Meningitis

By: Dr. Hawine Bekele

June 24,2017
Objective
At the end of this lecture students should be able
to:
• know the epidemiology, microbiology,
pathogenesis of meningitis
• Understand the transmission mode and
treatment of the infection
• be aware about the prevention methods
Outline
• Introduction
• Epidemiology
• Aetiology
• Transmission
• Pathogenesis
• Clinical presentation
• DDX
• Diagnosis
• Treatment
• Prognosis
Introduction
• Infections of the central nervous system can be
divided into 2 broad categories. Those primarily
involving the menings (meningitis) and those
primarily confined to the parenchyma
(encephalitis).
• Meningitis is an inflammatory disease of the
leptomeninges, the tissues surrounding the brain
and spinal cord, and is defined by an abnormal
number of white blood cells in the cerebrospinal
fluid (CSF)
• Meningitis is a clinical syndrome characterized by
inflammation of the menings, the 3 layers of
membranes that enclose the brain and spinal
cord.
• These layers consist of the following:
• Dura: a tough outer membrane, Arachnoid: a lacy,
web like middle membrane, subarachinoid space:
a delicate, fibrous inner layer that contains many
of blood vesseles that feed the brain and spinal
cord.
• Approximately 1.2 million cases of bacterial
meningitis occur annually worldwide.
• Meningitis is among the ten most common
infectious causes of death and is responsible for
approximately 135,000 deaths throughout the
world each year.
• Neurologic sequelae are common among
survivors.
•  From its original recognition in 1805 until the
early 1900s, bacterial meningitis was virtually
100 percent fatal.
• In 1913, Simon Flexner's introduction of
intrathecal meningococcal antiserum prevented
some deaths, but the clinical outcome did not
improve dramatically until the advent of
systemic antimicrobial therapy in the 1930s.
• Despite the effectiveness of current antibiotics in
clearing bacteria from the cerebrospinal fluid
(CSF), bacterial meningitis continues to cause
significant morbidity and mortality worldwide.
Epidemiology
• The incidence of meningitis varies according to the
specific ethiologic agent as well as in conjuction
with a nations medical resource.
• The incidence is presumed to be higher in
developing countries because of less access to
preventive services, such as vaccination.
• In these countries the incidence is has been
reported to be 10 times higher than in developed
countries.
• Menigitis affect people of all races
• Meningococcal meningitis is endemic in parts of
Africa, India and other developing areas.
• Periodic epidemics occur in the sub-saharan
“meningitis belt” as well as among religious
piligrims travelling to Saudi Arabia for the Haji.
• In parts of Africa, widespread epidemics of
meningococcal meningitis occur regularly.
• In 1996, the biggest wave of meningococcal meningitis
outbreaks ever recorded arose in West Africa. An
estimated 250,000 cases and 25,000 deaths occurred
in Niger, Nigeria, Burkina Faso, Chad and Mali.
• The incidence of neonatal bacterial meningitis is 0.25-1
cases per 1000 live births. In addition, the incidence is
0.15 cases per 1000 full term births and 2.5 cases per
1000 premature births.
• Approximately 30% of newborns with clinical sepsis
have associated bacterial meningitis.
•  The Centers for Disease Control and Prevention
examined the epidemiology of meningitis in the
United States based on population-based
surveillance from 1998 to 2007 via the Emerging
Infections Program Network [ 4 ]. Importantly,
the pneumococcal conjugate vaccine was
introduced in the US in 2000 as part of routine
childhood immunizations
• In eight surveillance areas, representing over 17 million
persons of all ages, bacterial meningitis incidence declined
from 2.0 to 1.38 cases per 100,000 population between
1998-1999 and 2006-2007.
• The median age of meningitis patients increased from 30
years to 42 years between 1998-1999 and 2006-2007.
• The overall case-fatality rate did not change significantly; it
was 15.7 percent in 1998-1999 and 14.3 percent in 2006-
2007.
• Among adults with bacterial meningitis, chronic or
immunocompromising conditions were common, occurring
in 33 and 23 percent, 
• Age  — In adults, the rates of bacterial meningitis increase with
increasing age. In a population-based surveillance study, between
2006 and 2007 in the United States, the following rates of bacterial
meningitis were observed:
• 18 to 34 years – 0.66 cases per 100,000 population
• 35 to 49 years – 0.95 cases per 100,000 population
• 50 to 64 years – 1.73 cases per 100,000 population
• ≥65 years – 1.92 cases per 100,000 population
• Between 2003 and 2007, the case-fatality rate of bacterial
meningitis among adults in the United States was 16.4 percent, and
increased linearly with increasing age; it was 8.9 percent among
patients between 18 and 34 years of age compared with 22.7 percent
in patients ≥65 years of age
• Impact of the pneumococcal conjugate
vaccine  — Surveillance after the introduction of the
pneumococcal conjugate vaccine (PCV7) to the standard
childhood immunization schedule in 2000 has shown
that the vaccine is effective in preventing invasive
pneumococcal disease (IPD) and providing herd
immunity .
• In 2003, it was estimated that 30,000 cases of vaccine
serotype IPD were prevented in the United States
through routine immunization; approximately two-thirds
of these cases were prevented through herd immunity.
• the rate of pneumococcal meningitis fell from 0.8 to
0.55 cases per 100,000 population (a 33 percent
reduction); the reduction was greatest in children under
5 years of age. These results were confirmed in another
study in which rates of pneumococcal meningitis fell
from 1.13 to 0.79 cases per 100,000 population from
1998-1999 and 2004-2005, respectively.
• A similar pattern was seen in another surveillance study
in which rates of pneumococcal meningitis in the
United States fell from 1.09 to 0.81 cases per 100,000
population between 1998-1999 and 2006-2007.
• However, there has been an increase in
pneumococcal meningitis cases caused by
serotypes not in the vaccine (specifically,
serotypes 19A, 22F, and 35B), including some
strains not susceptible to many antibacterial
agents. With the licensure of the 13-valent
pneumococcal conjugate vaccine in 2010, further
declines in the incidence of pneumococcal
meningitis may be seen
• In a United States surveillance study between 2003 and 2007, 1083
cases of bacterial meningitis were reported in adults; S. pneumoniae
was responsible for 71 percent of cases, Neisseria meningitidis for 12
percent, group B streptococcus for 7 percent, Haemophilus influenzae
for 6 percent, and Listeria monocytogenes for 4 percent.
• In a 2004 review of 696 cases of bacterial meningitis in adults in the
Netherlands, S. pneumoniae was responsible for 51 percent, N.
meningitidis for 37 percent, and L. monocytogenes for 4 percent of
cases.
• The remaining cases were primarily due to H. influenzae,
streptococci, Staphylococcus aureus, and gram-negative bacilli. A
similar distribution was noted in another study of community-
acquired bacterial meningitis in adults.
• In a multicenter study of patients with bacterial meningitis in the
United States in 1995, the frequency of the major pathogens
varied with age
• In adults up to age 60, S. pneumoniae was responsible for 60
percent of cases, followed by N. meningitidis (20 percent), H.
influenzae (10 percent), L. monocytogenes (6 percent), and group
B streptococcus (4 percent).
• In adults age 60 and above, almost 70 percent of cases were due
to S. pneumoniae, approximately 20 percent to L.
monocytogenes, and 3 to 4 percent each to N. meningitidis, group
B streptococcus, and H. influenzae. An increased prevalence of L.
monocytogenes in older adults has been noted in other reports as
well
• The high frequency of pneumococcal meningitis in adults
reflects the relatively high rate of pneumococcal infection in
the community. It has been estimated that meningitis occurs
in only 4 percent of invasive pneumococcal infections,
compared with 48 percent of invasive N. meningitidis
infections, 30 percent of invasive listeriosis, 10 percent of
invasive H. influenzae infections, and 4 percent of invasive
group B streptococcal infections.
• Invasive pneumococcal infection is defined as the isolation of
S. pneumoniae from a normally sterile site, such as the blood
or cerebrospinal fluid.
• Geography  — The distribution of pathogens depends
not only upon the age of the patient, but also upon the
region of the world. As an example, epidemics of
meningitis due to N. meningitidis occur throughout the
developing world, particularly in sub-Saharan Africa,
but are uncommon in the United States and Europe.
• In African countries with high rates of HIV infection,
the majority of meningitis cases are caused by S.
pneumoniae, which has been associated with a high
mortality rate. 
• NOSOCOMIAL  — Nosocomial meningitis is primarily a
disease of neurosurgical patients . Two large series reported
a meningitis incidence of 0.3 and 1.5 percent, respectively,
after neurosurgical procedures. Specific risk factors for the
development of nosocomial meningitis include craniotomy,
placement of ventricular or lumbar catheters, and head
trauma.
• The distribution of causative organisms is appreciably
different in nosocomial meningitis compared with
community-acquired meningitis. This was illustrated in a
study of 197 episodes of nosocomial meningitis between
1962 and 1988.
• Nosocomial infection was primarily defined as meningitis
that developed more than 48 hours after hospitalization or
within one week of hospital discharge. Gram-negative bacilli
accounted for 38 percent of single episodes of meningitis,
and streptococci, Staphylococcus aureus, and coagulase-
negative staphylococci accounted for 9 percent each.
• In contrast, S. pneumoniae accounted for only 5 percent of
cases, L. monocytogenes for 3 percent, and N. meningitidis
for 1 percent of cases. In contrast, the majority of meningitis
cases that occur after basilar skull fracture or early after
otorhinologic surgery care are caused by microorganisms
that colonize the nasopharynx, especially S. Pneumoniae.
• A later report evaluated 6243 consecutive craniotomies performed
between 1997 and 1999. Postoperative bacterial meningitis occurred
in 1.5 percent of cases; patients with ventriculitis related to a device
were excluded.
• When comparing patients from periods before and after antimicrobial
prophylaxis to prevent wound infection caused by gram-positive
bacteria, prophylaxis had no effect on the rate of meningitis but did
affect the cause of meningitis: mostly cutaneous organisms without
prophylaxis compared with mostly non cutaneous organisms with
prophylaxis; Enterobacteriaceae and, to a lesser degree, streptococci
and Pseudomonas aeruginosa accounted for more cases than
coagulase-negative staphylococci, S. aureus, and P. acnes.
Epidemiology of specific bacterial pathogens of acute
meningitis:
• [Link] meningitis primarily affects infants yonger
than 2 years.
• [Link] meningitis occurs principally during the
first 12 weeks of life but has also been reported in adults,
primarily affecting individuals older than age 60 years.
The overall case-fatality rate in adult is 34%.
• Among the bacterial agents that cause meningitis,
[Link] is associated is associated with one of the
highest moralities (19-26%)
Aetiology
• Causes of meningitis include bacteria, viruse,
fungi and parasites .
• Certain risk factors are associated with particular
pathogens.
• Hiv infection increases susceptibility to meningitis
from a Varity of pathogens, including cryptococci,
mycobacterium tuberculosis and listeria species.
• In addition HIV itself may cause aseptic
meningitis.
• Other viral causes of meningitis include:
• Enteroviruses
• West Nile virus
• Human Herpes virus
Heamophilus influenza meningitis
• [Link] is a small, pleomorphic, gram
negative coccobacillus that is frequently found as
part of the normal flora in the respiratory tract.
• The organism can spread from one individual to
the other in airborne droplets or by direct
contact with secretions.
• Meningitis is the most serious acute manifestation
of systemic infection with H. Influenza
• In the past [Link] was the major cause of
meningitis, and the encapsulated type b strain of
the organiam (Hib) accounted for the majority of
cases.
• Since the introduction of Hib vaccine in the US in
1990, the overall incidence has dereased by 35%
with Hib accounting for fewer than 9.4% of cases.
Pneumococcal meningitis:
• S. Pneumoniae, a gram positive coccus, is the
most common bacterial cause of meningitis. In
addition, it is the most common bacterial agents
in meningitis associated with with basillar skull
fructure and CSF leak.
• It is associated with other focal infections such
as pneumonia, sinusitis or endocarditis.
• [Link] is common colonizer of the
human nasopharynx; it is present in 5-10% of
healthy adults and 20-40% of healthy children.
• It causes meningitis by escaping local host
defences and phagocytic mechanisms, either
through choroid plexus seeding from
bacteraemia or through direct extension from
sinusitis or otitis media.
Patients with the following conditions are at
increased risk for [Link] meningitis:
• Hyposplenism, hypogammaglobulinemia,
multiple myeloma, DM, renal insufficiency,
alcoholism, malnutrition and chronic liver
disease.
Meningoccocal meningitis:
• N. Meningitidis is a gram negative diplococcus that is
carried in the nasopharynx of otherwise healthy
individuals. It initiates invasion by penetrating the
airway epithelial surface.
• Most sporadic cases of meningococcal meningitis (95-
97%) are caused by serogroups B,C and Y whereas the A
and C strains are observed in epidemics(< 3% of cases)
• Currently [Link] is the leading cause of
bacterial meningitis in children and young adults.
Risk factors for meningococcal meningitis include
the following:
• Deficiencies in terminal complement components
• Properdin defects that increase the risk of invase
disease
• Antecedent viral infection, chronic medical illness,
corticosteroid use, active or passive infection
• Crowded living conditions
Listeria monocytogens meningitis:
• Listeria monogytogens is a small gram positive
bacillus that causes 3% of bacterial cases and is
associated with one of the highest
mortalities(20%)
• The organism is widespread in nature and has
been isolated in the stool of 5% of healthy adults.
Most human cases appear to be food born.
• [Link] is a common food contaminant,
with a recovery rate upto 70% from raw meat,
vegetables and meats.
• Outbreaks have been associated with
consumption of contaminated milk and cheese.
• Groups at risk include pregnant women, infant
and children, elderly individual (>60 yrs),
patients with alcoholism, immunosuppresed,
CLD patients, DM patients.
Staphylococcal meningitis:
• Staphylococcal are gram- positive cocci that are
part of the normal skin flora.
• Meningitis caused by staphylococci associated
with risk factors like neurosurgery, head trauma,
presence of CSF shunts, Infective endocarditis
Aseptic meningitis:
• The term aseptic meningitis refers to patients who
have clinical and laboratory evidence for
meningeal inflammation with negative routine
bacterial cultures.
• The most common cause is enterovirus .
Additional etiologies include other infections,
(mycobacteria, fungi, spirochetes), parameningeal
infections, medications, and malignancy.
• Aseptic meningitis often has a similar presentation to
bacterial meningitis (eg, fever, headache, altered mental
status, stiff neck, photophobia), which can be a life-
threatening illness. However, in contrast to bacterial
meningitis, the majority of patients with aseptic
meningitis have a self-limited course that will resolve
without specific therapy.
• The assessment of patients with probable aseptic
meningitis is complicated by the large number of
potential etiologic agents and the relatively limited
diagnostic tools for identifying specific pathogens
VIRAL MENINGITIS: 
• A number of viruses produce aseptic meningitis
including enteroviruses, herpes simplex virus (HSV),
human immunodeficiency virus (HIV), West Nile virus
(WNV), varicella-zoster virus (VZV), mumps, and
lymphocytic choriomeningitis virus (LCM)
• Enteroviruses  — Aseptic meningitis occurring
during the summer or fall is most likely to be caused by
enteroviruses (e.g, Coxsackie, echovirus, other non-
poliovirus enteroviruses), the most common cause of
viral meningitis
• Enteroviruses continue to cause 6 to 10 percent of
cases of viral meningitis in the winter and spring
despite their predilection for inciting illness in the late
summer and fall
• The presenting signs and symptoms of enteroviral
meningitis are not distinctive. The onset of symptoms
is characteristically abrupt and typically includes
headache, fever, nausea or vomiting, malaise,
photophobia, and meningismus. Rash, diarrhea, and
upper respiratory symptoms may also be present.
• Cerebrospinal fluid (CSF) findings are typical of
other viral meningitides and include a white
blood cell (WBC) count that is generally less than
250 cells/microL, a modest elevation in CSF
protein concentration (generally less than
150 mg/dL), and a normal glucose concentration
• Up to two-thirds of patients with enteroviral
meningitis have a polymorphonuclear
predominance in the CSF when examined early in
the course of the illness.
• CSF PCR for enteroviruses yields a diagnosis in
up to 75 percent of patients with culture-
negative aseptic meningitis Among patients with
CNS manifestations and a negative CSF PCR,
upper respiratory tract and gastrointestinal tract
specimens for enterovirus PCR may be useful to
establish a diagnosis of enterovirus infection
HIV infection:
• Primary infection with HIV frequently presents
as a mononucleosis-like syndrome manifested by
fever, malaise, lymphadenopathy, rash, and
pharyngitis.
• A subset of these patients will develop
meningitis or meningoencephalitis, manifested
by headache, confusion, seizures or cranial nerve
palsies.
• In most patients with HIV-1 meningitis, the clinical
findings resolve without treatment, and patients may
be erroneously assumed to have a benign cause of viral
meningitis. Thus, clinicians should have a high index of
suspicion for primary HIV infection in patients at
increased risk for acquisition of this virus and all
patients should be questioned about possible risk
factors.
• The CSF profile characteristically has a lymphocytic
pleocytosis, an elevated protein concentration, and
normal glucose concentration.
Herpes simplex meningitis:
• Primary HSV has been increasingly recognized as a cause of
viral meningitis in adults. In contrast to HSV encephalitis,
which is almost exclusively due to HSV-1, viral meningitis in
immunocompetent adults is generally caused by HSV-2
• Between 13 and 36 percent of patients presenting with primary
genital herpes have clinical findings consistent with meningeal
involvement, including headache, photophobia and
meningismus.
• On the other hand, genital lesions are present in approximately
85 percent of patients with primary HSV-2 meningitis and
generally precede the onset of CNS symptoms by seven days.
• The CSF profile includes a pleocytosis with a predominance
of lymphocytes, and a normal CSF glucose concentration .
HSV meningitis can also occur without evidence of genital
lesions, although this is less common. Thus, the absence of
genital lesions should not deter the clinician from testing
for HSV-2 infection in a patient with aseptic meningitis.
• There is no standard approach to the treatment of HSV
meningitis . For hospitalized patients, we prefer
intravenous acyclovir at 10mg/kg administered every eight
hours. Patients can be switched to an oral agent on
discharge for a total of 10 to 14 days of treatment.
OTHER INFECTIONS:
• Spirochetes  — The two major spirochetes that need
to be considered in the differential diagnosis of
aseptic meningitis are Treponema pallidum, the
causative agent of syphilis, and Borrelia burgdorferi,
the spirochete that leads to Lyme disease.
• Fungal infections: The two major fungal infections
that should be considered in the differential diagnosis
of aseptic meningitis include cryptococcus and
coccidioidomycosis
Tuberculous meningitis:
• Patients with tuberculous meningitis frequently
have protracted headache, vomiting, confusion, and
varying degrees of cranial nerve signs. Mental
status changes can occur, leading to coma, seizures,
and at times hemiparesis. Signs of disseminated TB
are of diagnostic importance, but are often absent.
• CSF analysis typically shows elevated protein and
lowered glucose concentrations with a
mononuclear pleocytosis.
Pathogenesis
• N. meningitidis is transmitted among humans through
close contact via large respiratory droplets. Colonization of
the upper respiratory mucosal surfaces (e.g., nasopharynx)
by N. meningitidis is the first step in establishment of a
human carrier state and invasive meningococcal disease.
• Acquisition of meningococci through contact with
respiratory secretions or saliva can be transient, lead to
colonization (carriage), or result in invasive disease. The
inoculum size needed for transmission is unknown.
Meningococcal disease usually occurs within 1 to 14 days of
acquisition.
• Initial contact of meningococci with mucosal epithelial cells is
mediated by type IV pili. The structures provide mobility to
penetrate mucus and are the initial adhesins for epithelial cells;
the receptor for pili may be the I-domain of integrin α chains or
possibly CD46.
• Meningococci proceed to proliferate on the surface of human
nonciliated epithelial cells, forming small microcolonies at the
site of attachment; they can disseminate from colonies by post-
translational modification of pili and migrate to adjacent cells via
pili-mediated “twitching” motility. Meningococci can also spread
from the nasopharynx to adjacent epithelial surfaces and can
infrequently cause local infections, including pneumonia,
sinusitis, or otitis media.
• Close adherence of meningococci to the host epithelial
cells results in the formation of epithelial cell cortical
plaques and leads to the recruitment of factors
ultimately responsible for the formation and extension
of pseudopodia that can surround the meningococcus.
Intimate meningococcal association with the epithelial
cell is mediated by the bacterial opacity proteins Opa
and Opc with CD66/carcinoembryonic antigen–
related cell adhesion molecules (CEACAMs) and
integrins, respectively, on the surface of the cell.
• The formation of epithelial cell membrane protrusions and
pseudopodia stems from the organization of specific molecular
complexes involving the linkers ezrin and moesin, along with the
clustering of several membrane-integral proteins, including
CD44, intracellular adhesion molecule 1, and cortical actin
polymerization.
• These events can lead to internalization of N. meningitidis in
epithelial cells. Intracellular meningococci reside within a
membranous vacuole and are capable of translocating through
the epithelial layers within 18 to 40 hours. Meningococci are
capable of intracellular replication, due in part to the protective
capsule and the organism’s capacity to acquire iron through
specialized transport systems.
• Meningococci cross mucosal surfaces, enter the blood
stream, and, in some individuals, produce systemic
infection. Damage to the mucosal surface by
coinfection, drying (e.g., very low humidity), or smoke
exposure may increase this risk of invasion.
• The molecular interactions noted for epithelial cells also
occur with endothelial cells, and meningococci can
translocate across the blood-meninges barrier, possibly
at the choroid plexus or by opening of intercellular
junctions, and proliferate in the subarachnoid space,
resulting in meningitis.
• In vasculature and cerebrospinal fluid (CSF),
high levels of multiplying bacteria lead to an
intense inflammatory response, with
pronounced increases in concentrations of
tumor necrosis factor-α (TNF-α), interleukins
(IL-1β,IL-6, IL-8, and IL-10), different
chemokines, and other inflammatory mediators.
• Resistance to complement-mediated lysis and
phagocytosis is due to the expression of the
capsule and lipo-oligosaccharide.
• Meningococcal endotoxin released in blebs plays
a major role in the inflammatory events of
meningococcemia and meningococcal
meningitis. Meningococcal lipid A is responsible
for much of the biologic activity and toxicity of
meningococcal endotoxin.
• In contrast, an asymptomatic N. meningitidis carrier state
is found in 8 to 25% of healthy individuals. Meningococcal
carriage is affected by age, intimate personal contact,
crowding (e.g., bars, dormitories), and vaccination or
chemoprophylaxis interventions in the community. Variable
carriage rates have been reported, even during epidemics.
• Meningococcal carriage is a dynamic process, is less
common in young children than in adults and increases in
closed populations (e.g., military recruits, hajj pilgrims).
Rates as high as 36 to 71% have been reported in military
recruits.
Pathophysiology
Colonization of the nasopharynx

Bacteria are transported across epithelial cells

Invade the intravascular space & bacteremia

Infect choroid plexus epithelial cells & gain

access to the CSF
Clinical Presentation
• Meningitis can present as either an acute
fulminant illness that progresses rapidly in a few
hours or as a subacute infection that
progressively worsens over several days.
• The classic clinical triad of meningitis is
fever, headache, and nuchal rigidity
Decreased level of consciousness
Nausea and vomiting
Photophobia
Seizures- focal vs generalized
Raised ICP- leading to cerebral herniation in 1-
8%
Specific clinical features like rashs
• Examination for nuchal rigidity  — Although
patients may not complain specifically of a stiff neck,
it is easy to demonstrate nuchal rigidity. Passive or
active flexion of the neck will usually result in an
inability to touch the chin to the chest. Difficulty in
lateral motion of the neck is a less reliable finding.
• Tests to illustrate nuchal rigidity (such as Kernig's and
Brudzinski's signs) were originally developed and
tested in patients with severe, late stage meningitis
• The classic Brudzinski's sign refers to spontaneous flexion
of the hips during attempted passive flexion of the neck.
• The Kernig's sign refers to the inability or reluctance to
allow full extension of the knee when the hip is flexed
90º. Kernig's test is usually performed in the supine
position, but it can be tested in the seated patient.
• Suspected meningitis was defined as the presence of
clinical symptoms (eg, fever, headache, stiff neck,
photophobia, nausea, and/or vomiting) that led to
performance of an LP to exclude meningeal
inflammation.
 Infants with meningitis infection will have the
following signs and symptoms:
• Bulging of fontanelles
• Paradoxic irritability
• High pitch cry
• Hypotonia
Diagnosis
The diagnostic challenges in patients with clinical
findings of meningitis are as follows:
• Early identification and treatment of patients
with acute bacterial meningitis
• Assessing weather a treatable central nervous
system infection is present in those with
suspected sub acute or chronic meningitis
• Identifying the causative organism
• The diagnosis of bacterial meningitis is made by
examination of the CSF
• The need to obtain neuroimaging studies prior
to LP requires clinical judgment.
• A broad-range PCR can detect small numbers of
viable and nonviable organisms in CSF
• MRI/CT
DDx
Viral meningoencephalitis
Rocky Mountain spotted fever
Ehrlichioses
Focal suppurative CNS infections
Subarachnoid hemorrhage
drug-induced hypersensitivity meningitis
carcinomatous or lymphomatous meningitis
Inflammatory disorders such as sarcoid, SLE
Subacute meningitis
Management
• Empirical Antimicrobial Therapy - is initiated in
patients with suspected bacterial meningitis
before the results of CSF Gram's stain and
culture are known
Specific Antimicrobial Therapy
• Meningococcal Meningitis-
penicillin G remains the antibiotic of
choice for meningococcal meningitis
if resistance is found, cefotaxime or ceftriaxone
Rx for 7 days
The index case and all close contacts should
receive chemoprophylaxis
• Pneumococcal Meningitis
 Cephalosporin (ceftriaxone,
cefotaxime, or cefepime) and
vancomycin
Rx for 2 weeks
Cont’d
Adjunctive Therapy
• Dexamethasone 10 mg IV 15–20 min before
the first dose of an antimicrobial agent, and the
same dose repeated every 6 h for 4 days.
• Dexamethasone does not alter TNF
production once it has been induced.
• Therapy with dexamethasone should ideally be
started 20 min before, or not later than
concurrent with, the first dose of antibiotics. It is
unlikely to be of significant benefit if started >6 h
after antimicrobial therapy has been initiated
Increased Intracranial Pressure

• Emergency treatment of increased ICP includes:

Elevation of the patient's head to 30–45°
Intubation & hyperventilation (PaCO2 25–30
mmHg)
 Mannitol
Complication
Immediate complications of meningitis include
the following:
• Septic shock
• Coma with loss of protective airway reflex
• Seizure
• Cerebral edema
• Septic arthritis
• Pericardial effusion
• Hemolytic anemia
Delayed complications include the following:
• Dereased hearing or deafness
• Cranial nerves dysfynction
• Focal paralysis
• Subdural effussions
• Hydrocephalous
• Ataxia
• Blindness
• Peripheral gangerene
• Waterhouse-Friderichsen syndrome
Prevention
• Vaccination and chemoprophylaxis are 2 means
of preventing meningitis.
Prognosis

• Mortality
3–7% for meningitis caused by H. influenzae, N.
meningitidis, or group B streptococci;
15% for L. monocytogenes
20% for S. pneumoniae.
• Common sequelae – 25%
Decreased intellectual function
Memory impairment
Seizures
Hearing loss and dizziness
Gait disturbances
Thank you!!!