• • Headache.
• • Focal neurological signs.
• • decreased GCS or coma
Causes
• • Viral HSV-1 & 2, VZV, adenovirus, CMV, HIV, measles, mumps, rabies,
arboviruses
• • Non-viral infections Any bacterial meningitis, TB, malaria, listeria,
Lyme disease,
• legionella, leptospirosis, aspergillosis, cryptococcus, schistosomiasis,
• • Auto-immune (with tumour associations) Anti-NMDA receptor
(ovarian teratoma), anti-LGI-1 (thymoma), anti-Hu (small cell lung),
anti-Ma (testicular tumour)
• anti-GAD, acute disseminated, Bickersta!'s encephalitis.
Investigations
LP Imaging is not needed prior if no focal neurological signs, no papilloedema, no
seizures, and GCS >12.

Moderate CSF protein, high ymphocytes glucose often normal. Viral PCR including HSV (high
sensitivity and specificity, though
may be negative early in disease
• blood culture, serum for viral PCR, throat swab, toxoplasma IgM titre,
malaria film. Consider autoantibody testing.
• MRI Abnormal in 90% of HSV encephalitis. Normal or subtle abnormalities in autoimmune
encephalitis
• CT, if paraneoplastic cause suspected.
• EEG Di!use abnormalities are non-specific and can be abnormal in encephalopathy
due to other causes.
Management
Mortality in untreated viral encephalitis is >70%.
Aciclovir 10mg/kg/8h IV for 14d. Consider repeat CSF HSV PCR at 14 days to con-
firm discontinuation. May need longer (eg 21d) if immunosuppressed.
• Supportive therapy in high-dependency unit or critical care may be needed.
• Monitor kidney function with IV aciclovir (small risk of crystal nephropathy).
• CMV encephalitis: ganciclovir, foscarnet.
Symptomatic treatment: eg anticonvulsant medication for seizures (