[PPT]No Slide Title - Trinity College Dublin, the University of … · Web viewCNS INFECTION FM...
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CNS INFECTION
FM Brett MD., FRCPath
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ORGANISMSORGANISMS
~ PATHOGENIC - cause disease in every individual
~ OPPORTUNISTIC – Affect people with lower resistance
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CNS INFECTIONCNS INFECTION
Development and outcomeDevelopment and outcomedepends ondepends on
Organism Organism natureroute of entrydose
HostHost Anatomical defenses - skull, meninges
Physiological - immune defense mechanisms
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BacteriaBacteria
Entry into the cranial cavityEntry into the cranial cavity
Haematogenous -Haematogenous - distant foci e.g lung
Local spread -Local spread - Skull - middle ear, nasal sinus, osteomyelitis
Abnormal routesAbnormal routes - Trauma -fractures Surgery - shunts
Congenital sinus
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BACTERIAL INFECTIONSBACTERIAL INFECTIONS
Depending on their virulence/pathogenicity bacteria can induce:
1. Purulent lesions
2. Cellular inflammatory reactions with giant cells
3. Inflammatory oedema caused by toxins and other inflammatory substances released by bacterial secretions or lysis, in the absence
of bacterial replication
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PYOGENIC INFECTIONPYOGENIC INFECTION
1. BONE – EPIDURAL – usually spinal sec to osteomyelitis
2. DURA MATER - SUB DURAL - sec to sinusitis, otitis etc.
3. ARACHNOID – SUBARACHNOID – sec to haematogenous spread of bacteria
4. PIA - INTRAPARENCHYMAL - abscess
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SUBDURAL
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Three organisms responsible for acute meningitis in childhood or adult life
• Meningococcus
• Haemophilus influenza
• Pneumococcus
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Bacterial meningitis
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Bacterial meningitis
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Complications of acute meningitisComplications of acute meningitis in the neonatein the neonate
• Obstructive hydrocephalus
• Cavitating lesions in the white matter
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MeningococcusMeningococcus
NasopharynxNasopharynx
BloodBlood
BacteraemiaBacteraemia SepticaemiaSepticaemia
Chronic Meningitis Endotoxic shockimmune complexes acute meningitis DICarthritis, vasculitis
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CSFBacterial Viral TB
low N low glucose
v. high Slightly increased
Raised protein
neutrophils
lymphocytes
lymphocytes
cells
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Complications of bacterial meningitisComplications of bacterial meningitis
• Acute inflammation of adjacent structures
• Organisation of inflammatory structures
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Organisation of inflammatory exudate
Impedes flow of Impedes flow of CSF into CSF into venous sinusesvenous sinuses
Obstructs CSF outflow fromObstructs CSF outflow fromIV ventricleIV ventricle
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A twelve year review of central nervous system bacterial abscesses: presentation and aetiology.Roche M, Humphreys H, Smyth E, Phillips J et al
Clin Mic & Inf 2003;9:803-14
1988-2000
163 patients
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Cerebral abscess
~ Mean age – 35.2~ P/C – headaches, pyrexia, altered mental state (depends on site, number, and +/- secondary cerebral lesion)~ Site – frontal lobe commonest~ Majority – associated with sinusitis, mastoiditis
20% no source~ Bacteria isolated from 73%. Polymicrobial – 17.7%~ Anaerobes – 13.6%~ 9.8% died~ 11% developed epilepsy
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Cerebral abscess
Predisposing conditions
Local – otitis media, sinusitis, trauma
Systemic ~ chronic lung disease~ cyanotic congenital heart disease~ transplants~ immunosupression
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Parenchymal abscess formation
~ Early cerebritis (days 1-3)
~ Late cerebritis (days 4-9)
~ Early capsule formation (days 10-13)
~ Late capsule formation (days 14 onward)
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AIMS OF TREATMENT
~ Eliminate infectious process
~ Reduce mass effect within cranial cavity – thus reduce secondary injury
~ Treat infections
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Tuberculous meningitis
Usually M Tuberculosis
More commonly associated with documented history of tuberculosis exposure in children than adults
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CSF
Bacterial Viral TB
glucose low N low
protein v. high Slightly increased
Raised
cells neutrophils
lymphocytes
lymphocytes
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SyphylisSyphylis
• Asymptomatic CNS involvement• Syphylitic meningitis – 1-2 yrs• meningovascular syphylis – 7yrs• parenchymatous neurosyphylis• gummatous neurosyphylis
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1 syphylis1 syphylis – spirochaete dissemination – chancre
22ndnd – haematogenous dissemination - rash, adenopathy,
3 3 – CVS, CNS, gumma
Latent Latent – lasts mths – yrs. Pts may progress straight to the stage of latent syphylis without developing secondary syphylis
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SyphylisSyphylis
I syphylisI syphylis – spirochaete dissemination – chancre22ndnd – haematogenous dissemination - rash,
adenopathy, 3 3 – CVS, CNS, gummaLatent Latent – lasts mths – yrs. Pts may progress straight
to the stage of latent syphylis without developing secondary syphylis
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Neurosarcoidosis~ Chronic granulomatous disease of unknown aetiology
~ CNS involved in 5%. CNS disease often accompanied by PNS disease~ Usually base of the brain ~ Facial nerve palsy common. May develop deafness, vertigo, ataxia, DI, hypopituitrism
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Acute viral infectionsAcute viral infections
• Aseptic meningitisAseptic meningitis• PoliomyelitisPoliomyelitis• Herpesvirus Herpesvirus - - HSV, VCZ, EBV,
cytomegalo, HHV6
• RubellaRubella• RabiesRabies
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Aseptic meningitis-common Aseptic meningitis-common causescauses
• Echovirus• Coxsachie B virus• Coxsachie A virus• HSV-2• Mumps• Measles• Adenovirus
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CSF
bacterial Viral TB
glucose low N low
protein v. high Slightly increased
Raised
cells neutrophils
lymphocytes
lymphocytes
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PoliomyelitisPoliomyelitis
Precentral gyrus
Reticular formationMotor nuclei of pons and medulla
Ant horn cells of spinal cord
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HERPESVIRUS INFECTIONS
DNA VIRUSES - include HSV1, HSV2, EBV, CMV and HHV6
HSE
EncephalitisFocal neurologic signsMortality 25-50%
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HSE -HSE - oral labial vesicles - retrograde axonal spread – trigeminal ganglion- (latency)
ReactivationReactivation (spontaneously, trauma, UV light, systemic disease)
Entry of HSV-1 into CNS – olfactory nervesReactivation of latent virus in trigeminal nerveReactivation from temporal lobes
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Chronic viral infectionsChronic viral infections progress over mths - yearsprogress over mths - years
SSPESSPE – follows exposure to measles virus Age of onset – 5-15 yrs prognosis poor
PMLPML- JC virus affects immunosupressed individuals demyelination
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HIV~ First recognised in USA in 1981~ Widely distributed worldwide~ 30 million currently infected
~ 9000 infections daily - > 50% sub-saharan Africa~ USA and western Europe – homosexual, and IVDA
~ Elsewhere heterosexual~ Small proportion perinatal or breast feeding
~ Organ donors, blood etc
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HIV – retrovirusHIV – retrovirus
~ Infects cells carrying CD4 antigen i.e CD4+ T helper cells and monocytes/macrophages
~ This leads to a) cell mediated immunodeficiency – AIDSb) invasion of CNS by macrophage/monocytes
~ CNS disease – infection by virus- opportunistic infections- Lymphomas- HIV asssociated systemic disease affecting CNS e.g metabolic, cvs etc.- complications of treatment
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Commonest processes identified prior to HAART
~ Cryptococcus~ Toxoplasmosis~ PML~ HIVE~ HIVL~ Cytomegalovirus infection~ Vacuolar myelopathy
~ CNS Lymphoma
By and large did not have bacterial infections
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Commonest causes of a cerebral mass in a patient with HIV
ToxoplasmosisCNS lymphomaTuberculomaPMLCMVLesion not related to HIV - glioma
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Toxoplasma cyst
Toxoplasma ICC
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Introduction of HAART (1995-96) dramatically improvedThe course and prognosis of HIV infection
Restored functional immune system – so less opportunistic infection
Dramatic reduction in cerebral toxoplasmosis, CMV encephalitis and HIV encephalitis
Unchanged incidence of PML and NHL