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Meningitis
1
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
2
Epidemic Cerebrospinal
Meningitis
Summarization:
Meningococcal disease:
Infections also occur in the upper
and lower respiratory tracts, joints,
pericardium, eyes, and genitourinary
tract.
3
Epidemic Cerebrospinal
Meningitis
4
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)
5
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
6
ETIOLOGY
N. meningitidis is a gram-negative
diplococcus, commonly named the
meningococcus.
7
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.
8
ETIOLOGY
Resistance: very weak
Autolyze: specimen delivery
9
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
12
EPIDEMIOLOGY
Epidemiologic character:
The whole year especially winter &
spring
All over the world
13
PATHOGENESIS
Adhere
Bacteremia (capsular
polysaccharide)
Septicemia (endotoxin and
cytokines)
Get through the BBB
Meningitis
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PATHOGENESIS
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PATHOLOGY
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PATHOLOGY
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PATHOLOGY
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PATHOLOGY
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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
21
CLINICAL MANIFESTATIONS
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CLINICAL MANIFESTATIONS
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CLINICAL MANIFESTATIONS
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CLINICAL MANIFESTATIONS
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CLINICAL MANIFESTATIONS
Common type :
About 20 per cent of patients with
meningococcal disease have
meningococcemia without
meningitis.
27
CLINICAL MANIFESTATIONS
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CLINICAL MANIFESTATIONS
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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
30
CLINICAL MANIFESTATIONS
31
CLINICAL MANIFESTATIONS
Fulminant type:
Fulminant type is divided into two:
1.Shock type (Waterhouse-
friderichsen’s syndrome)
2. Meningitis-encephalitis type
32
CLINICAL MANIFESTATIONS
1.Shock type:
high fever with chills /
hypothermic
headache and vomit
diffusive petechiae
peripheral circulation failure
DIC
33
CLINICAL MANIFESTATIONS
1.Shock type:
Inapparent signs of meningeal
irritation
Clear CSF usually with a normal
cell count
Always with positive blood culture
34
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.
35
CLINICAL MANIFESTATIONS
Mild type:
36
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.
37
LABOLATORY TESTS
1. Blood routine test:
The peripheral white blood
cell count shows an apparent
leukocytosis (﹥20x109/L) and
neutrophilia is usually seen.
38
LABOLATORY TESTS
2. Cerebrospinal fluid:
appearance: turbid
pressure: increased
(normal?)
WBC count:﹥1000x106/L,
mainly neutrophil
39
LABOLATORY TESTS
2. Cerebrospinal fluid:
protein: elevated
glucose: obviously decreased
chloride: obviously decreased
40
LABORATORY TESTS
3. Bacteria examination:
① smear directly: CSF or
petechiae
② bacteria culture: cultures
of the blood or petechiae
41
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)
42
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
43
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.
44
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.
45
DIFFERENTIAL DIAGNOSIS
46
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.
47
DIFFERENTIAL DIAGNOSIS
Epidemic cerebrospinal
meningitis mainly expresses as
meningitis must be differentiated
from other infection of CNS.
48
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.
49
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
50
TREATMENT
Supportive therapy
Especially to patients with
fulminant meningococcemia
51
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.
52
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.
53
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.
54
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.
55