Acute viral neurological diseases

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Acute viral neurological diseases

• Dr. Mohammed Arif
• Associate professor
• Consultant virologist
• Head of the virology unit
• College of medicine KKUH

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Acute viral neurological diseases

• Aseptic meningitis
• Encephalitis
• Post-infectious encephalomyelitis
• Paralysis

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1-Aseptic meningitis

• Case definition
• A syndrome characterized by acute onset of
  meningeal symptoms, fever and cerebrospinal fluid
  pleocytosis, with no laboratory evidence of
  bacterial or fungal meningitis.

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Aseptic meningitis

• Inflammation of the meninges that cover the brain
  and spinal cord.
• Meninges duramatter, arachnoid and piamatter.
• It is a disease of children and young adults.

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Viral etiology

• Enteroviruses (85).
• Arboviruses.
• Mumps virus.
• Lymphocytic choriomeningitis.
• Herpes viruses (HSV-12, CMV EBV.HHV-6,7,8)

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Symptoms

• Severe headache.
• Fever.
• Stiffness of neck.
• Nausea.
• Vomiting.
• Sore throat.
• Myalgia.

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Symptoms ( CONT.)

• Prognosis recovery is usual in 5 14 days.
• Complication meningoencephalitis.

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CSF-picture

• Clear.
• Colorless.
• Pleocytosis (increased lymphocytes).
• Increased protein.
• Normal glucose.
• Negative for bacterial culture.

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2-Acute viral encephalitis

• Inflammation of the brain.
• Caused by direct viral invasion of the brain.
• The virus replicate in the brain, causing
  destructive lesions in the grey matter.

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Viral etiology

• HSV-12.
• Enteroviruses.
• Arboviruses.
• Rabies virus.
• Mumps virus.

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Clinical features

• The incubation period 3-7 days.
• Starts with the symptoms of aseptic meningitis
  followed by
• Drowsiness.
• Mental confusion.
• Alteration in the level of consciousness.

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Clinical features (cont.)

• Lack of coordination.
• Seizures.
• Coma.

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Prognosis

• The clinical outcome varies, some are mild with
  full recovery.
• Others are severe with permanent neurological
  sequalae.
• Permanent neurological impairments include
  memory, speech, vision, and muscle control.

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Pathology

• HSV-encephalitis is characterized by
• Edema, hemorrhage and necrosis confined primarily
  to the temporal lobes (bilateral or unilateral).
• Vascular destruction with infiltrates of
  neutrophils and lymphocytes.
• Glial proliferation.
• Eosinophilic intranuclear inclusion bodies.

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Pathology

• Rabies encephalitis is characterized by
• Perivascular infiltrate of neutrophils and
  lymphocytes.
• Glial proliferation.
• Negri bodies, intracytoplasmic inclusion bodies,
  most prominent in the hippocampus.

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Treatment

• For enteroviruses and arboviruses, treatment is
  supportive. There is no anti-viral drug therapy.
• For HSV, the recommended dose of acyclovir is 30
  mg/ kg per day, in three divided doses for 14 -
  21 days.

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Methods of Diagnosis

• Detection of the viral genome using PCR.
• Isolation of the virus in tissue culture,
  followed by identification of the isolated virus.
• MRI (magnetic resonance imaging) provides high
  quality picture of the brain, useful in the
  identification of edema, necrosis and hemorrhage.

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Methods of Diagnosis (cont.)

• CT-scan (computer assisted tomography), useful of
  identification of internal bleeding. Edema and
  necrosis.
• EEG (electroencephalography) shows spikes and
  wave activity.

Ewaves activity.
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3-Post-infectious encephalomyelitis

• It is uncommon complication of many viruses that
  do not usually affect the CNS including measles,
  mumps , rubella and varicella.
• Encephalitis develops within 6 10 days after
  symptoms of viral illness appear.

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Post- infectious encephalomyelitis

• The disease is believed to be an auto-immune
  phenomenon, in which the immune system is
  triggered by exposure to foreign antigen which is
  closely related to host proteins normally
  expressed in brain tissue.

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Pathology

• Characterized by wide spread demyelinating
  lesions in the brain and spinal cord.
• Lymphocytic infiltration and perivascular cuffing
  of adjacent blood vessels.

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Clinical features

• Similar to acute viral encephalitis.
• Fever.
• Headache.
• Stiffness of neck.
• Alteration in the level of consciousness.
• Mental confusion.
• Seizures and coma.

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Prognosis

• Not good.
• Recovery is not complete.
• Survivors are left with permanent neurological
  sequalae.

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Treatment

• Supportive therapy, there is no specific viral
  drug therapy.

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Lab. diagnosis

• By detection of the viral genome to measles,
  mumps and rubella.
• By detection of IgM-Ab to these viruses.

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Chronic viral neurological diseases

• Subacute sclerosing pan encephalitis (SSPE).
• Progressive multifocal leucoencephalopathy.
• Tropical spastic paraparesis (TSP).

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SSPE

• Caused by a mutant measles virus.
• Measles virus usually does not cause brain
  damage, but the mutant virus can invade the brain
  causing persistent infection and severe form of
  encephalitis and death.
• It affects only unvaccinated children.

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Clinical features

• It is a rare, slowly progressive disease of the
  CNS ending in death.
• SSPE develops 6 12 years after having a primary
  measles infection.
• It is due to reactivation of persistent measles
  virus in the brain.

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Clinical features

• The disease starts with personality changes and
  memory defects followed by
• Myoclonic.
• Intellectual impairment.
• Impairment of vision and speech.
• Seizures.
• Ataxia
• Coma death.

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Laboratory Diagnosis

• Presence of high Ab-titre to measles virus in CSF
  and serum.
• MRI provides high quality picture of the brain.
• Electro-encephalogram (ECG), is a test for the
  electrical activity of the brain, which shows a
  wave pattern whish is typical of SSPE.

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Treatment

• No cure for SSPE exist.
• A combination of Isoprinosine and alpha
  interferon injected directly into the brain
  ventricles appears to be the most effective
  treatment.

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Prevention

• Immunization of children against measles virus is
  the only known prevention of SSPE.

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Pathology

• SSPE is characterized by atrophy of the cortex,
  loss of white matter and ventricular enlargement.
• Perivascular lymphocytic infiltrate and intense
  gliosis.
• Intranuclear inclusion bodies.

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Progressive multifocal leukoencephalopathy

• Caused by a polyoma virus known as JC virus.
• The virus belongs to the family papovaviridae.
• Genus polyoma virus,
• The virus is opportunistic, causing brain
  disorder only in the immunosuppressive patients.
• Infection with JC virus is common, but
  asymptomatic.
• 50 60 of adults have Ab to the virus.

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Clinical features

• It is a slowly progressive disease of the CNS
  that is usually fatal.
• It is due to reactivation of latent virus in the
  brain.
• The disease is characterized by
• Hemiparesis
• Dementia
• Impaired
  vision and speech
• Dysphagia
• Lack of
  coordination seizures.

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Prognosis

• Death is very common 1 to 6 months when symptoms
  starts.

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Laboratory diagnosis

• Detection of the viral genome using PCR.
• MRI.

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Pathology

• Brain autopsy shows multiple demyelination foci
  prominent in the hemispheres and cerebellum.
• Destruction of the white matter.
• Prominent gliosis.
• Eosinophilic intranuclear inclusion bodies.