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pathophys.org http://www.pathophys.org/meningitis/

Katherine

Montgomery

Meningitis

Definition

An inflammation of the meninges, especially the arachnoid mater and the pia mater, often secondary to infection.

Edema and inflammatory infiltrates lead to fever, focal neurological deficits, decreased level of consciousness,

and seizure.

Infectious causes can be bacterial, viral, fungal, or parasitic

While the etiology is usually infectious, ultimately it is the inflammatory changes in the CNS that cause

morbidity and mortality

Etiology

Lancet 2003; 361: 213948.

Curr Opin Infect Dis 2007; 20(3):272-277.

Causative organisms vary by age group:

Neonates (65)

Group B

Streptococcus

Escherichia coli

Listeriamonocytogenes

Streptococcus pneumoniae(pneumococcus)

Neisseria meningitidis(meningococcus)

Haemophilus influenzae type B(less commonnow with the advent of the HiB vaccination)

Streptococcus

pneumoniae

Neisseria meningitidis

(these two organismscause 80% of cases)

Streptococcus

pneumoniae

Neisseriameningitidis

Listeriamonocytogenes

If no organism can be isolated with routine culture and sensitivity assays of cerebrospinal fluid (CSF), thecondition is called aseptic meningitis, and the etiology is likely viral (e.g. Enterovirus, HIV andHSV). Less

common etiologies for aseptic meningitis include tuberculous meningitis(Mycobacterium tuberculosis), Lyme

disease (Borreliaspp.), parasitic infections (e.g. Taenia solium,Toxoplasma gondii), and malignancy.

Pathogenesis

Ther Adv Neurol Disord. 2009; 2(6):401-412.

See figure.

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Clinical features and pathophysiology

JAMA.1999 Jul 14;282(2):175-81.

http://www.ncbi.nlm.nih.gov/pubmed/10411200http://www.ncbi.nlm.nih.gov/pubmed/10411200

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N Engl J Med 2004; 351:1849-1859.

Pediatrics.2010 Nov;126(5):952-60.

Symptom Sign Mechanism

Chills, rigors Fever (T>38) Endogenous cytokines (released during the immune response tothe invading pathogens) affect the thermoregulatory neurons ofthe hypothalamus, changing the central regulation of body

temperature.

Invading viruses or bacteria produce exogenous substances(pyrogens) that can also re-set the hypothalamic thermal set

point.

Nuchalrigidity (neckstiffness)

Brudzinski sign and Kernigsign

Flexion of the spine leads to stretching of the meninges.

In meningitis, traction on the inflamed meninges is painful,resulting in limited range of motion through the spine (especiallyin the cervical spine).

Alteredmentalstatus

Decreased Glasgow ComaScale (GCS)

ICP brain herniation damage to the reticular formation(structure in the brainstem that governs consciousness)

Focalneurologicaldeficits, e.g.vision loss

Examples: cranial nervepalsies, hemiparesis,hypertonia, nystagmus

Cytotoxic edema and ICP lead to neuronal damage.

Signs or symptoms depend on the affected area (cerebrum,

cerebellum, brainstem, etc.)

Seizures Inflammation in the brain alters membrane permeability, loweringthe seizure threshold. Exact seizure pathophysiology is unknown.

Headache Jolt accentuation ofheadache: headacheworse when patientvigorously shakes head

Bacterial exotoxins, cytokines, and ICP stimulate nociceptors inthe meninges (cerebral tissue itself lacks nerve endings thatgenerate pain sensation).

Photophobia Due to meningeal irritation. Mechanisms unclear; pathways arethought to involve the trigeminal nerve.

Nausea andvomiting

ICP stimulates the area postrema (vomiting centre), causingnausea and vomiting.

Petechial rash Meningococcemia (due to N. meningitidis)

In the pediatric population, all of the above signs and symptoms are applicable. Additional signs and symptoms in

children include:

Bulging fontanelles

Bones of the skull do not join fully (form sutures) until age 2

ICP meninges protrude through gaps in skull bones

http://www.ncbi.nlm.nih.gov.libaccess.lib.mcmaster.ca/pubmed/20974781http://www.ncbi.nlm.nih.gov.libaccess.lib.mcmaster.ca/pubmed/20974781

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