This document provides an overview of meningitis beyond the neonatal period. It discusses the epidemiology, etiology, pathogenesis, clinical manifestations, diagnosis, treatment, complications and prognosis of meningitis. The most common causative organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Clinical features may include fever, headache, vomiting, and signs of meningeal irritation. Diagnosis involves lumbar puncture and culture of CSF. Empiric antibiotic treatment is initiated while awaiting culture results. Complications can be early like seizures or late like hearing loss. Prognosis depends on causative organism, age of presentation, and presence of co-morbidities.

1. Meningitis Beyond
Neonatal Period
PRESENTED BY
DR. HAJA SOVULA

2.  Introduction
 Epidemiology
 Etiology
 Pathogenesis
 Clinical manifestation
 Diagnosis
 Differential diagnosis
 Treatment
 Complications
 Prognosis
 Prevention
 Conclusion.

3. Introduction
 Meningitis is an inflammatory disease of the
leptomeninges, and this may be caused by:
-Bacteria (highest burden)
-Viruses
-Fungi
-Protozoa
-Chemicals
It is an important cause of mortality and morbidity in
infants and older children and is associated with high rate
of complications.

4. Introduction
 The brain and spinal cord are covered by
connective tissue layers collectively called the
meninges which consist of 3 layers:
 1-the dura mater
 2-the arachnoid mater
 3-the pia mater

6. Epidemiology
 Annual incidence globally is 20 per 100,000 & btw 10-1000 per 100,000
in Africa
 Peak age is in infancy with about 95% of meningitis cases occurring in
children < 5yrs
 Incidence of meningitis due to N. meningitidis is highest in the region of
sub-saharan Africa known as the Meningitis belt.
 350 million people are at risk of meningitis during annual epidemics
across the meningitis belt
 Nigeria recorded 1689 suspected cases & 124 deaths(2022-23)

8. Epidemiology Contd.
 Higher incidence in pts with impaired splenic function:
HbSS,Nephrotic syndrome, congenital asplenia, post-
splenectomy,
 As a result of increased susceptibility to infections by
encapsulated organisms e.g. H.flu, Strept pneumo

9. ETIOLOGY
Causative organisms include:
 0-1 month:
 Group B streptococus
 Eschericha coli
 Listeria monocytogenes
 Klebsiella spp.
 Salmonella spp.

10.  2 months – 2 years:
 Streptococcus pneumonia
 Haemophilus influenza type B
 Neisseria meningitidis

11.  > 3 years :
 Streptococcus pneumonia
 Neisseria meningitidis
 Haemophilus influenza
 Mycobacterium tuberculosis.

12.  Others:
 Pseudomonas aeruginosa
 Staphyloccocus aureus
 Coagulase – negative staphyloccoci
 Mycoplasma pneumoniae
 Mycoplasma hominis.

13. Neisseria meningitidis
 Gram-negative, diplococcus.
 Commensal in the human nasopharynx in about 10%
of the population.
 N. meningitidis has 12 serogroups, however 6 of this
serogroups cause the great majority of infection in
people: A,B,C W135, X and Y.
 May be sporadic or occur in epidemics

14. CONT…
 Serotypes B, C and Y each account for approximately
30% of cases in the US.
 Epidemic disease especially in developing countries is
usually caused by serogroup A
 Associated with severe bacteremia called
meningococcemia.
 Most infection in children occur from contact with
infected adults.

15. STREPTOCOCCUS
PNEUMONIAE
 Encapsulated gram-positive organism
 Serotypes 4,6B,9V,14,18C,19F and 23F which were
contained in the initial 7-valent pneumococcal vaccine
were responsible for invasive disease
 13-valent PCV contains the serotype in PCV 7 plus
serotypes 1, 3, 5, 6A, 7F and 19A

16. Haemophilus influenzae
 Encapsulated Gram-negative, coccobacillary,
facultative anaerobic organism.
 Six serotypes have been identified; a, b, c, d,e and f,
with the most common cause of invasive disease
being serotype b.
 Before universal HIB vaccination, approximately 70%
of cases of bacterial meningitis were caused by this
pathogen.

17. Risk factors
 Overcrowding
 Male
 Age
 Infections e.g sinusitis, otitis media, mastoiditis, tonsillitis
 Immunosuppressed states like, HIV, SCD, DM,
chemotherapy, malignancy
 Head injury especially basal skull fracture
 Neural tube defect
 Congenital csf leak (lumbar dural sinus)
 Defective complement system(C5-C8)
 Iatrogenic especially after LP, V-P shunt

18. Route of Infection
 Infectious agent establishes a localized infection in the
host which may be infection of nasopharynx, respiratory
tract, sinuses, ear.
 Prior viral upper respiratory tract infection may enhance
the pathogencity of bacteria.
 Pathogens gain entry into CNS via; Invasion of blood
stream and subsequent haematogenous seeding of
CNS.
 Direct contiguous spread from neighboring
structures
 Retrograde neuronal pathway(olfactory and
peripheral nerves)

19. Pathogenesis
• Susceptibility of bacterial infection on
CNS in the children
– Immaturity of immune systems
• Nonspecific immune
– Insufficient barrier (Blood-brain barrier)
– Insufficient complement activity
– Insufficient chemo taxis of neutrophils
– Insufficient function of monocyte-macrophage
system
– Blood levels of diminished interferon
(INF) –γ and interleukin -8 ( IL-8 )

20. Contd. Pathogenesis
-Specific immune
• Immaturity of both the
Cellular and Humoral
immune systems
– Insufficient antibody-mediated
protection
– Diminished immunologic response
– Bacterial virulence

21. Contd Pathogenesis
 Bacterial toxics and
Inflammatory mediators are
released.
– Bacterial toxics
• Lipopolysaccharide, LPS
• Teichoic acid
• Peptidoglycan
– Inflammatory mediators
• Tumor necrosis factor, TNF
• Interleukin-1, IL-1
• Prostaglandin E2, PGE2

22. Pathology
 Diffuse bacterial infections involve the
leptomeninges, superficial cortical structures,
and brain parenchyma is also inflamed.
 Meningeal exudate of varying thickness is
found.
 There is purulent material around veins,
venous sinuses, convexity of brain and spinal
cord

23. Pathology
 Ventriculitis (purulent material within the
ventricles)
 Cerebral Infarction
 Subdural empyema may occur.
 Hydrocephalus is an common complication of
meningitis.
– Communicating hydrocephalus
– Obstructive hydrocephalus

24. Pathology
 Signs of cranial neuropathy is due to inflammation of
cranial nerves
 Signs of meningeal irritation is due to inflammation of
spinal nerve and nerve root
 Hypoglycorrhachia is due altered glucose transport to
brain tissue
 Elevated protein due to increased vascular
permeability of BBB

25. Pathology
 Cerebral edema in meningitis is multifactorial and
results from variable combination of;
-Vasogenic edema; from altered brain barrier permeability
-Cytotoxic edema; consequence of degranulation of WBC
and cerebral ischaemia
-Interstitial edema; increased hydrostatic pressure with
resultant trans-ependymal movement of CSF from
ventricular into surrounding brain parenchyma

26. Clinical manifestations
 Two predominant patterns;
SUDDEN ONSET
 Rapid progressive manifestations of shock
 Purpura
 Disseminated intravascular coagulopathy(DIC) with
reduced levels of consciousness often resulting in
progression to coma or death within 24 hours
GRADUAL ONSET (COMMON PATTERN)
Preceded by several days of fever accompanied by upper
respiratory tract or gastrointestinal symptoms.

27. Clinical Manifestations
NONSPECIFIC SYMPTOMS
Infants
 Fever
 Lethargy
 Irritability

28. Clinical Manifestations
 Restlessness
 Seizures
 Poor Feeding
 Coma
 Headache
 Irritability
 Nausea
 Vomiting
 Anorexia
 Photophobia
 Petechia/Purpura
 Myalgia

30. Signs
 Infants
 Irritable
 Unconscious
 Febrile Or Hypothermic
 Bulging Anterior Fontanel
 Diastasis Of Sutures

31. Signs
 Older children
 Meningeal signs
 - neck stiffness
 - positive kernig’s sign
 - positive brudzinski’s sign
 OTHER SIGNS
 Ptosis
 Diplopia
 Cranial Nerve 6 Palsy
 Cushing’s Triad (Bradycardia, Hypertension, Apnoea)
 Focal Neurologic Signs
 Seizures
 Altered Consciousness

33. Diagnosis
1).LP to obtain CSF is Mandatory for confirmation of diagnosis.
-Reveals micro-organisms on gram stain and culture, neutrophilic
pleocytosis, elevated protein and reduced glucose.
- CSF leukocyte count in bacterial meningitis usually is elevated>1000/mm3
and typically, there is neutrophilic predominance (75-95%).
-Turbid CSF is present when CSF leukocyte count exceed 200-400/mm3
Children have <5 WBC/mm3 Healthy neonates =20 WBC/mm3

37. Dx cont…
2. Blood culture; reveals the responsible bacteria in up to
80-90%.
3. Blood chemistry (RBS, E/U/CR)
4. C-reactive protein – Elevated
5. Procalcitonin; differentiates between bacterial and viral
meningitis
6. FBC
7. Clotting profile
8. Neuroimaging ; CT-scan may demonstrate areas of
cerebral edema and ischaemia

38. Contraindications to
Immediate LP
 Evidence of raised ICP
 Severe cardiopulmonary compromise
 Infection of the skin overlying the site for LP
 Thrombocytopenia (relative contraindication)

39. Differential diagnosis
 Encephalitis
 TBM
 Fungal meningitis
 Cerebral malaria
 Hypoglycemia
 Sub-arachnoid haemorrhage
 Brain abscess
 Brain tumor
 Subdural empyema
 Sarcoidosis
 Lymphoma

40. TREATMENT
 Meningitis is a medical emergency.
 If unconscious – ABC, maintain hydration, calories.
 Once suspected, aggressive antibiotics therapy using
broad spectrum antibiotics should be commenced as
soon as CSF and blood samples are taken for
investigation.
 Parenteral antibiotics are used

41. Emperical Treatment
 NEONATES - Combination of a 3rd Generation
Cephalosporin & an Aminoglycoside.
 IV Ceftriaxone or Cefotaxime or Ceftazidime + IM
Gentamycin or IV Amikacin
 Lysteria monocytogenes- IV AMPICILLIN
 INFANTS 1-2 MO - Treat as Neonate.

42. Treatment
 Age >2mo - IV Crystalline Penicillin 0.04MU/kg/D
 + IV Chloramphenicol 100mg/kg/D
 Intravenous Ceftriaxone 100mg/kg/day daily or divide 12
hourly
 Intravenous Vancomycin 60mg/kg/day divided 6 hourly
 Intravenous Cefotaxime 150-300mg/day 6 hourly

43. Duration of treatment
 Neisseria meningitidis – sensitive to penicillin and cephalosporin
given for 5-7 days
 Haemophilus influenzae – treated for 7-10 days
 Streptococcus pneumoniae – treated for 10-14 days
 Gram –ve – Treated for 21 days
 CSF should be sterile within 24-48hrs of initiation of appropriate
antibiotic therapy

44. Adjunct therapy
 Corticosteroids
 Intravenous dexamathasone 0.15mg/kg/dose 6
hourly x 2/7.
 Given 1-2 hours before antibiotics are initiated.
 Associated with shorter duration of fever, lower CSF
protein and reduces risk for sensorineural hearing loss.
 Stabilizes BBB
 Reduces CSF outflow resistance.

45. Adjunct therapy cont…
 Anti-convulsant
 IV Diazepam 0.1 – 0.3mg/kg/dose
 IV lorazepam 0.05mg-0.10mg/kg/dose
 IV phenytoin 15-20mg/kg loading dose, then 5mg/kg/day maintenance.
 Treatment of raised intracranial pressure
 IV mannitol 0.5 – 1g/kg
 Iv Lasix 1mg/kg 12 hrly

46. COMPLICATIONS
EARLY
 Seizures
 Raised ICP
 CN palsy
 Stroke
 Hydeocephalus
 Subdural effusion
 Disseminated intravascular coagulopathy
 SIADH
 Septic shock
 Waterhouse-Friderichsen syndrome

47. Complications cont…
LATE
 Cortical blindness
 Hearing loss (common)
 Cerebral Palsy
 Hemiplegia/quadriplegia
 Ataxia
 Cognitive impairment
 Mental retardation
 Speech impairment.

48. Prognosis
 Appropriate antibiotic therapy and supportive care
have reduced mortality of bacterial meningitis after
neonatal period by <10%.
 The highest mortality rates are observed with
pneumococcal meningitis.
 Sensorineural hearing loss is the most common
sequelae of bacterial meningitis and usually is already
present at presentation.

49. Prognosis
 Late presentation is associated with poor prognosis
 Seizures presenting after 4 days of illness is
associated with poor prognosis.
 Comatose patient – poor prognosis
 Co-morbidities or immunodeficiency – poor prognosis.

50. TB Meningitis
 TB meningitis is caused by
 Mycobacterium tuberculosis
 Infection mostly from the lungs
 1 – 2% of cases the bacteria travel via the
bloodstream.
 Unlike other types of meningitis its progresses very
slowly and symptoms are vague
 Prognosis is often Poor if patient is at Stage III
 BCG vaccine provides good protection (64%) against
TBM but doesn’t necessarily rule it out

51. TB Meningitis
 AntiTb medications:
 Isoniazid; rifampacin; pyrazinamide and streptomycin
x 9 months
 Corticosteriods (dexamethasone /prednisolone) can
be given in first 4-6weeks of treatment

52. Aseptic Meningitis
 Definition: A syndrome characterized by acute onset of
meningeal symptoms, fever, and cerebrospinal fluid
pleocytosis, with bacteriologically sterile cultures.
 Laboratory criteria for diagnosis:
CSF showing ≥ 5 WBC/cm3
No evidence of bacterial or fungal meningitis.

53. Aseptic Meningitis
 Aseptic meningitis is a syndrome of multiple
etiologies, but most cases are caused by a
viral agent ;
 Enteroviruses(most common 90%), Arbovirus,
Adenoviruses, HSV, Measles virus, VZV

54. Modes of transmission:
 -Primarily person to person and arthopod vectors for
Arboviruses
Incubation Period:
 -Variable. For enteroviruses 3-6 days, for arboviruses 2-
15 days
 Can affect anyone & mostly spread through respiratory
secretions or stool of infected persons
Treatment: No specific treatment available.
Most patients recover completely on their own

55. Levels of prevention for
Meningitis
GENERAL HEALTH PROMOTION
 Health education
 Avoid overcrowding
 Exclusive breastfeeding
 Adequate nutrition
 Promotion of good health seeking behavior.

56. SPECIFIC PROTECTION
 Routine immunization
 Mass vaccination
 Chemoprophylaxis
 Vaccination of specific risk group

57. EARLY DIAGNOSIS AND TREATMENT
 Prompt initiation of antibiotics.
LIMITATION OF DISABILITY
 Treatment of cerebral edema
 Anticonvulsant
 Use of steroids
 Ophthalmic evaluation.

58. REHABLITATION
 Use of glasses
 Hearing aids
 Wheel chair
 Physiotherapy.
 Speech therapy
 Occupational therapy
 Psychotherapy
 Special schools
 Use of brail.

59. chemoprophylaxis
 Meningococcal meningitis; chemoprophylaxis is
recommended for unvaccinated persons during outbreak.
 Also recommended for household contacts of confirmed
meningococcus.
Drugs;
Rifampicin 10mg/kg 12hourly for 2 days or
Ceftriaxone 250mg IV or IM or
Ciprofloxacin 500mg orally stat or
Azithromycin 500mg orally stat

60.  Vaccination
i) Meningococcal infection; tetravalent polysaccharide
vaccine(A,C, W135,Y) is recommended for people with
asplenia, sickle cell anemia, terminal complement
deficiencies and travelers to areas with hyperendemic
or epidemic disease
ii )Streptococcal pneumonia; pneumococcal vaccine is
recommended in persons with asplenia, chronic
illness(DM, HIV)

61. conclusion
 Paediatric bacterial meningitis is a medical emergency
which requires a high index of suspicion.
 It is an important cause of morbidity and mortality with
serious long term complications
 Early diagnosis and treatment is therefore essential
 Safe vaccination is a cheap means of preventing long

62. THANK
YOU!!!!!!!!!!
!!!!!!!!!!!!!!

63. REFRENCES
 Nelson’s textbook of paediatrics 21st Edition
 Medscape Meninigits:
https://emedicine.medscape.com/article/232915-
overview
 NCDC: Cerebrospinal meningitis outbreak in Nigeria:
situation report Available
at: http://ncdc.gov.ng/themes/common/files/sitreps/153
667690b5c184d9fab417f65a25b1e.pdf. Accessed 30
October 2017.81–
S88, https://doi.org/10.1093/cid/ciz474