Meningitis, Bacterial

Article Author:
Tyler Runde
Article Editor:
John Hafner
12/4/2017 7:33:54 PM
PubMed Link:
Meningitis, Bacterial


Bacterial meningitis is a bacterial infection of the meninges, which is the protective covering for the brain and spinal cord resulting in inflammation. It is a serious and life-threatening condition that requires prompt diagnosis and treatment.


Bacterial meningitis is caused by a bacterial infection of the meninges, resulting in inflammation. The infection is either community-acquired or nosocomial. Community-acquired bacterial meningitis is the result of the invasion of the bacteria into the meninges from bacteremia or direct extension from local infection. The most common bacterial culprit varies by age. Streptococcus pneumoniae is common in adults older than age 60. Neisseria meningitidis is common in patients 17 to 59 years old. Listeria monocytogenes and gram-negative bacteria such as Escherichia coliKlebsiella, Enterobacter, Pseudomonas aeruginosa are other less common causes. Nosocomial infections are caused by S. pneumonia, Staphylococcus aureus, Staphylococcus albus, and gram-negative bacilli. Infectious meningitis may also be caused by viruses, fungi, and protozoa. Meningitis may also be non-infectious in etiology and can be caused by cancer, medications, or inflammatory conditions.


Bacterial meningitis was previously more common in pediatric patients. However, vaccinations have increased the median age of patients infected. In 2006 there were 72,000 meningitis-related hospitalizations in the United States. The majority of these cases were due to viral infection (54.6%). Bacterial infections accounted for 21.8% of cases, and 7.3% were due to fungi and parasite infections, while 17.2% were due to an unspecified cause. There was an 8% in-hospital mortality rate for patients with bacterial meningitis, and it rose substantially for patients older than 45. 

Several possible risk factors for bacterial meningitis have been identified. Patients with an abnormal communication between the nasopharynx and subarachnoid space are thought to be at increased risk. This abnormal communication can be due to a congenital abnormality or a result of trauma. Patients who have undergone neurosurgery, sustained skull fractures, or have cochlear implants are also at increased risk. Other at-risk patient populations are the immunosuppressed and people that live in close personal contact with others in places like college dorms or military barracks.


Bacteria require access to the meninges to cause meningitis. There are several mechanisms for entry. Bacteremia, or bacteria in the blood, can result in bacteria crossing the blood-brain barrier. This can only be accomplished by certain bacteria, most notably N. meningitidis and S. pneumoniae. Direct extension of otitis media or sinusitis to the central nervous system (CNS) may also occur. Dural defects, either congenital or acquired, allow bacteria to enter the CNS. Nosocomial bacterial meningitis is the result of manipulation of the meninges during neurosurgical procedures. Invasion of bacteria into the subarachnoid space results in inflammation of the meninges. This causes the patient to experience headaches and fevers. Blood-brain barrier breakdown occurs secondary to the infection and inflammatory response. This causes cerebral edema and increases the patient's intracranial pressure and decreases cerebral blood flow. Altered mental status, seizures, and focal neurologic deficits occur due to the decreased perfusion and increased intracranial pressure. 

History and Physical

Fever, neck stiffness, and altered mental status are the classic triad of symptoms for meningitis; however, all three are only present in 41% of cases of bacterial meningitis. The triad is most commonly seen in elderly patients. Seventy percent of patients will present with at least one of these symptoms. Common early symptoms of the disease include fever, headache, and confusion which can progress to obtundation, focal neuro deficits, and seizures. History should include questioning about any recent neurosurgical procedures, immunization status, and living arrangements. A physical exam may reveal nuchal rigidity or positive Kernig's or Brudzinski's signs. However, the absence of these does not reliably rule out the disease. Brudzinski's sign occurs when passive flexion of the neck causes involuntary flexion of the knee. Kernig's sign is resistance or pain with knee extension when the patient is supine, and their hip is flexed to 90 degrees. These signs are thought to be secondary to meningeal irritation. The fundoscopic exam may reveal papilledema due to increased intracranial pressure. A rapidly spreading petechial rash, known as purpura fulminans, would suggest a Meningococcal infection.


Patients presumed to have bacterial meningitis should receive a lumbar puncture to obtain a cerebrospinal fluid (CSF) sample. The CSF should be sent for Gram stain, culture, complete cell count (CBC), and glucose and protein levels. Bacterial meningitis typically results in low glucose and high protein levels in the cerebrospinal fluid. A neutrophil predominance on cell count would be expected. The diagnosis would be confirmed with bacteria identified on gram stain or culture. A non-contrast CT scan of the head should be performed before lumbar puncture if the patient has a risk of herniation. Risk factors include papilledema on the exam, new onset seizures, focal neurologic deficits, or is immunocompromised. Consider delaying the lumbar puncture if the patient has unstable vital signs, coagulation abnormalities, or has had a recent seizure. Treat with antibiotics empirically if testing is going to be delayed. Blood cultures should be obtained as 53% of patients have concurrent bacteremia. Elevated C-reactive protein or procalcitonin levels would suggest a bacterial rather than viral etiology.

Treatment / Management

Timely administration of antibiotics is essential. Delays in the administration of 3 to 6 hours are associated with increased mortality. The identified bacteria determine antibiotic selection. Empiric treatment with ceftriaxone and vancomycin should strongly be considered if the diagnosis is going to be delayed. Patients who are immunocompromised or older than 50 should also receive ampicillin. Patients with bacterial meningitis due to head trauma or post-neurosurgical procedure need to be covered for methicillin-resistant Staphylococcus aureus and aerobic gram-negative organisms. They should receive vancomycin and ceftazidime or cefepime. Acyclovir can also be administered for HSV coverage. Antibiotics can then be narrowed once the culture and sensitivities have resulted. Dexamethasone may increase survival if given at the time of antibiotic administration for S. pneumoniae infections. It has not been shown to improve outcomes for meningitis caused by other bacteria. Patients suspected of having meningococcal meningitis should be placed in droplet precautions until they have received 24 hours of antibiotics. Close contacts should also be treated prophylactically. Ciprofloxacin, rifampin, or ceftriaxone may be used. Close contacts are defined as people within 3 feet of the patient for more than 8 hours during the seven days before and 24 hours after receiving antibiotics. People exposed to the patient's oral secretions during this time should also be treated.