Infections of the Central Nervous System

Infections of the Central Nervous System
Presentation by:Charles S. Bryan, M.D.

* Pleocytosis: increased WBCs in the CSF
* Hypoglycorrhachia: low CSF glucose
* Meningitis: inflammation of meninges
* Encephalitis: inflammation of the brain
* Meningoencephalitis: both of the above
* Myelitis: inflammation of the spinal cord
* Encephalomyelitis: encephalitis + myelitis
* Parameningeal infection: localized infection “beside the meninges”, e.g. brain abscess, subdural empyema, epidural abscess,suppurative intracranial thrombophlebitis, mycotic aneurysm

The CSF formula
* Red cells (normally 0)
* WBCs (normally < 5/cmm)
* Differential (normally all mononuclear cells)
* Protein (normally 15 to 45 mg/dL)
* Glucose (normally 40 to 70 mg/dL or about 2/3 of simultaneous blood glucose)

Some pointers on the LP
* If you think of it, it’s generally best to do it!
* In chronic problems, rule out localized intracranial pathology; for acute problems, don’t delay if there are no localizing signs!
* Save an extra tube (the Golden Rule)!

Acute bacterial meningitis
* A MEDICAL EMERGENCY
* Consider in every patient with a history of URI interrupted by one of the “meningeal symptoms”: vomiting, headache, lethargy, confusion, stiff neck
* Clinical picture is often unimpressive when the patient is first seen

Triad of acute bacterial meningitis
* Fever (bacterial invasion of blood & CSF)
* Stiff neck (nuchal rigidity due to protective reflexes from inflammation of the subarachnoid space)
* Brain dysfunction (nausea/vomiting, headache, irritability/excitability; obtundation)

Kernig’ sign
Brudzinski’s sign
LP in acute bacterial meningitis
Gram’s stain of CSF in meningitis
Pathogenesis of meningitis
* Mucosal colonization
* Mucosal invasion
* Bacteremia
* Meningeal invasion
* Bacterial replication in CSF
* Host response to bacterial antigens
* Subarachnoid space inflammation

Pathogen offensive strategies in acute bacterial meningitis
* IgA protease secretion
* Ciliostasis
* Adhesive pili
* Evasion of alternative complement pathway by polysaccharide capsule

Host defensive strategies in acute bacterial meningitis
* Secretory IgA
* Ciliary activity
* Mucosal epithelium
* Complement (serum bactericidal system)
* Cerebral endothelium: Blood-brain barrier

The blood-brain barrier in meningitis
* 99% of bacteremic adults do not develop meningitis
* However, 1/3 of bacteremic infants develop meningitis suggesting immaturity of blood-brain barrier
* Barrier seems to function unidirectionally (inoculation of subarachnoid space causes bacteremia 1/3 of the time)
* Normal functions: active transport, facilitated diffusion, aqueous secretion of CSF, homeostasis
* Major sites: arachnoid membrane, choroid plexus, and endothelial cells of cerebral microvascular
* Meningitis: cytokines (especially interleukin-1) increase permeability

Cytokines in meningitis
Why is bacterial meningitis so devastating?
Complications of meningitis
Causes of bacterial meningitis by age
“The big three” of bacterial meningitis
Haemophilus influenzae meningitis
H. influenzae meningitis: current issues
Invasive meningococcal disease
Epidemiology of meningococcal disease
Meningococcal disease: indications for preventive
Pneumococcal meningitis
Neonatal meningitis due to gram-negative bacilli
Listeria monocytogenes meningitis
Epidemiology of bacterial meningitis: some associations
Aseptic meningitis: etiology of the term
Aseptic meningitis: current operational definition
Causes of viral meningitis
Pearls on viral meningitis
Other causes of aseptic meningitis syndrome
* Partially-treated bacterial meningitis
* Tuberculous or fungal meningitis
* Parameningeal infection
* Syphilis or leptospirosis
* Toxoplasmosis, amebiasis
* Sarcoidosis
* Drug reactions
The syndrome of chronic meningitis
Causes of chronic meningitis
Tuberculous meningitis
Cryptococcal meningitis
Syphilitic meningitis
Herpes simplex encephalitis
Brain abscess
Subdural empyema
Cavernous sinus thrombosis
Spinal epidural abscess

Infections of the Central Nervous System.ppt