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Acute Bacterial Meningitis


John E. Greenlee

, MD, University of Utah School of Medicine

Last full review/revision Dec 2020| Content last modified Dec 2020

Acute bacterial meningitis is rapidly progressive bacterial infection of the meninges and subarachnoid space. Findings typically include headache, fever, and nuchal rigidity. Diagnosis is by cerebrospinal fluid (CSF) analysis. Treatment is with antibiotics and corticosteroids given as soon as possible.

(See also Overview of Meningitis and Neonatal Bacterial Meningitis.)

Pathophysiology of Acute Bacterial Meningitis

Most commonly, bacteria reach the subarachnoid space and meninges via hematogenous spread. Bacteria may also reach the meninges from nearby infected structures or through a congenital or acquired defect in the skull or spine (see Route of entry).

Because white blood cells (WBCs), immunoglobulins, and complement are normally sparse or absent from cerebrospinal fluid (CSF), bacteria initially multiply without causing inflammation. Later, bacteria release endotoxins, teichoic acid, and other substances that trigger an inflammatory response with mediators such as WBCs and tumor necrosis factor (TNF). Typically in CSF, levels of protein increase, and because bacteria consume glucose and because less glucose is transported into the CSF, glucose levels decrease. Brain parenchyma is typically affected in acute bacterial meningitis.

Inflammation in the subarachnoid space is accompanied by cortical encephalitis and ventriculitis.

Complications of bacterial meningitis are common and may include

  • Hydrocephalus (in some patients)
  • Arterial or venous infarcts due to inflammation and thrombosis of arteries and veins in superficial and sometimes deep areas of brain
  • Abducens palsy due to inflammation of the 6th cranial nerve
  • Deafness due to inflammation of the 8th cranial nerve or structures in the middle ear
  • Subdural empyema
  • Increased intracranial pressure (ICP) due to cerebral edema
  • Brain abscess (if the infection penetrates into brain parenchyma)
  • Brain herniation (the most common cause of death during the acute stages)
  • Systemic complications (which are sometimes fatal), such as septic shock, disseminated intravascular coagulation (DIC), or hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Etiology of Acute Bacterial Meningitis

Likely causes of bacterial meningitis depend on

  • Patient age
  • Route of entry
  • Immune status of the patient


In neonates and young infants, the most common causes of bacterial meningitis are

  • Group B streptococci, particularly Streptococcus agalactiae
  • Escherichia (E.) coli and other gram-negative bacteria
  • Listeria monocytogenes

In older infants, children, and young adults, the most common causes of bacterial meningitis are

  • Neisseria meningitidis
  • Streptococcus pneumoniae

N. meningitidis meningitis occasionally causes death within hours. Sepsis caused by N. meningitidis sometimes results in coagulopathy and bilateral adrenal hemorrhagic infarction (Waterhouse-Friderichsen syndrome).

Haemophilus influenzae type B, previously the most common cause of meningitis in children < 6 years and overall, is now a rare cause in the US and Western Europe, where the H. influenzae vaccine is widely used. However, in areas where the vaccine is not widely used, H. influenzae is still a common cause, particularly in children aged 2 months to 6 years.

In middle-aged and in older adults, the most common cause of bacterial meningitis is

  • S. pneumoniae

Less commonly, N. meningitidis causes meningitis in middle-aged and older adults. As host defenses decline with age, patients may develop meningitis due to L. monocytogenes or gram-negative bacteria.

In people of all ages, Staphylococcus aureus occasionally causes meningitis.

Causes of Bacterial Meningitis by Patient Age

Age Group


Neonates and young infants

Group B streptococci, particularly Streptococcus agalactiae

Escherichia (E.) coli

Listeria monocytogenes

Older infants, children, and young adults

Neisseria meningitidis

Streptococcus pneumoniae

Staphylococcus aureus*

Haemophilus influenzae (rare in developed countries but still seen in countries where the H. influenzae type B vaccine is not widely used)

Middle-aged adults

S. pneumoniae

S. aureus*

N. meningitidis (less common in this age group)

Older adults

S. pneumoniae

S. aureus*

L. monocytogenes

Gram-negative bacteria

* S. aureus occasionally causes severe meningitis in patients of all ages. It is the most common cause of meningitis that develops after a penetrating head wound.

Route of entry

Routes of entry include the following:

  • By hematogenous spread (the most common route)
  • From infected structures in or around the head (eg, sinuses, middle ear, mastoid process), sometimes associated with a CSF leak
  • Through a penetrating head wound
  • After a neurosurgical procedure (eg, if a ventricular shunt becomes infected)
  • Through congenital or acquired defects in the skull or spine

Having any of the above conditions increases the risk of acquiring meningitis.

Causes of Bacterial Meningitis by Route



Infection in or around the head (eg, sinusitis, otitis, mastoiditis), sometimes with a leak of cerebrospinal fluid

Streptococcus pneumoniae

Haemophilus influenzae

Anaerobic and microaerophilic streptococci

Bacteroides species

Staphylococcus aureus

Penetrating head wound

S. aureus

Damaged skin (eg, skin infections, abscesses, pressure ulcers, large burns)

S. aureus

An infected shunt

S. epidermidis

A neurosurgical procedure

Gram-negative bacteria (eg, Klebsiella pneumoniae, Acinetobacter calcoaceticus, Escherichia coli)

Immune status

Overall, the most common causes of bacterial meningitis in immunocompromised patients are

  • S. pneumoniae
  • L. monocytogenes
  • Pseudomonas aeruginosa
  • Mycobacterium tuberculosis
  • N. meningitidis
  • Gram-negative bacteria

But the most likely bacteria depend on the type of immune deficiency:

  • Defects in cell-mediated immunity (eg, in AIDS, Hodgkin lymphoma, or drug-induced immunosuppression): L. monocytogenes or mycobacteria
  • Defects in humoral immunity or splenectomy: S. pneumoniae or, less frequently, N. meningitidis (both can cause fulminant meningitis)
  • Neutropenia: P. aeruginosa or gram-negative enteric bacteria

In very young infants (particularly premature infants) and older adults, T-cell immunity may be weak; thus, these age groups are at risk of meningitis due to L. monocytogenes.

Symptoms and Signs of Acute Bacterial Meningitis

In most cases, bacterial meningitis begins with 3 to 5 days of insidiously progressive nonspecific symptoms including malaise, fever, irritability, and vomiting. However, meningitis may be more rapid in onset and can be fulminant, making bacterial meningitis one of the few disorders in which a previously healthy young person may go to sleep with mild symptoms and never awaken.

Typical symptoms and signs of meningitis include

  • Fever
  • Tachycardia
  • Headache
  • Photophobia
  • Changes in mental status (eg, lethargy, obtundation)
  • Nuchal rigidity (although not all patients report it)
  • Back pain (less intense than and overshadowed by headache)

However, fever, headache, and nuchal rigidity may be absent in neonates and infants (see Neonatal Bacterial Meningitis). So-called paradoxical irritability, in which cuddling and consoling by a parent irritates rather than comforts the neonate, suggests bacterial meningitis.

Seizures occur early in up to 40% of children with acute bacterial meningitis and may occur in adults. Up to 12% of patients present in coma.

Severe meningitis increases intracranial pressure (ICP) and typically causes papilledema, but papilledema may be absent early or be attenuated because of age-related or other factors.

Accompanying systemic infection by the organism may cause

  • Rashes, petechiae, or purpura (which suggest meningococcemia)
  • Pulmonary consolidation (often in meningitis due to S. pneumoniae)
  • Heart murmurs (which suggest endocarditis—eg, often caused by S. aureus or S. pneumoniae)

Atypical presentations in adults

Fever and nuchal rigidity may be absent or mild in immunocompromised or older patients and in alcoholics. Often, in older patients, the only sign is confusion in those who were previously alert or altered responsiveness in those who have dementia. In such patients, as in neonates, the threshold for doing lumbar puncture should be low. Brain imaging (MRI or, less optimally, CT) should be done if focal neurologic deficits are present or increased ICP is suspected.

If bacterial meningitis develops after a neurosurgical procedure, symptoms often take days to develop.

Diagnosis of Acute Bacterial Meningitis

  • Cerebrospinal fluid (CSF) analysis

As soon as acute bacterial meningitis is suspected, blood cultures and lumbar puncture for CSF analysis (unless contraindicated) are done. Blood should be analysed when lumbar puncture is done so that blood glucose levels can be compared with CSF glucose levels. Treatment should be started as follows:

  • If bacterial meningitis is suspected and the patient is very ill, antibiotics and corticosteroids are given immediately, even before lumbar puncture.
  • If bacterial meningitis is suspected and lumbar puncture will be delayed pending CT or MRI, antibiotics and corticosteroids should be started after blood cultures but before neuroimaging is done; the need for confirmation should not delay treatment.

Clinicians should suspect bacterial meningitis in patients with typical symptoms and signs, usually fever, changes in mental status, and nuchal rigidity. However, clinicians must be aware that symptoms and signs are different in neonates and infants and may be absent or initially mild in older patients, alcoholics, and immunocompromised patients. Diagnosis can be challenging in the following patients:

  • Those who have had a neurosurgical procedure because such procedures can also cause changes in mental status and neck stiffness
  • Older patients and alcoholics because changes in mental status may be due to metabolic encephalopathy (which may have multiple causes) or to falls and subdural hematomas

Focal seizures or focal neurologic deficits may indicate a focal lesion such as a brain abscess.

Because untreated bacterial meningitis is lethal, tests should be done if there is even a small chance of meningitis. Testing is particularly helpful in infants, older patients, alcoholics, immunocompromised patients, and patients who had neurosurgical procedure because symptoms may be atypical.

Pearls & Pitfalls

  • Do a lumbar puncture even if clinical findings are not specific for meningitis, particularly in infants, older patients, alcoholics, immunocompromised patients, and patients who have had neurosurgery.

If findings suggest acute bacterial meningitis, routine tests include

  • CSF analysis
  • Complete blood count and differential
  • Metabolic panel
  • Blood cultures plus polymerase chain reaction (PCR), if available

Lumbar puncture

Unless contraindicated, lumbar puncture is done immediately to obtain CSF for analysis, the mainstay of diagnosis.

Contraindications to immediate lumbar puncture are signs suggesting markedly increased ICP or an intracranial mass effect (eg, due to edema, hemorrhage, or tumor); typically, these signs include

  • Focal neurologic deficits
  • Papilledema
  • Deterioration in consciousness
  • Seizures (within 1 week of presentation)
  • Immunocompromise
  • History of central nervous system disease (eg, mass lesion, stroke, focal infection)

In such cases, lumbar puncture may cause brain herniation and thus is deferred until neuroimaging (typically CT or MRI) is done to check for increased ICP or a mass effect. When lumbar puncture is deferred, treatment is best begun immediately (after blood sampling for culture and before neuroimaging). After ICP, if increased, has been lowered or if no mass effect or obstructive hydrocephalus is detected, lumbar puncture can be done.

CSF should be sent for analysis: cell count, protein, glucose, Gram staining, culture, PCR, and other tests as indicated clinically. A new multiplex film-array PCR panel can provide rapid screening for multiple bacteria and viruses plus Cryptococcus neoformans in a CSF sample. This test, which is not always available, is used to supplement, not replace, culture and traditional tests. Simultaneously, a blood sample should be drawn and sent to have the CSF:blood glucose ratio determined. CSF cell count should be determined as soon as possible because white blood cells (WBCs) may adhere to the walls of the collecting tube, resulting in a falsely low cell count; in extremely purulent CSF, WBCs may lyse.

Typical CSF findings in bacterial meningitis include the following (see table CSF Findings in Meningitis):

  • Increased pressure
  • Fluid that is often turbid
  • A high WBC count (consisting predominantly of polymorphonuclear neutrophils)
  • Elevated protein
  • A low CSF:blood glucose ratio

A CSF:blood glucose level of < 50% suggests possible meningitis. A CSF glucose level of ≤ 18 mg/dL or a CSF:blood glucose ratio of < 0.23 strongly suggests bacterial meningitis. However, changes in CSF glucose may lag 30 to 120 minutes behind changes in blood glucose. In acute bacterial meningitis, an elevated protein level (usually 100 to 500 mg/dL) indicates blood-brain barrier injury.

CSF cell count and protein and glucose levels in patients with acute bacterial meningitis are not always typical. Atypical CSF findings may include

  • Normal in early stages except for the presence of bacteria
  • Predominance of lymphocytes in about 14% of patients, particularly in neonates with gram-negative meningitis, patients with meningitis due to L. monocytogenes, and some patients with partially treated bacterial meningitis
  • Normal glucose in about 9% of patients
  • Normal WBC counts in severely immunosuppressed patients

When initial CSF findings are equivocal, a repeat lumbar puncture 12 to 24 hours later can sometimes clarify which direction CSF changes are heading or whether there was a laboratory error.

CSF Findings in Meningitis


Predominant Cell Type*



Specific Tests

Normal CSF

All lymphocytes† (0–5 cells/mcL)

> 50% of blood glucose


Bacterial meningitis

Leukocytes (usually PMNs), often greatly increased


< 50% of blood glucose (may be extremely low)

Gram staining (yield is high if 105 colony-forming units of bacteria/mL are present)

Bacterial culture

PCR or multiplex PCR panel if available

Viral meningitis

Lymphocytes (may be mixed; PMNs and lymphocytes during the first 24–48 hours)


Usually normal

Multiplex PCR panel or conventional PCR (to check for enteroviruses or herpes simplex, herpes zoster, or West Nile virus)

IgM (to check for West Nile virus or other arboviruses)

Tuberculous meningitis‡

PMNs and lymphocytes (usually mixed pleocytosis)


< 50% of blood glucose (may be extremely low)

Acid-fast staining


Mycobacterial culture (ideally using a CSF sample of ≥ 30 mL)

Interferon-gamma tests of serum and (if available) CSF

Xpert MTB/RIF§

Fungal meningitis

Usually lymphocytes


< 50% of blood glucose (may be extremely low)

Cryptococcal antigen test

Multiplex PCR panel if available (an adjunctive test, not to replace other tests)

Serologic tests for Coccidioides immitis or Histoplasma species antigen, especially if patients have recently spent time in an endemic area

Fungal culture (ideally using a CSF sample of ≥ 30 mL)

India ink (for Cryptococcus sp)

* Changes in cell count, glucose, and protein may be minimal in severely immunocompromised patients.

† In tuberculous meningitis, CSF acid-fast staining can be insensitive, sensitivity of PCR is only about 50%, and culture requires up to 8 weeks. Positive CSF interferon-gamma tests indicate tuberculous meningitis, but serum interferon-gamma tests may only indicate prior infection. Thus, confirming a diagnosis of tuberculous meningitis is difficult, and if it is strongly suspected, even if not confirmed, it is treated presumptively.

‡ A small number of cells may be present normally in neonates or after a seizure.

§ Xpert MTB/RIF (an automated rapid nucleic acid amplification test) may be used to detect M. tuberculosis DNA in CSF.

CSF = cerebrospinal fluid; PCR = polymerase chain reaction; PMNs = polymorphonuclear neutrophils.

Identification of the causative bacteria in CSF involves Gram staining, culture, and, when available, PCR. Gram staining provides information rapidly, but the information is limited. For bacteria to be reliably detected with Gram stain, about 105 bacteria/mL must be present. Results may be falsely negative if any of the following occur:

  • CSF is handled carelessly.
  • Bacteria are not adequately resuspended after CSF has been allowed to settle.
  • Errors in decolorization or reading of the slide occur.

If clinicians suspect an anaerobic infection or other unusual bacteria, they should tell the laboratory before samples are plated for cultures. Prior antibiotic therapy can reduce the yield from Gram staining and culture. PCR, if available, and latex agglutination tests to detect bacterial antigens may be a useful adjunctive tests, especially in patients who have already received antibiotics.

Determination of antibiotic sensitivity requires bacterial culture.

Until the cause of meningitis is confirmed, other tests using samples of CSF or blood may be done to check for other causes of meningitis, such as viruses (particularly herpes simplex), fungi, and cancer cells.

Other tests

Samples from other sites suspected of being infected (eg, urinary or respiratory tract) should also be cultured.

Prognosis for Acute Bacterial Meningitis

With antibiotic treatment, the mortality rate for children < 19 years may be as low as 3% but is often higher; survivors may be deaf and neuropsychologically impaired. The mortality rate, even with antibiotic treatment, is about 17% for adults < 60 years but up to 37% in those > 60. Community-acquired meningitis due to S. aureus has a mortality rate of 43%.

In general, mortality rate correlates with depth of obtundation or coma. Factors associated with a poor prognosis include

  • Age > 60 years
  • Coexisting debilitating disorders
  • A low Glasgow coma score at admission (see tables Glasgow Coma Scale and Modified Glasgow Coma Scale)
  • Focal neurologic deficits
  • A low CSF cell count
  • Increased CSF pressure (particularly)

Seizures and a low CSF:serum glucose ratio may also indicate a poor prognosis.

Treatment of Acute Bacterial Meningitis

  • Antibiotics
  • Corticosteroids to decrease cerebral inflammation and edema

Antibiotics are the mainstay of therapy for acute bacterial meningitis. In addition to antibiotics, treatment includes measures to decrease brain and cranial nerve inflammation and increased intracranial pressure (ICP).

Most patients are admitted to an intensive care unit (ICU).


Antibiotics must be bactericidal for the causative bacteria and must be able to penetrate the blood-brain barrier.

If patients appear ill and findings suggest meningitis, antibiotics (see table Initial Antibiotics for Acute Bacterial Meningitis) and corticosteroids are started as soon as blood cultures are drawn and even before lumbar puncture. Also, if lumbar puncture is delayed pending neuroimaging results, antibiotic and corticosteroid treatment begins before neuroimaging.

Pearls & Pitfalls

  • If patients appear ill and acute meningitis is suspected, treat them with antibiotics and corticosteroids as soon as blood for cultures is drawn.

Appropriate empiric antibiotics depend on the patient's age and immune status and route of infection (see table Initial Antibiotics for Acute Bacterial Meningitis). In general, clinicians should use antibiotics that are effective against S. pneumoniae, N. meningitidis, and S. aureus. In pregnant women, neonates, older patients, and immunocompromised patients, Listeria meningitis is possible; it requires specific antibiotic treatment, usually ampicillin. Herpes simplex encephalitis can clinically mimic early bacterial meningitis; thus, acyclovir is added. Antibiotic therapy may need to be modified based on results of culture and sensitivity testing.

Commonly used antibiotics include

  • 3rd-generation cephalosporins for S. pneumoniae and N. meningitidis
  • Ampicillin for L. monocytogenes
  • Vancomycin for penicillin-resistant strains of S. pneumoniae and for S. aureus

Initial Antibiotics for Acute Bacterial Meningitis

Patient Group

Suspected Bacteria

Provisional Antibiotics


< 3 months

Streptococcus agalactiae

Escherichia coli or other gram-negative bacteria

Listeria monocytogenes

Staphylococcus aureus*



Ceftriaxone or cefotaxime

3 mo–18 years

Neisseria meningitidis

S. pneumoniae

S. aureus*

Haemophilus influenzae

Cefotaxime or ceftriaxone



18–50 years

S. pneumoniae

N. meningitidis

S. aureus*

Ceftriaxone or cefotaxime



> 50 years

S. pneumoniae

L. monocytogenes

S. aureus

Gram-negative bacteria

N. meningitidis (unusual in this age group)

Ceftriaxone or cefotaxime






Sinusitis, otitis, CSF leaks

S. pneumoniae

H. influenzae

Gram-negative bacteria including Pseudomonas aeruginosa

Anaerobic or microaerophilic streptococci

Bacteroides fragilis

S. aureus*



Ceftazidime or meropenem



Penetrating head wounds, neurosurgical procedures, shunt infections

S. aureus

S. epidermidis

Gram-negative bacteria including P. aeruginosa

S. pneumoniae




Immune status

AIDS, other conditions that impair cell-mediated immunity

S. pneumoniae

L. monocytogenes

Gram-negative bacteria including P. aeruginosa

S. aureus*






* S. aureus is an uncommon cause of meningitis except when the route is a penetrating head wound or a neurosurgical procedure. However, it can cause meningitis in all patient groups. Thus, vancomycin or other antistaphylococcal antibiotics should be given if clinicians think that these bacteria are a possible, even if unlikely, cause.

H. influenzae should be considered in children < 5 years with no record of H. influenzae type b conjugate vaccination.

S. pneumoniae is the most common causative bacteria in patients with a CSF leak or acute otitis. Such patients may be treated with vancomycin and ceftriaxone or cefotaxime. However, when meningitis is accompanied by subdural empyema or develops after a neurosurgical procedure, other bacteria, such as P. aeruginosa or Bacteroides, may also be present; in such cases, initial treatment should include vancomycin plus ceftazidime plus metronidazole. Subdural empyemas should be promptly drained.

CSF = cerebrospinal fluid.

Specific Antibiotics for Acute Bacterial Meningitis


Age Group



Gram-positive bacteria (unidentified)

Children and adults



Ceftriaxone (cefotaxime) and ampicillin†

Gram-negative bacilli (unidentified)

Children and adults

Cefotaxime (or ceftriaxone, meropenem, or ceftazidime)


Gentamicin, tobramycin, or amikacin‡ if systemic infection is suspected

Haemophilus influenzae type b

Children and adults

Ceftriaxone (cefotaxime)

Neisseria meningitidis

Children and adults

Ceftriaxone (cefotaxime)

Penicillin G is used for susceptible strains after sensitivities are known.

Streptococcus pneumoniae

Children and adults

Vancomycin and ceftriaxone (cefotaxime)

Penicillin G may be used for susceptible strains after sensitivities are known. Vancomycin covers strains that are highly resistant to penicillin and that ceftriaxone and cefotaxime may not cover. These strains can account for up to 50% of community-acquired infections.

Staphylococcus aureus and S. epidermidis

Children and adults

Vancomycin with or without rifampin

Vancomycin is used for methicillin-resistant strains, or nafcillin or oxacillin may be used after sensitivities are known.

Rifampin is added if no improvement occurs with vancomycin or nafcillin.

Listeria species

Children and adults

Ampicillin (penicillin G)



Penicillin G is used for susceptible strains after sensitivities are known.

Trimethoprim/sulfamethoxazole is used in patients who are allergic to penicillin.

Enteric gram-negative bacteria (eg, Escherichia coli, Klebsiella species, Proteus species)

Children and adults

Ceftriaxone (cefotaxime)


Gentamicin, tobramycin, or amikacin‡ if systemic infection is suspected

Pseudomonas species

Children and adults

Meropenem (ceftazidime or cefepime), usually alone but sometimes with an aminoglycoside



* Alternative antibiotics are in parentheses.

† If gram-positive bacteria are pleomorphic, ampicillin is included to cover Listeria species.

‡ Amikacin is used in areas where gentamicin resistance is common. Because aminoglycosides have poor cerebrospinal fluid penetration, they are infrequently used for treatment of meningitis. When required, they may have to be given intrathecally or via an Ommaya reservoir, especially in patients with Pseudomonas meningitis. When aminoglycosides are used, renal function should be monitored.

Common IV Antibiotic Dosages for Acute Bacterial Meningitis*



Children > 1 month



50 mg/kg every 12 hours

2 g every 12 hours


50 mg/kg every 6 hours

2 g every 4–6 hours


50 mg/kg every 8 hours

2 g every 8 hours


2 g every 12 hours

2 g every 8–12 hours


75 mg/kg every 6 hours

2–3 g every 4 hours

Penicillin G

4 million units every 4 hours

4 million units every 4 hours

Nafcillin and oxacillin

50 mg/kg every 6 hours

2 g every 4 hours


15 mg/kg every 6 hours

10–15 mg/kg every 8 hours


40 mg/kg every 8 hours

2 g every 8 hours

Gentamicin and tobramycin†

2.5 mg/kg every 8 hours

2 mg/kg every 8 hours


10 mg/kg every 8 hours

7.5 mg/kg every 12 hours


6.7 mg/kg every 8 hours

600 mg every 24 hours

* For neonatal dosages, see table Recommended Dosages of Selected Parenteral Antibiotics for Neonates.

† Renal function should be monitored.


Dexamethasone is used to decrease cerebral and cranial nerve inflammation and edema; it should be given when therapy is started. Adults are given 10 mg IV; children are given 0.15 mg/kg IV. Dexamethasone is given immediately before or with the initial dose of antibiotics and every 6 hours for 4 days.

Use of dexamethasone is best-established for patients with pneumococcal meningitis.

Other measures

The effectiveness of other measures is less well-proved.

Patients presenting with papilledema or signs of impending brain herniation are treated for increased ICP:

  • Elevation of the head of the bed to 30˚
  • Hyperventilation to a PCO2 of 27 to 30 mm Hg to cause intracranial vasoconstriction
  • Osmotic diuresis with IV mannitol

Usually, adults are given mannitol 1 g/kg IV bolus over 30 minutes, repeated as needed every 3 to 4 hours or 0.25 g/kg every 2 to 3 hours, and children are given 0.5 to 2.0 g/kg over 30 minutes, repeated as needed.

Additional measures can include

  • IV fluids
  • Antiseizure drugs
  • Treatment of concomitant infections
  • Treatment of specific complications (eg, corticosteroids for Waterhouse-Friderichsen syndrome, surgical drainage for subdural empyema)

Prevention of Acute Bacterial Meningitis

Use of vaccines for H. influenzae type B and, to a lesser extent, for N. meningitidis and S. pneumoniae has reduced the incidence of bacterial meningitis.

Physical measures

Keeping patients in respiratory isolation (using droplet precautions) for the first 24 hours of therapy can help prevent meningitis from spreading. Gloves, masks, and gowns are used.


Vaccination can prevent certain types of bacterial meningitis.

A conjugated pneumococcal vaccine effective against 13 serotypes, including > 80% of organisms that cause meningitis, is recommended for all children (see table Recommended Immunization Schedule for Ages 0–6 Years).

Routine vaccination against H. influenzae type b is highly effective and begins at age 2 months.

A quadrivalent meningococcal vaccine is given to

  • Children who are 2 to 10 years if they have an immunodeficiency or functional asplenia
  • All children at age 11 to 12 years with a booster dose at age 16
  • Older children, college students living in dormitories, and military recruits who have not had the vaccine previously
  • Travelers to or residents of endemic areas
  • Laboratory personnel who routinely handle meningococcal specimens

During a meningitis epidemic, the population at risk (eg, college students, a small town) must be identified, and its size must be determined before proceeding to mass vaccination. The effort is expensive and requires public education and support, but it saves lives and reduces morbidity.

The meningococcal vaccine does not protect against serotype B meningococcal meningitis; this information should kept in mind when a vaccinated patient presents with symptoms of meningitis.


Anyone who has prolonged face-to-face contact with a patient who has meningitis (eg, household or day care contacts, medical personnel and other people who are exposed to the patient's oral secretions) should be given postexposure chemoprophylaxis.

For meningococcal meningitis, chemoprophylaxis consists of one of the following:

  • Rifampin 600 mg (for children > 1 month, 10 mg/kg; for children < 1 month, 5 mg/kg) orally every 12 hours for 4 doses
  • Ceftriaxone 250 mg (for children < 15 years, 125 mg) IM for 1 dose
  • For adults, a fluoroquinolone (ciprofloxacin or levofloxacin 500 mg or ofloxacin 400 mg) orally for 1 dose

For meningitis due to H. influenzae type b, chemoprophylaxis is rifampin 20 mg/kg orally once a day (maximum: 600 mg/day) for 4 days. There is no consensus on whether children < 2 years require prophylaxis for exposure at day care.

Chemoprophylaxis is not usually needed for contacts of patients with other types of bacterial meningitis.

Key Points

  • Common causes of acute bacterial meningitis include N. meningitidis and S. pneumoniae in children and adults and Listeria species in infants and older adults; S. aureus occasionally causes meningitis in people of all ages.
  • Typical features may be absent or subtle in infants, alcoholics, older patients, immunocompromised patients, and patients who develop meningitis after a neurosurgical procedure.
  • If patients have focal neurologic deficits, obtundation, seizures, or papilledema (suggesting increased ICP or an intracranial mass effect), defer lumbar puncture pending results of neuroimaging.
  • Treat acute bacterial meningitis as soon as possible, even before the diagnosis is confirmed.
  • Common empirically chosen antibiotic regimens often include 3rd-generation cephalosporins (for S. pneumoniae and N. meningitidis), ampicillin (for L. monocytogenes), and vancomycin (for penicillin-resistant strains of S. pneumoniae and for S. aureus).
  • Routine vaccination for H. influenza, S. pneumoniae, and N. meningitidis and chemoprophylaxis against N. meningitidis help prevent meningitis.

More Information

The following are some English-language resources that may be useful. Please note that THE MANUAL is not responsible for the content of these resources.

  • Practice Guidelines for the Management of Bacterial Meningitis: This article reviews the recommendations for the diagnosis and management of bacterial meningitis, including the initial approach, indications for CT before lumbar puncture, tests to distinguish viral from bacterial meningitis, specific tests to identify the causative bacteria, timing of antimicrobial drugs for suspected meningitis, specific drugs to be used to treat suspected or confirmed bacterial meningitis, and the role of dexamethasone.
  • 2017 Infectious Diseases Society of America’s Clinical Practice Guidelines for Healthcare-Associated Ventriculitis and Meningitis: This article reviews the literature, evaluates the evidence, and presents recommendations. It specifically discusses the approach to infections associated with cerebrospinal fluid shunts, cerebrospinal fluid drains, intrathecal drugs (eg, baclofen), deep brain stimulation hardware, neurosurgery, and head trauma.

Drugs Mentioned In This Article

Drug Name Select Trade
ciprofloxacin CILOXAN, CIPRO
Metronidazole FLAGYL
Dexamethasone OZURDEX
Trimethoprim No US brand name
Ceftriaxone ROCEPHIN
tobramycin TOBI, TOBREX
Gentamicin GENOPTIC
cefotaxime CLAFORAN
Vancomycin VANCOCIN
Aztreonam AZACTAM
meropenem MERREM
ofloxacin FLOXIN OTIC
acyclovir ZOVIRAX
cefepime MAXIPIME
baclofen LIORESAL

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