Acute CNS infection can cause meningitis, meningoencephalitis, or brain abscess. Common causes in children include viruses, bacteria, and fungi. Clinical features may include fever, altered mental status, neck stiffness, photophobia, and seizures. Diagnosis involves lumbar puncture and CSF analysis showing pleocytosis and characteristic findings. Treatment involves identifying the specific cause and administering antivirals, antibiotics, or antifungals as needed. Complications can include increased intracranial pressure, neurological deficits, and long-term sequelae.

2. Acute CNS infection

3. • What is it?
• What causes it?
• What happens in the system?
• How to recognize it?
• How to prove it?
• How to treat it?
• How to prevent?

4. Significance
• Significant morbidity & mortality in
children [1.2m cases worldwide]
• Diagnosis, challenging in young children
• High incidence of sequalae

5. • Fever with altered sensorium
• Virus > bacteria > fungi & parasite
• Meningitis
• Meningoencephalitis
• Brain abscess
• Common symptoms
photophobia, neckpain/rigidity, fits,
stupor
• Diagnosis by CSF

7. Pyogenic meningitis

8. Etiology
• < 2months
• Maternal flora, NICU/PNW flora;
• GBS, GDS, gram-ve, listeria, HIB,
• 2m-12m
• Pneumococci, meningococci, HIB[now less]
• Pseudomonos, staph.aureus, CONS.

9. Reasons for infection
• Less immunity
• Contact with people with invasive disease
• Occult bacteremia [infants]
• Immunodeficiency
• Splenic dysfunction
• CSF leak , Meningomyelocele
• CSF shunt infection

10. Risk of infection
• Pneumococci
OM, sinusitis, pneumonia, CSF rhinorrhea.
• Meningococci
contact with adults, nasopharyngeal carriage
• HIB
Contact in daycare center

11. Pathogenesis
• Colonisation of nasopharynx
• Prior/concurrent viral URTI
• Bacteremia
• Hematogenous dissemination
• Contiguous spread from sinus, otitis, orbit
vertebral trauma, meningocele.

12. Why few only get meningitis?
• Defective opsonic phagocytosis
– Developmental defects
– Absent preformed anticapsular antibodies
– Deficient complement/properdin system
– Splenic dysfunction

13. Pathogenesis
• Bacteria enter through choroid plexus of LV
• Circulate to extra cerebral CSF &
subarachnoid space
• Rapidly multiply in CSF
• Release of inflammatory mediators
• Neutrophilic infiltrates
• Increase vascular permeability
• Altered BBB
• Vascular thrombosis

14. Pathology
• Thick exudate covering all areas
• Ventriculitis, arteritis, thrombosis
• Vascular occlusion, sinus occlusion.
• Cortical necrosis, cerebral infarct
• Subarachnoid hemorrhage
• Hydrocephalus
• ICT, inflammation of spinal nerves

15. Clinical features
• Nonspecific
– Fever,anorexia,myalgia,arthralgia,headache,
– Purpura , petechiae, rash, photophobia.
• Meningeal signs
– Neck rigidity, backache.
– Kernig sign
– Brudzinski sign
– Crossed leg sign

20. ICT signs
 Headache, vomiting, drowsy, Fits
 Ptosis, squint,
 AF bulge, widened sutures
 Hypertension, bradycardia
 Stupor, coma
 Abnormal posturing
 Papilloedema [only in chronic ICT]

21. • Focal neurological deficit
• Cranial neuropathy
– 3rd nerve
– 6th nerve
– 7th nerve
– 8th nerve

22. Diagnosis
• LP & CSF analysis
– Gram stain
– Culture
– Cell count
– Glucose, protein
– [Contraindications for LP]
• Blood culture

24. CSF analysis
• Cell count
– Normal
• NB >30/mm3
• Child >5/mm3
– Meningitis >1000/mm3
• Turbid 200-400/mm3
• Early; lymphocytic predominance
• Later; neutrophilic predominance
• low in severe sepsis

29. CSF analysis in prior antibiotic
therapy
• Culture, gramstain altered
• Pleocytosis, protein, glucose unaltered

30. Traumatic LP
• Cell count, protein level altered
• Glucose, bacteriology unaltered.

31. Condition Pressure
mm-h2o
Cell count/mm3 Glucose
mg/dl
Protein
mg/dl
microbiology
Normal 50-80 <5,lymphocyte >50, 75% of
blood level
20-40mg
Bacterial
meningitis
100-300 100-1000, >75%
neutrophils
<40mg 100-500 Gram stain+ve
Partially
treated
meningitis
N /
elevated
5-1000,
Lymphocytes?
N /decreased 100-500 Gramstain ,
c/s maybe -ve
Antigens +ve
Viral
meningitis
Normal Less cells,
lymphocytes
N, less in
mumps
<200
TBM More <500,
lymphocytes
<40 100-3000 Stain –ve
Culture ± ve
Fungal More 5-500 N More? Culture

32. Treatment
• Rapidly progressive [ ~24h]
LP  antibiotics
ICT , FND  CTbrain & antibiotics
Manage shock, ARDS
• Subacute course [4-7d]
• Assess for ICT, FND
• Antibiotics  CT  LP

33. Supportive care
• Monitoring
– Vitals
– BUN,electrolytes,HCO3,IO, CBC,Platelets,Ca
– Periodic neurologic assessment
• PR,sensorium,power,cranial N ex, head circ,
• Supportive care
– IVF  restrict for ICT,SIADH, more for shock
– ICT ETI & ventilation,frusemide,mannitol
– Seizures  diazepam,phenytoin

34. Antibiotic therapy
• Vancomycin & cefataxime/ceftrioxone
– Pneumococci,meningococci,HIB.
• Ampicillin / cotrimaxazole I.V
– Listeria
• Ceftazidime & aminoglycoside
– Immunocompromised

35. Duration of therapy
 Pneumococci : 7-10 days
 Menigococci: 5-7 days
 HIB; 7-10 days
 E.coli,Pseudomonos ; 3 weeks
 Antibiotics started before LP [partially
treated meningitis] ; ceftrioxone 7-10 days.

36. Repeat LP
• After 48h
• For ; resistant pneumococci,
gram-ve meningitis

37. Corticosteroids
• Rapid bacterial killing
• Cell lysis
• Release of inflammatory mediators
• Edema
• Neutrophilic infiltration
• 1-2h before antibiotics
• Dexamathasone q6h for 2 days.
• Less fever, less deafness.

38. Complications
• ICT, Herniation
• Fits, Cranial N palsy
• Dural Vein sinus thrombosis
• Subdural effusion
• SIADH
• Pericarditis, Arthritis
• Anemia, DIC

39. Prognosis
• Mortality >10% [more in pneumococci]
• Prognosis poor in
– Infants
– Fits >4days
– Coma, FND on presentation
• Neurological sequalae 20%
– Behavior changes 50%
– Deafness [pneumo,HIB], visual loss
– MR,fits,

40. Prevention
• Meningococci
– Rifampacin for close contacts [10mg/kg/day q12h for
2days]
– Quadrivalent vaccine for high risk children
• HIB
– Rifampacin for contacts for 4days
– Conjugate vaccine
• Pneumococci
– Heptavalent conjugate vaccine

41. Thank you

42. TBM
• Subacute / ?chronic meningitis
• From lymphohematogenous dissemination
• Caseous lesion in cortex / meninges
• Discharge of TB bacilli in CSF
• Thick exudate infiltrate blood vessels
• Inflammation,obstruction,infarct.

43. • Brainstem affected
• Cranial N dysfunction
• Hydrocephalus
• Infarcts
• Cerebral edema
• SIADH
• Dyselectrolytemia

44. Features
• 6m-4yrs
• 3 stages
• Prodrome stage; 1-2 wks, nonspecific
symptoms, stagnant development
• Abrupt stage;lethargy,fits,meningeal signs
focal ND,cranial neuropathy,hydrocephalus.
Encephalitic picture
• Coma stage; posturing,hemi/paraplegia,poor
vital signs

45. Diagnosis
• Contact with adult TB
• Mx nonreactive 50%
• CSF – lymphocytes
• Glucose <40mg/dl
• Protein high: 400-5000mg/dl
• AFB +ve 30%

46. Thank you

47. Meningoencephalitis

48. • Acute inflammation of meninges & brain
tissue
• CSF – pleocytosis
• Gram stain & culture negative
• Mostly self limiting

49. Etiology
• Enterovirus
• Arbovirus
• Herpes virus

50. Pathogenesis
• Direct invasion & destruction by virus
• Host reaction to viral antigens
• Meningeal congestion
• Mononuclear infiltration
• Neuronal disruption
• Neuronophagia
• Demyelination

51. Structures affected
• HSV; temporal lobe
• Arbovirus; entire brain
• Rabies; basal parts

52. Clinical features
• Depends on parenchymal involvement
• Preceding mild febrile illness & exantheme
• Acute onset of high fever, headache,
irritability,lethargy,nausea,myalgia
• Convulsions,stupor,coma
• Fluctuating FND,emotional outburst
• Ant.horn cell injuryflaccid paralysis [west
nile,entero virus]

53. DD
• Meningitis of various organisms

54. Diagnosis
• CSF: lymphocytic predominance
– Protein: normal,high in HSV
– Glucose: normal,low in mumps
– Culture of organism [entero V]
– Viral antigen by PCR
– Culture from NPswab,feces,urine
• EEG: focal seizures [temporal];HSV
• CT/MRI: swollen brain parenchyma

55. Treatment
• Acyclovir for HSV
• Non aspirin analgesic
• Nursing in a quiet room