Meningitis is an inflammation of the meninges that can be caused by bacteria, viruses, fungi or other pathogens. Bacterial meningitis requires urgent treatment and has the highest risk of complications. Common bacterial causes include streptococcus pneumoniae, neisseria meningitidis, and haemophilus influenzae. Viral meningitis is generally milder and self-limiting. Tubercular meningitis has a subacute onset and causes thick basal exudates. Fungal meningitis occurs more often in immunocompromised individuals. Diagnosis involves CSF analysis showing pleocytosis and characteristic findings depending on the cause. Treatment involves antibiotics, antivirals or antitubercular drugs depending on the

1. Meningitis
By: Dr. Ram Gopal Maurya

2. Definition
• Meningitis is an inflamation of leptomeninges (
arachnoid and pia) and CSF fluid residing in the
space that it encloses.
• As the subarachnoid space is continous around
the brain, the spinal cord and the optic nerves, an
infective agent may extend immediately to all of
it. Therefore meningitis is always cerebrospinal.
• It also reaches the ventricles, either directaly or
by reflux through the basal foramens of
magendie and luschka.

4. Classification
• Based on its causes
1. Bacterial
2. Viral
3. Tubercular
4. Rickettsial: typhus fever
5. Protozoal: naegleria, toxoplasma, plasmodium
6. Fungal: Cryptococcosis, aspergillus, candida,
histoplasma, mucormycosis
7. Malignant : leukaemic meningitis, metastatic

5. 8. Other non infectious cause
• Drugs induced: mainly NSAID’S
• Physiacal injury: SAH
• Vasculitis: wegener granulomatosis, churg-
strauss syndrome
• Connective tissue disease: SLE, Rheumatiod
arthritis, sjogrens syndrome.

6. BASED ON ONSET
• Acute meningitis – with onset over hours to
days.
mainly bacterial meningitis
• Subacute meningitis- with onset days to
weeks
mainly viral, fungal and tubercular
meningtis.

7. Route of infection
• Infectious agents can invade the CSF by at least three
routes.
1. First, the vascular structures of the choroid plexus and pia
and the vessels that traverse the subarachnoid space may
serve as conduits during systemic bacteremia.
2. A second route is by direct invasion across the protective
meninges. Physical disruption of the dura by trauma or
surgery allows for the direct invasion of the subarachnoid
space and should be considered in patients with a history
of CSF leakage or rhinorrhea, in addition to those who
have undergone recent neurosurgical interventions.

8. 3. Emissary veins provide another pathway for
bacteria to spread from contiguous foci into
the subarachnoid space. These veins traverse
the skull and dura, directly connecting the soft
tissues of the head and neck with the venous
system of the brain and meninges, including
the arachnoid villi.

10. Bacterial meningitis
• Bacterial meningitis is a medical emergency.
• Mainly present acute manifestation.

11. Aetiology
• Common organisms
1. Streptococcus pneumoniae (30-50%)
2. Neisseria meningitidis (10-35%) { meningococcus }
3. Haemophilus influenzae (1-3%)
• Less common organisms
1. Staphylococcus
2. Group B Streptococcus
3. E. Coli
4. Klebsiella
5. Proteus
6. Pseudomonas
7. Citerobacter

12. • Neonate: gram negative bacilli- E.coli, Proteus.
group B Streptococci
• Pre-school child: Haemiphilus influenzae,
Neisseria meningitidis, Streptococcus,
• Older child and adult: Neisseria meningitidis,
Streptococcus pneumoniae

13. Predisposing factors
• Acute otitis media
• Mastoiditis
• Recent head injury
• Diabetes
• Immune deficiency
• Splenectomy
• Chronic alcoholism
• Neurosurgical procedure: staph. aureus
meningitis

14. Pathophysiology
• Once in the CSF, bacteria induce leukocyte migration
into the subarachnoid space, which can cause
occlusion of cortical blood vessels, damage to nerve
roots that traverse the subarachnoid space and
impaired CSF flow.
• The activation of leukocytes leads to an inflammatory
cascade, with the release of cytokines, oxidants, and
proteolytic enzymes, which contribute to the damage
caused by the infection. The resultant edema can lead
to increased intracranial pressure and a risk of
herniation.

15. Clinical features

16. Skin lesion in meningococcal
meningitis with “ GLASS TEST ”

17. Signs of meningeal irritation
• Neck stiffness.
• Kernig’s sign
• Brudzinski’s neck sign
• Brudzinski’s leg sign

20. CSF finding
• Turbid
• Elevated pressure
• Cell count >1000/mm3
• Neutrophil leucocytes predominate
• Protein level raised
• sugar level low

21. Other test
• Raised ESR
• Total leucocytes count raised
• CT scan may detect evidence of hydrocehalus,
brain abscess, increased contrast
enhancement of meninges.

22. treatment
• Airway protection
• Oxygenation
• Volume resuscitation
• Control of seizure
• Reduction of hyperthermia
• Measure to reduce icp
head end elevation, manitol, glycerol,
frusemide
• antibiotics

23. antibiotics

25. • Duration of treatment is 10 to 14 days.
• Ceftriaxone is the DOC in any patient with
acute meningitis

26. • Steroids: found to reduce meningitis
assosiated complication.
dexamethasone .15 mg/kg every 6 hr for 4
days.

27. complication
• Cerebrovascular involvement
• Cranial nerve palsies
• Focal neurological deficits
• Cerebral edema and hydrocephalus
• Systemic complication include septic
shock,ARDS

28. VIRAL MENINGITIS
• ASEPTIC TYPE
• SUBACUTE TYPE
• CSF lymphocytic pleocytosis with no apparent cause
after CSF stains and cultures.
• Aetiology :
enteroviruses (coxsackie, echovirus)
arboviruses
HIV
herpes virus
mumps virus
japanese encephalitis virus

29. Sign and symptoms
• Same as bacterial meningitis, but less sever
than bacterial meningitis.
• Viruses are the most common cause of
meningitis, usually resulting in a benign and
self-limiting illness requiring no specific
therapy.

30. CSF finding
• Clear fluid
• Normal to elevated pressure
• Cell count 100 to 500/mm3
• Lymphocytes predominant
• Normal to slightly low sugar
• Normal to slightly high protein

31. treatment
• Mainly supportive
• Use of Acetaminophen/NSAID’S ( for fever and
pain)
• Acyclovir for herpes virus.

32. Tubercular meningitis
• Caused by Mycobacterium tuberculosis.
• Mainly occur as part of widespread
haematogenous spread of Mycobacteria in
children.
• In adult it most of cases it occurs by re-
activation of a subpial focus of dormant lesion
( rich’s focus ).

33. Pathology
• Subarachnoid space throughout CNS is involved.
• Basal cisterns and sylvian fissure are maximally
involved.
• Thick exudates cover the base of brain, lead to
communicating hydrocephalus
• Exudates may also block foramina of luschka and
magendie or any point of CSF pathway resulting
in non-communicating hydrocephalus.

34. Clinical feature
• Sub acute or chronic course
• Same as bacterial meningitis but slower onset
with early manifestations like lack of interest,
malaise, fever, anorexia
• Cranial nerve palsies more common
• Seizure s common
• SIADH

36. INVESTIGATION
• CT Scan:
meningial enhancement
basal exudates
hydrocephalus

37. CSF finding
• Opaque or clear fluid, with cobweb formation on
lond standing.
• Wbc count: 100 to 500/microliter
rarely >1000
• Lymphocytic predominant
• Levated protein level
• Low sugar level
• Csf culture sterile for bacteria
• AFB STAIN POSITIVE.

38. • CSF ADENOSIN DEAMINASE { ADA} LEVEL
1. produce by T lymphosites
2. It has good resulst in diagnosis of pleural, peritoneal
and pericardial fluid for tubercular disease.
3. ADA activity could not distinguish between TBM and
other bacterial meningitis.
4. ADA values from 1 to 4 U/L can help to exclude TBM
and values >8 U/L can improve the diagnosis of TBM.

39. • TUBERCULOSTEARIC ACID
CELL WALL COMPONANT OF MYCOBACTERIUM
has high sensitivity and specificity but costly.
• Nucleic acid amplification test ( NAAT ) on CSF- PCR
test for mycobacterial nucleic acid.

40. treatment
• Anti – tb chemotherapy should be started:
with early phase ( first 2 months ) intensive
therary combination rifampicin, INH,
PYRAZINAMIDE AND streptomycin then
maintance by rifampicin and INH for next 8 to
10 months.
• Ethambutol dose not penetrate blood brain
barrier effectively.

42. Fungal meningitis
• Less common
• Hematogenous, infected paranasal sinus.
• Occur in immunosuppression : diabetes
mellitus, hematopoietic malignancy,
prolonged immunosuppression in transplant
patients, or chronic steroid therapy
• Chronic meningitides : afebrile,cranial nerve
involvement, arteritis with thrombosis,
infarction, and hydrocephalus.

43. • Cryptococcosis – Headache, fever, stiff neck,
increase intracranial pressure, ataxia,
confusion state
• CSF for india ink(60%), serumcryptcoccal Ag
• RX : amphotericin B IV(0.7 mg/kg),
voriconazole for 2 Wk

44. • Coccidioidomycosis –
progresses from the typical influenza-like illness
with pulmonary infiltration to the disseminated
form of the disease
• Candidiasis –
Cause meningitis very rare
parenchymal abscesses and noncaseating
granulomas
Mortality rate very high

45. • CSF – Mirror to tuberculos meningitis –
Pressure elevate, moderate pleocytosis of
lymphocytic predominance,protein is elevated
and glucose is low
• KOH, culture, PCR

46. CSF ANALYSIS
• Composition of Normal CSF:
protein 15- 45 mg/dl
glucose 50-80 mg/dl
Urea 6.0-16 mg/dl
Uric acid .5-3.0 mg/dl
Creatinine .6-1.2 mg/dl
Cholesterol .2-0.6 mg/dl
ammonia 10-35 μg/dL

47. Sodium 135-150 mEq/L
Potasium 2.6-3.0 mEq/L
Chloride 115-130 mEq/L
Cell 0 to 5 /μL
Appearance Clear colourless
s. Gravity 1.003 -1.004
Ph 7.28-7.32

48. IMAGING AND LABORATORY STUDIES
PRIOR TO LP
• Patients with an altered level of
consciousness, a focal neurologic deficit, new-
onset seizure, papilledema, or an
immunocompromised state are at increased
risk for potentially fatal cerebellar or tentorial
herniation following LP.
• Neuroimaging should be obtained in these
patients prior to LP to exclude a focal mass
lesion or diffuse swelling.

49. • In patients with suspected meningitis who require
neuroimaging prior to diagnostic LP, administration of
antibiotics, preferably following blood culture, should
precede the neuroimaging study.
• Patients with coagulation defects including
thrombocytopenia are at increased risk of post-LP
spinal subdural or epidural hematomas, either of which
can produce permanent nerve injury and/or paralysis.
If a bleeding disorder is suspected, the platelet count,
international normalized ratio (INR), and partial
thromboplastin time should be checked prior to LP.

50. • Bleeding complications rarely occur in patients
with platelet counts ≥50,000/μL and an INR
≤1.5.

52. Thank you