Bacterial meningitis

Teacher:Dongmei-Zhang
Department:the third hospital
affiliated to ZhengZhou university
 Clinical features
1. fever
2. seizure(focus or generalize)
3. disturbance of consciousness
4. increased ICP
5. meningeal irritation
6. purulent alterations of CSF
 Etiololgy (1)
[Three major types of bacteria]
 Neisseria meningitis
 Group B streptococcus pneumoniae
 Haemophilus influenzae type B
 Etiololgy(2)
[ The pathogens of meningitis are various
based on age,season, and region ]
 [ Pathogen and Age factor ]
 <2m
 streptococcus pneumoniae
 Gram-negative enteric bacilli
 Etiololgy(3)
 2m~12y
 Haemophilus influenzae type B
 Neisseria meningitis
 Streptococcus pneumoniae
 >12y
 Neisseria meningitis
 group B streptococcus pneumoniae
 Epidemiology(1)
 [Age ]
 Bacterial meningitis may occur throughout
life . Above 90% of cases occur between
the ages of 1mo~5y
 [Season]
 Cases occur throughout the year but occur
most frequently in winter and spring
 Epidemiology(2)
 [Transmission]

The mode of transmission is probably

person to person contact through respiratory
tract secretions or droplets
 Epidemiology (3)
 [risk factor]
1. A major risk factor for meningitis is the
lack of immunity to specific pathogens
associated with young age.
 Epidemiology (4)
2. Addition risks include recent colonization
with pathogenic bacteria,close contact
with individuals having invasive disease,
crowding, poverty, possibly absence of
breast-feeding for 2~ 5 mo of age
 Pathogenesis(1)
[The pathways of invasion]
 Hematogenous dissemination of micro-
organism from a distant site infection
1) Upper respiratory tract infection– most
common
2) Skin infection-- newborn infant
3) Gut infection—newborn infant
 Pathogenesis(2)
 A contiguous focus of infection
—less common
 Paranasal sinusitis,otitis media,mastoiditis
 Direct pathway
 Penetrating cranial trauma,dermal sinus
tract,Meningo-myelocele
 Pathogenesis(3)
Inflammatory
response
a think and fibrinous exudate
brain edema and hyperemia

a layer of purulent exudate

covers the surface of the brain
invasion into cranial nerves

blindness ,deafness,facial
paralysis
A layer of gray purulent exudate covers the surface of
the brain .The brain becames edematous and hyperemic
 Clinical manifestion(1)
 [Two onset patterns]
1. Sudden onset is less common with rapidly
progressive manifestations of shock,
purpura, DIC, and reduced levels of
consciousness frequently resulting in death
within 24 hours.
[Pathogen]
Meningococcus - purpura
 Clinical manifestion(2)
2. Subacute onset– Antecedent infection
More common onset is preceded by
several days of upper respiratory tract or
gastrointestinal symptomsfollowed by
nonspecific signs of CNS infection such
as increasing lethargy and irritability
 Clinical manifestion(3)
[ In early stages ---Nonspecific Sympotms]
 fever , drowsiness, irritability, vomiting ,
poor feeding
[In progressive stages]
 [meningeal irritation]
 Neck stiffness,Kerning sign ,Brudzinski
sign
 Clinical manifestion(1)
 [Increased ICP ]
• Symptoms--headache ,vomiting
• Physical Examination--bulging fontanel or
diastasis(widening) of the sutures ,even signs of
herniation
 [ focal neurologic sign ]
 cranial nerve paralysis—
ocular,oculomotor,abducence,facial,auditory
 nerves paralysis
 Clinical manifestion(2)
 [seizures(focus or generalize)]
 due to cerebritis, infarction, or electrolyte
disturbances.
 >4d—poor prognosis
 [disturbance of consciousmess]
 Irritability, lethargy, stupor, coma
 Neonatal Bacterial meningitis
 [Symptoms]—atypical
 Fever or hypothermia
 marked irritability,weak cry,inactivity, vomiting,poor feeding
,sudden shock,apnea,frequent atypical seizures
[Physical Examination]
A bulging fontanel—most diagnostic
 meningeal irritation signs—vague
 Complications
 Subdural effusions
 Hydrencephalus
 Inappropriate antidiuretic hormone
subdural (SIADH)
 Ependymitis
 Complications
--[Subdural effusion]
 [Symptoms]

 85~90% cases of subural effusion are

asymptomatic
 After treating and getting a good effect by antibiotic,
then the patients manifest the symptoms and signs of PM
again
 fever, seizures, alternation of mental status
 Complications
--[Subdural effusion]
[Physical Examination]
 A bulging fontanel
 diastasis(widening) of the sutures
 enlarging head circumference,
 abnormal results of cranial transillumination
 [Diagnosis]
 CT or MRI scanning
 Complications-- Hydrocephalus
 Most of them are communicating, someone are
non- communicating.
 irritability, lethargy, vomiting, seizures,
progressing enlarging head circumference,
bulging fontanel and widening of the sutures
 Cerebral cortex may become atrophy,
dysfunction and mental deficiency
 Complications-- SIADH
 [Pathogenesis]
 Itis a result of hypothalamic or pituitary
dysfunction
 Hyponatremia and decrease of serum osmolality

 Exacerbate
cerebral edma,hyponatremic
[Symptoms] seizures
 Complications-- Ependymitis
 It is occurred in the patients who are
not treated in time.
 The symptoms and signs of PM are not
improved and even progressed using
effective antibiotics
Laboratory Tests
 DIAGNOSIS
[the earlier diagnosis and the earlier treatment are
very important. When PM is suspected, lumbar
puncture(LP) should be performed to get CSF]

1. CSF:
1) Turbid or purulent
2) High ICP
3) Elevated leukocyte count: greater than
1000/mm3 (300~2000/mm3) and a
neutrophilic predominance (75~95%)
4) Elevated protein (100~500mg/dl)
5) Reduced glucose concentrations
6) Gram stain may be positive with bacteria
7) Bacteria culture may be positive
2. Other potentially valuable diagnostic tests
1) Peripheral blood: WBC↑, NC↑
2) Blood cultures
3) Bacteria on the smear of cutaneous
petechiae
4) CT or MRI of brain:
Maybe normal except of complications
When the cases are difficult to diagnosis,
the examinations are necessary
DIFFERENTIAL
DIAGNOSIS
 DIFFERENTIAL DIAGNOSIS
[CSF is the most important examination]
 1. Viral meningitis
• CSF:normal or slight changes,
predominanted by lymphocytes
• Bacteria culture is negative
• specific test: viral serology, culture
2. Tuberculosis meningitis:
a contact history with tuberculosis
the clinical progression is gradual
a relative long course of disease
Cranial nerves (facial, abducent,
auditory nerves) paralysis are more
common
 CSF changes:
• slight turbit or frosted glass appearance;
• the leukocyte count usually
ranges from 50-500/mm3
predominanted by lymphocytes
• simultaneous decrease is the typical change of
tuberculosis meningitis
• CSF anti-acid stain (+)
• anti-PPD antibody(+)
• culture of mycobacteria tubercule (+)
 Table:CSF findings in common CNS disorders
Condition Pressure Leucocytes Protein Glucose Appearance Pandy Others
(mmH2O) (mm3 ) (mg/dl) (mg/dl) test

normal 50~80 <5, >75%L 20~45 >50 clear -

PM usually↑ ↑100~10000 ↑100~500 ↓ turbid +~+++ Gram stain

 100~300 300~2000NCs <40 bacterial culture

Partialy normal ↑5~10000 ↑100~500 normal slight +~++ like PM, but
Treated PM or ↑ NCs or ↓ turbit down positive

Viral normal normal or↑ normal or normal clear - ~+ PCR or

meningitis or ↑ LCs or NCs ↑50~200 or ↓ antibody

Tuberculous ↑ ↑10~500 ↑100~3000 ↓<50 slight turbit +~+++ culture

meningitis NCs, LCs frosted glass anti-PPD(+)

Cryptococcal ↑ ↑10~500 ↑100~3000 ↓<50 slight +~+++ culture

meningitis NCs, LCs turbit ink stain(+)
1.Initial Antibiotic Therapy
 [Principle of Antibiotic therapy ]
 Senstive to pathogens
 Treatment started early and in time
 intravenous antibiotic therapy
 Antibiotics penetrating freely into the CSF
 Enough duration of Antibiotic therapy
TREATMENT
[Initial
therapy for suspected
meningitis of undetermined etiology]
A third-generation cephalosporin e.g
 Cefotamine—200mg/kg.d
 Ceftriaxone---100mg/kg.d
[The initial choice of antibiotic after
determined etiology]
 Ifthe result of bacterial culture has been
received, the antibiotics choice is simple,
selecting the antibiotics of sensitivity to the
bacteria and easy penetrating the blood-
brain barrier
 streptococcus pneumoniae
1) A third-generation cephalosporin –most commonly selected
2) panicillin --only when drug sensitive test demonstrates it is
sensitive to panicillin
 Meningococal
1) panicillin –more common
2) Resistance to panicillin -- A third-generation cephalosporin
 Haemophilus influenzae
1) Sensitive to amipicllin —amipicllin
2) Resistance to amipicllin—A third-generation
cephalosporin or chlormycetin
 Others
If gram-negative bacterial PM is suspected,
selected antibiotics might include ceftazidime
and aminoglycoside
 [Duration of Antibiotic therapy]
 group B streptococcus pneumoniae10~14d
 Haemophlius influenzae type B10~14d
 Neisseria meningitis7d
 Gram-negative bacilli21d
 Staphylococcus aureus （ SA ） 21d
2. Corticosteroids
 The corticosteroids can limit production of
inflammatory mediators and fibrosis

 The common usage is intravenous

dexamethasone (0.15mg/kg.dose) given
every 6 hr for 2~3 days.
3. Supportive care
 Repeated medical assessments of patients
with PM are essential to identify early signs
of cardiovascular, CNS, and metabolic
complications, such as pulse rate, blood
pressure, respiratory rate, pupillary reflexes,
level of consciousness, motor strength,
cranial nerve signs, and evaluation for
seizures.
 Maintain the balances of fluids,
electrolytes, and plasma osmotic pressure.

4. Symptomatic treatment
1) Anticonvulsant—phenbarbital diazapam
2) Dehydrant-- --mannitol
3) Antifebrile--acetaminophen
5.Treatment of complications
Subdural Effusion : aspiration through the
open fontanel and antibiotic therapy
SIADH: transfuse natrium fluid of high
osmolarity (till 3%, when it is necessary)
Hydrocephalus: drainage operation
Ependymitis : ventriculopuncture and
introventricular antibiotic infusion
 Prevention
 Preventionof bacterial meningitis depends
on vaccines,rapid diagnosis,and prompt
treatment of close personal contact.