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HAMISI MKINDI
MD5,SFUCHAS
INTRODUCTION
• 60 yrs male,Headache, fever, irritability, and
altered mental status and seizures.No prior hx
of illness.
• No neck stiffness,kerning –ve,brudziki –ve.
• CSF with lymphocytes, red blood cells and
elevated protein.
• BS-ve & MRDT -ve, VDRL –ve, HIV –ve and
normal blood glucose level
DIFFERENTIALS????????????
Introduction
• Encephalitis -An acute inflammation of the
brain parenchyma.
• The causative virus is not known in >50% of
cases.
Aetiology
• Viral: Frequent and common HSV 1(close
contact,pred.encephalitis,older) and
2(ST,pred.meningitis,infants),VZV, EBV,
measles virus, mumps virus, and rubella
virus,HH6 and WNV
• Bacterial: Mycoplasma species.
• Parasites: Toxoplasma
• Non infectious: acute disseminated
encephalitis
Pathophysiology
• Most cases of HSE are thought to be reactivation
of HSV lying dormant in the trigeminal ganglia.
• Varicella-zoster virus (VZV) and cytomegalovirus
(CMV), an immune-compromised state is usually
necessary to develop clinically apparent
encephalitis.
• Virus replicates outside the CNS and gains entry
to the CNS either by hematogenous spread or by
travel along neural pathways.
• Once across the blood-brain barrier, the virus
enters neural cells, with resultant disruption in
cell functioning, perivascular congestion,
hemorrhage, and a diffuse inflammatory
response that disproportionately affects gray
matter over white matter.
• Regional tropism eg. HSV predilection for the
inferior and medial temporal lobes.
• Acute disseminated encephalitis and post
infectious encephalomyelitis (PIE), most
commonly due to measles infection and
associated with Epstein-Barr virus (EBV) and
CMV infections, are immune-mediated
processes that result in multifocal
demyelination of perivenous white matter.
Clinical features
Acute or sub acute non-specific febrile illness characterised by headache and
fever.
Diffuse or focal. Typical findings include the following:
• Altered mental status
• Personality changes (very common)
• Focal findings (eg, hemiparesis, focal seizures)
• Movement disorders (eg, St Louis encephalitis, eastern equine
encephalitis, and western equine encephalitis)
• Ataxia
• Cranial nerve defects
• Dysphagia, particularly in rabies
• Meningismus (less common and less pronounced than in meningitis)
• Unilateral sensorimotor dysfunction (postinfectious encephalomyelitis
Diagnosis
• Clinical findings and a characteristic CSF with
lymphocytes, red blood cells and elevated
protein.
• Infection in the CSF may be demonstrated by
PCR, serologically and viral culture.
• An EEG can be diagnostic. CT/MRI of the head
typically shows oedema and haemorrhage in
the temporal/frontal lobe
DDx
• HIV related CNS infections
• TB meningitis
• partially treated acute bacterial meningitis
• cerebral malaria and brain abscess.
Management
• Aciclovir 10-15 mg/kg/iv 8 hourly is given for
14 days as soon as possible after the onset of
symptoms if HSE is thought to be at all likely
and for 21days if HIV positive.
• Seizures are treated as in status epilepticus.
• Rehabilitation.
• Steroids-evidence of raised or increasing
intracranial pressure.
• viruses are leading cause of encephalitis
worldwide & mainly affect children
• transmission is by close physical contact:
inhalation, ingestion, insect bites & sexual
contact
• diagnosis is clinical in combination with CSF &
serology findings
• outcome is variable in encephalitis depending
on the virus

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Enephalitis

  • 2. INTRODUCTION • 60 yrs male,Headache, fever, irritability, and altered mental status and seizures.No prior hx of illness. • No neck stiffness,kerning –ve,brudziki –ve. • CSF with lymphocytes, red blood cells and elevated protein. • BS-ve & MRDT -ve, VDRL –ve, HIV –ve and normal blood glucose level DIFFERENTIALS????????????
  • 3. Introduction • Encephalitis -An acute inflammation of the brain parenchyma. • The causative virus is not known in >50% of cases.
  • 4. Aetiology • Viral: Frequent and common HSV 1(close contact,pred.encephalitis,older) and 2(ST,pred.meningitis,infants),VZV, EBV, measles virus, mumps virus, and rubella virus,HH6 and WNV • Bacterial: Mycoplasma species. • Parasites: Toxoplasma • Non infectious: acute disseminated encephalitis
  • 5. Pathophysiology • Most cases of HSE are thought to be reactivation of HSV lying dormant in the trigeminal ganglia. • Varicella-zoster virus (VZV) and cytomegalovirus (CMV), an immune-compromised state is usually necessary to develop clinically apparent encephalitis. • Virus replicates outside the CNS and gains entry to the CNS either by hematogenous spread or by travel along neural pathways.
  • 6. • Once across the blood-brain barrier, the virus enters neural cells, with resultant disruption in cell functioning, perivascular congestion, hemorrhage, and a diffuse inflammatory response that disproportionately affects gray matter over white matter. • Regional tropism eg. HSV predilection for the inferior and medial temporal lobes.
  • 7. • Acute disseminated encephalitis and post infectious encephalomyelitis (PIE), most commonly due to measles infection and associated with Epstein-Barr virus (EBV) and CMV infections, are immune-mediated processes that result in multifocal demyelination of perivenous white matter.
  • 8. Clinical features Acute or sub acute non-specific febrile illness characterised by headache and fever. Diffuse or focal. Typical findings include the following: • Altered mental status • Personality changes (very common) • Focal findings (eg, hemiparesis, focal seizures) • Movement disorders (eg, St Louis encephalitis, eastern equine encephalitis, and western equine encephalitis) • Ataxia • Cranial nerve defects • Dysphagia, particularly in rabies • Meningismus (less common and less pronounced than in meningitis) • Unilateral sensorimotor dysfunction (postinfectious encephalomyelitis
  • 9. Diagnosis • Clinical findings and a characteristic CSF with lymphocytes, red blood cells and elevated protein. • Infection in the CSF may be demonstrated by PCR, serologically and viral culture. • An EEG can be diagnostic. CT/MRI of the head typically shows oedema and haemorrhage in the temporal/frontal lobe
  • 10. DDx • HIV related CNS infections • TB meningitis • partially treated acute bacterial meningitis • cerebral malaria and brain abscess.
  • 11. Management • Aciclovir 10-15 mg/kg/iv 8 hourly is given for 14 days as soon as possible after the onset of symptoms if HSE is thought to be at all likely and for 21days if HIV positive. • Seizures are treated as in status epilepticus. • Rehabilitation. • Steroids-evidence of raised or increasing intracranial pressure.
  • 12. • viruses are leading cause of encephalitis worldwide & mainly affect children • transmission is by close physical contact: inhalation, ingestion, insect bites & sexual contact • diagnosis is clinical in combination with CSF & serology findings • outcome is variable in encephalitis depending on the virus

Notes de l'éditeur

  1. Viral Main article: Viral encephalitis Viral encephalitis can occur either as a direct effect of an acute infection, or as one of the sequelae of a latent infection. The most common causes of acute viral encephalitis are rabies virus, Herpes simplex, poliovirus, measles virus,[4] varicella zoster virus, and JC virus.[citation needed] Other causes include infection by flaviviruses such as Japanese encephalitis virus, St. Louis encephalitis virus or West Nile virus, or by Togaviridae such as Eastern equine encephalitis virus (EEE virus), Western equine encephalitis virus (WEE virus) or Venezuelan equine encephalitis virus (VEE virus), variola minor virus and variola major virus. Henipaviruses; Hendra (HeV) and Nipah (NiV),[5] are also known to cause viral encephalitis. Bacterial: It can be caused by a bacterial infection, such as bacterial meningitis, spreading directly to the brain (primary encephalitis), or may be a complication of a current infectious disease syphilis (secondary encephalitis). Certain parasitic or protozoal infestations, such as toxoplasmosis, malaria, or primary amoebic meningoencephalitis, can also cause encephalitis in people with compromised immune systems. Lyme disease and/or Bartonella henselae may also cause encephalitis. Cryptococcus neoformans is notorious for causing fungal encephalitis in the immunocompromised. Streptococci, Staphylococci and certain Gram-negative bacilli cause cerebritis prior to the formation of a brain abscess
  2. HERPES ENCEPHALITIS This is the most common form of fatal sporadic encephalitis worldwide and is important because it is treatable if diagnosed early. The frequency is not known in Africa but may be less there possibly because of early exposure in childhood. There are two main types, HSV-1 and HSV-2. Humans are the reservoir for both types; HSV-1 is more common and affects mainly older adults, whereas HSV-2 affects neonates. HSV-I is spread by close physical contact and causes predominantly encephalitis, whereas HSV-2 is considered a sexually transmitted disease and predominantly causes meningitis. The source of encephalitis is mostly reactivation of latent ganglionic infection or less commonly a primary infection. It spreads in a retrograde way either via the trigeminal or olfactory nerves to the temporal and frontal areas of the brain .