CNS infections

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The CNS is particularly sensitive to infection and the infective agents can be bacterial, viral and fungal or agents such as prions (small-chain deoxyribose nucleic acid (DNA) fragments) which are the suspected causative agents in Creutzfeldt-Jakob disease. Bacteria and fungi cause meningitis or brain abscess, viruses lead to encephalitis and prions to spongiform encephalopathies.


Acute bacterial meningitis

An acute infection of the subarachnoid space which invokes an inflammatory reaction from the meninges. Bacteria gain access to the CSF pathways through a variety of routes such as through the sinuses, if the dura has been breached such as through a CSF fistula, or most commonly indirectly through the bloodstream. The common infecting organisms vary at different stages of life. In neonates gram negative bacilli such as E. coli, in children haemophilus influenzae, in adults pneumo-coccus or meningococcus. In immuno-compromised patients, for example those on immune suppressing therapy and those with HIV infection, the bacteria may be opportunistic, that is usually commensal elsewhere in the body of a healthy patient and thus harmless, but in these patients somehow gain access to the CSF and grow. In this context, it should be realized that one of the commonest causes of death in a patient with HIV infection is intracranial infection with the commonest bacterium being Listeria monocytogenes.

A purulent exudates forms in the basal cisterns and the brain becomes oedematous and ischaemic. The process of acute inflammation in the subarachnoid space can lead to an external obstructive hydrocephalus. Infarction of the brain can occur as the inflammation leads to an arteritis or venous thrombophlebitis.

Clinically, meningitis manifests as fever, headache, neck stiffness, photophobia and a deteriorating level of consciousness. A transient petechial skin rash can occur in meningococcal meningitis. Seizures, cranial nerve signs including deafness can develop. Focal neurological deficits can occur usually from focal ischaemia or the development of an abscess.

Diagnosis is suspected clinically and confirmation is by examination of the CSF by lumbar puncture. If there is focal neurological deficit, decreased conscious level or papil-loedema, it is essential to perform a CT brain scan first to look for any space-occupying lesion. The CSF must be taken immediately to microbiology where a white cell count will be performed together with a Gram-stained film (gram +ve cocci - pneumococcus, gram — ve bacilli - haemophilus, gram —ve intra and extracellular cocci - meningococcus). A raised white cell count in the CSF is diagnostic (100-10 000 cells/mm3); the glucose is reduced; the causative organisms can only be correctly identified by culture. Further investigations are then needed to determine the source of the infection for example chest X-ray, sinus X-ray, skull X-ray.

The main mode of treatment is with antibiotics which should be started immediately after diagnosis. Antibiotics must penetrate the blood brain barrier, be in appropriate doses, and the causal organism must be sensitive. Benzylpenecillin, cefo-taxime, and Gentamicin are the most commonly used drugs. Treatment is continued until the patient is asymptomatic and a follow-up lumbar puncture shows resolution of the white cell count; the minimum period should be at least 10 days.

Tuberculous meningitis

Tuberculosis involves the CNS in 10% of infected patients. Following a bacteraemia foci of infection can lodge in the meninges, cerebral or spinal tissue, or choroids plexus. The basal meninges are most severely affected and hydrocephalus is common. The illness is progressive over months with a dementia. In the CSF a lymphocyte pleocytosis is present, the CSF protein is elevated, the CSF glucose is usually significantly lowered compared to the blood glucose. Microscopy using a Ziehl Neelsen stain can reveal the acid fast bacilli, CSF culture confirms the diagnosis but takes many weeks, most laboratories have polymerase chain reaction (PCR) tests available to detect the bacterial DNA. Treatment is with antibiotics usually including Isoniazid, Rifampicin and Pyrzinamide, steroids may be used if the conscious level is deteriorating and hydrocephalus may need CSF drainage.

Viral meningitis

CNS involvement in viral infection can occur through massive viraemia or along peripheral nerves. The infection not only can lead to meningitis but also cause encephalitis, cerebritis or myelitis. Infection of the motor neurons and spinal nerves is poliomyelitis and of the dorsal root ganglia radiculitis. The commonest causal organisms are enteroviruses, mumps virus, or herpes simplex. The meningeal phase of infection with headache photophobia and drowsiness usually lasts about 7-10 days. CSF cell count is elevated and if obtained early can contain the virus. Treatment is for the symptoms apart from severe herpes simplex meningitis where acyclovir is used.


Intracerebral abscess can occur either as a result of haema-togenous emboli of bacteria with for example congenital heart disease, bronchiectasis or by direct spread from the nose and paranasal sinuses or from the middle ear and mastoid cavities (Fig. 21.20), through compound depressed fractures, infected dental caries. In either event the bacteria grow and initially lead to an area of septic encephalitis. Thereafter, the centre liquefies and the surrounding brain reacts by forming a gliotic capsule and thus a true abscess develops. In direct spread from sinusitis or mastoiditis, the bacteria either spread intracranially through a hole in the dura or by retrograde spread along a draining emissary vein and the commonest sites are in the frontal or temporal lobes. Also direct spread can lead to extradural or subdural abscess formation; occasionally the bone is involved and develops osteomyelitis (see Chapter 20).

Clinically, an abscess is suspected in a patient with symptoms and signs of raised intracranial pressure, focal neurological deficit and only occasionally fevers. Systemic signs of infection can be often absent. An infectious source may or may not be apparent. Diagnosis is by CT scanning although MRI is able to show multiple lesions not seen on CT and lumbar puncture is contraindicated. Emergency referral should be made to a neurosurgeon who in the majority of cases will perform a burr hole and aspirate the pus for microbiological analysis. Treatment is by appropriate antibiotics, abscess drainage. The infectious source must be found and dealt with early to prevent further abscesses forming. Persistent abscesses may require excision by craniotomy particularly those in the cerebellum as do subdural and extradural abscesses. Intracerebral and subdural empyema are accompanied by a very high incidence of epilepsy and anticonvulsants are usually necessary. The patient must be informed that he should report himself to the Driving Licensing Authority before recommencing driving.

Creutzfeldt-Jakob disease

One of the prion diseases characterized by the accumulation of a modified cell membrane protein within the central nervous system. The infective agent is resistant to heat and

Figure 21.20. CT scan of a 40-year-old-man who 8 years previously had a head injury with fracture of the frontal bone. Note the frontal intra-cerebral abscess (arrows).

radiation therefore is potentially transmissible through contaminated surgical instruments. Creutzfeldt-Jakob disease (CJD) has an incidence of 1 in 1 million and presents with rapidly progressive myoclonus, ataxia, and dementia. The new variant form vCJD presents in younger patients with a slower time course and has been linked to bovine spongi-form encephalopathy (BSE). Other prion diseases include Gestmann Straussler syndrome similar to CJD and Kuru spread by cannibalism in Papua New Guinea.

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