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ACUTE CNS INFECTION
P.POOJA SWETHA
MBBS IV YEAR
INTRODUCTION
Encephalopathy => cerebral dysfunction due to
circulatory toxins, poisons, abnormal
metabolites.
Intrinsic biochemical disorder affecting neurons
without inflammatory response
Inflammation of meninges – meningitis
Involvement of brain parenchyma –
meningoencephalitis
ETIOLOGY OF ENCEPHALOPATHIES
Infections
Acute disseminated encephalomyelitis
Postinfectious : typhoid, shigella, Reye syndrome
Hypoxic encephalopathy, heat hyperpyrexia
Metabolic : diabetic acidosis, uremic coma, hepatic coma,
neonatal hyperbilirubinemia, lactic acidosis, mitochondrial
disorders, inborn error of metabolism
Fluid and electrolyte disturbances: water intoxication,
hypernatremia, hyponatremia, alkalosis, acidosis
Toxic: heavy metals, insecticides, carbon monoxide
Post vaccination
ACUTE BACTERIAL MENINGITIS
AGE AND INCIDENCE
Age: – 90% between 1month to 5 yrs
Incidence: – 5.4 to 7.3/1,00000 population
Decreased after use of conjugate Hemophilus
Influenza b vaccine
ETIOLOGY
Depends on
Age
Immune Status of the host
Environmental factors
ETIOLOGICAL ORGANISMS
NEONATAL PERIOD:
Group B streptococcus,
Gram negative enteric organisms,
Listeria monocytogenes, Hemophilus influenza.
2MONTHS ‐12YRS:
Hemophilus influenza(<5yrs),
Streptococcus pneumoniae, Neisseria meningitidis,
Rarely : Staph.aureus, S.typhi, Pseudomonas
RISK FACTORS
Lack of immunity
Close contact with invasive disease caused by He
mophilus influenza, Neisseria meningitidis.
Overcrowding
Occult bacteremia in infants
PREDISPOSING FACTORS AND
ORGANISMS
ROUTES OF SPREAD
Blood spread
• pneumonia
• Cochlear
implant,
osteomyelitis
Direct spread
• Trauma,
neuro surgery
• sinusitis
Others
• Csf
rhinorrhea
• Myelo
menigocele
PATHOGENESIS
Meninges infiltrated with inflammatory cells
Cortex shows edema , proliferation of microglia,
destruction of ependymal cells.
PATHOLOGICAL CHANGES
Exudate
Subpial toxemia
Vasculitis and thrombosis
EXUDATES
Sites of collection
• Cerebral vessels
• Sylvian fissures
• Base and
surface of brain
• cerebellum
Manifestations
• Meningeal
irritation
• Raised ICT
Complications
• Internal
hydrocephalus
• Neurodeficits
VASCULAR CHANGES
Subintimal changes in the small vessels & arte
ries,
Thrombosis and
thrombophlebitis of small cortical veins,
Subarachnoid haemorrhage,
Hemiparesis due to ischemia
SUBCELLULAR PATHOGENIC MECHANISM
Subpial toxemia: TNF and cytokine production
Bacterial pathogen release endotoxin and
peptidoglycans => extensive host damage
Cerebral edema
Cytotoxins-
cytotoxic edema
Increased
vascular
permeability-
vasogenic edema
DIFFERENTIAL DIAGNOSIS OF MENINGITIS
Tubercular meningitis
Viral encephalitis
Meningism
Aseptic meningitis
Cryptococcal meningitis
Lyme disease
Subarachnoid hemorrhage
TUBERCULAR MENINGITIS
Tuberculosis -major global health problem
2nd leading cause of death among
infectious disease worldwide ‐ after HIV
In 2013 –9.0 million new TB cases &
1.5 million TB deaths
Infection of the CNS is one of the most devastating clini
cal manifestations of tuberculosis
EPIDEMIOLOGY
Approximately 95% of tuberculosis cases occur in the devel
oping world.
Worldwide (2013) ‐‐ 8.7 million incident cases,
‐‐ 12 million prevalent cases,
‐‐ 1.4 million deaths from tuberculosis
India accounts for 1/5 of the global TB burden
The global burden is influenced by the HIV pandemic; MDR
TB;
Most common between 6 and 24 months of age
ETIOPATHOGENESIS
 TB Bacillemia (primary or late reactivation)
 Subependymal tubercles
Rupture into the subarachnoid space
Meningitis
ENCEPHALITIS
Inflammation of brain parenchyma
ETIOLOGY
RNA viruses : mumps, measles, rubella, enterovirus
DNA viruses : HSV , CMV , EBV
Arthropod borne viruses: JE, west nile, equine virus
HIV, Rabies, prion infections , dengue virus
Lymphocytic meningitis
Rickettsia; cryptococcus; toxoplasma
THANK YOU

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Acute central nervous system infection

  • 1. ACUTE CNS INFECTION P.POOJA SWETHA MBBS IV YEAR
  • 2. INTRODUCTION Encephalopathy => cerebral dysfunction due to circulatory toxins, poisons, abnormal metabolites. Intrinsic biochemical disorder affecting neurons without inflammatory response Inflammation of meninges – meningitis Involvement of brain parenchyma – meningoencephalitis
  • 3. ETIOLOGY OF ENCEPHALOPATHIES Infections Acute disseminated encephalomyelitis Postinfectious : typhoid, shigella, Reye syndrome Hypoxic encephalopathy, heat hyperpyrexia Metabolic : diabetic acidosis, uremic coma, hepatic coma, neonatal hyperbilirubinemia, lactic acidosis, mitochondrial disorders, inborn error of metabolism Fluid and electrolyte disturbances: water intoxication, hypernatremia, hyponatremia, alkalosis, acidosis Toxic: heavy metals, insecticides, carbon monoxide Post vaccination
  • 5. AGE AND INCIDENCE Age: – 90% between 1month to 5 yrs Incidence: – 5.4 to 7.3/1,00000 population Decreased after use of conjugate Hemophilus Influenza b vaccine
  • 6. ETIOLOGY Depends on Age Immune Status of the host Environmental factors
  • 7. ETIOLOGICAL ORGANISMS NEONATAL PERIOD: Group B streptococcus, Gram negative enteric organisms, Listeria monocytogenes, Hemophilus influenza. 2MONTHS ‐12YRS: Hemophilus influenza(<5yrs), Streptococcus pneumoniae, Neisseria meningitidis, Rarely : Staph.aureus, S.typhi, Pseudomonas
  • 8. RISK FACTORS Lack of immunity Close contact with invasive disease caused by He mophilus influenza, Neisseria meningitidis. Overcrowding Occult bacteremia in infants
  • 10. ROUTES OF SPREAD Blood spread • pneumonia • Cochlear implant, osteomyelitis Direct spread • Trauma, neuro surgery • sinusitis Others • Csf rhinorrhea • Myelo menigocele
  • 11. PATHOGENESIS Meninges infiltrated with inflammatory cells Cortex shows edema , proliferation of microglia, destruction of ependymal cells. PATHOLOGICAL CHANGES Exudate Subpial toxemia Vasculitis and thrombosis
  • 12. EXUDATES Sites of collection • Cerebral vessels • Sylvian fissures • Base and surface of brain • cerebellum Manifestations • Meningeal irritation • Raised ICT Complications • Internal hydrocephalus • Neurodeficits
  • 13. VASCULAR CHANGES Subintimal changes in the small vessels & arte ries, Thrombosis and thrombophlebitis of small cortical veins, Subarachnoid haemorrhage, Hemiparesis due to ischemia
  • 14. SUBCELLULAR PATHOGENIC MECHANISM Subpial toxemia: TNF and cytokine production Bacterial pathogen release endotoxin and peptidoglycans => extensive host damage Cerebral edema Cytotoxins- cytotoxic edema Increased vascular permeability- vasogenic edema
  • 15. DIFFERENTIAL DIAGNOSIS OF MENINGITIS Tubercular meningitis Viral encephalitis Meningism Aseptic meningitis Cryptococcal meningitis Lyme disease Subarachnoid hemorrhage
  • 16. TUBERCULAR MENINGITIS Tuberculosis -major global health problem 2nd leading cause of death among infectious disease worldwide ‐ after HIV In 2013 –9.0 million new TB cases & 1.5 million TB deaths Infection of the CNS is one of the most devastating clini cal manifestations of tuberculosis
  • 17. EPIDEMIOLOGY Approximately 95% of tuberculosis cases occur in the devel oping world. Worldwide (2013) ‐‐ 8.7 million incident cases, ‐‐ 12 million prevalent cases, ‐‐ 1.4 million deaths from tuberculosis India accounts for 1/5 of the global TB burden The global burden is influenced by the HIV pandemic; MDR TB; Most common between 6 and 24 months of age
  • 18. ETIOPATHOGENESIS  TB Bacillemia (primary or late reactivation)  Subependymal tubercles Rupture into the subarachnoid space Meningitis
  • 19. ENCEPHALITIS Inflammation of brain parenchyma ETIOLOGY RNA viruses : mumps, measles, rubella, enterovirus DNA viruses : HSV , CMV , EBV Arthropod borne viruses: JE, west nile, equine virus HIV, Rabies, prion infections , dengue virus Lymphocytic meningitis Rickettsia; cryptococcus; toxoplasma