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Infection of central nervous system|bacterial infection of central nervous system |viral infection of central nervous system|Medical World

Infection of the Central Nervous System

Introduction

The brain and spinal cord are relatively well protected from microbial infection by the blood-stream barrier.


CNS infections are usually bacterial or viral but may also be protozoal or fungal. Infections may originate in the meninges or in the brain, then spread from one site to the other.


Bacterial infections

Entry of bacteria into the CNS may be:


Direct-through a compound skull fracture or through the skull bones from, e.g. middle ear or paranasal sinus infections, mastoiditis.


Blood-borne from infection elsewhere in the body, e.g. septicaemia, bacterial endocarditis Iatrogenic- introduced during an invasive procedure, e.g. lumber puncture.


Bacterial meningitis

The term meningitis usually refers to inflammation of the sunarchnoid space and is most commonly transmitted through contact with an infected individual. Bacterial meningitis is usually preceded by a mild upper respiratory tract infection during which a few bacteria enter the bloodstream and are carried to the meninges.


Common microbes include:
  • Haemophilus influenza in children between the ages of 2 and 5 years
  • Neisseria meningitis in those between 5 and 30 years, the most common type
  • Streptococcus pneumoniae in people over 30 years.

Other pathogenic bacteria can also cause meningitis, e.g. those causing tuberculosis and syphilis. Meningitis can also affect the dura mater, especially when spread is direct blood through a compound skull fracture as leakage of CSF and blood from the site also provides a route of entry for microbes. CSF and blood may escape through the:

  • Skin, in compound skull fracture
  • Middle ear, in fracture of the temporal bone
  • Nose, in fracture of the sphenoid, ethmoid or frontal bones when air sinuses are involved
  • It may also arise from nearly infection, e.g. of the ear.if an extradural or subdural abscess forms, the infection may spread further locally should it rupture.
  • The onset is usually sudden with severe headache, neck stiffness, photophobia and fever. This is sometimes accompanied by a petechial rash.CSF appears cloudy owing to the presence of many bacteria and neutrophils. Mortality and morbidity rates are considerable.

Viral infections

Entry of viruses in CNS is usually blood-borne from viral infection elsewhere in the body and, less commonly, through the nervous system. In the latter situation, neurotropic viruses, i.e. those with an affinity for nervous tissue, travel along peripheral nerve from a site elsewhere, e.g. poliovirus. They enter the body via:

  • the alimentary tract, e.g. poliomyelitis
  • The respiratory tract, e.g. shingles
  • Skin abrasions, e.g. rabies


The effect of viral infections vary according to the site and the amount of tissue destroyed. Viruses may damage neurones by multiplying within them or stimulating an immune reaction which may explain why signs of some infections do not appear until is a high antibody titre, 1-2 weeks after infection.



Viral meningitis

This is the most common form of meningitis, which is usually relatively mild and followed by complete recovery.


Viral encephalitis

Viral encephalitis is a rare and usually associated with a recent viral infection. Most cases are mild and recovery is usually complete. More serious cases are usually associated with rabies or herpes simplex viruses. Many different sites can be affected and, as neurones cannot be replaced, loss of function reflects the extent of damage. In severe infections neurones and neuroglia may be affected, followed by necrosis and gliosis. If the individual survives the initial acute phase there may be residual dysfunction, e.g. cognitive impairment and epilepsy. If vital centres in the medulla are involved the condition can be fatal.

Herpes zoster

Herpes zoster viruses cause chickenpox, mainly in children, and zoster in adults. Susceptible children may contact chickenpox from a person with shingles but not the reverse. Infected adults may show no immediate signs of disease. The viruses may remain dormant in posterior root ganglia of the spinal nerves then become active years later, causing zoster. Reactivation may be either spontaneous or associated with intercurrent illness or depression of the immune system, e,g. By drugs, old age, AIDS.


The posterior root ganglion becomes acutely inflamed. From there the viruses travel along the sensory nerve to the surface tissues supplied, e.g. skin, cornea. The infection is usually unilateral and the most common sites are:


Nerves supplying the trunk, sometimes two or three adjacent dermatomes. The ophthalmic division of the trigeminal nerve, causing trigeminal neuroglia, and, if vesicles from on the cornea, there may be ulceration, scarring and residual interference with vision.


Poliomyelitis

This disease is usually caused by polioviruses and, occasionally, by other enteroviruses. The infection is spread by food contaminated by infected faecal matter and, initially, viral multiplication occurs in the alimentary tract. The viruses are then blood-borne to the nervous system and invade anterior horn cells in the spinal cord. Usually there is a mild febrile illness with no indication of nerve damage. In mild cases there is complete recovery but there is permanent disability in many others. Irreversible damage to lower motor neurones causes muscle paralysis unopposed tonal contraction of antagonistic muscles. Death may occur owing to respiratory paralysis if the intercostal muscles are affected. Vaccination programmes have now almost eradicated this disease in developed countries.


Rabies

All warm-blooded animals are susceptible to the rabies virus, which is endemic in many. Countries but not in the UK. The main reservoir of this virus are wild animals, some of which may be carriers. When these infect domestic pets they then become the source of human infection. The viruses multiply in the salivary glands and are present in large numbers in saliva. They enter the body through skin abrasions and are believed to travel to the brain along peripheral nerves.


incubation period varies from about 2 weeks to several months, possibly reflecting the distance viruses travel between the site of entry and the brain. There is acute encephalomyelitis with extensive damage to the basal ganglia, midbrain and medulla oblongata. Involvement of the posterior root ganglia of the peripheral nerves causes meningeal irritation, extreme hyperaesthesia , muscle spasm and convulsions.


Hydrophobia and overflow of saliva from the mouth are due to painful spasm of the throat muscles that inhibit swallowing. In the advanced stages muscle spasm may alternate with flaccid paralysis and death is usually due to respiratory muscle spasm or paralysis.



Human immunodeficiency virus (HIV)

The brain is often affected in individual with AIDS resulting in opportunistic infection and dementia.


Creutzfeldt-Jakob disease

This infection condition may be caused by a 'slow' virus, the nature and transmission of which is poorly under-stood. It is thought to be via a heat-resistant transmissible particle known as a prion protein. It is a rapidly progressive form of dementia for which there is no known treatment so the condition is always fatal.


Myalgic encephalitis (ME)

This condition is also known as post-viral syndrome or chronic fatigue syndrome. It affects mostly teenagers and young adults and the aetiology is unknown. Sometimes the condition follows a viral illness. The effects include malaise, severe fatigue, poor concentration and myalgia. Recovery is usually spontaneous but sometimes results in chronic disability.

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