2. OBJECTIVES
By the end of this lecture you will be able to
understand the followings:
• Etiology, clinical manifestations, investigations, and
treatment of acute bacterial meningitis.
• Etiology, clinical manifestations, laboratory findings,
diagnosis and management of encephalitis.
• Slide and video demonstration of some neurological
manifestations.
3. Acute Bacterial MeningitisAcute Bacterial Meningitis
Etiology:
First 2 months of life: Group B Streptococcus, gram negative bacilli, S.
pneumoniae, Neisseria meningitides, Haemophilus influenzae type b. and
L. monocytogenes.
Children 2 mo-12yr of age 1- S. pneumoniae
2- N. meningitides
Alterations of host defense:
Pseudomonas aeruginosa, Staphylococcus aureus, Salmonella spp., and L.
monocytogenes.
Mode of infection: Bacterial meningitis most commonly results from
hematogenous dissemination of microorganisms from a distant site of
infection.
Etiology:
First 2 months of life: Group B Streptococcus, gram negative bacilli, S.
pneumoniae, Neisseria meningitides, Haemophilus influenzae type b. and
L. monocytogenes.
Children 2 mo-12yr of age 1- S. pneumoniae
2- N. meningitides
Alterations of host defense:
Pseudomonas aeruginosa, Staphylococcus aureus, Salmonella spp., and L.
monocytogenes.
Mode of infection: Bacterial meningitis most commonly results from
hematogenous dissemination of microorganisms from a distant site of
infection.
4. Clinical Manifestations: The onset of acute bacterial
meningitis has two predominant patterns:
1- The more dramatic less common presentation is sudden
onset with rapidly progressive manifestations of shock,
purpura, DIC, unconsciousness, and frequently resulting in
death within 24 hours.
2- More often, meningitis: is preceded by several days of fever
with upper respiratory or GIT symptoms followed by
nonspecific signs of CNS infection such as lethargy or
irritability.
Non specific findings: Fever, anorexia, poor feeding,
myalgia, arthralgia, tachycardia, hypotension, and
petechiae,or an erythematous macular rash.
7. Signs of meningeal irritation:
• Nuchal rigidity and back pain
• Kernig’s sign: flexion of the hip 90 degrees with
subsequent pain and limitation with extension of the
leg.
• Brudzinski sign: involuntary flexion of the knees and
hips after passive flexion of the neck while the
patient in supine position.
Symptoms and Signs of increased ICP:
1- Headache, and vomiting
2- Bulging fontanel or widening of the sutures
3- Cranial nerve neuropathies.
4- Hypertension with bradycardia
5- Apnea or hyperventilation, stupor and coma.
Signs of meningeal irritation:
• Nuchal rigidity and back pain
• Kernig’s sign: flexion of the hip 90 degrees with
subsequent pain and limitation with extension of the
leg.
• Brudzinski sign: involuntary flexion of the knees and
hips after passive flexion of the neck while the
patient in supine position.
Symptoms and Signs of increased ICP:
1- Headache, and vomiting
2- Bulging fontanel or widening of the sutures
3- Cranial nerve neuropathies.
4- Hypertension with bradycardia
5- Apnea or hyperventilation, stupor and coma.
12. Seizures (focal or generalized) due to, cerebritis, infarction or
electrolyte disturbances. Seizures that occur on presentation
or within the first 4 days of onset are usually of no prognostic
significance.
Diagnosis:
Lumbar puncture for CSF analysis should be performed:
1- Microorganisms on gram stain and culture.
2- Neutrophil pleocytosis (300-2000/mm3
).
3- Elevated protein (100-500mg/dL)
4- Reduced glucose concentration (<50% of S. glucose)
5- Physical appearance:Turbid with elevated pressure (100-300
mm H2O).
Normal CSF shows: Normal pressure (50-80 mm H2O), leucocytes
(<5/mm3
), proteins (20-45 mg/dl) and glucose (75% of the level
of serum glucose).
Seizures (focal or generalized) due to, cerebritis, infarction or
electrolyte disturbances. Seizures that occur on presentation
or within the first 4 days of onset are usually of no prognostic
significance.
Diagnosis:
Lumbar puncture for CSF analysis should be performed:
1- Microorganisms on gram stain and culture.
2- Neutrophil pleocytosis (300-2000/mm3
).
3- Elevated protein (100-500mg/dL)
4- Reduced glucose concentration (<50% of S. glucose)
5- Physical appearance:Turbid with elevated pressure (100-300
mm H2O).
Normal CSF shows: Normal pressure (50-80 mm H2O), leucocytes
(<5/mm3
), proteins (20-45 mg/dl) and glucose (75% of the level
of serum glucose).
14. Treatment: 1- Initial Antibiotic Therapy:
-Ampicillin 200mg/kg with either cefotaxime or
ceftriaxone100mg/kg, if gram-ve bacilli present give
Ampicillin with Gentamycin for neonatal meningitis.
-Vancomycin 60mg/kg/24hr given every 6 hr in combination
With either cefotaxime (200mg/kg/24hr given every 6 hours)
or ceftriaxone (100mg/kg/24hr once or twice daily) in older
infants and children.
-Patients allergic to β- Lactam antibiotics can be treated with
chloramphenicol, 100mg/kg/d, given every 6 hr. Duration of
therapy: At least for 7-14 days I.V.
-Corticosteroids: I.V dexamethasone 0.15 mg/kg/dose given every 6hr for
2 days for children older than 6wk with acute bacterial meningitis caused
by H. influenzae type b to decrease the permanent auditory nerve
damage.
15. 2-Supportive and symptomatic therapy:
A-Good evaluation and monitoring are essential.
B-Correction of dehydration and electrolyte
disturbances and proper nutrition.
C-Control of seizures
D- Management of neurological complications
Prevention:
- Vaccination and antibiotic prophylaxis for susceptible
at –risk contacts.
Close contact should be treated with Rifampin
10mg/kg/dose every 12hr, for 2 days (in N.
meningitides) and 20mg/kg/day for 4 days in H.
influenzae type b.
2-Supportive and symptomatic therapy:
A-Good evaluation and monitoring are essential.
B-Correction of dehydration and electrolyte
disturbances and proper nutrition.
C-Control of seizures
D- Management of neurological complications
Prevention:
- Vaccination and antibiotic prophylaxis for susceptible
at –risk contacts.
Close contact should be treated with Rifampin
10mg/kg/dose every 12hr, for 2 days (in N.
meningitides) and 20mg/kg/day for 4 days in H.
influenzae type b.
16. ENCEPHALITIS
Definition: Infection involving cerebral parenchyma, in some
patients the meninges involved with the parenchyma
causing meningoencephalitis.
Etiology:
1- Arthropod born virus: Arbovirus; Flavivirus:
-St. Louis encephalitis. Birds (culex mosquitoes).West-Nile virus.
- Western equine encephalitis.Birds (Colisata mosquitoes).
- Eastern equine encephalitis. Birds ( Culisata mosquitoes).
- Venezuelan equine encephalitis. Hoarses ( 10 species mosquitoes).
- California encephalitis (Bunya virus). Chipmunks (Aedes mosquitoes).
- Clorado tick fever (Wood tick).
ENCEPHALITIS
Definition: Infection involving cerebral parenchyma, in some
patients the meninges involved with the parenchyma
causing meningoencephalitis.
Etiology:
1- Arthropod born virus: Arbovirus; Flavivirus:
-St. Louis encephalitis. Birds (culex mosquitoes).West-Nile virus.
- Western equine encephalitis.Birds (Colisata mosquitoes).
- Eastern equine encephalitis. Birds ( Culisata mosquitoes).
- Venezuelan equine encephalitis. Hoarses ( 10 species mosquitoes).
- California encephalitis (Bunya virus). Chipmunks (Aedes mosquitoes).
- Clorado tick fever (Wood tick).
20. Clinical manifestations:
- Duration of illness: 2-5 days ----------up 3 weeks.
- Abrupt onset of fever, chills, headache, nausia, vomiting.
- Generalized weakness, seizures, coma, ataxia, cranial nerve palsies.
- Meningeal signs in some cases; (Meningoencephalitis).
Laboratory findings:
- Lymphocytosis in blood picture.
- CSF: 100-500 WBCs/ul pleocytosis (lymphocytes).
- Serology: Specific antibodies( IgM) in the 1st
week.
- PCR for viral antigens.
- Neuroimaging CT or MRI for brain.
- EEG for temporal lobe lesion of herpes simplex.
- Brain biopsy for undiagnosed cases.
Clinical manifestations:
- Duration of illness: 2-5 days ----------up 3 weeks.
- Abrupt onset of fever, chills, headache, nausia, vomiting.
- Generalized weakness, seizures, coma, ataxia, cranial nerve palsies.
- Meningeal signs in some cases; (Meningoencephalitis).
Laboratory findings:
- Lymphocytosis in blood picture.
- CSF: 100-500 WBCs/ul pleocytosis (lymphocytes).
- Serology: Specific antibodies( IgM) in the 1st
week.
- PCR for viral antigens.
- Neuroimaging CT or MRI for brain.
- EEG for temporal lobe lesion of herpes simplex.
- Brain biopsy for undiagnosed cases.
21. Complications:
*Acute disseminated encephalomyelitis ADEM usually follow
measles or varicella diseases or vacination.
*Mortality is variable according to the type of encephalitis 2-
5% in St. Louis and 20% in Venezuelan equine. And 50% in
Eastern equine.
*Neurological sequelea ranging from 1% to more than 50% in
Eastern equine encephalitis.
Therapy:
Supportive except in Herpes Simplex;and varicella-zoster
infections, Acyclovir is used.
