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466 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

TABLE 17.7 Classification of acute meningitis

Acute meningitis Bacterial – notifiable disease Viral
Aetiology Neisseria meningitis Enteroviruses: 85–95% of cases
● Serogroups A,B,C – 90% invasive isolates Herpes simplex 1 & 2
● Serogroup B – most disease Varicella zoster
● Serogroup A – epidemic disease and indigenous Cytomegalovirus
haemophilus influenzae type B Epstein–Barr
streptococcus pneumoniae HIV infection can also present as aseptic meningitis
listeria monocytogenes Postinfectious encephalomyelitis: may occur following a
variety of viral infections, usually of the respiratory tract.
Cryptococcus neoformans
Fungal isolates
Pathophysiology Rapid recognition and diagnosis of meningitis is The physical signs are not so marked and the illness is not
imperative. as severe and prolonged as bacterial meningitis.
Quick and insidious progress of disease Viral infection of mucosal surfaces of respiratory or
Colonisation of mucosal surfaces (nasopharynx) gastrointestinal tract
Haematogenous or contiguous spread Virus replication in tonsillar or gut lymphatics
Specific antibodies important defence Viraemia with haematogenous dissemination to the CNS
Bacterial invasion of meninges: inflammatory response, Meningeal inflammation, BBB breakdown, cerebral
breakdown of the BBB, cerebral oedema, intracranial oedema, vasculitis and spasm
hypertension
Vasculitis, spasm and thrombosis in cerebral blood vessels
Clinical Presents with sepsis: headache, fever, photophobia, Presents with non-specific symptoms, viral respiratory
presentation and vomiting, neck stiffness, alteration of mental status. illness, diarrhoea, fever, headache, photophobia,
progression Meningococcaemia is characterised by an abrupt onset of vomiting, anorexia, rash, cough and myalgia.
fever (with petechial or purpuric rash). Occurs in summer or late autumn.
Progresses to purpura fulminans, associated with the Enteroviral, pleurodynia, chest pain, hand-foot-mouth
rapid onset of hypotension, acute adrenal disease
haemorrhage syndrome, and multiorgan failure. HSV-2: acute genital herpes
Kernig’s sign
Brudzinski’s sign
Cranial nerve palsy (III, IV, VI, VII) uncommon and develop
after several days
Focal neurological signs in 10–20% cases
Seizures in 30% of cases
Signs of intracranial hypertension: coma, altered
respiratory status
Leads to hypertension and bradycardia before herniation,
or brain death, leads to irreversible septic shock
Treatment If meningococcal infection is suspected, the best way to Administer intravenous aciclovir.
reduce mortality is to administer Dexamethasone may be prescribed: reduces BBB
Empirical IV therapy immediately permeability.
Ceftriaxone 2g IV 12hrly or Supportive treatment and resuscitation
Cefatoxime 2g IV 6hrly or immediately Management of intracranial hypertension/ischaemia
Consequent dose, times and type of antibiotic need to be
modified after full investigation and a detailed
examination have taken place.
Dexamethasone may be prescribed: Needs to be at same
time of antibiotic as outcome neurologically is reduced
if given after antibiotic. Reduces BBB permeability.
Supportive treatment and resuscitation
Management of intracranial hypertension/ischaemia

● Murray Valley encephalitis (MVE) virus causes sea- ● Mycobacterium tuberculosis, the yeast Cryptococcus
sonal epidemics of encephalitis at times of high neoformans and Treponema pallidum (syphilis) may
regional rainfall. This arthropod-borne virus is the also affect the brain parenchyma but usually
commonest flavivirus to cause encephalitis in produce chronic or subacute meningitis in such
Australia. circumstances.
● Since 2005, the distribution of Japanese B ence phalitis
virus has expanded into Australia via the Torres Strait
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Islands. It causes disease clinically similar to MVE. Pathophysiology
In addition, two novel encephalitis viruses were In the majority of encephalitis cases, the offending organ-
recently identified in Australia, the Hendra virus and ism finds access to the brain via the nasopharyngeal epi-
Australian bat lyssavirus. These should be considered thelium and the olfactory nerve system. Arboviruses are
if there is a history of animal exposure, or if no other transmitted from infected animals to human through bite
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pathogen can be implicated. of infected animals. The cytokine storm results in