An infection of the central nervous system can be a life-threatening condition, especially for children with weakened immune systems. These infections need ...

1. Nervous System infections
 Meningitis
 Encephalitis
 Brain abscess
 Others

2. Meningitis infections
• Bacterial
• Viral
• Fungal
• Parasitic

3. BACTERIAL VIRAL
FUNGAL,
OTHER

4. Routes of Entry
– Hematogenous
– Neighboring focus
– Anatomic defect
• congenital
• traumatic
• surgical
– Intraneural pathways

5. Risk Groups
 Neonates (first few weeks of life)
 Elderly
 Immunosuppressed

6. Common etiologic agents of bacterial
meningitis
• Most common
– Neisseria meningitidis
– St. pneumoniae
– H.influenzae
• Other Gram Positive
– Group B Streptococcus
– Listeria monocytogenes
– Staphylococcus aureus
• Other Gram Negative
– E. Coli
– Klebsiella
– Pseudomonas
– Proteus
– Salmonella

8. COMMON BACTERIAL PATHOGENS BASED ON
PREDISPOSING FACTOR IN PATIENTS WITH
MENINGITIS
Predisposing Factor
Age
0-4 wk
4-12 wk
3 mo to 18 yr
18-50 yr
>50 yr
Common Bacterial Pathogens
Streptococcus agalactiae, Escherichia coli,
Listeria monocytogenes, Klebsiella
pneumoniae, Enterococcus spp.,
Salmonella spp.
S. agalactiae, E. coli, L. monocytogenes,
Haemophilus influenzae, Streptococcus
pneumoniae, Neisseria meningitidis
H. influenzae, N. meningitidis, S.
pneumoniae
S. pneumoniae, N. meningitidis
S. pneumoniae, N. meningitidis, L.
monocytogenes, aerobic gram-negative
bacilli

9. Etiology - in Adults
 S. pneumoniae 30-50%
 N. meningitidis 10-35%
 H. influenzae 1-3%
 G -ve bacilli 1-10%
 Listeria species 5%
 Streptococci 5%
 Staphylococci 5-15%

10. COMMON BACTERIAL PATHOGENS BASED ON
PREDISPOSING FACTOR IN PATIENTS WITH
MENINGITIS
Predisposing Factor
Immunocompromised state
Basilar skull fracture
Head trauma; postneurosurgery
Cerebrospinal fluid shunt
Common Bacterial Pathogens
S. pneumoniae, N. meningitidis, L.
monocytogenes, aerobic gram-
negative bacilli (including P.
aeruginosa)
S. pneumoniae, H. influenzae, group A
β- hemolytic streptococci
Staphylococcus aureus, Staphylococcus
epidermidis, aerobic gram-negative
bacilli (including P. aeruginosa)
S. epidermidis, S. aureus, aerobic gram-
negative bacilli (including P.
aeruginosa), P. acnes

11. BACTERIAL
Incidence:
Primary meningitis:
spread via the bloodstream
Secondary meningitis:
Pneumonia, Ears, sinuses,
trauma, Surgery
Main pathogens:
Neisseria meningitidis
Strept. pneumoniae
Haemophilus influenzae

12. Meningococcal meningitis
 Gram negative diplococcus, some within
neutrophils (intracellular)
 Reservoir nasopharynx (2-25% carriage)
 Person to person transmission, Respiratory
droplet spread
 Most common cause of acute bacterial
meningitis
 Most cases in children and young adults
 3 main serological types A, B. C
 Incubation period 1-3 days

13. Higher carriage rates in:
 Children
 Overcrowding
 Schools, universities, other
institutions
 Military

14. Nasopharyngeal carriage
Bloodstream infection
Meningitis

15. N. meningitidis
N. meningitidis –
Epidemic strains/endemic strains -
“meningitis” belt in sub-Saharan Africa (type A)
Sporadic cases – types B, A, W135,
Gram negative (LPS) - Rapid uptake by the epithelial cells -
Receptor mediated endocytosis- Sepsis
Encapsulated - requires IgG + complement to phagocytose
Carriers in the population - increased carriage - disease
in those lacking antibody

16. Meningococcal meningitis
 Most cases are sporadic
 Close family contacts of cases at risk
 Outbreaks may occur in eg, schools
 Group B serotype traditionally most
frequent cause
 Group C serotype has become
increasingly common
 Epidemics occur in eg, Africa, South
America

17. Gram stain of CSF - note PMN’s and intracellular bacteria

18. N. meningitidis
Vaccine against group C now widely in use and for
overseas travellers , group A vaccine may be indicated
Development of protective immunity - cross reactive CHO’s
commensal flora (Neisseria lactamica)
Vaccines - (epidemic types) - A and C, Y, W 135
Not B - associated with sporadic cases
Sialic acid epitopes - look like self
Who to vaccinate? College students? Military, travellers
to endemic areas
Prophylaxis - Rifampin, ciprofloxacin, ceftriaxone
achieve levels in nasopharyngeal secretions

19. Pneumococcal meningitis
 Strep pneumoniae is the cause, a
capsulate gram positive coccus
 Highest incidence in those at extremes of
age, infants <3yrs and elderly
 Alcoholism, debilitation, malnutrition,
hyposplenism
 May spread from middle ear or sinus
infection Or following trauma causing
basal skull #

20. Etiology - General
 Pneumococcus (Streptococcus
Pneumoniae)
• Most common in adults >20yr
• Account for ½ of reported cases
• 2° to pneumonia/otitis, splenectomy/DM2
• ’ing incidence of pen-resistance in
pneumococcus (25-45% to pen, 10% to
Ceph,+ to chloramphenicol)

21. Pneumococcal meningitis: clinical
features
 Acute onset with rapid development of loss of
consciousness
 Skin rash not a feature
 May be a history of ear infection, splenectomy
 Bacteraemia a feature
 Higher mortality than other causes
 High incidence of complications in survivors

22. Pneumococcal meningitis
Sporadic cases - NP colonization - bacteremia - meningeal
seeding - Inflammation -
Treatment - Achieve 20x MIC of the organism in the CSF
Penicillin MIC = 1.0 - need level of 20 micrograms/ml
only get 10% of the blood level -

23. Prevention of S. pneumoniae infections
Infants/children – Prevnar – Pneumococcal Vaccine
8 – capsular types + protein conjugate vaccine
Immunogenic
Effective
Adults – 23-valent polysaccharide vaccine

24. Prevention
 Pneumovax for surgical or functional
asplenia (sickle cell, chronic illness,
immunosuppression, older age…)

26. Haemophilus influenzae meningitis
 Gram negative coccobacillus, capsulated strains
(type b used predominate)
 Peak incidence 2 years old, range 3 months to 5
years
 Incidence has declined greatly since the
successful introduction of Hib vaccine
 More insidious onset, no rash, lower mortality
 Diagnostic approach as for other causes
 Treament with cefotaxime or ceftriaxone

27. Etiology - General
 HiB (Haemophilus Influenzae type B)
• most common case in US 45% of meningitis
caused by Hib
• After vaccination, Now accounts for less than
10%
• still in elderly, HIV pts

28. Meningitis - Haemophilus influenzae type B
Antibody - polyribose phosphate capsule
Allows efficient phagocytosis
Development of conjugate vaccines:
PRP - Diphtheria toxin
Meningococcal OMP
Sporadic cases - adults who lack Ab

30. Clinical features that suggest the
diagnosis of acute meningitis
 Headache
 Irritable
 Neck stiffness
 Photophobia
 Fever
 Vomiting
 Varying levels of consciousness
 Rash

31. Clinical Features
 Fever
 Headache
 Nuchal rigidity
 Altered mental status
 Photophobia
 Non-specific symptoms/signs
 Focal neurological signs
 Seizures
 Specific clinical stigmata according to etiological agent
 Children / elderly

32. NEONATAL MENINGITIS
 Group B streptococcus (S agalactiae) and Esch coli are
the principal causes
 Travel via the bloodstream but direct infection may occur
 Premature rupture of membranes, pre-term delivery are
risk factors
 May complicate maternal infection
 High morbidity and mortality
 Clinical features can be non-specific
 Early onset Group B infection more common than late
onset disease
 Other causes: Listeria, Staph, Salmonella, other GNB
 Treat: Cephalosporin, or penicillin + aminoglycoside

33. Bacterial Infections of the CNS
• Neonatal bacterial meningitis
– Common organisms
• Gram negative bacilli
• Streptococci
– Significant long-term morbidity 35%
– 30-60% mortality

34. GBS – Streptococcus agalactiae
Common commensal flora – childbearing women
Lack of preformed Ab – sepsis – meningitis in neonate
Early onset disease – Sepsis – pneumonia
Late onset disease – Sepsis – MENINGITIS
Vertical transmission – most important - Preventable

35. E.coli – K1
(not all E. coli - specific capsular type)
Maternal fecal flora – ascending infection
CHO – capsule – lack of antibody
High grade bacteremia – meningitis –
specific receptors on meninges -
Problem with antibiotic resistance

36. Meningitis - neonate
Listeria monocytogenes -
Gram positive bacillus - motile
Found in animal feces - very common !
Contamination of unpasteurized animal products
- organic produce - Mexican cheese
Epidemiology -
2000 cases/year
Associated with a “flu-like” illness in the mother
Immunocompromised patients - T cell function

37. Listeria - pathogenesis
Preterm delivery (not always)
Pneumonia - sepsis - meningitis
Intracellular pathogen - ? Lack of T cell function
in the neonate
Cell to cell spread - like Shigella -
breaks out of phagosome - avoids Ab -
Need T cell function- macrophage
activation
Maternal infection

38. Meningitis - neonate/young infant
Greater incidence of sepsis - immature immune function
Greater incidence of meningitis - “Sepsis” work-up -
includes LP - difficult to distinguish viral from
bacterial disease
Clinical clues – high or low WBC
irritability – non specific sx’s

39. Very small premature infants
Complex congenital heart diseas
Premature infants – improved ventilatory support
Coagulase negative staphylococci – sepsis/meningitis
Enterococci – selection by antibiotics
Fungi

40. Other bacterial causes of
meningitis in adults and children
 Post trauma or surgery
Staph aureus, streps, anaerobes, coliforms,
Pseudomonas
 Immunocompromised
Listeria monocytogenes
 Others
M tuberculosis, Leptospira, Borrelia burgdorferi

41. Tuberculous meningitis
 Higher incidence in immigrant populations who come
from countries with a higher incidence of TB
 Insidious onset
 High frequency of complications, cranial nerve palsies
 Delayed diagnosis makes complications more likely
 CSF shows predominantly lymphocytic response but
polymorphs also present
 High protein, low/absent sugar
 Treat: probably with 3 agents eg, isoniazid, rifampicin,
pyrazinamide
 Note occasional reports of MDR TB

42. From: Neuropathology Illustrated 1.0
Fite stained mycobacteria
Leptomeningeal inflammation
Tuberculosis meningitis

43. Syphilis
• Asymptomatic CNS involvement
– CSF pleocytosis
• Meningitis
– 1-2 years post primary infection
– Rarely symptomatic
• Meningovascular syphilis
– Peak incidence 7 years post primary infection
– Chronic meningitis and multifocal arteritis
• Parenchymatous neurosyphilis and Tabes Dorsalis
– Peak incidence 10-20 years after initial infection
– General paresis of the insane
• Gummatous neurosyphilis

44. From: Neuropathology Illustrated 1.0
Plasmacytic infiltrate
Spirochetes
Neurosyphilis

45. Lyme Disease
• Borrelia burgdorferi
• Stage 1: Days to weeks
– Maculopapular rash
• Stage 2: Weeks to months
– Meningitis with cranial nerve palsies
• Stage 3: Months to years
– Axonopathy, encephalopathy, polyarthritis

46. VIRAL MENINGITIS
 Primarily affects children and young adults
 Milder signs and symptoms
 May start as respiratory or intestinal
infection then viraemia
 CSF shows raised lymphocyte count (50-
200/cu mm); protein and sugar usually
normal
 Full recovery expected

47. Causes of viral meningitis
 Enteroviruses: Echo, coxsackie A ,B, polio
 Paramyxovirus: mumps
 Herpes simplex, VZV
 Adenoviruses
 Other: arboviruses, lymphocytic
choriomeningitis, HIV

48. Etiology
followed by
mumps
arboviruses
herpesviruses
lymphocytic choriomeningitis(LCM)
HIV at the time of seroconversion

49. VIRAL MENINGITIS/ENCEPHALITIS
Enteroviruses
Polioviruses
Coxsackieviruses
Echoviruses
Togaviruses
Eastern equine
Western equine
Venezuelan equine
St. Louis
Powasson
California
West Nile
Herpesviruses
Herpes simplex
Varicella-zoster
Epstein Barr
Cytomegalovirus
Myxo/paramyxoviruses
Influenza/parainfluenzae
Mumps
Measles
Miscellaneous
Adenoviruses
LCM
Rabies
HIV

50. Fungal meningitis
 Cryptococcus neoformans is main cause
 HIV and immunosuppressed pts at risk
 Insidious onset of headache, fever, neck
stiffness
 Diagnosis made on CSF examination
 Shows raised lymphocyte count, protein,
low sugar, capsulate yeasts, antigen
 Treat with amphotericin B +flucytosine

51. Cryptococcosis
• Encapsulated organism
• Stains with PAS & Mucicarmine
Encapsulated organisms
From: Neuropathology Illustrated 1.0

52. Candidiasis
• Usually systemic nidus
– Intestinal overgrowth secondary to antibiotics
– Catheterization or surgery
• Seldom in immunologically intact
• Microabcesses with hematogenous dissemination
From: Neuropathology Illustrated 1.0
Grocott
Pseudo
Hyphae

53. Coccidioidomycosis or Histoplasmosis
• Soil organisms
• Inhaltion leades to primary pulmonary nidus
– Pregnancy, diabetes or other immunosuppression
From: Neuropathology Illustrated 1.0
Encapsulated 50 micron cyst

54. Parasitic Infections
• Amebic Infections
– Cerebral amebic abscess
– Primary amebic meningoencephalitis
– Granulomatous amebic encephalitis

55. Cerebral amebic abscess
• Entamoeba histolytica
– Common intestinal parasite
– CNS abscess is rare and late complication
– Hematogenous dissemination of trophozoites
– Trophozoites identifiable in abscess wall

56. Primary amebic meningoencephalitis
• In immunocompetent host, etiologic agent
– Naegleria fowleri
– Ubiquitous environmental contaminant that
seeds nasal passages
• Follows swimming in fresh water
– Ascends into CNS through cribiform plate
– Acute fulminant presentation with death in 72
hours

57. Granulomatous amebic
encephalitis
• In immunocompromised host
– Acanthamoeba or Balamuthia madrillaris
• Hematogenous dissemination into CNS from lower
respiratory tract or skin
– Subacute or chronic disease
• Focal deficits or seizures
• Usually fatal

58. Cerebral Malaria
Any of four species of malaria
1-10% of P. falciparum have CNS
involvement
– Usually in children
– Incubation period 1-3 weeks
– Clinical presentation secondary to
increased intracerebral pressure
Pathogenesis
– Occlusion of CNS capillaries by infected
RBCs
– Mortality 20-50%
From: Neuropathology Illustrated 1.0
From: Neuropathology Illustrated 1.0
Blood vessel with infected RBCs

59. Cerebral Toxoplasmosis:
Congenital
• Only a minority of cases show classical triad
– hydrocephalus, calcifications and chorioretinits
• Results from transplacental spread in primary
maternal infection
• Pathology
– Multifocal necrosis
• Periventricular and sub-pial
• tachyzoites
– Microcephaly

60. Cysticercosis
• Commonest parasitic infection of CNS
– Larval form of pork tapeworm Taenia solium
– Humans are usually definitive host
– Pig intermediate host
• Cysts = Cysticerci most commonly in
muscle
– 1-2 cm in diameter with single scolex
– Calcifies

61. Viral Encephalitis
 Etiology
 C/F
 CSF findings
 Neuroimaging

62. ENCEPHALITIS
 Affects children and adults mostly
 A variety of symptoms and signs
 Drowsiness, confusion, coma, fits, nerve
palsies, paresis
 May have sequelae eg, memory loss,
motor impairment, death
 EEG, brain scan, CSF exam, brain biopsy
may establish diagnosis

63. Causes of encephalitis
• Sporadic:
 Herpes simplex, mumps, VZV, EBV rabies
• Epidemic:
 Togaviruses: equine, louping ill, Japanese B,
enteroviruses
• Post-infectious:
 Measles, rubella, post-vaccination
• Degenerative:
 Measles (SSPE), vCJD, JC virus (PML)

64. Herpes simplex encephalitis
 Most common cause of sporadic
encephalitis in previously healthy
 May be evidence of herpes infecion of
skin, mucosae
 Causes severe haemorrhagic encephalitis
affecting temporal lobe,
 Focal signs and epilepsy features
 High mortality so treatment urgently
needed with aciclovir

65. Other causes
 VZV
 Mumps
 Rabies
 Mycoplasma pneumoniae
 Rickettsiae
 Toxoplasma

66. Viral Encephalitis
 C/F
Fever 90%
Headache 80%
Altered mentation 70%
Personality changes 70-80%
Seizures 40-67%
Memory disturbance 25-45%
Motor deficit 30-40%
Aphaisa 33%
Olfactory hallucination

67. Subacute sclerosing
panencephalitis (SSPE)
 A rare complication of measles infection
 Usually affects children
 Intellectual impairment, involuntary
movements
 High titres of measles antibody
 Brain biopsy shows measles virus
 Fatal outcome

68. Prion diseases
 Degenerative disorders
 Long incubation periods
 Slow progressive spongiform
encephalopathy
 Fatal outcome

69. • Kuru: occurred in New Guinea, diue to
cannibalism, eating human brain
• Sporadic Creutzfeldt-Jacob disease (CJD): rare
degenerative disease in over 50’s
• Recipients of growth hormone at increased risk,
use of surgical instruments contamined with
prion protein
• Prions are (Prp) proteins in abnormal
configuration resistant to destruction
• Mutations of genes encoding these proteins can
be inherited

70. New variant CJD
 In 1980’s emergence of bovine spongiform
encephalopathy (BSE)
 Could be experimentally transmitted from brains
of sheep with scrapie
 Similarities between BSE and nvCJD
 Occurs in young people rapidly fatal
 Possibly acquired from eating infected beef/ beef
products
 Diagnosis on brain biopsy (? Tonsillar tissue)
 No treatment

71. Brain abscess
 Can arise from direct inoculation of infection
following trauma, surgery; from spread of
infection of ear or sinuses; or haematogenous
spread from eg, lungs, heart (endocarditis)
 May be non-specific signs, neurological
symptoms
 Needs urgent investigation by CT/MRI scan
 Surgical treatment +antibiotics

72. Causes of brain abscess
 Trauma/surgery: Staph aureus
 Chest: strep, staph, pneumococci
 Ear: mixed anaerobes, coliforms
 Sinus: pneumococci, streptococci

73. Brain Abscess
• Increasing CNS pressure + localizing
signs
• If direct spread: frontal or temporal lobes
• Hematogenous spread: gray-white
junction
• 50% morbidity
– 20% mortality

74. Brain Abscess: Pathogenesis
• Half result from direct spread from sinus
– Etiology
• Streptococcus, Bacteroides, Actinomyces, aerobic gram
negative bacilli
• 25% result from hematogenous spread
– Children with congenital heart defects
– Adults lung abcess or endocarditis
• Streptococcus
– Etiologies:
• Toxoplasma, Nocardia, Listeria, Gram negative bacilli,
mycobacteria, fungi

75. Microbiological diagnosis
 CSF and blood cultures should be taken
 Gram stain of CSF deposit shows gram
positive cocci in short chains
 Culture on blood and choc agar in CO2
gives alpha haemolytic (green) colonies
with “draughtsmen”
 Direct sensitivities for penicillin,
cefotaxime, ceftriaxone, ampicillin

76. Nervous system infection
Meningitis
Collection of CSF specimen

77. Position of patient

79. CSF
color
Boiling in water bath centrifugation(3000rpm/5min)
For 5min
Centrifugation supernatant sediment
(3000rpm/5min)
Supernatant protein sugar culturing staining
BA/Mac/L.J Gs/AFs
LAT cytology
(>5cell/ml)

81. CSF findings

82. CSF
 ↑ pressure 20-50 mm H20
 ↑ WBC (100-10000 wbc/mm3,
mainly PMN)
 ↓ glucose (less than 40% of serum
glu)
 ↑ Protein (1.0-5.0 mg/dl)
 Positive gram stain/culture in 70-
90%
• Less if Abx before; sterile only after 12h

83. CSF Abnormalities in Meningitis
Condition Appearance Cells/cu mm Gram Protein Glucose
Normal Clear,
colourless
0-5
lymphocytes
Bacterial Cloudy,
turbid
100-2000
polymorphs
Orgs High Low
‘Aseptic’
(viral)
Clear,
slightly
cloudy
10-500
lymphocytes
Normal Normal
TB Clear,
slightly
cloudy
10-500
lymphocytes
High Low
Cryptococcal Clear 10-200
lymphocytes
Normal,
slightly
elevated
Normal,
slightly
reduced

84. CSF Abnormalities in Meningitis
Condition Appearance Cells/cu mm Gram Protein Glucose
Normal Clear,
colourless
0-5
lymphocytes
Bacterial Cloudy,
turbid
100-2000
polymorphs
Orgs High Low
‘Aseptic’
(viral)
Clear,
slightly
cloudy
10-500
lymphocytes
Normal Normal
TB Clear,
slightly
cloudy
10-500
lymphocytes
High Low
Cryptococcal Clear 10-200
lymphocytes
Normal,
slightly
elevated
Normal,
slightly
reduced

85. CSF SMEARS & STAINS
 GmS + in 60-90% of pts with
untreated bacterial meningitis
 With prior ATB Rx, positivity of
GmS decreases to 40-60%
 REMEMBER: + GmS = Heavy
organism burden & worse
prognosis

86. CSF ANTIGEN SCREENS
 Bacterial antigen screens detect
S. pneumoniae, N. meningitidis, Hib; +
in 50-100% of pts (esp. useful in pts with
prior ATB Rx)
 Crypto antigen screen detects C.
neoformans; + in 90-95% of pts with
crypto meningitis
 Should NOT be a ordered routinely

87. Additional lab investigations
 Latex agglutination test on CSF to detect
meningo polysaccharide antigen
 PCR to amplify bacterial DNA in blood (EDTA
sample) or CSF which may be positive even
after start of antibiotics
 Save serum sample for antibody tests with a
subsequent “convalescent” sample
 Set up antibiotic sensitivities to penicillin,
cephalosporins, ampicillin, chloramphenicol and
others

88. TREATMENT OF ACUTE BACTERIAL
MENINGITIS KEYPOINTS:
 Once the diagnosis is clinically suspected don’t
delay treatment
 If the causative agent is not clear eg, no rash,
give ceftriaxone or cefotaxime
 This provides cover of the 3 main causes until a
microbiological diagnosis is made
 If meningococcal meningitis confirmed then a
change to high doses of benzylpenicillin can be
considered
 Chloramphenicol can be an alternative if allergy
to beta lactams

89. Age of patient Likely organism Antimicrobial therapy*
0-12 weeks
Group B Strep
E. Coli
L. Monocytogenes
3rd generation cephalosporin +
ampicillin (+ dexamethasone first 2
days in >4-8-week-old infant)
3 months-50 years
S. Pneumoniae
N. Meningitidis
H. Influenzae
3rd generation ceph + vancomycin (±
ampicillin )
>50 years
S. Pneumoniae
L. Monocytogenes
Gram-neg. bacilli
3rd generation ceph + vancomycin +
ampicillin
Base of skull
fracture
Staphylococci
Gram-neg. bacilli
S. pneumoniae
3rd generation cephalosporin +
vancomycin
Immunocompromi
sed state
L. Monocytogenes
Gram-neg. bacilli
S. Pneumoniae
Vancomycin + ampicillin + ceftazidime
Treatment

90. EMPIRIC THERAPY OF MENINGITIS IN THE
ADULT
Clinical Setting Likely Pathogens Therapy
Community-acquired S. pneumoniae Ceftriaxone
N. meningitidis 2 gm q12h
[Listeria] +
[H. influenzae] Ampicillin 2 gm q4h
Closed head trauma S. pneumoniae Pen G 3-4 mu q4h
Streptococci +
Vancomycin 1-2 gm q12h

91. EMPIRIC THERAPY OF MENINGITIS IN THE
ADULT
Clinical Setting Likely Pathogens Therapy
High risk patients S. aureus Vancomycin 2-3 gm/d
Compromised hosts Gram negative +
Neurosurgical bacilli Ceftazidime 2 gm q8h or
Open head injury Listeria Cefepime 2 gm q8h
Nosocomial [Ceftriaxone 2 gm q12h]
Elderly [Cefotaxime 2 gm q4h]
+/-
Ampicillin 2 gm q4h

92. Role of Steroids
 The addition of anti-inflammatory agents has been
attempted as an adjuvant in the treatment of
meningitis
 Early administration of corticosteroids for pediatric
meningitis has shown no survival advantage, but
there is a reduction in the incidence of severe
neurologic complications and deafness
 Less bilateral deafness late neurological sequelae in
controls compared to children treated with steroids

93. Thank You!
Questions?