Purulent Leptomeningitis

Purulent leptomeningitis refers to an inflammation of the pia and arachnoid with a purulent exudate in the subarachnoid space. Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae are responsible for about 75% of these infections.

TABLE 6.2.

Age Prevalence of Major

Pyogenic Infections




Escherichia coli

6 mos.-2 yrs. Children-young adults Adults

B. streptococcus Listeria monocytogenes Staphylococcus aureus Haemophilus influenzae Neisseria meningitidis Streptococcus pneumoniae

Clinical Features

Purulent leptomeningitis occurs at all ages from birth through old age. The age-related preferences of common bacteria are listed in Table 6.2. The onset is sudden, with fever, headaches, photophobia, and nuchal rigidity. Severe cases are complicated by an altered state of consciousness, seizures, cranial nerve deficits, and focal neurologic symptoms and signs. The cerebrospinal fluid (CSF) shows elevated cell count, chiefly with polymorphonuclear leukocytes (PNLs), increased protein levels, and decreased glucose levels. The causative microorganisms are identified in the sediment of the CSF using Gram stain and by culturing the CSF and blood. Polymerase chain reaction (PCR) and immunologic techniques identify the bacteria within hours of onset.

Once the bacteria have reached the subarachnoid space, they evoke an acute inflammatory reaction that produces a purulent exudate, vascular-circulatory changes, and edema. The exudate is composed of PNLs, plasma fluid, protein, and a few erythrocytes. The cerebral blood flow increases, and the blood vessels dilate and become engorged. The release of toxic substances from bacteria and disintegrating leukocytes produces cytotoxic edema. The breakdown of the blood-brain barrier allows an escape of fluid and protein into the extracellular compartment and produces vasogenic edema. Subsequently, the brain volume increases, and the intracranial pressure rises. When it becomes severe, herniations develop, carrying the risk of sudden death.


Grossly, the brain is swollen, the blood vessels are congested, and a purulent greenish yellow exudate fills the subarachnoid space and the basal cisterns, obscuring the cortical surface (Fig. 6.1).

Histologically, the subarachnoid space is filled with PNLs, phagocytic cells, fibrin, and a few erythrocytes. The inflammation may involve the arterial and venous walls, and the exudate may extend into the parenchyma along the perivascular spaces (see Fig. 6.1).

With time, the vascular congestion and exudate gradually resolve, usually without sequelae. In some severe cases, late complications may develop, such as (a) internal hydrocephalus due to leptomeningeal fibrosis and obstruction to CSF circulation in the sub-arachnoid space; (b) infarction due to vasculitis and arterial and venous thrombosis; or (c) subdural effusion, a common complication of Haemophilus influenzae meningitis.

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