4. Introduction
• Infection of the CNS may be diffuse or focal.
– diffuse infection
– Meningitis, encephalitis ,or both
– Focal infection of the CNS
– Brain abscess
5. Etiology
• Viral infections > bacterial > fungal &
parasitic
• Factors affecting etiologic agent
– Age of the host
– Immune status of the host
– Vaccination status
– Predisposing factors/anatomic factors
7. Epidemiology
Transmission
• Person-to-person contact through respiratory tract
secretions or droplets.
Risk factors
• Young age
• Male gender
• Black race
• Poverty
• Over crowding
• Recent colonization with pathogenic bacteria
• Bacterima and/or close contact with N.meningitids or
H.inflenza meninigitis
8. Cont…..
Anatomic defects
Lumbosacral dremal sinus
Ruptured meningomylocele
Ventriculo peritoneal shunts
Otitis media
Cochlear transplants(30x)
Midline cranial or facial defects
Basal skull fracture
Complement deficiency(C5-8)
T cell lymphocyte defect or chemotherapy
Anatomic or functional asplenia
9. invasive pneumococcal infections
• Peaks incidence 6 months-2 yrs
• Risks
– anatomic or functional asplenia
– HIV
– otitis media, sinusitis, pneumonia, CSF otorrhea
or rhinorrhea,
– cochlear implant
– chronic graft versus host disease
10. NEISSERIA MENINGITIDIS
• Five serogroups : A, B, C, Y, and W-135
• sporadic or epidemic.
• Epidemic disease in developing countries is
caused by serogroup A.
• More common in winter and spring
• Risk of infection in close Contact is 1%
(1000x)
11. HAEMOPHILUS INFLUENZAE TYPE B
• 70% of meningitis in U5 children is caused by
H. inf. type b(prior to vaccination)
• Age predilected:2 mo–2 yr of age
• peak incidence 6–9 mo of age
• Risks
– Contacts with H. influenzae type b disease.
– Incompletely vaccinated
– not vaccinated
– HIV infection.
13. Pathology
• Direct damage to CNS by the inflammatory
process
– neutrophilic infiltration,
– increased vascular permeability,
– alterations of the blood-brain barrier, and
– vascular thrombosis.
• Immune mediated damage induced by
bacterial components.
15. Mechanism of cerebral injury
Damage to the cerebral cortex may be due to the
focal or diffuse effects of
vascular occlusion (infarction, necrosis, lactic
acidosis),
hypoxia,
bacterial invasion (cerebritis),
toxic encephalopathy (bacterial toxins),
elevated ICP,
ventriculitis, and
transudation (subdural effusions).
16. Effects of cerebral injury
• Impaired consciousness/comma
• Seizures
• Cranial nerve deficits
• Motor and sensory deficits
• later psychomotor retardation.
17. Clinical feature
• Clinical manifestations of bacterial meningitis are
variable and nonspecific.
• Non specific s & s
– Preceding history of URTI.
– Fever , nausea, vomiting, irritability, anorexia,
headache
– Petechiae, purpura, DIC
• Meningeal irritation signs
– back pain, nuchal rigidity
– Confusion ,Convulsion(33%)
18. Cont….
• Kerning and Brudzinski signs are inconsistently
found in younger children less than 12–18
mo.
• Meningeal irritation signs are present in 60 to
80 percent of children with bacterial
meningitis and in approximately 25 percent of
children with normal CSF findings.
19. DIAGNOSIS.
• The diagnosis of acute pyogenic meningitis is
confirmed by analysis of the CSF, which
typically reveals microorganisms on Gram
stain and culture, a neutrophilic pleocytosis,
elevated protein, and reduced glucose
concentrations.
20. Contraindications for LP
• (1) evidence of increased ICP (other than a
bulging fontanel)
• (2) severe cardiopulmonary compromise
• (3) infection at the site of the LP.
• Thrombocytopenia is a relative
contraindication.
21. Lumbar Puncture
• Normal CSF WBC finding
– Neonates up to 30 leukocytes/mm3
– older children <5 leukocytes/mm3.
• Turbid CSF is present when the CSF leukocyte count
exceeds 200–400/mm3.
• In Most bacterial meningitis
• CSF leukocyte count >1,000/mm3 with neutrophilic
predominance (75–95%).
• Pleocytosis may be absent in patients with severe
overwhelming sepsis and meningitis.
• Gram stain is positive in 70–90% of patients with
untreated bacterial meningitis.
23. Tratment
• Emperic therapy
– Crystaline pencillin loading dose 250,000IU/kg stat
followed by 500,000 IU/kg divided in 8 doses
– Chlorapmpheniclo 50 mg/kg loading followed by
100mg/kg qid
– Dexamethasone 0.6 mg/kg qid for 48 hours
– Modify antibiotic based on culture and sensitivity result.
• Suportive therapy : maintainace fluid 2/3 of daily
requirment.
• Manage complications like increased ICP and seizure
24. Duration of therapy
• N. meningitidis meningitis 5–7 days .
• H. influenzae type b meningitis 7–10 days.
• Partialy treated meningitis treat with
ceftriazone or cefotaxime for 7–10 days.
• Gram-negative bacillary meningitis for 3 wks
or for at least 2 wk after CSF sterilization.
27. Poor Prognostic factors
• Age less than 6 mo.
• high concentrations of bacteria/bacterial
products in their CSF.
• seizures lasting more than 4 days into
therapy.
• coma or focal neurologic signs at
presentation.
• Pneumococcal meningitis
