CLINICAL APPROACH IN MENINGITIS
Excluding open CNS trauma or neurosurgical procedures, bacteria causing acute meningitis
reach the CSF hematogenously. Many bacteria have a bacteremic potential, i.e., bacteremias are
part of their infection process, but relatively few are able to cross the blood/brain barrier and
cause meningitis. ABM usually involves the leptomeninges or the covering of the brain.
Leptomeningeal irritation is responsible for the nuchal rigidity, Kernig’s and Brudzinski’s
signs associated with ABM (7,8) Because the leptomeninges cover the brain parenchyma,
meningitis is not associated with changes in mental status that require parenchymal invasion.
The majority of pathogens causing ABM are respiratory tract organisms.
ABM may also result from contiguous spread from a local source in close proximity to
the brain. Infections that cause meningitis by contiguous spread include sinusitis or
mastoiditis. Cracks in the cribriform plate are another example of a mode of entry via a
contiguous bacterial source. Meningitis may also occur by hematogenous spread of
nonrespiratory pathogens, e.g.,Listeria monocytogenes, Escherichia coli, Staphylococcus aureus,as
part of secondary bacteremia with CNS seeding. Acute bacterial endocarditis due toS. aureusis
not infrequently complicated by acute purulent bacterial meningitis as a suppurative
complication (1,2,9). The insertion of CNS shunts for hydrocephalus/increased intracranial
pressure, if complicated by meningitis, reflects either the flora of the skin introduced during the
insertion process, or the flora at the distal end of the shunt, i.e., a ventricular peritoneal shunt.
Open head trauma introduces the bacteria into the CSF/brain parenchyma (1–5,10–13) (Table 1).
Meningoencephalitis due toL. monocytogenesis recognizable by clues from the CSF
profile and is common in the elderly/immunosuppressed.M. pneumoniaemeningoencephalitis
is being recognized as part of the clinical presentation ofM. pneumoniaeatypical pneumonia.
M. pneumoniaemeningoencephalitis occurs in patients withMycoplasmacommunity–acquired
pneumonia with very high cold agglutinin levels (>1:512) (1,2,5).
The viruses, e.g., enteroviruses, that cause meningitis are relatively few compared with
their bacterial counterparts. Some viruses, i.e., HSV-1 cause a spectrum of CNS infections in
normal hosts from aseptic meningitis to encephalitis. Partially treated meningitis is bacterial
meningitis following initial treatment for meningitis. Partially treated bacterial meningitis is
diagnosed by history, and findings in the CSF, i.e., pleocytosis with a variably decreased
glucose and a moderately elevated CSF lactic acid (4–6 mmol/L). Partially treated meningitis
requires re-treatment with antimicrobials with the same spectrum and dosage as to treat ABM
(1,5,6,14,15).
THE MIMICS OF MENINGITIS
Because a stiff neck or nuchal rigidity is the hallmark of ABM, any condition that is associated
with neck stiffness may mimic meningitis. Patients with acute torticollis, muscle spasm of the
head/neck, cervical arthritis, or meningismus due to a variety of head and neck disorders can
all mimic bacterial meningitis. Fortunately, most of these causes of neck stiffness or
meningismus are not associated with fever. Fever plus nuchal rigidity is the distinguishing
hallmark of ABM. It may be difficult in elderly patients to rule out meningitis on the basis of
fever and nuchal rigidity alone since many elderly individuals have fever due to a variety of
non-CNS infections, and may have a stiff neck due to cervical arthritis. In such situations,
analysis of the CSF profile will readily distinguish the mimics of meningitis from actual
infection (1,4,5,18).
Table 1 Symptoms and Signs of ABM
Symptoms Signs
Headache Fever
Photophobia Meningismus
Nausea and vomiting Kernig’s sign
Brudzinski’s sign
Acute deafness
Cranial nerve palsies
Seizures
Meningitis and Its Mimics in Critical Care 135