Definition of Meningococcal Meningitis Diagnosis of Meningococcal Meningitis • Are exposed to areas where the the meninges.
ed to areas where the the meninges.
Meningococcal meningitis is a severe bacterial
infection of the bloodstream and meninges (a
thin lining covering the brain and spinal cord).
The microorganism that causes this condition
is called meningococcus or Neisseria
meningitidis (N. meningitidis).
Description of Meningococcal Meningitis
The meningococcus bacteria is spread by
direct close contact with nose or throat
discharge of an infected person. Many people
carry this particular bacteria in their nose and
throat without any signs of illness, while
others may develop serious symptoms.
Causes and Risk Factors of Meningococcal
Meningitis
Meningococcal meningitis occurs as a and Meningococcemia are major causes of
communicable disease between humans. It is
often found in young military recruits living
together, or among college students living in
close quarters in dormitories.
When the cerebrospinal fluid is invaded by this
blood-borne organism. Originating in the
respiratory tract, the meningococcus bacteria
travels, via the blood, into the cerebrospinal
fluid (the watery liquid that surrounds the
brain and spinal cord). During infection, the
bacterium releases a toxin into the fluid
causing an inflammatory reaction.
If the bacteria invades the blood it can lead
to arthritis, heart infections and pneumonia. If
it damages the nerves leading into the brain it
could cause hearing loss, learning disabilities,
motor impairment or mental retardation.
Symptoms of Meningococcal Meningitis
The most common symptoms
of meningococcal meningitis are:
• Fever
• Chills
• Headache
• Vomiting
• Stiff neck
• Rash
• Confusion
Symptoms may also include:
• Seizures
• Coma
• Inability to completely extend the
legs
• Stiffness in knees and hips
• Shock
The symptoms may appear 2 to 10 days after
exposure, but usually within 5 days.
Infected fluid from the
A medical history and physical examination
are useful but not specific enough to make the
diagnosis. Typically a lumbar puncture (also
called a spinal tap) must be done. This
procedure is done by injecting local anesthetic
(numbing medicine) into the skin of the lower
back, then inserting a hollow needle into the
lower part of the spinal canal and withdrawing
some cerebrospinal fluid. The fluid is then
stained and cultured to determine the
causative organism and to look for signs of
infection (white blood cells, bacteria, protein).
Cultures of blood, sputum and urine will also
be obtained. In all patients with suspected
meningitis, chest films and CT scans of the
brain are done to look for other sources of
infections and to rule out other diagnoses.
Treatment of Meningococcal Meningitis
Bacterial meningitis is a medical
emergency. Every hour of delay in starting
antibacterial (antibiotic) therapy increases the
risk of complications and permanent
neurological damage. Treatment with
intravenous antibiotics (such as penicillin G or
ceftriaxone) should be started immediately, in
some cases even before the lumbar puncture.
The regimen of intravenous antibiotics may be
continued for up to 7-10 days.
Postexposure Prevention
Household members, close friends at school
and at home with intensive exposure, and - if
the child attends child care - all preschool
children who are cared for in the same room,
should receive an antibiotic such as rifampin,
ceftriaxone or ciprofloxacin as soon as
possible (preferably within 24 hours of the
diagnosis) as a preventive measure.
Prevention of Meningococcal Meningitis
A vaccine called meningococcal
polysaccharide is used to prevent infection by
certain groups of meningococcal bacteria. The
vaccine works by causing the body to produce
its own antibodies against the disease. This
vaccine only applies to the Groups A, C, Y and
W-135 of the meningococcal bacteria. The
vaccine will not protect against Group B. The
vaccine is recommended for persons who:
• Are age two (2) or older
• Are susceptible to certain conditions
that may cause meningococcal
meningitis
• Are living in, working in, or visiting an
area where there is a high incidence
of meningococcal infection
epidemic is occurring and the cases
are due to Groups A, C, Y, and W-135
• Are military recruits
• Have no spleen
Meningococcal disease describes infections
caused by the bacterium Neisseria
meningitidis (also termed meningococcus). It
carries a high mortality rate if untreated.
Whilst best known as a cause of meningitis,
widespread blood infection (sepsis) is more
damaging and dangerous. Meningitis
illness, death, and disability in both developed
and under developed countries worldwide.
The disease's host/pathogen interaction is not
fully understood. The pathogen originates
harmlessly in a large number of the general
population, but thereafter can invade the
blood stream and the brain, causing serious
illness. Over the past few years, experts have
made an intensive effort to understand
specific aspects of meningococcal biology and
host interactions, however the development of
improved treatments and effective vaccines
will depend on novel efforts by workers in
many different fields.[1]
The incidence of endemic meningococcal
disease during the last 13 years ranges from 1
to 5 per 100,000 in developed countries, and
from 10 to 25 per 100,000 in developing
countries. During epidemics the incidence of
meningococcal disease approaches 100 per
100,000. There are approximately 2,600 cases
of bacterial meningitis per year in the United
States, and on average 333,000 cases in
developing countries. The case fatality rate
ranges between 10 and 20 per cent.[2]
While Meningococcal disease is not as
contagious as the common cold (which is
spread through casual contact), it can be
transmitted through saliva and occasionally
through close, prolonged general contact with
an infected person.
Pathogenesis
Meningococcal disease causes life-threatening
meningitis and sepsis conditions. In the case
of meningitis, bacteria attack the lining
between the brain and skull called
meninges then passes into the spinal cord,
causing symptoms including stiff
neck, fever andrashes. The meninges (and
sometimes the brain itself) begin to swell,
which affects the central nervous system.
Even with antibiotics, approximately 1 in 10
victims of meningococcal meningitis will die;
However, about as many survivors of the
disease lose a limb or their hearing, or suffer
permanent brain damage.[3] The sepsis type of
infection is much more deadly, and results in a
severe blood poisoningcalled meningococcal
sepsis that affects the entire body. In this
case, bacterial toxins rupture blood vessels
and can rapidly shut down vital organs. Within
hours, patient's health can change from
seemingly good to mortally ill.[4]
The N. meningitidis bacterium is surrounded
by a slimy outer coat that contains disease-
causing endotoxin. While many bacteria
produce endotoxin, the levels produced by
meningococcal bacteria are 100 to 1,000
times greater (and accordingly more lethal)
than normal. As the bacteria multiply and
move through the bloodstream, it sheds
concentrated amounts of toxin. The endotoxin
directly affects the heart, reducing its ability
to circulate blood, and also causes pressure on
blood vessels throughout the body. As some
blood vessels start to hemorrhage, major
organs like the lungs and kidneys are
damaged.
Patients suffering from meningococcal disease
are treated with a large dose of antibiotic. The
systemic antibiotic flowing through the
bloodstream rapidly kills the bacteria but, as
the bacteria are killed, even more toxin is
released. It takes up to several days for the
toxin to be neutralized from the body by using
continuous liquid treatment and antibiotic
therapy.[5]
There are many mental signs of
meningococcal such as paranoia and other
mental instabilities.
[edit]Meningitis
The patient with meningococcal meningitis
typically presents with high
fever, meningism (stiff neck),Kernig's sign,
severe headache, vomiting, purpura,
photophobia, and sometimes chills, altered
mental status, or seizures. Diarrhea or
respiratory symptoms are less common.
Petechiae is often also present, but does not
always occur, so its absence should not be pneumonia, sometimes associated with septic
used against the diagnosis of meningococcal shock. With prompt treatment with penicillin
disease. Anyone with symptoms of or chloramphenicol, the prognosis is
meningococcal meningitis should receive excellent. Pericarditis can appear, either as a
intravenus antibiotics pending results septic pericarditis with grave prognosis or as a
of lumbar puncture, as delay in treatment rective pericarditis in the wake of meningitis
worsens the prognosis. or septicaemia. Myocarditis can be a use proper precautions should receive anti-
complication of meningococcemia and can be
[edit]Meningococcemia
contributive to shock seen in this form of
disease. Pharyngitis and conjunctivitis can also
This section requires expansion.
appear and can constitute the portal of entry
for the bacterium. Septic arthritis due to N.
Symptoms of meningococcemia are, at least meningitidis can be seen, usually
initially, similar to those of influenza. Typically, accompanying disseminated infection. Other
the first symptoms include fever, nausea, forms of disease can rarely be seen,
myalgia, headache, arthralgia, chills, diarrhea, like osteomyelitis,endophthalmitis and urethrit
is.
stiff neck, and malaise. Later symptoms
include septic shock, purpura, hypotension, Prevention
cyanosis, petechiae, seizures, anxiety,
and multiple organ dysfunction
The most important form of prevention is a
syndrome. Acute respiratory distress
vaccine against N. meningitidis. Different
syndrome and altered mental status may also
countries have different strains of the bacteria
occur. Meningococcal sepsis has a higher
and therefore use different vaccines. Five
mortality rate then meningococcal meningitis,
serogroups, A, B, C, Y and W135 are
but the risk of neurologic sequelae is much
responsible for virtually all cases of the
lower.[citation needed]
disease in humans. Vaccines are currently
available against four of the five strains, and a
[edit]Types of infection
vaccine against the B strain is in
[edit]Meningococcemia development. Menactra,Menomune of Sanofi-
Aventis, Mencevax of GlaxoSmithKline and Nm
Meningococcemia, like many gram- Vac4-A/C/Y/W-135 (has not been licensed in
negative blood infections, can the US) of JN-International Medical
cause disseminated intravascular Corporation are the commonly used vaccines.
coagulation (DIC), a condition where blood Vaccines offer significant protection from
starts to clot throughout the body, sometimes three to five years (plain polysaccharide
causingischemic tissue damage. DIC also vaccine Menomune, Mencevax and NmVac-4)
causes bleeding, when the clotting factors are
to more than eight years (conjugate vaccine
used up, causing the
Menactra).[14][15]
characteristic purpuric rash.
[edit]Vaccinations
[edit]Meningitis
[edit]Children
Meningococcal meningitis is a consequence of
Children 2–10 years of age who are at high
bacteria entering the cerebrospinal fluid (CSF)
risk for meningococcal disease such as certain
and irritating the meninges - the membranes
chronic medical conditions and travel to or
that line the brain and spinal cord. Sub-
reside in countries with hyperendemic or
Saharan Africa, Americas, Western Europe, UK
epidemic meningococcal disease should
and Ireland face multifarious challenges, 200
receive primary immunization. Although safety
years after the discovery of bacterial
and efficacy of the vaccine have not been
meningitis.[6]
established in children younger than 2 years
[edit]Other types of age and under outbreak control, the
unconjugated vaccine can be considered....[16]
As with any gram negative bacterium, N. [17][18][19]
meningitidis can infect a variety of sites.
Meningococcal pneumonia can appear during
influenza pandemics and in military camps.
This is a multilobar, rapidly evolving
[edit]Children and adolescents 11 years of Meningitis A,C,Y and W-135 vaccines and
age or older those older than 55 years of age. Under
certain circumstances if unvaccinated health-
It is recommended that primary immunization
care personnel cannot get vaccinated and who
against meningococcal disease with Meningitis
have intensive contact with oropharyngeal
A,C,Y and W-135 vaccines for all young
secretions of infected patients and who do not
adolescents at 11–12 years of age and all
unvaccinated older adolescents at 15 years of
infective prophylaxis against meningococcal
age. Although conjugate vaccines are the
infection (i.e., 2-day regimen of oral rifampin
preferred meningococcal vaccine in
or a single dose of IM ceftriaxone or a single
adolescents 11 years of age or older,
dose of oral ciprofloxacin).[17][22]
polysaccharide vaccines are an acceptable
alternative if the conjugated vaccine is [edit]Military recruits
unavailable.[17][18][20][20]
Because the risk of meningococcal disease is
[edit]Adults increased among military recruits, all military
recruits routinely receive primary
College Students who plan to live in
immunization against the disease.[23]
dormitories receive primary immunization with
Meningitis A,C,Y and W-135 vaccines. [edit]Travelers and tourists
Although the risk for meningococcal disease
Immunization against meningococcal disease
for is similar to 18–24 years of age that for the
is not a requirement for entry into any
general population of similar age. The college
country, unlike Yellow fever. Only Saudi Arabia
students consider vaccination against
require that travelers to their country for the
meningococcal disease to reduce their risk for
annual Hajj and Umrah pilgrimage have a
the disease and stated that college health-
certificate of vaccination against
care providers should take a proactive role in
meningococcal disease issued not more than 3
providing information about meningococcal
disease to students and their parents. years and not less than 10 days before arrival
[21]
Routine primary immunization against in Saudi Arabia.
meningococcal disease is recommended for Travelers to or residents of areas where N.
most adults live in endemic areas and meningitidis is highly endemic or epidemic are
planning to travel such areas. Although at risk of exposure should receive primary
conjugate vaccines are the preferred immunization against meningococcal disease.
meningococcal vaccine in adults 55 years of [18][24]
age or younger, polysaccharide vaccines are
an acceptable alternative for adults in this age [edit]HIV-infected individuals
group if the conjugated vaccine is unavailable.
HIV-infected individuals are likely to be at
Since safety and efficacy of conjugate
increased risk for meningococcal disease; HIV-
vaccines in adults older than 55 years of age
infected individuals who wish to reduce their
have not been established to date,
risk of meningococcal disease may receive
polysaccharide vaccines should be used for
primary immunization against meningococcal
primary immunization in this group.[17][18]
disease.[22] Although efficacy of Meningitis
[edit]Medical staff and laboratory personnel A,C,Y and W-135 vaccines have not been
evaluated in HIV-infected individuals to date,
Health care people should receive routine
HIV-infected individuals 11–55 years of age
immunization against meningococcal disease
may receive primary immunization with the
for laboratory personnel who are routinely
conjugated vaccine.[22] Vaccination against
exposed to isolates of N. meningitidis.
meningitis do not decrease CD4+ T-cell counts
Laboratory personnel and medical staff are at
or increase viral load in HIV-infected
risk of exposure to N. meningitides or to
individuals and there has been no evidence
patients with meningococcal disease. Hospital that the vaccines adversely affect survival.[25]
Infection Control Practices Advisory [26][27]
Committee (HICPAC) recommendations
regarding immunization of health-care workers
that routine vaccination of health-care
personnel is recommended, Any individual 11–
55 years of age who wishes to reduce their
risk of meningococcal disease may receive
[edit]Household and other close contacts of
individuals with invasive
meningococcal disease
Protective levels of anticapsular antibodies are
not achieved until 7–14 days following
administration of a meningococcal vaccine,
vaccination cannot prevent early onset
disease in these contacts and usually is not
recommended following sporadic cases of
invasive meningococcal disease. Unlike,
developed countries, in sub-Saharan Africa
and other under developed countries, entire
family live in a single room of a house.[28]
[29]
Meningococcal infection is usually
introduced into a household by an
asymptomatic person. Carriage then spreads
through the household, reaching infants
usually after one or more other household
members have been infected. Disease is most
likely to occur in infants and young children
who lack immunity to the strain of organism
circulating and who subsequently acquire
carriage of an invasive strain.[30] By preventing
susceptible contacts from acquiring infection
by directly inhibiting colonization. Close
contacts are defined as those persons who
could have had intimate contact with the
patient’s oral secretions such as through
kissing or sharing of food or drink. The
importance of the carrier state in
meningococcal disease is well known. In
developed countries the disease transmission
usually occurs in day care, schools and large
gatherings where usually disease transmission
could occur. Because the meningococcal
organism is transmitted by respiratory
droplets and is susceptible to drying, it has
been postulated that close contact is
necessary for transmission. Therefore, the
disease transmission to other susceptible
person cannot be prevented. Meningitis occurs
sporadically throughout the year, and since
the organism has no known reservoir outside
of man, asymptomatic carriers are usually the
source of transmission.[31] Additionally,
basic hygienemeasures, such as handwashing
and not sharing drinking cups, can reduce the
incidence of infection by limiting exposure.
When a case is confirmed, all close contacts
with the infected person can be
offered antibiotics to reduce the likelihood of
the infection spreading to other people.
However, rifampin-resistant strains have been
reported and the indiscriminate use of
antibiotics contributes to this problem.
Chemoprophylaxis is commonly used to those
close contacts who are at highest risk of
carrying the pathogenic strains. Vaccinations
are the only answer for reducing the
transmission of the Meningococcal disease.[32]
[33]
[edit]Treatment and prognosis
When meningococcal disease is suspected,
treatment must be started immediately and
should not be delayed while waiting for
investigations. Treatment in primary care
usually involves prompt intramuscular
administration of benzylpenicillin, and then an
urgent transfer to hospital for further care.
Once in hospital, the antibiotics of choice are
usually IV broad spectrum 3rd
generationcephalosporins,
e.g. cefotaxime or ceftriaxone. Benzylpenicillin
and chloramphenicol are also effective.
Supportive measures include IV fluids, oxygen,
inotropic support, e.g. dopamine
dobutamine and management
raised intracranial pressure. Steroid therapy
may help in some adult patients, but is
unlikely to affect long term outcomes.
Complications following meningococcal
disease can be divided into early and late
groups. Early complications include: raised
intracranial pressure, disseminated
intravascular coagulation, seizures, circulatory
collapse and organ failure. Later complications
are: deafness, blindness, lasting neurological
deficits, reduced IQ, and gangrene leading to
amputations.
Background
Meningococcal meningitis (International
Classification of Disease-9 [ICD-9] code:
036.0) has been recognized as a serious
problem for almost 200 years. It was first
identified definitely by Vieusseux in Geneva in
1805. The causative organism, Neisseria
meningitidis,was isolated first in 1887.
Meningococcal disease still is associated with
a high mortality rate and persistent
neurological defects, particularly among
infants and young children.
The first successful treatment of meningitis
with intravenous and intrathecal penicillin was
reported in 1944, and the first clinical trials
using high doses of intravenous penicillin as
monotherapy for the treatment of meningitis
were reported in 1950. Since then, penicillin
has remained the drug of choice for the
treatment of meningococcal meningitis.1
For related information, see eMedicine
article Meningococcal Infections.
Pathophysiology
N meningitidis is a gram-negative, aerobic,
encapsulated diplococcus that grows best on
enriched media such as Mueller-Hinton or
chocolate agar, at 37° and in an atmosphere
of 5-10% carbon dioxide.
or
of
Meningococci comprise numerous serogroups
that are based on the composition of their
polysaccharide capsular antigens. They differ
in their agglutination reactions to sera
directed against polysaccharide antigens. At
least 13 serogroups have been described: A,
B, C, D, E, H, I, K, L, W-135, X, Y, and Z.
Serogroups B and C have caused most cases
of meningococcal meningitis in the United
States since the end of World War II; before
that, group A was more prevalent. More than
99% of meningococcal infections are caused
by serogroups A, B, C, 29E, or W-135.
The natural habitat and reservoir for
meningococci is the mucosal surfaces of the
human nasopharynx and, to a lesser extent,
the urogenital tract and anal canal.
Approximately 5-10% of adults are
asymptomatic nasopharyngeal carriers, but
that number increases to as many as 60-80%
of members of closed populations (eg, military
recruits in camps).
The modes of infection include direct contact
or respiratory droplets from the nose and
throat of infected people. Meningococcal
disease most likely occurs within a few days of
acquisition of a new strain, before the
development of specific serum antibodies.
The incubation period averages 3-4 days
(range 1-10 days), which is the period of
communicability. Bacteria can be found for 2-4
days in the nose and pharynx and for up to 24
hours after starting antibiotics. Treatment with
penicillin may not eradicate the bacteria from
the nasopharyngeal carriers.
After adherence to the nasopharyngeal
mucosa, meningococci are transported to
membrane-bound phagocytic vacuoles. Within
24 hours, they can be seen in the submucosa,
close to vessels and local immune cells. In
most cases, meningococcal colonization of
mucosal surfaces leads to subclinical infection
or mild symptoms. In approximately 10-20% of
cases, N meningitidis enters the bloodstream.
In the vascular compartment, they may be
killed by bactericidal antibodies, complement,
and phagocytic cells or may multiply, initiating
the bacteremic phase. Organisms replicate
rapidly.
Systemic disease appears with the
development of meningococcemia and usually
precedes meningitis by 24-48 hours. This can
lead to systemic infection in the form of
bacteremia, metastatic infection that
commonly involves the meninges (see Media
file 3), or severe systemic infection with
circulatory collapse and disseminated
intravascular coagulation (DIC).
Meningococcemia leads to diffuse vascular
injury, which is characterized by endothelial
necrosis, intraluminal thrombosis, and
perivascular hemorrhage.
Invasive disease depends on host factors.
Infants are protected from meningococcal
disease for the first few months of life by
transferred maternal antibodies and low rate
of meningococcal acquisition. Subsequently,
susceptibility peaks at age 6-12 months and
decreases again after colonization of closely
related nonpathogenic bacteria such
as Neisseria lactamica that have surface
antigens in common with virulent strains.
Colonization withN meningitidis gradually
replaces the nonpathogenic bacteria and
induces antibodies to the infecting strain, thus
reinforcing natural immunity. Invasive disease
occurs if no protective bactericidal antibodies
are mounted against the infecting strain.
Meningococci that elaborate a capsule can
lead to invasive disease. The capsule protects
them from desiccation and from host immune
mechanisms. Adhesins and endotoxins also
enhance their pathogenic potential.
Dysfunctional properdin (ie, component of the
alternative pathway of complement), HIV
infection, functional or anatomical asplenia,
and congenital complement deficiencies also
predispose individuals to meningococcal
disease.
Individuals acquire the infection if they are
exposed to virulent bacteria and have no
protective bactericidal antibodies. Smoking
and concurrent viral infection of the upper
respiratory tract diminish the integrity of the
respiratory mucosa and increase the likelihood
of invasive disease. Crowding living conditions
also facilitate disease spread, since individuals
from different areas have different strains of
meningococci. The risk of invasive disease is
higher in the first few days after exposure to a
new strain.
Clinical
History
• In a 2008 published cohort study
from Netherlands (the Meningitis
Cohort Study), only 70% of the
patients had the classic triad of fever,
neck stiffness, and change in mental
status. If the presence of rash was
added, 89% of the patients had 2 of
the 4 features.5
• Meningococcal meningitis is
characterized by acute onset of
intense headache, fever, nausea,
vomiting, photophobia, and stiff neck.
• Lethargy or drowsiness frequently is
reported. Stupor or coma is less
common. If coma is present, the
prognosis is poor.
• Patients also may complain of skin
rash, which usually points to disease
progression.
• The clinical pattern of bacterial
meningitis is quite different in young
children: Bacterial meningitis usually
presents as a subacute infection that
progresses over several days.
o Irritability is a common
presenting feature, and
headache and neck stiffness
may not be present.
Projectile vomiting may
occur.
o Seizures occur in 40% of
children with meningitis,
typically during the first few
days. The majority of
seizures have a focal onset.
o In infants, the illness may
have an insidious onset; stiff
neck may be absent. In
children, even when the
combination of convulsive
status epilepticus and fever
is present, the classic signs
and symptoms of acute
bacterial meningitis may not
be present.6
Physical
• Neurological signs include nuchal
rigidity, lethargy, delirium, coma, or
convulsions.
o Most adult patients have an
altered mental state, clinical
signs of nuchal rigidity (eg,
Kernig sign, Brudzinski sign),
and fever.
o Elderly patients are prone to
have an altered mental state
and a prolonged course with
fever.
• Patients older than 30 years were
noted to have petechiae (62%) less
frequently than younger patients
(81%).
• A more severe but less common form
of meningococcal disease is
meningococcal septicemia, which is
characterized by rapid circulatory
collapse and a hemorrhagic rash.
• The Waterhouse-Friderichsen
syndrome may develop in 10-20% of
children with meningococcal
infection. This syndrome is
characterized by large petechial
hemorrhages in the skin and mucous
membranes, fever, septic shock, and
DIC.
• A petechial or purpuric rash usually is
found on the trunk, legs, mucous
membranes, and conjunctivae.
Occasionally, it is on the palms and
soles. The rash may progress to
purpura fulminans, when it usually is • Perform a neuroimaging study (either
associated with multiorgan failure (ie, MRI or CT scan) prior to lumbar
Waterhouse-Friderichsen syndrome). puncture in all patients in whom
meningitis is suspected. CT scan
findings are usually normal. However,
Workup
imaging is an important cause
of delay of therapy.
Laboratory Studies
• MRI with contrast is preferred to CT
scan because MRI better
• Laboratory examination of the demonstrates meningeal lesions,
cerebrospinal fluid (CSF) usually cerebral edema, and cerebral
confirms the presence of meningitis. ischemia. T1 may show obliterated
Typical CSF abnormalities in cisterns. Contrast enhances the
meningitis include the following: cisterns, and extension of enhancing
subarachnoid exudate deep into the
o Increased opening pressure
sulci may be seen in severe cases.
(>180 mm water)
Strokes can be seen with the
o Pleocytosis of
development of vasculitis and
polymorphonuclear cerebritis. CNS complications that
leukocytes (WBC counts can be visualized by MRI include
between 10 and 10,000 hydrocephalus, aqueductal
cells/µL, predominantly
neutrophils)
obstruction, ventriculitis (especially in
neonates), choroid plexitis, subdural
o Decreased glucose effusion, and empyema.
concentration (<45 mg/dL)
• Indications for performing CT scan
o Increased protein prior to lumbar puncture include
concentration (>45 mg/dL) altered level of consciousness,
• Gram stain and culture of CSF papilledema, focal neurological
identify the etiological organism, N deficits, and/or focal or generalized
meningitides. In bacterial meningitis, seizure activity.
Gram stain is positive in 70-90% of
untreated cases, and culture results
Other Tests
are positive in as many as 80% of
cases.
An electroencephalogram (EEG) study is
• More specialized laboratory tests, sometimes useful to document irritable
which may include culture of CSF and electrical patterns that may predispose the
blood specimens, are needed for patient to seizures. Periodic complexes and
identification of N meningitidis and periodic lateralizing epileptiform discharges
the serogroup of meningococci, as (PLEDs) may be suggestive of encephalitis
well as for determining its caused by herpes simplex virus.
susceptibility to antibiotics.
• Polymerase chain reaction (PCR)8 may
Histologic Findings
be used to complement standard
laboratory procedures for the During the first few days, the subarachnoid
diagnosis of meningococcal and ventricular exudate contains large
meningitis.9 The IS1106 PCR is a rapid numbers of neutrophils and necrotic debris.
and sensitive test for confirmation of Intracellular and extracellular bacteria can be
the diagnosis; its sensitivity is not demonstrated. The exudate extends along the
affected by prior antibiotic perivascular spaces into the cortex and
treatment.10 PCR of the nspA gene cerebral cortex. Purulent material usually is
was also reported to be a fast observed in the choroid plexus. With time, the
diagnostic test.11 number of mononuclear leukocytes increases,
and they predominate by the end of the first
Imaging Studies week. Fibroblasts also proliferate.
Inflammatory cells infiltrate leptomeningeal
and cortical arteries and veins and accumulate
in the intima. Thrombosis of small vessels
leads to infarction. This pattern is common in
autopsied cases.
Treatment
Medical Care
Meningococcal disease is potentially fatal and
always should be viewed as a medical
emergency. Admission to a hospital is
necessary. To prevent serious neurological
morbidity and death, prompt institution of
antibiotic therapy is essential when the
diagnosis of bacterial meningitis is suspected.
• Institute antimicrobial therapy as
soon as possible after the lumbar
puncture is performed.
• If imaging studies are indicated
before lumbar puncture, draw blood
for culture and begin administration
of empiric antibiotics. Administration
of empiric antibiotics is unlikely to
decrease diagnostic sensitivity if CSF
is tested for bacterial antigens early
in the course of the illness.
• Long delays may occur in the
emergency department before
initiation of antibiotics in patients
with suspected bacterial meningitis.
In general, these delays appear to be
physician generated and, to a great
extent, potentially avoidable.12
• In children and adults, the
recommended initial empiric therapy
consists of third-generation
cephalosporins, but the addition of
ampicillin is required in patients in
whom a Listeria species pathogen is
suspected (eg, patients older than 50
years, neonates). Once the organism
is identified, the antibiotic regimen
can be changed appropriately.
• A recent study has suggested that at
least in children, CSF sterilization
may occur more rapidly after
initiation of parenteral antibiotics
than previously suggested, with
complete sterilization of
meningococcus within 2 hours and
the beginning of sterilization of
pneumococcus by 4 hours.
Surgical Care
Surgical interventions may be necessary for
the management of complications such as
subdural effusions, empyema, and
hydrocephalus.
Medication
At presentation, meningitis due to N
meningitidis may be impossible to
differentiate from other types of meningitis.
Thus, empirical treatment with an antibiotic
with effective CNS penetration should be
based on age and underlying disease status,
since delay in treatment is associated with
adverse clinical outcome.
Standard empirical therapy varies according
to age, as follows:
• In infants younger than 4 weeks, it
consists of ampicillin plus cefotaxime
or an aminoglycoside.
• Infants aged 4-12 weeks should be
treated with ampicillin plus a third-
generation cephalosporin.
• In children aged 12 weeks to 18
years, a third-generation
cephalosporin or ampicillin plus
chloramphenicol is an appropriate
combination.
• Adults aged 18-50 years and
individuals with basilar skull fracture
should be treated with a third-
generation cephalosporin, while
individuals older than 50 years should
be treated with ampicillin plus a
third-generation cephalosporin.
Once the accurate diagnosis of meningococcal
meningitis is established, appropriate changes
can be made. Currently, penicillin is the drug
of choice for the treatment of meningococcal
meningitis and septicemia. Unresponsiveness
to penicillin has not been observed in the
United States. Routine testing for
susceptibility of meningococcal isolates is not
necessary, unless the patient does not exhibit
appropriate clinical response.
Therapy should be changed to ceftriaxone (or The infection occurs more often in winter or
cefotaxime) if the isolate is resistant to spring. It may cause local epidemics at
penicillin. boarding schools, college dormitories, or
military bases.
The use of dexamethasone in the
management of bacterial meningitis in adults Risk factors include recent exposure to
remains controversial. It may be used in meningococcal meningitis and a recent upper
children, especially in those with meningitis respiratory infection.
caused by Haemophilus influenzae. In adults
Symptoms
with suspected bacterial meningitis, especially
in high-risk cases, the adjunctive use of
Symptoms usually come on quickly, and may
dexamethasone may be beneficial.
include:
Person-to-person transmission can be
interrupted by chemoprophylaxis, which • Fever and chills
eradicates the asymptomatic nasopharyngeal • Mental status changes
carrier state. Rifampin, quinolones, and • Nausea and vomiting
ceftriaxone are the antimicrobials used to
eradicate meningococci from the • Purple, bruise-like areas (purpura)
nasopharynx. • Rash, pinpoint red spots (petechiae)
• Sensitivity to light (photophobia)
Antibiotics • Severe headache
• Stiff neck (meningismus)
Penicillin is the drug of choice for the
treatment of meningococcal meningitis and
septicemia. Chemoprophylactic antimicrobials Other symptoms that can occur with this
disease:
most commonly used to eradicate
meningococci include rifampin, quinolones
(eg, ciprofloxacin), and sulfonamides. (Also
included in this category are ceftriaxone, • Agitation
minocycline, and spiramycin.) • Bulging fontanelles
• Decreased consciousness
• Poor feeding or irritability in children
• Rapid breathing
Meningococcal meningitis is an infection
• Unusual posture with the head and
that results in swelling and neck arched backwards
irritation (inflammation) of the (opisthotonos)
membranes covering the brain and
spinal cord.
Exams and Tests
Causes Physical examination will show:
Meningococcal meningitis is caused by the
bacteria Neisseria meningitidis (also known as
• Fast heart rate
meningococcus).
• Fever
Most cases of meningococcal meningitis occur • Mental status changes
in children and adolescents. Meningococcus is • Rash
the most common cause of bacterial
meningitis in children and the second most
• Stiff neck
common cause of bacterial meningitis in
adults. For any patient who is suspected of having
meningitis, it is important to perform a lumbar
puncture ("spinal tap"), in which spinal fluid
(known as cerebrospinal fluid, or CSF) is • Myocarditis
collected for testing.
• Seizures
Tests that may be done include: • Subdural effusion (buildup of fluid
between the skull and brain)

• Blood culture When to Contact a Medical Professional

• Chest x-ray
Call the local emergency number (such as
• CSF examination for cell count, 911) or go to an emergency room if you
glucose, and protein suspect meningitis in a young child who has
• CT scan of the head the following symptoms:
• Gram stain, other special stains,
andculture of CSF
• Feeding difficulties
• White blood cell (WBC) count
• High-pitched cry
• Irritability
Treatment
• Persistent unexplained fever
Treatment with antibiotics should be started
as soon as possible. Ceftriaxone is one of the
Call the local emergency number if you
most commonly used antibiotics for
develop any of the serious symptoms listed
meningococcal meningitis. Penicillin in high
above. Meningitis can quickly become a life-
doses is almost always effective, too.
threatening illness.

If the antibiotic is not working and the health

care provider suspects antibiotic resistance,
chloramphenicol may be used. Sometimes
corticosteroids may be used, especially in
children.
People in close contact with someone who has
meningococcal meningitis should be given
antibiotics to prevent infection. Such people
include:
• Household members
• Roommates in dormitories
• Those who come into close and long-
term contact with an infected person
Prevention
All family and close contacts (especially in
health care or school settings) of people with
this type of meningitis should begin antibiotic
treatment as soon as possible to prevent
spread of the infection. Ask your health care
provider about this during the first visit.
Close contacts in the same household, school,
or day care center should be watched for early
signs of the disease as soon as the first case is
diagnosed. Always use good hygiene habits,
such as washing hands before and after
changing a diaper, or after using the
bathroom.

Vaccines are effective for controlling

Outlook (Prognosis)
Early treatment improves the outcome. The
death rate ranges from 5% - 15%. Young
children and adults over 50 have the highest
risk of death.
Possible Complications
epidemics. They are currently recommended
for:
• College students in their first year
living in dormitories
• Military recruits
• Travelers to certain parts of the world

• Brain damage
• Hearing loss
• Hydrocephalus