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Epidemic Cerebrospinal

Meningitis

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Epidemic Cerebrospinal
Meningitis
 Summarization:
 Meningococcal disease:
 Meningococcal infections are
caused by Neisseria meningitidis.
 The best known syndromes are
meningococcal meningitis ("epidemic
cerebrospinal meningitis")
 And fulminant meningococcemia

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Epidemic Cerebrospinal
Meningitis

 Summarization:
 Meningococcal disease:
 Infections also occur in the upper
and lower respiratory tracts, joints,
pericardium, eyes, and genitourinary
tract.

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Epidemic Cerebrospinal
Meningitis

 Today, our mainly topic is


epidemic cerebrospinal meningitis.

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Epidemic Cerebrospinal
Meningitis
 Summarization:
 The main clinical manifestations:
 High fever
 Severe headache
 Frequent `vomit
 Petechiae
 Triad signs of meningeal irritation
(stiff-neck rigidity, Kernig sign &
Brudzinski sign)
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Epidemic Cerebrospinal
Meningitis

 Summarization:
 The main clinical manifestations:
 In severe cases, septic shock and
damage of the brain parenchyma
may occur.
 CSF shows`purulent changes
 With the highest morbidity in
`purulent meningitis
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ETIOLOGY
 N. meningitidis is a gram-negative
diplococcus, commonly named the
meningococcus.

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ETIOLOGY
 The cell wall of pathogenic
meningococci contains a toxic
lipopolysaccharide or endotoxin.
 Meningococcal endotoxin appears to be
chemically identical to endotoxin of
enteric bacilli, but meningococcal
endotoxin has greater `potency for
inducing the dermal
Shwartzman reaction than enteric
endotoxin.
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ETIOLOGY
 Resistance: very weak
 Autolyze: specimen delivery

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EPIDEMIOLOGY
 Source of infection:
 The human nasopharynx is the
only known reservoir of
meningococcal infection.

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EPIDEMIOLOGY
 Route of transmition:
 Meningococci are spread from
person to person by airborne
droplets of infected nasopharyngeal
secretions.

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EPIDEMIOLOGY
 Susceptible groups:
 From 6 months to 2 years
 A permanent post-infection
immunity

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EPIDEMIOLOGY

 Epidemiologic character:
 The whole year especially winter &
spring
 All over the world

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PATHOGENESIS

 Adhere
 Bacteremia (capsular
polysaccharide)
 Septicemia (endotoxin and
cytokines)
 Get through the BBB
 Meningitis

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PATHOGENESIS

 The incubation period from


initiation of nasopharyngeal infection
to bloodstream dissemination is
probably under 10 days.

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PATHOLOGY

 The pathologic findings in acute


meningococcemia are observed
when shock and disseminated
intravascular coagulation have
occurred.

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PATHOLOGY

 The skin lesions show evidence of


fibrin thrombi and vasculitis in small
blood vessels.
 N. meningitidis can be seen in
endothelial cells and in neutrophils
surrounding damaged vessels.

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PATHOLOGY

 The prominent `purpura has


been attributed to the enhanced
capacity to elicit the dermal
Shwartzman reaction of its endotoxin
compared to endotoxin from enteric
gram-negative bacilli.

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PATHOLOGY

 Hemorrhagic adrenal infarction is


often observed in patients with
fulminant meningococcemia
(Water-house-Friderichsen
syndrome).

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CLINICAL MANIFESTATIONS
 According to the clinical
manifestations, epidemic
cerebrospinal meningitis is divided
into the following four types:
 common type: 99%
 fulminant type
 mild type
 type of chronic meningococcemia

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CLINICAL MANIFESTATIONS

 The most common clinical


syndromes are acute
meningococcemia, acute
purulent meningitis, and a
combination of the two
(meningococcemia-meningitis).

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CLINICAL MANIFESTATIONS

 The clinical picture may be


dominated by manifestations of
either meningccoccemia or
meningitis. In the latter instance
the findings are similar to those of
meningitis caused by any of the
common pyogens.

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CLINICAL MANIFESTATIONS

 Common type is divided into four


phases:
 Prodromal stage
 Septicemia stage
 Meningitis stage
 Convalescent stage

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CLINICAL MANIFESTATIONS

 Common type (99%):


 Prodromal stage (stage of the
upper respiratory infection):
 low fever
 sore throat
 cough etc.

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CLINICAL MANIFESTATIONS

 Septicemia stage of common


type:
 This is the most common form of
meningococcemia, characterized by
the rapid development of malaise,
fever, chills, myalgias, and
arthralgias, often following a minor
upper respiratory infection.
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CLINICAL MANIFESTATIONS

 Septicemia stage of common type :


 In more severe infections, purpura and
ecchymotic areas with gunmetal gray necrotic
centers always appear.
 Petechiae appear initially on the
extremities, rapidly increase in number and
coalesce as new ones appear in the
conjunctiva and buccal mucosa.

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CLINICAL MANIFESTATIONS

 Common type :
 About 20 per cent of patients with
meningococcal disease have
meningococcemia without
meningitis.

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CLINICAL MANIFESTATIONS

 Meningitis stage of common type:


 Meningitis always follows or
overlaps meningococcemia.

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CLINICAL MANIFESTATIONS

 Meningitis stage of common type:


 Most cases occur in children
between three months of age and
adolescence.
 Isolated meningitis is less
common than meningococcemia-
meningitis.

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CLINICAL MANIFESTATIONS
 Meningitis stage of common type:
 High fever and toxic symptoms
 CNS symptoms:
 severe headache
 serious vomit
 dysphoria
 convulsions
 triad signs of meningeal irritation
(stiff-neck rigidity, Kernig sign & Brudzinski sign)
 disturbance of consciousness
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CLINICAL MANIFESTATIONS

 Convalescent stage of common type:

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CLINICAL MANIFESTATIONS

 Fulminant type:
 Fulminant type is divided into two:
 1.Shock type (Waterhouse-
friderichsen’s syndrome)
 2. Meningitis-encephalitis type

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CLINICAL MANIFESTATIONS

 1.Shock type:
 high fever with chills /
hypothermic
 headache and vomit
 diffusive petechiae
 peripheral circulation failure
 DIC

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CLINICAL MANIFESTATIONS

 1.Shock type:
 Inapparent signs of meningeal
irritation
 Clear CSF usually with a normal
cell count
 Always with positive blood culture

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CLINICAL MANIFESTATIONS

 2.Meningitis-encephalitis type:
 disturbance of consciousness
 disturbance of vital signs
 pupil changing
 cardiac (myocarditis) and
respiratory (“shock lung”) failure
may be terminal events.

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CLINICAL MANIFESTATIONS

 Mild type:

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CLINICAL MANIFESTATIONS
 Chronic meningococcemia:
 The clinical expression of
meningococcemia varies from an acute
process to a chronic, indolent, relapsing
disease that may go on for months.
 This uncommon form of
meningococcemia is characterized by
intermittent febrile episodes lasting one
to six days, or, rarely, by sustained
fevers for several weeks.
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LABOLATORY TESTS
 1. Blood routine test:
 The peripheral white blood
cell count shows an apparent
leukocytosis (﹥20x109/L) and
neutrophilia is usually seen.

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LABOLATORY TESTS
 2. Cerebrospinal fluid:
 appearance: turbid
 pressure: increased
(normal?)
 WBC count:﹥1000x106/L,
mainly neutrophil

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LABOLATORY TESTS
 2. Cerebrospinal fluid:
 protein: elevated
 glucose: obviously decreased
 chloride: obviously decreased

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LABORATORY TESTS
 3. Bacteria examination:
 ① smear directly: CSF or
petechiae
 ② bacteria culture: cultures
of the blood or petechiae

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PROGNOSIS
 Indications of poor prognosis:
 1. petechiae for less than 12 hours
prior to hospitalization (rapid
development of crops of new
petechiae and purpura from one hour
to the next is ominous)

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PROGNOSIS
 Indication of poor prognosis:
 2. shock
 3. fever above 40℃
 4. absence of meningitis
 5. leukopenia
 6. thrombocytopenia or evidence of
DIC
 7. extremes of age
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DIAGNOSIS
 Discovery of N. meningitidis from
cultures of the blood or petechiae is
the usual means for establishing the
diagnosis of meningococcemia.
Positive blood cultures may not be
obtained until late in the course of
chronic meningococcemia.

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DIAGNOSIS
 Detection of group-specific
meningococcal antigen in serum offers
a new and rapid means of diagnosis.
Studies have shown that serum from
patients with fulminant
meningococcemia contains detectable
levels of the polysaccharide antigen.

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DIFFERENTIAL DIAGNOSIS

 Epidemic cerebrospinal meningitis


mainly expresses as meningococcemia with
purpura or petechiae must be differentiated
from bacterial endocarditis, hemorrhagic
fevers due to arboviruses, enteroviral
infection with exanthem, thrombotic
thrombocytopenic purpura, and
anaphylactoid purpura.

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DIFFERENTIAL DIAGNOSIS

 Epidemic cerebrospinal
meningitis mainly expresses as
meningococcemia without purpura or
petechiae must be differentiated
from those fever of unknow origin
especially other septicemia.

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DIFFERENTIAL DIAGNOSIS

 Epidemic cerebrospinal
meningitis mainly expresses as
meningitis must be differentiated
from other infection of CNS.

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TREATMENT
 Specifc antimicrobial therapy
should be instituted promptly when
the clinical features are suggestive of
meningococcemia.
 The preferred drug for the
treatment of meningococcal disease
is penicillin G, and it should be given
intravenously.
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TREATMENT
 Alternate therapy in penicillin-
allergic patients is chloramphenicol.
 Actually, cephalosporin, especially
its third generation is in more
common use than chloramphenicol in
stead of penicillin G:
 ceftriaxone

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TREATMENT
 Supportive therapy
 Especially to patients with
fulminant meningococcemia

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PROPHYLAXIS
 Meningococcal disease can be prevented
by vaccination with group-specific
meningococcal polysaccharides and by
chemoprophylaxis. Purified polysaccharides
of group A and group C meningococci have
been used to stimulate group-specific
humoral
bactericidal antibodies.

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PROPHYLAXIS
 Vaccination with these polysaccharide
antigens appears to be a highly
effective means of preventing disease
caused by these serogroups of
meningococci. A single dose of vaccine,
however, does not protect younger
children, especially those under two
years of age.

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PROPHYLAXIS
 Nevertheless, use of the vaccines
is indicated for the population at risk
whenever an outbreak caused by
group A or group C meningococci
becomes evident. Efforts to obtain a
satisfactory vaccine for group B
meningococcal disease have been
unsuccessful.

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PROPHYLAXIS
 Person-to-person transmission can
be interrupted by chemoprophylaxis,
which eradicates the asymptomatic
nasopharyngeal carrier state.
 Sulfonamides, rifampin, and
minocycline are the only drugs that
have been shown to eradicate
meningococci from the nasopharynx.
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