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 by inflammatory responses in acute bacterial meningitis.
Inflammation in the subarachnoid space may be 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 compression or inflammation of the 6th cranial nerve
Deafness due to inflammation of the 8th cranial nerve or structures in the middle ear
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
Age
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 United States 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 | Bacteria |
|---|---|
Neonates and young infants | Group B streptococci, particularly Streptococcus agalactiae Escherichia (E.) coli Listeria monocytogenes, Staphylococcus aureus |
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
Route | Bacteria |
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 severe HIV infection, 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 preterm 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. If meningitis becomes severe in neonates and infants, skull fontanelles may bulge because of increased intracranial pressure.
Seizures occur early in up to 40% of children with acute bacterial meningitis and may occur in adults. Up to 14% of adult patients present in coma (1).
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 patients with alcohol use disorder. 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.
Symptoms and signs reference
1. van de Beek D, de Gans J, Spanjaard L, et al. Clinical features and prognostic factors in adults with bacterial meningitis. N Engl J Med..351(18):1849-1859, 2004. doi: 10.1056/NEJMoa040845. Erratum in: N Engl J Med352(9):950, 2005
Diagnosis of Acute Bacterial Meningitis
Cerebrospinal fluid (CSF) analysis
Bacterial meningitis is a medical emergency; administration of antibiotics should occur within 30 minutes of presentation.
Blood cultures and lumbar puncture for CSF analysis (unless contraindicated) may be done after initiating antimicrobial therapy because a lumbar puncture within 4 hours of treatment is still likely to yield positive cultures of the etiologic agent. Ideally, blood should be sampled at the time of lumbar puncture so that blood glucose levels can be compared with CSF glucose levels. Treatment should be started as follows:
If bacterial meningitis is suspected, 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, in patients with alcohol use disorder, and in 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 patients with alcohol use disorder 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, patients with alcohol use disorder, immunocompromised patients, and patients who had neurosurgical procedure because symptoms may be atypical.
Pearls & Pitfalls
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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 (see also How To Do Lumbar Puncture) is done immediately to obtain CSF for analysis, the mainstay of diagnosis.
Contraindications to immediate lumbar puncture are signs suggesting markedly increased intracranial pressure (ICP) or an intracranial mass effect (eg, due to edema, hemorrhage, or tumor). Thus, lumbar puncture should be considered high risk with any of the following:
Papilledema
Focal neurologic deficits
Focal seizures
A known central nervous system mass lesion
Large stroke
Suspected central nervous system 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. Because Treponema pallidum requires long-term in vitro culture methods, a CSF VDRL (venereal disease research laboratory) test should be performed (1). A 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 Cerebrospinal Fluid 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 glucose level of ≤ 18 mg/dL or a CSF:blood glucose ratio of < 0.23 strongly suggests bacterial meningitis. 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 (2):
Normal findings 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 the direction in which CSF changes are heading or whether there was a laboratory error.
Cerebrospinal Fluid Findings in Meningitis
Condition | Predominant Cell Type* | Protein* | Glucose* | Specific Tests |
|---|---|---|---|---|
Normal CSF | All lymphocytes† (0–5 cells/mcL) | < 40 mg/dL | > 50% of blood glucose | None |
Bacterial meningitis | Leukocytes (usually PMNs), often greatly increased | Elevated | < 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 Multiplex PCR panel if available |
Viral meningitis | Lymphocytes (may be mixed; PMNs and lymphocytes during the first 24–48 hours) | Elevated | Usually normal | Multiplex PCR panel (if available) and/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) | Elevated | < 50% of blood glucose (may be extremely low) | Acid-fast staining PCR 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 | Elevated | < 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. Blood glucose should be measured when lumbar puncture is done so that the CSF:serum glucose ratio can be determined. | ||||
† A small number of cells may be present normally in neonates or after a seizure. | ||||
‡ 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. § 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 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.
Diagnosis references
1. Edmondson DG, Hu B, Norris SJ. Long-Term In Vitro Culture of the Syphilis Spirochete Treponema pallidum subsp. pallidum. mBio. 2018;9(3):e01153-18. Published 2018 Jun 26. doi:10.1128/mBio.01153-18
2. de Almeida SM, Furlan SMP, Cretella AMM, et al. Comparison of Cerebrospinal Fluid Biomarkers for Differential Diagnosis of Acute Bacterial and Viral Meningitis with Atypical Cerebrospinal Fluid Characteristics. Med Princ Pract. 2020;29(3):244-254. doi:10.1159/000501925
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
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
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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
Third-generation cephalosporins for S. pneumoniae and N. meningitidis
Ampicillin for L. monocytogenes
Vancomycin for penicillin-resistant strains of S. pneumoniae and for S. aureus
For patients who develop meningitis or another infection after a neurosurgical procedure (including shunt implantation), the recommended empiric therapy is vancomycin plus an antipseudomonal beta-lactam (such as cefepime, ceftazidime, or meropenem); the choice of empiric beta-lactam agent should be based on local in vitro susceptibility patterns (1).
Initial Antibiotics for Acute Bacterial Meningitis
Patient Group | Suspected Bacteria | Provisional Antibiotics |
|---|---|---|
Age | ||
< 3 months | Streptococcus agalactiae Escherichia coli or other gram-negative bacteria Listeria monocytogenes Staphylococcus aureus* | Ampicillin plus Ceftriaxone or cefotaxime |
3 months–18 years | Neisseria meningitidis S. pneumoniae S. aureus* Haemophilus influenzae† | Cefotaxime or ceftriaxone plus Vancomycin |
18–50 years | S. pneumoniae N. meningitidis S. aureus* | Ceftriaxone or cefotaxime plus Vancomycin |
> 50 years | S. pneumoniae L. monocytogenes S. aureus Gram-negative bacteria N. meningitidis (unusual in this age group) | Ceftriaxone or cefotaxime plus Ampicillin plus Vancomycin |
Route | ||
Sinusitis, otitis, CSF leaks | S. pneumoniae‡ H. influenzae Gram-negative bacteria including Pseudomonas aeruginosa Anaerobic or microaerophilic streptococci Bacteroides fragilis S. aureus* | Vancomycin plus Ceftazidime or meropenem plus Metronidazole |
Penetrating head wounds, neurosurgical procedures, shunt infections | S. aureus S. epidermidis Gram-negative bacteria including P. aeruginosa S. pneumoniae | Vancomycin plus Ceftazidime |
Immune status | ||
AIDS, other conditions that impair cell-mediated immunity | S. pneumoniae L. monocytogenes Gram-negative bacteria including P. aeruginosa S. aureus* | Ampicillin plus Ceftazidime plus Vancomycin |
* 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
Bacteria | Age Group | Antibiotics* | Comments |
|---|---|---|---|
Gram-positive bacteria (unidentified) | Children and adults | Vancomycin plus Ceftriaxone (cefotaxime) and ampicillin† | — |
Gram-negative bacilli (unidentified) | Children and adults | Cefotaxime (or ceftriaxone, meropenem, or ceftazidime) plus 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 plus ceftriaxone or 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) or Trimethoprim/sulfamethoxazole | 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) plus 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 or Aztreonam | — |
* 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*
Antibiotic | Dosage | |
|---|---|---|
Children > 1 month | Adults | |
Ceftriaxone | 50 mg/kg every 12 hours | 2 g every 12 hours |
Cefotaxime | 50 mg/kg every 6 hours | 2 g every 4–6 hours |
Ceftazidime | 50 mg/kg every 8 hours | 2 g every 8 hours |
Cefepime | 2 g every 12 hours | 2 g every 8–12 hours |
Ampicillin | 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 |
Vancomycin† | 15 mg/kg every 6 hours | 10–15 mg/kg every 8 hours |
Meropenem | 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 |
Amikacin† | 10 mg/kg every 8 hours | 7.5 mg/kg every 12 hours |
Rifampin | 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. | ||
Corticosteroids
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 with the following:
Elevation of the head of the bed to 30˚
Hyperventilation to a PCO2 of 27 to 30 mm Hg for not more than 24 hours to cause intracranial vasoconstriction
Osmotic diuresis with IV mannitol
Hyperventilation is used until other measures become effective and is not used for more than 24 hours. When stopped, the PCO2 should be gradually increased to normal because a sudden increase may cause a significant increase in ICP.
Usually, adults are given intravenous mannitol to cause an osmotic diuresis and reduce brain swelling.
Additional measures can include
IV fluids
Antiseizure medications
Treatment of concomitant infections
Treatment of specific complications (eg, corticosteroids for Waterhouse-Friderichsen syndrome, surgical drainage for subdural empyema)
Treatment reference
1. Tunkel AR, Hasbun R, Bhimraj A, et al. 2017 Infectious Diseases Society of America's Clinical Practice Guidelines for Healthcare-Associated Ventriculitis and Meningitis. Clin Infect Dis. 2017;64(6):e34-e65. doi:10.1093/cid/ciw861
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 21% for adults (1). Community-acquired meningitis due to S. aureus has a mortality rate in the range 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 for Infants and Children)
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.
Prognosis reference
1. van de Beek D, de Gans J, Spanjaard L, et al: Clinical features and prognostic factors in adults with bacterial meningitis [published correction appears in N Engl J Med. 2005 Mar 3;352(9):950]. N Engl J Med. 2004;351(18):1849-1859. doi:10.1056/NEJMoa040845
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
Vaccination can prevent certain types of bacterial meningitis.
A conjugated pneumococcal vaccine effective against 20 serotypes, including > 80% of organisms that cause meningitis, is recommended for all children (see Centers for Disease Control and Prevention [CDC]: Child and Adolescent Immunization Schedule by Age).
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.
Chemoprophylaxis
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 1 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, patients with alcohol use disorder, 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 third-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 English-language resources 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: These guidelines provide 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 medications for suspected meningitis, specific medications 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 guideline 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 medications (eg, baclofen), deep brain stimulation hardware, neurosurgery, and head trauma.
