Neurosurgery notes/Infection/Cranial infection/Viruses

Viruses

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Acquired immune deficiency syndrome (AIDS)
HSV encephalitis
Herpes encephalitis

Viruses

  • Obligate intracellular parasites that depend on the host cell for protein synthesis and energy.
  • They may contain either DNA or ribonucleic acid (RNA).
  • They have no organelles or nucleus and are not cells.
  • They are surrounded by a capsid with protein subunits (capsomeres).

Neurotropic RNA viruses

  • Single strand, with sense, without envelope
    • Picornavirus (poliovirus, echovirus, and Coxsackie virus)
  • Single strand, with sense, with envelope
    • Togavirus (rubella and eastern, western, and Venezuelan equine encephalopathies), retrovirus (HIV), and flavivirus (St. Louis and Japanese encephalopathies)
  • Single-strand, without sense, with envelope
    • Paramyxovirus (measles, SSPE, mumps), rhabdovirus (rabies), bunyavirus (California encephalopathy), orthomyxovirus (influenza), and arenavirus (lymphocytic choriomeningitis)

Neurotropic DNA viruses

  • Circular without envelope
    • Papovavirus JC and SV40
  • Circular with envelope
    • Poxvirus
  • Linear without envelope
    • Adenovirus
  • Linear with envelope
    • Herpes group with HSV-1 and 2

Infection transmission

  • Respiratory route
    • Measles
    • Mumps
    • Varicella-zoster
  • GI route
    • Poliovirus
  • Subcutaneous inoculation
    • Rabies
    • Arbovirus

Virus access to the CNS

  • Blood — poliovirus
  • Peripheral nerves — rabies

Virus detection

  • By in situ hybridization with radioactive complementary DNA or RNA
  • By polymerase chain reaction (PCR) used to amplify their DNA segments. HSV is persistent so it can always be recovered. Varicella-zoster becomes latent so it is intermittently recovered.

Viral (aseptic) meningitis

  • 70% are caused by enterovirus (picornavirus: polio, echovirus, Coxsackie virus) and mumps.
  • Symptoms
    • It is self-limited and usually lasts up to 1 week.
    • Fever
    • Headache
    • Nuchal rigidity
    • No features of encephalitis such as
      • Decreased mental status
      • Seizures
      • Focal deficits.
  • CSF evaluation
    • Lymphocytic pleocytosis, normal protein, and glucose (except decreased glucose with mumps and lymphocytic choriomeningitis virus in rodent handlers) and no bacteria or fungus on culture.
  • Epidemiology
    • It is most common in August and September.
  • Aetiology
    • Adjacent sinus or mastoid bacterial infection
    • Syphilis
    • Cryptococcus
    • TB
    • Borrelia
    • Leukemia
    • Lymphoma
    • Behçet disease

Viral encephalitis

  • Aetiology
    • The most frequent epidemic cause is arbovirus
    • The most frequent sporadic cause is HSV-1.
  • In immunocompromised patients, the most common viruses are HIV, CMV, and papovavirus
  • (There are also infections from Toxoplasma , Aspergillus , and Listeria ).
  • Symptoms
    • Seizures
    • Decreased mental status
    • Focal deficits.
  • There is a 5–20% mortality (HSV has 50% mortality) and 20% incidence of permanent sequelae.

Arboviruses

  • “Arthropod borne” by mosquitoes, ticks, etc.
  • Reservoirs are birds, small mammals, and horses.
  • Humans are dead-end hosts.
  • Eg:
    • Togavirus, flavivirus, bunyavirus, and reovirus.
  • Eastern encephalopathy
    • The most severe and occurs in late summer on the eastern seaboard of the United States and has a 70% mortality
  • Western encephalopathy
    • Milder and occurs on the west coast of Canada, the United States, and Central America
  • Venezuelan equine encephalopathy
    • Mild, occurs in Central and South America and has <1% mortality
  • LaCrosse encephalitis
    • The second most frequent encephalitis in the United States after enterovirus, has a low mortality, and occurs in the Midwest and New York
  • St. Louis encephalitis
    • Transmitted by birds and occurs in the summer in the Midwest and South
  • Japanese encephalitis
    • The most frequent epidemic encephalitis in the world and has a 50% mortality rate
  • Pathologic findings of all these viruses
    • Perivascular mononuclear infiltrates

Rabies

  • Acquired from
    • The bites of
      • Skunks
      • Foxes
      • Coyotes
      • Bats
    • Transmitted by
      • Aerosolized vectors inside caves where bats live.
  • The virus travels through the peripheral nerves to the CNS
  • Has an incubation period of 1 to 3 months.
  • The prodrome phase is followed by either a paralytic (Guillain–Barré-like) form or encephalitic (more frequent) form that progresses to coma and death 2 to 25 days after the onset of symptoms.
  • Pathological features
    • The virus destroys mainly limbic neurons.
    • Negri bodies
      • Intracytoplasmic eosinophilic collections of ribonucleoproteins
      • Seen in 80% of cases
      • Are especially prominent in the
        • Cerebellum (Purkinje cells),
        • Brainstem,
        • Hippocampus
  • Symptoms
    • Initially: pain or paresthesias at the site of the animal bite.
    • Furious form (80%)
      • Hydrophobia
        • Viral multiplication in the salivary glands results in painful spasms of throat/larynx, especially when saliva production is increased associated with drinking or the thought of it.
        • Dehydration is no longer likely because intravenous fluids can be given to completely replace what the hydrophobic patient cannot consume by mouth.
      • With the classic form of the disease, the patient will also exhibit intermittent hyperactivity.
    • Paralytic form (20%)
      • Disease that progresses to quadriplegia (dumb rabies)
  • Treatment
    • Washing the wound with soap, water, and benzyl ammonium chloride (inactivates virus)
    • Watching the biting animal for 10 days.
      • If it becomes symptomatic, it should be euthanized and the brain examined.
      • If there are signs of rabies, treat with rabies immune globulin to provide 10 to 20 days of passive immunization.
    • If one is at high risk, consider a vaccine.
      • Post-exposure prophylaxis consists of a single dose of rabies immunoglobulin and 3-4 doses of rabies vaccine.
    • Patients have also been treated by inducing a coma (Milwalkee protocol) with some success even without post-exposure prophylaxis.

Enteroviruses

  • The human GI tract is the reservoir
  • Most common cause of viral meningitis
  • Poliovirus (single-stranded RNA virus)
    • Numbers
      • <10 cases/year in the USA
        • Mostly in unvaccinated
        • Risk of paralytic disease with the live attenuated oral vaccine is 1 in 2.5 million
      • Incubation is 7 to 21 days.
      • 10% of cases develop viremia.
    • Clinical
      • Most infections are subclinical (nonparalytic form).
      • The CNS is involved in 0.1–1% of cases with aseptic meningitis, encephalitis, and paralysis.
    • Pathology
      • Anterior horn cells
        • The most susceptible because they have increased numbers of viral receptors on their surface.
        • The virus may also infect Betz cell (Largest pyramidal cell) and brainstem nuclei (10–35% of patients develop bulbar palsy).
      • Pathologic examination reveals perivascular mononuclear infiltrates and neuronophagia.
      • There is no virus detected in the CSF.
    • Outcome
      • Mortality: 5–10%.
      • Motor strength usually returns in 4 months.
  • Coxsackie and echoviruses
    • Cause
      • Meningoencephalitis
      • Polymyositis
    • + CSF culture
    • Incidence is increased in patients with humoral immunity deficiencies.

Mumps

  • 10% of the patients with mumps parotiditis develop meningitis. Before the routine use of the mumps vaccine, it accounted for 25% of viral encephalitis cases. It can be cultured from the CSF.

Measles

  • A postinfectious encephalomyelitis develops after the rash in 1 in 1000 cases. It is immune mediated and not directly caused by the virus.
  • SSPE
    • Occurs in children and adolescents (ages 5–15 years) after a measles infection that has usually occurred before 2 years of age.
  • Chronic encephalitis
    • Develops with deteriorating school performance and behavioral changes followed by myoclonus, seizures, weakness, and death in 1–3 years.
  • Pathology
    • It affects both the gray and white matter with perivascular lymphocytes, neuronophagia, demyelination, and oligodendrocyte destruction.
    • There are intranuclear and intracytoplasmic inclusions in the neurons and oligodendrocytes. The CSF has oligoclonal antibodies to the measles virus, no cells, and increased protein
  • Diagnosis can be made by periodic 2–3 electroencephalographic (EEG) spikes per second, increased CSF immunoglobulin, and increased serum and CSF measles antibody titers.

Transmissible spongiform encephalitis

  • The incubation is months to years, but once deterioration is started it progresses rapidly to death. These are a heterogeneous collection of probable infections caused by SSPE and HIV, but most commonly prions.

Postinfectious encephalitis

  • SSPE (subacute sclerosing panencephalitis)
    • It develops several years after a measles infection. There are increased neutralized measles virus immunoglobulin titers in the serum and CSF. Pathologic examination demonstrates atrophy, perivascular lymphocytosis, demyelination, and increased eosinophilic intranuclear and intracytoplasmic inclusions in the neurons and oligodendrocytes. It affects children and young adults and develops in 1 in 1,000,000 cases of measles. Findings are as described above. Death occurs within 1–3 years.
  • Acute disseminated encephalomyelitis
    • Immune-mediated disease that occurs after a viral infection or a vaccination
      • It most commonly occurs after varicella-zoster, measles, upper respiratory infection, rabies vaccination, diphtheria, smallpox, tetanus, typhoid, and influenza.
      • Pathologic examination demonstrates perivascular mononuclear infiltrates with a zone of demyelination along the course of the venules.