Acute community-acquired bacterial meningitis in adults: An evidence-based review
ABSTRACTCommunity-acquired bacterial meningitis is still a significant cause of morbidity and mortality. Clinicians should know how to quickly diagnose it, perform a lumbar puncture, order the necessary tests, and start appropriate empiric therapy promptly.
KEY POINTS
- The most common organisms that cause community-acquired bacterial meningitis are Streptococcus pneumoniae and Neisseria meningitidis. The incidence of Listeria infection increases in patients over age 50 and in those with compromised cell-mediated immunity.
- Symptoms and signs are not sensitive or specific enough to diagnose community-acquired bacterial meningitis. A lumbar puncture for cerebrospinal fluid studies is needed to reach the diagnosis, to identify the organism, and to determine antimicrobial susceptibilities.
- Gram stain of cerebrospinal fluid may quickly identify the causative organism. It is not very sensitive, but it is specific.
- Lumbar puncture should be performed as soon as possible. Computed tomography of the head is not necessary in all patients, only in immunocompromised patients and those who have features suggestive of or who are at risk of increased intracranial pressure.
- Try to obtain blood and cerebrospinal fluid cultures before staring antimicrobial therapy, but do not delay therapy if obtaining them is not feasible.
Although the incidence and rates of morbidity and death from acute community-acquired bacterial meningitis have dramatically declined, probably as a result of vaccination and better antimicrobial and adjuvant therapy, the disease still has a high toll. From 10% to 20% of people who contract it in the United States still die of it.1,2
In the United States, meningitis from all causes accounts for about 72,000 hospitalizations and up to $1.2 billion in hospital costs annually.3 However, the incidence of bacterial meningitis has declined from 3 to 5 per 100,000 per year a few decades ago to 1.3 to 2 per 100,000 per year currently.2 In less-developed countries, rates are much higher.
In the early 1900s in the United States, the death rate from bacterial meningitis was 80% to 100%. The use of intrathecal equine meningococcal antiserum during the first decades of the 1900s dramatically reduced the rate of death from meningococcal meningitis. With the advent of antimicrobial drugs in the 1930s and 1940s, the death rate from bacterial meningitis further declined.
The organisms that cause community-acquired bacterial meningitis differ somewhat by geographic region and by age. In a recent paper based on surveillance data, in the United States, from 1998 to 2007, the most common cause of bacterial meningitis among adults was Streptococcus pneumoniae. Among young adults, Neisseria meningitidis is nearly as common as S pneumoniae. The incidence of Listeria infections increases with age in adults.2
The epidemiologic features of bacterial meningitis have changed dramatically over the past decades with the advent of the Haemophilus influenzae vaccine. In 1986, about half the cases of acute bacterial meningitis were caused by H influenzae, but a decade later the incidence of H influenzae meningitis had been reduced by 94%.4
Meningitis is inflammation of the pia and arachnoid (the inner two layers of the meninges). Acute community-acquired meningitis can develop within hours to days and can be viral or bacterial. Viral meningitis usually has a good prognosis, whereas bacterial meningitis is associated with significant rates of morbidity and death, so it is critical to recognize and differentiate them promptly.
PATHOGENESIS
Most cases of community-acquired bacterial meningitis begin with colonization of the nasopharyngeal mucosa. In certain individuals this leads to mucosal invasion and bacteremia. Not all organisms that cause bacteremia are capable of breaching the blood-cerebrospinal fluid barrier to enter the subarachnoid space to cause meningitis. Very few organisms have this capacity, but N meningitidis and S pneumoniae do.5
Some patients are at higher risk of meningitis because of an abnormal communication between the nasopharynx and the subarachnoid space due either to trauma or a congenital anatomic abnormality. The organisms in these instances can directly spread from the nasopharynx to the meninges. Patients without a spleen or with an immunoglobulin deficiency are also more prone to infections from encapsulated organisms such as pneumococci and meningococci. The opsonizing immunoglobulins coat the capsule, helping phagocytes in the spleen to remove them from the bloodstream. A patient presenting with multiple episodes of bacterial meningitis merits evaluation for these conditions.
In contrast, Listeria spp and, rarely, gramnegative bacteria enter the bloodstream through the gastrointestinal tract and then spread to the meninges.
Once in the subarachnoid space, bacteria elicit a profuse inflammatory response, which can be damaging.5 The inflammation in the subarachnoid space can extend along the Virchow-Robin spaces surrounding the blood vessels deep into the brain parenchyma. This perivascular inflammation can cause thrombosis in both the arterial and venous circulation.
Thus, the inflammation can lead to intracranial complications such as cerebral edema, hydrocephalus, and stroke. The complications of bacterial meningitis can be remembered by the acronym HACTIVE: hydrocephalus, abscess, cerebritis and cranial nerve lesions, thrombosis, infarct, ventriculitis and vasculopathy, and extra-axial collection.5,6
