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HO 3rd year lecture
Meningitis
Prepared by: Dr Elbet
Content
Introduction
Epidemiology
Etiology
Clinical feature
Diagnosis
Complication
Management
• DEFINITION
-Acute &diffuse bacterial infection of the
CNS with primary involvement of the
meninges .
Introduction
• Infection of the CNS may be diffuse or focal.
– diffuse infection
– Meningitis, encephalitis ,or both
– Focal infection of the CNS
– Brain abscess
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
Cont….
 Birth-2 months
 GBS (Streptococcus agalactiae)
 E.coli, klebsella
 L.Monocytogens
 Group D streptococus
 2months-12years
 H.influenza
 S.Pneumonia
 N.Meninigitis
 Others: s.aureus, pseudomonas, CONS,
salmonella
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
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
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
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)
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.
Pathogenesis
1)Hematogneous spread
Nasopharyngeal colonization with pathogenic
organisms (H.inf , n.meningitids, s.pneumoniae)
2)from a contiguous focus of infection.
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.
Damages caused by meningitis
• Extensive exudates in the CSF circulation path
ways
• Communicating hydrocephalus
• Subdural effusion/ empyema
• Ventriculitis
• Necrotizing arteritis subarachinoid hemmorage
• Cranial neuropathies
• Cerebral infarction
• Increased intracranial pressure
• Cerebral herniation
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).
Effects of cerebral injury
• Impaired consciousness/comma
• Seizures
• Cranial nerve deficits
• Motor and sensory deficits
• later psychomotor retardation.
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%)
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.
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.
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.
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.
Differential diagnosis
• Viral meningoencephalities
• Tuberculous meningitis
• Para meningeal infections
• Brain tumor
• Tuberculoma
• Fungal meningitis
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
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.
Complications
• seizures,
• increased ICP,
• cerebral edema,
• ischemia,
• subdural effusion/ empyema
• disseminated illness (septic arthritis, pericarditis,
etc.).
• DIC
• SIADH
Neurologic Sequelae
• Sensory neural hearing loss,
• mental retardation,
• recurrent seizures,
• delay in acquisition of language,
• visual impairment,
• behavioral problems
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
Prevention
• Vaccination
• antibiotic prophylaxis for susceptible at-risk
contacts
-meningitis-1.ppt

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-meningitis-1.ppt

  • 1. HO 3rd year lecture Meningitis Prepared by: Dr Elbet
  • 3. • DEFINITION -Acute &diffuse bacterial infection of the CNS with primary involvement of the meninges .
  • 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
  • 6. Cont….  Birth-2 months  GBS (Streptococcus agalactiae)  E.coli, klebsella  L.Monocytogens  Group D streptococus  2months-12years  H.influenza  S.Pneumonia  N.Meninigitis  Others: s.aureus, pseudomonas, CONS, salmonella
  • 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.
  • 12. Pathogenesis 1)Hematogneous spread Nasopharyngeal colonization with pathogenic organisms (H.inf , n.meningitids, s.pneumoniae) 2)from a contiguous focus of 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.
  • 14. Damages caused by meningitis • Extensive exudates in the CSF circulation path ways • Communicating hydrocephalus • Subdural effusion/ empyema • Ventriculitis • Necrotizing arteritis subarachinoid hemmorage • Cranial neuropathies • Cerebral infarction • Increased intracranial pressure • Cerebral herniation
  • 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.
  • 22. Differential diagnosis • Viral meningoencephalities • Tuberculous meningitis • Para meningeal infections • Brain tumor • Tuberculoma • Fungal 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.
  • 25. Complications • seizures, • increased ICP, • cerebral edema, • ischemia, • subdural effusion/ empyema • disseminated illness (septic arthritis, pericarditis, etc.). • DIC • SIADH
  • 26. Neurologic Sequelae • Sensory neural hearing loss, • mental retardation, • recurrent seizures, • delay in acquisition of language, • visual impairment, • behavioral problems
  • 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
  • 28. Prevention • Vaccination • antibiotic prophylaxis for susceptible at-risk contacts