Viral infections myelitis and poliomyelitis

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MYELITIS

Acute viral transverse myelitis is rare. It can occur in association with measles, mumps, Epstein-Barr, herpes zoster/simplex, enterovirus infections or small pox. Fever, back and limb pain precede paralysis, sensory loss and bladder disturbance. Initially paralysed limbs are flaccid, but over 1-2 weeks spasticity and extensor plantar responses develop. Good recovery occurs in 30%. Death from respiratory failure is rare (5%).

Investigations

Myelography when performed is normal. MRI may demonstrate focal cord signal changes. CSF shows elevated protein with a neutrophil or lymphocytic response. Serological tests will occasionally identify the causal virus. Electrophysiology distinguishes from Guillain-Barre syndrome.

Treatment

Supportive; the place of steroids remains unproven.

It is not clear whether the pathological effects (perivenous demyeiination) result from direct or delayed (immunological) reactions to the virus.

POLIOMYELITIS

An acute viral infection in which the anterior horn cells of the spinal cord and motor nuclei of the brain stem are selectively involved. A major cause of paralysis and death 30 yrs ago, now rare with the introduction of effective vaccines.

Causative viruses:

The poliovirus is an enterovirus (RNA virus).

Three immunologically distinct strains have been isolated. Immunity to one does not result in immunity to the other two. Coxsackie and echoviruses may produce a clinically identical disorder.

Pathology

Initially - inflammatory meningeal changes, followed by - inflammatory cell infiltration (polymorphs and lymphocytes) around the brain stem nuclei and anterior horn cells. Neurons may undergo necrosis or central chromatolysis.

Microglial proliferation follows.

Epidemiology

A highly communicable disease which may result in epidemics. Seasonal incidence - late summer/autumn.

World-wide distribution, although more frequent in northern temperate climates.

Prophylactic vaccination has produced a dramatic reduction in incidence in the last 25 years. In developing countries without a vaccination programme, the disease remains a problem.

Clinical features

Infection may result in:

- Subclinical course + resultant immunity (majority)

- Mild non-specific symptoms of viraemia + resultant immunity

- Meningism without paralysis (PREPARALYTIC) + resultant immunity

- Meningism followed by paralysis

(PARALYTIC) + resultant immunity. 491

Mode of spread

Spread by faecal/oral route. Once ingested the virus multiplies in the nasopharynx and

G1 tract results in viraemia but CNS involvement occurs in only a very small proportion. Most infected patients are asymptomatic. Virus excretion continues in the faeces for as long as three months after the initial infection - carrier state.

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