- With appropriate treatment, mortality from Haemophilus influenzae
and Neisseria meningitidis should be below 5%. However, N.
meningitidis septicaemia can be rapidly fatal if the diagnosis is
- H. influenzae - recurrence of fever, hydrocephalus, convulsions
- N. meningitidis - deafness, intellectual deficit, skin necrosis and
- Streptococcus pneumoniae has the highest mortality (>20%)
and deafness, cranial nerve palsies and hydrocephalus are
- CSF should be obtained if possible but treatment of suspected
meningitis should not be delayed.
- Total and differential white cell count, Gram stain, Ziehl-
Neelsen, India ink, nucleic acid amplification test (NAAT) and
antigen detection methods should be used.
- Blood should be taken for culture, rapid antigen detection and
glucose determination. Meningococcal disease can be diagnosed
by NAAT on whole blood.
- Neonatal meningitis (likely Escherichia coli, group B Streptococcus
and Listeria): cefotaxime and an aminoglycoside, plus ampicillin
if Listeria is suspected.
- Adult: ceftriaxone 2 g per day.
- If penicillin-resistant S. pneumoniae is suspected: vancomycin
can be added.
- Cryptococcal meningitis: amphotericin and 5-flucytosine.
- Tuberculous meningitis: rifampicin, pyrazinamide, isoniazid and
ethambutol (see Pathogenic mycobacteria
- Shunt-related meningitis: treatment according to the identity
and susceptibilities of the organisms.
- Protein-conjugated polysaccharide vaccines are available for H.
influenzae and N. meningitidis serogroups A and C, but not serogroup
B, which causes most cases in the UK.
- Family (close) contacts of meningococcal and Haemophilus meningitis
patients require antimicrobial prophylaxis (ciprofloxacin or
Brain abscesses arise from parameningeal suppuration, foreign
bodies or haematogenous spread from distant sepsis. Infection
is polymicrobial with anaerobic cocci, Prevotella spp.
streptococci (S. anginosus/S. constellatus group) and
Diagnosis and Treatment
- Headache, fever and reduced consciousness.
- Focal neurological signs depend on the location of the abscess.
- Signs of raised intracranial pressure may develop followed by
Lesions are localized by CT scanning. A lumbar puncture is contraindicated
because of the risk of cerebellar herniation. Drainage
should be performed if feasible and pus sent for culture, NAAT
and sensitivity testing.
A regimen of cefotaxime, metronidazole and penicillin or a combination
of benzylpenicillin, chloramphenicol and metronidazole
may be used.
Meningitis and encephalitis may arise from infection with enteroviruses,
mumps, herpes simplex, arboviruses, influenza and, rarely,
rubella or Epstein-Barr virus (EBV). Viral meningitis can be part
of the natural history of polio infection (see Enterovirus and viruses that infect the gastrointestinal tract
present with headache, photophobia, fever and neck stiffness. The
CSF shows an increase in lymphocytes, a mildly raised protein
level and normal glucose level. Throat swabs, CSF and stool specimens
should be sent for NAAT and serological testing. management
is symptomatic as most patients recover without residual
deficit within a few days.
Viral encephalitis is caused
by a variety of viruses including herpesvirus
and arbovirus (see Herpesviruses II
and Tropical, exotic or arbovirus infections
). Patients are
febrile with headache, neck stiffness and impaired consciousness.
Focal neurological signs may develop; convulsions are common.
Virus may be detected in CSF, stool and throat specimens by
NAAT and serological techniques. Aciclovir is used for Treatment
of herpetic encephalitis and has led to reductions in both mortality
and the number of patients left with severe residual disability.
Some viruses are associated with encephalitis after a systemic
infection has resolved, known as postinfectious encephalitis (e.g.
measles, varicella zoster, rubella, EBV, mumps and influenza).
Clinically similar to viral meningitis, this condition is thought to
be mediated by an autoimmune reaction.
The prion protein is a protease-resistant form of a protein that is
a normal constituent of the brain. When ingested, the prion protein
induces a conformational change in the host brain protein, which
leads to spongiform degeneration in the brain. There is an extended
incubation period of more than 5 years.
Kuru was a disease seen in Papua New Guinea among people
who ate human tissue, including brain. Variant Creutzfeldt-Jakob
disease (vCJD) arose after animal brain protein was fed to cattle,
the disease being transmitted to humans by ingestion of contaminated
beef products. The animal disease, bovine spongiform
encephalopathy (BSE), has been eliminated in countries with effective
control measures. The size and scale of any human epidemic
is uncertain but likely to be small.