Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Meningitis Workup

  • Author: Rodrigo Hasbun, MD, MPH; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Feb 16, 2016
 

Approach Considerations

The diagnostic challenges in patients with clinical findings of meningitis are as follows:

  • Early identification and treatment of patients with acute bacterial meningitis
  • Assessing whether a treatable central nervous system (CNS) infection is present in those with suspected subacute or chronic meningitis
  • Identifying the causative organism

Bacterial meningitis must be the first and foremost consideration in the differential diagnosis of patients with headache, neck stiffness, fever, and altered mental status. Acute bacterial meningitis is a medical emergency, and delays in instituting effective antimicrobial therapy result in increased morbidity and mortality.

In general, whenever the diagnosis of meningitis is strongly considered, a lumbar puncture should be promptly performed. Examination of the cerebrospinal fluid (CSF) is the cornerstone of the diagnosis. The diagnosis of bacterial meningitis is made by culture of the CSF sample. The opening pressure should be measured and the fluid sent for cell count (and differential count), chemistry (ie, CSF glucose and protein), and microbiology (ie, Gram stain and cultures).

A concern regarding LP is that the lowering of CSF pressure from withdrawal of CSF could precipitate herniation of the brain. Herniation can sometimes occur in acute bacterial meningitis and other CNS infections as the consequence of severe cerebral edema or acute hydrocephalus. Clinically, this is manifested by an altered state of consciousness, abnormalities in pupil reflexes, and decerebrate or decorticate posturing. The incidence of herniation after LP, even in patients with papilledema, is approximately 1%.

A screening computed tomography (CT) scan of the head may be performed before LP to determine the risk of herniation. A prospective study involving 301 adults with suspected meningitis found that the following baseline patient characteristics were associated with an abnormal finding on head CT[16] :

  • Age ≥60 years
  • Immunocompromise (ie, HIV infection/AIDS, immunosuppressive therapy, or transplantation)
  • A history of CNS disease
  • A history of seizure within 1 week before presentation
  • Any abnormality on neurologic examination

These factors have been included in the Infectious Diseases Society of America guidelines to decide who should undergo CT before LP.[17]

The decision to obtain a brain CT scan before LP should not delay the institution of antibiotic therapy; such delay can increase mortality. It should be also noted that herniation can occur in patients with bacterial meningitis who have a normal brain CT scan. The most reliable clinical signs that indicate the risk of herniation include deteriorating level of consciousness, brainstem signs, and a very recent seizure.

Other laboratory tests, which may include blood cultures, are needed to complement the CSF culture. These bacterial cultures are used for identification of the offending bacteria and occasionally its serogroup, as well as for determination of the organism’s susceptibility to antibiotics. Special studies, such as serology and nucleic acid amplification, may also be performed, depending on clinical suspicion of an offending organism.

As many as 50% of patients with pneumococcal meningitis also have evidence of pneumonia on initial chest radiography. This association occurs in fewer than 10% of patients with meningitis caused by H influenzae or N meningitidis and in approximately 20% of patients with meningitis caused by other organisms. (See Imaging in Bacterial Meningitis.)

Next

Blood Studies

In patients with bacterial meningitis, a complete blood count (CBC) with differential will demonstrate polymorphonuclear leukocytosis with a left shift. Useful elements of the metabolic panel include the following:

  • Serum electrolytes, to determine dehydration or syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
  • Serum glucose (which is compared with the CSF glucose)
  • Blood urea nitrogen (BUN) or creatinine and liver profile, to assess organ function and adjust antibiotic dosing

The serum glucose level may be low if glycogen stores are depleted, or they may be high in infected patients with diabetes.

A coagulation profile and platelet count are indicated in cases of chronic alcohol use, chronic liver disease, or suspected disseminated intravascular coagulation (DIC). Patients with coagulopathies may require platelets or fresh frozen plasma (FFP) before LP.

Previous
Next

Cultures and Bacterial Antigen Testing

Obtaining cultures before instituting antibiotics may be helpful if the diagnosis is uncertain. The utility of cultures is most evident when LP is delayed until head imaging can rule out the risk of brain herniation, in which cases antimicrobial therapy is rightfully initiated before CSF samples can be obtained. These cultures include the following:

  • Blood - 50% positive in meningitis caused by H influenzae, S pneumoniae, or N meningitidis
  • Nasopharynx
  • Respiratory secretions
  • Urine
  • Skin lesions

Latex agglutination or counterimmunoelectrophoresis (CIE) of blood, urine, and CSF for specific bacterial antigens is occasionally recommended if diagnosis is challenging or in patients with partially treated meningitis. The Binax NOW S pneumoniae antigen test, if done on CSF, has a 99%-100% sensitivity and specificity and can even be positive despite prior antibiotic therapy.[18]

The use of nucleic acid amplification (eg, polymerase chain reaction [PCR] testing) has revolutionized the diagnosis of herpes simplex virus (HSV) meningitis. The availability of this technique has confirmed HSV as the cause of the recurrent Mollaret meningitis. This technique has also been applied to the diagnosis of enteroviral infections and the other herpesvirus infections. The PCR assay for enteroviruses has been demonstrated to be substantially more sensitive than culture and is 94-100% specific.

Previous
Next

Syphilis Testing

Perform serologic tests to detect syphilis. Screening for syphilis is done with the nontreponemal tests: rapid plasma reagent (RPR) or Venereal Disease Research Laboratory (VDRL). Positive results are confirmed with one of the following specific treponemal tests:

  • Fluorescent treponemal antibody absorption (FTA-Abs)
  • T pallidum hemagglutination (TPHA)
  • Microhemagglutination– T pallidum (MHA-TP)
  • The newer immune-capture enzyme immunoassay (ICE Syphilis) recombinant antigen test

In patients with syphilis, initial results on nontreponemal tests can serve as a baseline for gauging the success of therapy. Titers decrease and usually revert to negative or undetectable levels following effective treatment.

Previous
Next

Serum Procalcitonin Testing

Increasing data suggest that serum procalcitonin (PCT) levels can be used as a guide to distinguish between bacterial and aseptic meningitis in children. Elevated serum PCT levels predict bacterial meningitis. The results of serum PCT testing, combined with other findings, could be helpful in making clinical decisions.[19]

In an analysis of retrospective, multicenter, hospital-based cohort studies, Dubos et al confirmed that measurement of the PCT level is the best biologic marker for differentiating bacterial meningitis from aseptic meningitis in children in the emergency department (ED). With a threshold of 0.5 ng/mL, the sensitivity and specificity of the PCT level in distinguishing between bacterial and aseptic meningitis were 99% and 83%, respectively.[19]

Previous
Next

Lumbar Puncture and CSF Analysis

Elevated opening pressure correlates with increased risk of morbidity and mortality in bacterial and fungal meningitis. In bacterial meningitis, elevated opening pressure (reference range, 80-200 mm H2 O) suggests increased intracranial pressure (ICP) from cerebral edema. In viral meningitis, the opening pressure is usually within the reference range. The CSF opening pressure may be elevated at times in cryptococcal meningitis, suggesting increased ICP, and it is usually elevated in tuberculous meningitis.

The CSF cell count varies according to the offending pathogen (see Tables 5 and 6 below). It is usually in the few hundreds (100-1000/µL) with a predominance of lymphocytes in patients with viral meningitis. Some cases of echovirus, mumps, and HSV meningitis may produce a neutrophilic picture early in the course of disease. (See Lumbar Puncture.)

Table 5. CSF Findings in Meningitis by Etiologic Agent (Open Table in a new window)

Agent Opening Pressure (mm H2 O) WBC count (cells/µL) Glucose (mg/dL) Protein (mg/dL) Microbiology
Bacterial meningitis 200-300 100-5000; >80% PMNs < 40 >100 Specific pathogen demonstrated in 60% of Gram stains and 80% of cultures
Viral meningitis 90-200 10-300; lymphocytes Normal, reduced in LCM and mumps Normal but may be slightly elevated Viral isolation, PCR assays
Tuberculous meningitis 180-300 100-500; lymphocytes Reduced, < 40 Elevated, >100 Acid-fast bacillus stain, culture, PCR
Cryptococcal meningitis 180-300 10-200; lymphocytes Reduced 50-200 India ink, cryptococcal antigen, culture
Aseptic meningitis 90-200 10-300; lymphocytes Normal Normal but may be slightly elevated Negative findings on workup
Normal values 80-200 0-5; lymphocytes 50-75 15-40 Negative findings on workup
LCM = lymphocytic choriomeningitis; PCR = polymerase chain reaction; PMN = polymorphonuclear leukocyte; WBC = white blood cell.

Table 6. Comparison of CSF Findings by Type of Organism (Open Table in a new window)

Normal Finding Bacterial Meningitis Viral Meningitis* Fungal Meningitis**
Pressure (mm H2 O)



50-150



Increased Normal or mildly increased Normal or mildly increased in tuberculous meningitis; may be increased in fungal; AIDS patients with cryptococcal meningitis have increased risk of blindness and death unless kept below 300 mm H2 O
Cell count (mononuclear cells/µL)



Preterm: 0-25



Term: 0-22



>6 months: 0-5



No cell count result can exclude bacterial meningitis; PMN count typically in 1000s but may be less dramatic or even normal (classically, in very early meningococcal meningitis and in extremely ill neonates); lymphocytosis with normal CSF chemistries seen in 15-25%, especially when cell counts < 1000 or with partial treatment; ~90% of patients with ventriculoperitoneal shunts who have CSF WBC count >100 are infected; CSF glucose is usually normal, and organisms are less pathogenic; cell count and chemistries normalize slowly (over days) with antibiotics Cell count usually < 500, nearly 100% mononuclear; up to 48 hours, significant PMN pleocytosis may be indistinguishable from early bacterial meningitis; this is particularly true with eastern equine encephalitis; presence of nontraumatic RBCs in 80% of HSV meningoencephalitis, though 10% have normal CSF results Hundreds of mononuclear cells
Microscopy



No organisms



Gram stain 80% sensitive; inadequate decolorization may mistake Haemophilus influenzae for gram-positive cocci; pretreatment with antibiotics may affect stain uptake, causing gram-positive organisms to appear gram-negative and decrease culture yield by average of 20% No organism India ink is 50% sensitive for fungi; cryptococcal antigen is 95% sensitive; AFB stain is 40% sensitive for tuberculosis (increase yield by staining supernatant from at least 5 mL CSF)
Glucose



Euglycemia: >50% serum



Hyperglycemia: >30% serum



Wait 4 hr after glucose load



Decreased Normal Sometimes decreased; aside from fulminant bacterial meningitis, lowest levels of CSF glucose are seen in tuberculous meningitis, primary amebic meningoencephalitis, and neurocysticercosis
Protein (mg/dL)



Preterm: 65-150



Term: 20-170



>6 months: 15-45



Usually >150, may be >1000 Mildly increased Increased; >1000 with relatively benign clinical presentation suggestive of fungal disease
AFB = acid-fast bacillus; CSF = cerebrospinal fluid; HSV = herpes simplex virus; RBC = red blood cell; PMN = polymorphonuclear leukocyte.



*Some bacteria (eg, Mycoplasma, Listeria, Leptospira spp, Borrelia burgdorferi [Lyme], and spirochetes) produce spinal fluid alterations that resemble the viral profile. An aseptic profile also is typical of partially treated bacterial infections (>33% of patients have received antimicrobial treatment, especially children) and the 2 most common causes of encephalitis—the potentially curable HSV and arboviruses.



**In contrast, tuberculous meningitis and parasites resemble the fungal profile more closely.



CFS sample handling

After drawing the CSF sample, do the following with the tubes:

  • Tube 1 – Send to the chemistry laboratory for glucose and protein
  • Tube 2 – Send to the hematology laboratory for a cell count with differential
  • Tube 3 – Send to the microbiology and immunology laboratory
  • Tube 4 – Hold for a repeat cell count with differential, if needed (or for other subsequent studies not initially ordered)

Microbiology and immunology studies for tube 3 include the following:

  • Gram stain
  • Bacterial culture
  • Acid-fast bacillus (AFB) stain and tuberculosis cultures
  • India ink stain
  • Cryptococcal antigen testing
  • Fungal cultures, counterimmunoelectrophoresis ( CIE), VDRL, and cryptococcal antigen, if indicated

Tumor necrosis factor alpha (TNF-α), interleukin (IL)-1, and other cytokines have received increasing attention as mediators of the inflammatory response during bacterial meningitis. Leist et al reported detecting TNF-α in the CSF of 3 of 3 patients with bacterial meningitis, but in 0 of 7 patients with viral meningitis. Lopez-Cortez et al demonstrated that a TNF-α level higher than 150 pg/mL and an IL-1β level higher than 90 pg/mL showed sensitivities of 74% and 90%, respectively, in discriminating viral from aseptic meningitis.

Mustafa et al demonstrated that IL-1β can be detected in the CSF of 95% of infants and children with bacterial meningitis and that levels higher than 500 pg/mL were correlated with an increased risk of neurologic sequelae.[20]

These findings, though requiring both confirmation and amplification, suggest that analysis of TNF and other cytokines, in particular IL-1β, may prove valuable in differentiating acute bacterial meningitis from viral meningitis and possibly in detecting patients at particular risk for an adverse outcome. Their role in guiding adjunctive therapy, such as corticosteroids and nonsteroidal treatment of blood-brain barrier injury, is also under investigation.

CSF characteristics of acute bacterial meningitis

Examination of the CSF in patients with acute bacterial meningitis reveals the characteristic neutrophilic pleocytosis (cell count usually ranging from hundreds to a few thousand, with >80% PMNs). In some (25-30%) cases of L monocytogenes meningitis, a lymphocytic predominance may occur. A low CSF white blood cell (WBC) count (< 20/µL) in the presence of a high bacterial load suggests a poor prognosis.

According to Seupaul, the following 3 findings on CSF analysis have clinically useful likelihood ratios for the diagnosis of bacterial meningitis in adults[21] :

  • CSF glucose−to−blood glucose ratio of 0.4 or lower
  • CSF WBC count of 500/µL or higher
  • CSF lactate level of 31.53 mg/dL or higher

CSF characteristics of viral meningitis

In viral meningitis, the opening pressure is 90-200 mm H2 O, and the WBC count is 10-300/µL. Although the glucose concentration is typically normal, it can be below normal in meningitis from lymphocytic choriomeningitis virus (LCM), herpes simplex virus (HSV), mumps virus, and poliovirus. The protein concentration tends to be slightly elevated, but it can be within the reference range.

CSF characteristics of fungal meningitis

The diagnosis of cryptococcal meningitis relies on the identification of the pathogen in the CSF. The CSF is characterized by a lymphocytic pleocytosis (10-200/µL), a reduced glucose level, and an elevated protein level. The CSF picture of other fungal meningitides is similar to that of cryptococcal meningitis, usually with lymphocytic pleocytosis. Eosinophilic pleocytosis has rarely been associated with C immitis meningitis.

The definitive diagnosis usually relies on the demonstration of the specific fungal agent (eg, H capsulatum, C immitis, B dermatitidis, or Candida species) from clinical specimens, including the CSF. This could be in the form of fungal culture isolation (eg, C albicans growth from CSF).

More commonly, fungal serology (eg, presence of histoplasma antigen in the CSF) is used in the diagnosis of many cases of fungal meningitis because isolating these organisms from culture has proved difficult. It should be noted, however, that the serology for B dermatitidis is not accurate and a negative serology finding does not rule out the diagnosis.

A test used to detect fungal infection in the blood was successfully used in the diagnosis of fungal meningitis in an outbreak caused by contaminated steroids.[22] This outbreak involved 13,534 US patients who underwent epidural steroid injection and were exposed to methylprednisolone acetate from lots contaminated with environmental fungi; hundreds of these individuals developed serious CNS complications. The test (Fungitell, Beacon Diagnostics Laboratories), which measures levels of b-D-glucan (a glycoprotein found in the fungal cell wall), was used in CSF samples from patients exposed to the contaminated steroids who had negative fungal culture and polymerase chain reaction results. All patients with fungal meningitis had detectable b-D-glucan in their CSF.[22]

CSF characteristics of eosinophilic/parasitic meningitis

Primary amebic meningoencephalitis (PAM) caused by N fowleri is characterized by a neutrophilic pleocytosis, low glucose levels, elevated protein levels, and red blood cells (RBCs). Mononuclear pleocytosis may be observed in patients with subacute or chronic forms of PAM. Demonstration of the trophozoites, with the characteristic ameboid movement, on wet preparations of the CSF has been used for diagnosis. Alternatively, the ameba may be demonstrated in biopsy specimens.

In the presence of exposure, profound peripheral blood eosinophilia, and characteristic eosinophilic pleocytosis, suspicion of meningitis caused by A cantonensis, G spinigerum, or B procyonis should be entertained. Demonstrating the larvae ante mortem is usually difficult, and diagnosis relies on clinical presentation and a compatible epidemiologic history. Serologic tests may aid in the diagnosis. G spinigerum meningitis may mimic cerebrovascular disease in that it may cause cerebral hemorrhage.

CSF characteristics of Lyme meningitis

In patients with Lyme meningitis, the CSF is characterized by low-grade lymphocytic pleocytosis, low glucose levels, and elevated protein levels. Oligoclonal bands reactive to B burgdorferi antigens may be present. Demonstration of the specific antibody to B burgdorferi aids in the diagnosis.

Comparison between the antibody response in the CSF and that in the serum is a helpful diagnostic test. A CSF-to-serum ratio greater than 1 suggests intrathecal antibody production and neuroborreliosis.

CSF characteristics of tuberculous meningitis

In patients with tuberculous meningitis, the CSF is characterized by a predominantly lymphocytic pleocytosis; an elevated protein level, especially if a CSF block is present; and a low glucose level (< 40 mg/dL). PCR testing can provide a rapid diagnosis, though false-negative results may occur in samples containing very few organisms (< 2 colony-forming units [cfu]/mL). (See Tuberculous Meningitis.)

CSF glucose and protein

In bacterial meningitis, the CSF glucose level (reference range, 40-70 mg/dL) is less than 40 mg/dL in 60% of patients. A simultaneous blood glucose determination should be obtained for the purposes of comparison. In patients with elevated blood glucose levels as a result of diabetes mellitus, the CSF-to-blood glucose ratio may not be predictive. The CSF glucose level is usually within the reference range in viral meningitis, but it may be low in some cases of LCM, HSV, mumps virus, or poliovirus infection.

The CSF protein level (reference range, 20-50 mg/dL) is usually elevated in bacterial meningitis. In viral meningitis, these levels are also usually elevated, though they can be within the reference range. In syphilitic meningitis, abnormal CSF protein levels (elevated) and CSF glucose levels (decreased) may be observed in 10-70% of cases.

CSF Gram stain and acid-fast bacillus stain

Gram staining of the CSF permits rapid identification of the bacterial cause in 60-90% of patients with bacterial meningitis. The presence of bacteria is 100% specific, but the sensitivity of this test for detection is variable. The likelihood of detection is higher in the presence of a higher bacterial concentration and diminishes with prior antibiotic use.

The demonstration of AFB (eg, with auramine-rhodamine stain, Ziehl-Neelsen stain, or Kinyoun stain) in the CSF is difficult and usually requires a large volume of CSF. Meningeal biopsy, with the demonstration of caseating granulomas and AFB on the smear, offers a higher yield than the CSF AFB smear.

CSF culture and antigen testing

CSF bacterial cultures yield the bacterial cause in 70-85% of cases. The yield diminishes by 20% in patients who have received antimicrobial therapy. In these cases, some experts advocate the use of a CSF bacterial antigen assay. This is a latex agglutination technique that can detect the antigens of H influenzae type B (Hib), S pneumoniae, N meningitidis, E coli K1, and S agalactiae (group B streptococcus [GBS]). Its theoretical advantage is the detection of the bacterial antigens even after microbial killing, as is observed after antibacterial therapy.

Another attractive alternative is using the Binax NOW for S pneumoniae in the CSF. This assay has a 99-100% sensitivity and specificity for ruling out the most common cause of bacterial meningitis.[18]

Others studies, however, have shown that the CSF bacterial antigen assay may not be better than the Gram stain. Although it is specific (a positive result indicates a diagnosis of bacterial meningitis), a negative finding on the bacterial antigen test does not rule out meningitis (50-95% sensitivity).

Cryptococcal meningitis

C neoformans may be cultured from the CSF in cryptococcal meningitis. Other methods of identification include India ink preparation and the detection of CSF cryptococcal antigen. India ink has a sensitivity of only 50%, but it is highly diagnostic if positive.

Because of the low sensitivity of the India ink preparation, many centers have adapted the use of CSF cryptococcal antigen determination, a test with a sensitivity exceeding 90%. However, the CSF cryptococcal antigen determination is not universally available.

In instances when the India ink results are negative but the degree of clinical suspicion for cryptococcal meningitis is high, the CSF specimen may be sent to reference laboratories that can perform CSF cryptococcal antigen determination to confirm the diagnosis. In addition, the titer of the antigen could serve to monitor the response to treatment. Blood cultures and serum cryptococcal antigen should be obtained to determine whether cryptococcal fungemia is present.

Syphilitic meningitis

In syphilitic meningitis, isolating T pallidum from the CSF is extremely difficult and time-consuming. The spirochete could be demonstrated by using dark-field or phase-contrast microscopy on specimens collected from skin lesions (eg, chancres and other syphilitic lesions).

The diagnosis is usually supported by the CSF VDRL test, which has a sensitivity of 30-70% (a negative result on the CSF VDRL test does not rule out syphilitic meningitis) and a high specificity (a positive test result suggests the disease). Care must always be taken not to contaminate the CSF with blood during spinal fluid collection (eg, traumatic tap).

Lyme meningitis

CSF culture for B burgdorferi has a low yield. The CSF Lyme PCR assay, if available, offers a rapid, sensitive, and specific method of diagnosis. This assay is gaining popularity as the method of choice for diagnosing Lyme meningitis.

Cohn et al validated a clinical prediction rule for differentiating Lyme meningitis from aseptic meningitis. Their “rule of 7s” classifies children at low risk for Lyme meningitis when all of the following 3 criteria are met[23] :

  • < 7 days of headache
  • < 70% CSF mononuclear cells
  • Absence of cranial nerve VII palsy or other cranial nerve palsy

Tuberculous meningitis

Culture for Mycobacterium usually takes several weeks and may delay definitive diagnosis. M tuberculosis detection assays involving nucleic acid amplification have become available and have the advantages of rapidity, high sensitivity, and high specificity. There remains a need for mycobacterial growth in cultures because this method offers the advantage of performing drug susceptibility assays.

Viral isolation from CSF

Isolation of viruses from the CSF has a sensitivity of 65-70% for enteroviruses. Alternatively, isolation of enteroviruses from throat and stool viral cultures may also indirectly implicate enterovirus as the cause of the meningitis. Culture of mumps virus from the CSF has a low sensitivity (30-50%). LCM virus may be cultured in blood early in the disease or in urine at a later stage.

Previous
Next

Neuroimaging

Computed tomography (CT) of the head and magnetic resonance imaging (MRI) of the brain generally do not aid in the diagnosis of meningitis. Some patients may show meningeal enhancement, but its absence does not rule out the condition. Routinely obtaining CT scans of the head may lead to unnecessary delay in the performance of diagnostic lumbar puncture and the initiation of antibiotic therapy; the latter may be detrimental to the outcome in these patients.

Cerebral herniation following the lumbar tap procedure is rare in individuals with no focal neurologic deficits and no evidence of increased ICP. If it occurs, it usually does so within 24 hours after the LP; thus, herniation should always be considered in the differential diagnosis if the patient’s neurologic status deteriorates during that time frame.

According to the Infectious Diseases Society of America guidelines, the following are indications for screening head CT before LP in adult patients[17] :

  • Immunocompromised state
  • History of CNS disease (eg, mass lesion, stroke, or focal infection)
  • Seizure within 1 week of presentation
  • Papilledema
  • Abnormal level of consciousness
  • Focal neurologic deficit (eg, dilated nonreactive pupil, gaze palsy, or arm or leg drift)

In patients with suspected bacterial meningitis, blood cultures should be obtained and treatment initiated before imaging studies and LP. Neuroimaging may yield normal results or demonstrate small ventricles, effacement of sulci, and contrast enhancement over convexities (see the images below). Late findings include venous infarction and communicating hydrocephalus. Brain abscess, sinus or mastoid infection, skull fracture, and congenital anomalies must be ruled out. (See Imaging in Bacterial Meningitis.)

Acute bacterial meningitis. This axial nonenhanced Acute bacterial meningitis. This axial nonenhanced computed tomography scan shows mild ventriculomegaly and sulcal effacement.
Acute bacterial meningitis. This axial T2-weighted Acute bacterial meningitis. This axial T2-weighted magnetic resonance image shows only mild ventriculomegaly.
Acute bacterial meningitis. This contrast-enhanced Acute bacterial meningitis. This contrast-enhanced, axial T1-weighted magnetic resonance image shows leptomeningeal enhancement (arrows).

Finally, neuroimaging studies are helpful in the detection of CNS complications of bacterial meningitis, such as the following (see the images below):

  • Hydrocephalus
  • Cerebral infarct
  • Brain abscess
  • Subdural empyema
  • Venous sinus thrombosis
    Chronic mastoiditis and epidural empyema in a pati Chronic mastoiditis and epidural empyema in a patient with bacterial meningitis. This axial computed tomography scan shows sclerosis of the temporal bone (chronic mastoiditis), an adjacent epidural empyema with marked dural enhancement (arrow), and the absence of left mastoid air.
    Subdural empyema and arterial infarct in a patient Subdural empyema and arterial infarct in a patient with bacterial meningitis. This contrast-enhanced axial computed tomography scan shows left-sided parenchymal hypoattenuation in the middle cerebral artery territory, with marked herniation and a prominent subdural empyema.
Previous
 
 
Contributor Information and Disclosures
Author

Rodrigo Hasbun, MD, MPH Associate Professor of Medicine, Section of Infectious Diseases, University of Texas Medical School at Houston

Disclosure: Received honoraria from Medicine''''''''s Company for speaking and teaching; Received honoraria from Cubicin for speaking and teaching; Received honoraria from Theravance for speaking and teaching; Received honoraria from Pfizer for speaking and teaching.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Suur Biliciler, MD Neuromuscular Fellow, Department of Neurology, Baylor College of Medicine

Disclosure: Nothing to disclose.

Timothy S Brannan, MD Director, Department of Neurology, Jersey City Medical Center; Professor, Department of Neurology, Seton Hall School of Graduate Medical Education

Disclosure: Nothing to disclose.

Robert Cavaliere, MD Assistant Professor of Neurology, Neurosurgery and Medicine, Ohio State University College of Medicine

Disclosure: Nothing to disclose.

Sidney E Croul, MD Director of Neuropathology, Professor, Department of Pathology and Laboratory Medicine, Medical College of Pennsylvania Hahnemann University

Disclosure: Nothing to disclose.

Francisco de Assis Aquino Gondim, MD, MSc, PhD Associate Professor of Neurology, Department of Neurology and Psychiatry, St Louis University School of Medicine

Francisco de Assis Aquino Gondim, MD, MSc, PhD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and Movement Disorders Society

Disclosure: Nothing to disclose.

Alan Greenberg, MD Director, Associate Professor, Department of Internal Medicine, Jersey City Medical Center, Seton Hall University

Alan Greenberg, MD is a member of the following medical societies: Alpha Omega Alpha and American College of Physicians

Disclosure: Nothing to disclose.

Ronald A Greenfield, MD Professor, Department of Internal Medicine, University of Oklahoma College of Medicine

Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist Honoraria Speaking and teaching; Forest Pharmaceuticals Speaking and teaching

J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Lutfi Incesu, MD Professor, Department of Radiology, Ondokuz Mayis University School of Medicine; Chief, Neuroradiology and MR Unit, Department of Radiology, Ondokuz Mayis University Hospital, Turkey

Lutfi Incesu, MD is a member of the following medical societies: American Society of Neuroradiology and Radiological Society of North America

Disclosure: Nothing to disclose.

Uma Iyer, MD Resident Physician, Department of Neurology, State University of New York Upstate Medical Center

Disclosure: Nothing to disclose.

Pieter R Kark, MD, MA, FAAN, FACP Instructor in Palliative Care, The Lifetime Healthcare Companies

Disclosure: Nothing to disclose.

Michael R Keating, MD Associate Professor of Medicine, Chair, Division of Infectious Diseases, Department of Medicine, Mayo Clinic College of Medicine

Michael R Keating, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, American Society of Transplantation, Infectious Diseases Society of America, and International Immunocompromised Host Society

Disclosure: Nothing to disclose.

Anil Khosla, MBBS, MD Assistant Professor, Department of Radiology, St Louis University School of Medicine, Veterans Affairs Medical Center of St Louis

Anil Khosla, MBBS, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Neuroradiology, North American Spine Society, and Radiological Society of North America

Disclosure: Nothing to disclose.

John W King, MD Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center

John W King, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Association of Subspecialty Professors, Infectious Diseases Society of America, and Sigma Xi

Disclosure: MERCK None Other

Marjorie Lazoff, MD Editor-in-Chief, Medical Computing Review

Marjorie Lazoff, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American Medical Informatics Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Glenn Lopate, MD Associate Professor, Department of Neurology, Division of Neuromuscular Diseases, Washington University School of Medicine; Director of Neurology Clinic, St Louis ConnectCare; Consulting Staff, Department of Neurology, Barnes-Jewish Hospital

Glenn Lopate, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and Phi Beta Kappa

Disclosure: Baxter Grant/research funds Other; Amgen Grant/research funds None

Joseph Richard Masci, MD Professor of Medicine, Professor of Preventive Medicine, Mount Sinai School of Medicine; Director of Medicine, Elmhurst Hospital Center

Joseph Richard Masci, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Association of Professors of Medicine, and Royal Society of Medicine

Disclosure: Nothing to disclose.

C Douglas Phillips, MD Director of Head and Neck Imaging, Division of Neuroradiology, New York Presbyterian Hospital, Weill Cornell Medical College

C Douglas Phillips, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Society of Head and Neck Radiology, American Society of Neuroradiology, Association of University Radiologists, and Radiological Society of North America

Disclosure: Nothing to disclose.

Tarakad S Ramachandran, MBBS, FRCP(C), FACP Professor of Neurology, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Chair, Department of Neurology, Crouse Irving Memorial Hospital

Tarakad S Ramachandran, MBBS, FRCP(C), FACP is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners, American College of International Physicians, American College of Managed Care Medicine, American College of Physicians, American Heart Association, American Stroke Association, Royal College of Physicians, RoyalCollegeofPhysicians and Surgeons of Canada, Royal College of Surgeons of England, and Royal Society of Medicine

Disclosure: Abbott Labs None None; Teva Marion None None; Boeringer-Ingelheim Honoraria Speaking and teaching

Raymund R Razonable, MD Consultant, Division of Infectious Diseases, Mayo Clinic of Rochester; Associate Professor of Medicine, Mayo Clinic College of Medicine

Raymund R Razonable, MD is a member of the following medical societies: American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and International Immunocompromised Host Society

Disclosure: Nothing to disclose.

Norman C Reynolds Jr, MD Neurologist, Veterans Affairs Medical Center of Milwaukee; Clinical Professor, Medical College of Wisconsin

Norman C Reynolds Jr, MD is a member of the following medical societies: American Academy of Neurology, Association of Military Surgeons of the US, Movement Disorders Society, Sigma Xi, and Society for Neuroscience

Disclosure: Nothing to disclose.

Robert Stanley Rust Jr, MD, MA Thomas E Worrell Jr Professor of Epileptology and Neurology, Co-Director of FE Dreifuss Child Neurology and Epilepsy Clinics, Director, Child Neurology, University of Virginia School of Medicine; Chair-Elect, Child Neurology Section, American Academy of Neurology

Robert Stanley Rust Jr, MD, MA is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Headache Society, American Neurological Association, Child Neurology Society, International Child Neurology Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Prem C Shukla, MD Associate Chairman, Associate Professor, Department of Emergency Medicine, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Manish K Singh, MD Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience

Manish K Singh, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American Association of Physicians of Indian Origin, American Headache Society, American Medical Association, and American Society of Regional Anesthesia and Pain Medicine

Disclosure: Nothing to disclose.

Niranjan N Singh, MD, DNB Assistant Professor of Neurology, University of Missouri-Columbia School of Medicine

Niranjan N Singh, MD, DNB is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Mark S Slabinski, MD, FACEP, FAAEM Vice President, EMP Medical Group

Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State Medical Association

Disclosure: Nothing to disclose.

James G Smirniotopoulos, MD Professor of Radiology, Neurology, and Biomedical Informatics, Program Director, Diagnostic Imaging Program, Center for Neuroscience and Regenerative Medicine (CNRM), Uniformed Services University of the Health Sciences

James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of University Radiologists, and Radiological Society of North America

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Florian P Thomas, MD, MA, PhD, Drmed Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, and National Multiple Sclerosis Society

Disclosure: Nothing to disclose.

Frederick M Vincent Sr, MD Clinical Professor, Department of Neurology and Ophthalmology, Michigan State University Colleges of Human and Osteopathic Medicine

Frederick M Vincent Sr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Legal Medicine, American College of Physicians, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Amir Vokshoor, MD Staff Neurosurgeon, Department of Neurosurgery, Spine Surgeon, Diagnostic and Interventional Spinal Care, St John's Health Center

Amir Vokshoor, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American Medical Association, and North American Spine Society

Disclosure: Nothing to disclose.

Cordia Wan, MD Adult Neurologist, Kaiser Permanente Hawaii, Kaiser Permanente Southern California

Cordia Wan, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Eric L Weiss, MD, DTM&H Medical Director, Office of Service Continuity and Disaster Planning, Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman, SUMC and LPCH Bioterrorism and Emergency Preparedness Task Force, Clinical Associate Progressor, Department of Surgery (Emergency Medicine), Stanford University Medical Center

Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Lawrence A Zumo, MD Neurologist, Private Practice

Lawrence A Zumo, MD is a member of the following medical societies: American Academy of Neurology, American College of Physicians, American Medical Association, and Southern Medical Association

Disclosure: Nothing to disclose.

References
  1. Mann K, Jackson MA. Meningitis. Pediatr Rev. 2008 Dec. 29(12):417-29; quiz 430. [Medline].

  2. Ginsberg L, Kidd D. Chronic and recurrent meningitis. Pract Neurol. 2008 Dec. 8(6):348-61. [Medline].

  3. Berkhout B. Infectious diseases of the nervous system: pathogenesis and worldwide impact. IDrugs. 2008 Nov. 11(11):791-5. [Medline].

  4. Koedel U, Klein M, Pfister HW. New understandings on the pathophysiology of bacterial meningitis. Curr Opin Infect Dis. 2010 Jun. 23(3):217-23. [Medline].

  5. Thigpen MC, Whitney CG, Messonnier NE, Zell ER, Lynfield R, Hadler JL, et al. Bacterial meningitis in the United States, 1998-2007. N Engl J Med. 2011 May 26. 364(21):2016-25. [Medline].

  6. Jaijakul S, Arias CA, Hossain M, Arduino RC, Wootton SH, Hasbun R. Toscana meningoencephalitis: a comparison to other viral central nervous system infections. J Clin Virol. 2012 Nov. 55(3):204-8. [Medline]. [Full Text].

  7. Thigpen, M, Rosenstein, NE, Whitney, CG. Bacterial meningitis in the United States--1998-2003. Presented at the 43rd Annual Meeting of the Infectious Diseases Society of America, San Francisco, CA. October 2005;65.

  8. West Nile Virus. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/ncidod/dvbid/westnile/index.htm. Accessed: March 29, 2013.

  9. La Crosse encephalitis. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/lac/. Accessed: March 29, 2013.

  10. Schut ES, Brouwer MC, Scarborough M, Mai NT, Thwaites GE, Farrar JJ, et al. Validation of a Dutch risk score predicting poor outcome in adults with bacterial meningitis in Vietnam and Malawi. PLoS One. 2012. 7(3):e34311. [Medline]. [Full Text].

  11. Worsøe L, Cayé-Thomasen P, Brandt CT, Thomsen J, Østergaard C. Factors associated with the occurrence of hearing loss after pneumococcal meningitis. Clin Infect Dis. 2010 Oct 15. 51(8):917-24. [Medline].

  12. van de Beek D, de Gans J, Spanjaard L, Weisfelt M, Reitsma JB, Vermeulen M. Clinical features and prognostic factors in adults with bacterial meningitis. N Engl J Med. 2004 Oct 28. 351(18):1849-59. [Medline].

  13. Thomas KE, Hasbun R, Jekel J, Quagliarello VJ. The diagnostic accuracy of Kernig's sign, Brudzinski's sign, and nuchal rigidity in adults with suspected meningitis. Clin Infect Dis. 2002 Jul 1. 35(1):46-52. [Medline].

  14. Moses S. Meningitis: acute bacterial meningitis. Accessed February 8, 2011. Available at http://www.fpnotebook.com/neuro/ID/Mngts.htm.

  15. Ramirez-Avila L, Slome S, Schuster FL, Gavali S, Schantz PM, Sejvar J, et al. Eosinophilic meningitis due to Angiostrongylus and Gnathostoma species. Clin Infect Dis. 2009 Feb 1. 48(3):322-7. [Medline].

  16. Hasbun R, Abrahams J, Jekel J, Quagliarello VJ. Computed tomography of the head before lumbar puncture in adults with suspected meningitis. N Engl J Med. 2001 Dec 13. 345(24):1727-33. [Medline].

  17. [Guideline] Tunkel AR, Hartman BJ, Kaplan SL, Kaufman BA, Roos KL, Scheld WM, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis. 2004 Nov 1. 39(9):1267-84. [Medline].

  18. Moïsi JC, Saha SK, Falade AG, Njanpop-Lafourcade BM, Oundo J, Zaidi AK, et al. Enhanced diagnosis of pneumococcal meningitis with use of the Binax NOW immunochromatographic test of Streptococcus pneumoniae antigen: a multisite study. Clin Infect Dis. 2009 Mar 1. 48 Suppl 2:S49-56. [Medline]. [Full Text].

  19. Dubos F, Korczowski B, Aygun DA, Martinot A, Prat C, Galetto-Lacour A, et al. Serum procalcitonin level and other biological markers to distinguish between bacterial and aseptic meningitis in children: a European multicenter case cohort study. Arch Pediatr Adolesc Med. 2008 Dec. 162(12):1157-63. [Medline].

  20. Mustafa MM, Lebel MH, Ramilo O, Olsen KD, Reisch JS, Beutler B, et al. Correlation of interleukin-1 beta and cachectin concentrations in cerebrospinal fluid and outcome from bacterial meningitis. J Pediatr. 1989 Aug. 115(2):208-13. [Medline].

  21. Seupaul RA. Evidence-based emergency medicine/rational clinical examination abstract. How do I perform a lumbar puncture and analyze the results to diagnose bacterial meningitis?. Ann Emerg Med. 2007 Jul. 50(1):85-7. [Medline].

  22. Hughes S. Blood assay used for CSF detection in fungal meningitis. Medscape Medical News. Available at http://at http://www.medscape.com/viewarticle/781179. Accessed: April 3, 2013.

  23. Cohn KA, Thompson AD, Shah SS, Hines EM, Lyons TW, Welsh EJ, et al. Validation of a clinical prediction rule to distinguish Lyme meningitis from aseptic meningitis. Pediatrics. 2012 Jan. 129(1):e46-53. [Medline].

  24. Gilbert DN, Moellering RC Jr, Sande MA. Antimicrobial Therapy. In: Sanford Guide to Antimicrobial Therapy. 33rd ed. March 15, 2003.

  25. van de Beek D, Brouwer MC, Thwaites GE, Tunkel AR. Advances in treatment of bacterial meningitis. Lancet. 2012 Nov 10. 380(9854):1693-702. [Medline].

  26. Mera RM, Miller LA, Amrine-Madsen H, Sahm DF. Impact of new Clinical Laboratory Standards Institute Streptococcus pneumoniae penicillin susceptibility testing breakpoints on reported resistance changes over time. Microb Drug Resist. 2011 Mar. 17(1):47-52. [Medline].

  27. Gouveia EL, Reis JN, Flannery B, Cordeiro SM, Lima JB, Pinheiro RM, et al. Clinical outcome of pneumococcal meningitis during the emergence of pencillin-resistant Streptococcus pneumoniae: an observational study. BMC Infect Dis. 2011 Nov 21. 11:323. [Medline]. [Full Text].

  28. Brouwer MC, Heckenberg SG, de Gans J, Spanjaard L, Reitsma JB, van de Beek D. Nationwide implementation of adjunctive dexamethasone therapy for pneumococcal meningitis. Neurology. 2010 Oct 26. 75(17):1533-9. [Medline].

  29. van de Beek D, de Gans J, McIntyre P, Prasad K. Steroids in adults with acute bacterial meningitis: a systematic review. Lancet Infect Dis. 2004 Mar. 4(3):139-43. [Medline].

  30. Brouwer MC, McIntyre P, de Gans J, Prasad K, van de Beek D. Corticosteroids for acute bacterial meningitis. Cochrane Database Syst Rev. 2010 Sep 8. CD004405. [Medline].

  31. van de Beek D, Farrar JJ, de Gans J, Mai NT, Molyneux EM, Peltola H, et al. Adjunctive dexamethasone in bacterial meningitis: a meta-analysis of individual patient data. Lancet Neurol. 2010 Mar. 9(3):254-63. [Medline]. [Full Text].

  32. Peltola H, Roine I. Improving the outcomes in children with bacterial meningitis. Curr Opin Infect Dis. 2009 Jun. 22(3):250-5. [Medline].

  33. van de Beek D, Drake JM, Tunkel AR. Nosocomial bacterial meningitis. N Engl J Med. 2010 Jan 14. 362(2):146-54. [Medline].

  34. Sloan D, Dlamini S, Paul N, Dedicoat M. Treatment of acute cryptococcal meningitis in HIV infected adults, with an emphasis on resource-limited settings. Cochrane Database Syst Rev. 2008 Oct 8. CD005647. [Medline].

  35. Kauffman CA, Bustamante B, Chapman SW, Pappas PG. Clinical practice guidelines for the management of sporotrichosis: 2007 update by the Infectious Diseases Society of America. Clin Infect Dis. 2007 Nov 15. 45(10):1255-65. [Medline].

  36. Treatment of tuberculosis. MMWR Recomm Rep. 2003 Jun 20. 52:1-77. [Medline].

  37. Report from the Advisory Committee on Immunization Practices (ACIP): decision not to recommend routine vaccination of all children aged 2-10 years with quadrivalent meningococcal conjugate vaccine (MCV4). MMWR Morb Mortal Wkly Rep. 2008 May 2. 57(17):462-5. [Medline].

  38. [Guideline] Updated recommendations for use of meningococcal conjugate vaccines --- Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. 2011 Jan 28. 60(3):72-6. [Medline].

  39. FDA News Release: First vaccine approved by FDA to prevent serogroup B Meningococcal disease. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm420998.htm. Accessed: October 29, 2014.

  40. FDA News Release. FDA approves a second vaccine to prevent serogroup B meningococcal disease. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm431370.htm. Accessed: January 23, 2015.

  41. Nuorti JP, Whitney CG. Prevention of pneumococcal disease among infants and children - use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine - recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2010 Dec 10. 59:1-18. [Medline].

  42. Tomczyk S, Bennett NM, Stoecker C, Gierke R, Moore MR, Whitney CG, et al. Use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine among adults aged =65 years: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep. 2014 Sep 19. 63(37):822-5. [Medline]. [Full Text].

  43. Kim SW, Jin JH, Kang SJ, Jung SI, Kim YS, Kim CK, et al. Therapeutic efficacy of meropenem for treatment of experimental penicillin-resistant pneumococcal meningitis. J Korean Med Sci. 2004 Feb. 19(1):21-6. [Medline]. [Full Text].

  44. Abdelnour A, Silas PE, Lamas MR, Aragón CF, Chiu NC, Chiu CH, et al. Safety of a quadrivalent meningococcal serogroups A, C, W and Y conjugate vaccine (MenACWY-CRM) administered with routine infant vaccinations: Results of an open-label, randomized, phase 3b controlled study in healthy infants. Vaccine. 2014 Jan 4. [Medline].

  45. Douglas D. Meningitis Vaccine Safe in Young Infants. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/819521. Accessed: January 27, 2014.

  46. Jones SC, Morris J, Hill G, Alderman M, Ratard RC. St. Louis encephalitis outbreak in Louisiana in 2001. J La State Med Soc. 2002 Nov-Dec. 154(6):303-6. [Medline].

  47. Nkoumou MO, Clevenbergh P, Betha G, Kombila M. Bacterial meningitis in HIV positive compared to HIV negative patients in an internal medicine ward of Librevile, Gabon. Int Conf AIDS: International Conference on AIDS. Jul 7-12 2002;abstract no. ThPeB7368.

  48. Scheld WM, Koedel U, Nathan B, Pfister HW. Pathophysiology of bacterial meningitis: mechanism(s) of neuronal injury. J Infect Dis. 2002 Dec 1. 186 Suppl 2:S225-33. [Medline].

  49. van de Beek D, de Gans J, Tunkel AR, Wijdicks EF. Community-acquired bacterial meningitis in adults. N Engl J Med. 2006 Jan 5. 354(1):44-53. [Medline].

 
Previous
Next
 
Pneumococcal meningitis in a patient with alcoholism. Courtesy of the CDC/Dr. Edwin P. Ewing, Jr.
Acute bacterial meningitis. This axial nonenhanced computed tomography scan shows mild ventriculomegaly and sulcal effacement.
Acute bacterial meningitis. This axial T2-weighted magnetic resonance image shows only mild ventriculomegaly.
Acute bacterial meningitis. This contrast-enhanced, axial T1-weighted magnetic resonance image shows leptomeningeal enhancement (arrows).
Chronic mastoiditis and epidural empyema in a patient with bacterial meningitis. This axial computed tomography scan shows sclerosis of the temporal bone (chronic mastoiditis), an adjacent epidural empyema with marked dural enhancement (arrow), and the absence of left mastoid air.
Subdural empyema and arterial infarct in a patient with bacterial meningitis. This contrast-enhanced axial computed tomography scan shows left-sided parenchymal hypoattenuation in the middle cerebral artery territory, with marked herniation and a prominent subdural empyema.
Table 1. Infectious Agents Causing Aseptic Meningitis
Category Agent
Bacteria Partially treated bacterial meningitis



Listeria monocytogenes



Brucella spp



Rickettsia rickettsii



Ehrlichia spp



Mycoplasma pneumoniae



Borrelia burgdorferi



Treponema pallidum



Leptospira spp



Mycobacterium tuberculosis



Nocardia spp



Parasites Naegleria fowleri



Acanthamoeba spp



Balamuthia spp



Angiostrongylus cantonensis



Gnathostoma spinigerum



Baylisascaris procyonis



Strongyloides stercoralis



Taenia solium (cysticercosis)



Fungi Cryptococcus neoformans



Coccidioides immitis



Blastomyces dermatitidis



Histoplasma capsulatum



Candida spp



Aspergillus spp



Viruses Enterovirus Poliovirus



Echovirus



Coxsackievirus A



Coxsackievirus B



Enterovirus 68-71



Herpesvirus (HSV) HSV-1 and HSV-2



Varicella-zoster virus



Epstein-Barr virus



Cytomegalovirus



HHV-6 and HHV-7



Paramyxovirus Mumps virus



Measles virus



Togavirus Rubella virus
Flavivirus West Nile virus



Japanese encephalitis virus



St Louis encephalitis virus



Bunyavirus California encephalitis virus



La Crosse encephalitis virus



Alphavirus Eastern equine encephalitis virus



Western equine encephalitis virus



Venezuelan encephalitis virus



Reovirus Colorado tick fever virus
Arenavirus LCM virus
Rhabdovirus Rabies virus
Retrovirus HIV
HHV = human herpesvirus; HSV = herpes simplex virus; LCM = lymphocytic choriomeningitis.
       
Table 2. Causes of Chronic Meningitis
Category Agent
Bacteria Mycobacterium tuberculosis



Borrelia burgdorferi



Treponema pallidum



Brucella spp



Francisella tularensis



Nocardia spp



Actinomyces spp



Fungi Cryptococcus neoformans



Coccidioides immitis



Blastomyces dermatitidis



Histoplasma capsulatum



Candida albicans



Aspergillus spp



Sporothrix schenckii



Parasites Acanthamoeba spp



Naegleria fowleri



Angiostrongylus cantonensis



Gnathostoma spinigerum



Baylisascarisprocyonis



Schistosoma spp



Strongyloides stercoralis



Echinococcus granulosus



Table 3. Changing Epidemiology of Acute Bacterial Meningitis in United States*
Bacteria 1978-1981 1986 1995 1998-2007
Haemophilus influenzae 48% 45% 7% 6.7%  
Listeria monocytogenes 2% 3% 8% 3.4%  
Neisseria meningitidis 20% 14% 25% 13.9%  
Streptococcus agalactiae (group B streptococcus) 3% 6% 12% 18.1%  
Streptococcus pneumoniae 13% 18% 47% 58%  
*Nosocomial meningitis is not included; these data include only the 5 major meningeal pathogens.    
Table 4. Most Common Bacterial Pathogens on Basis of Age and Predisposing Risks
Risk or Predisposing Factor Bacterial Pathogen
Age 0-4 weeks Streptococcus agalactiae (GBS)



Escherichia coli K1



Listeria monocytogenes



Age 4-12 weeks S agalactiae



E coli



Haemophilus influenzae



Streptococcus pneumoniae



Neisseria meningitidis



Age 3 months to 18 years N meningitidis



S pneumoniae



H influenzae



Age 18-50 years S pneumoniae



N meningitidis



H influenzae



Age >50 years S pneumoniae



N meningitidis



L monocytogenes



Aerobic gram-negative bacilli



Immunocompromised state S pneumoniae



N meningitidis



L monocytogenes



Aerobic gram-negative bacilli



Intracranial manipulation, including neurosurgery Staphylococcus aureus



Coagulase-negative staphylococci



Aerobic gram-negative bacilli, including Pseudomonas aeruginosa



Basilar skull fracture S pneumoniae



H influenzae



Group A streptococci



CSF shunts Coagulase-negative staphylococci



S aureus



Aerobic gram-negative bacilli



Propionibacterium acnes



CSF = cerebrospinal fluid; GBS = group B streptococcus.
Table 5. CSF Findings in Meningitis by Etiologic Agent
Agent Opening Pressure (mm H2 O) WBC count (cells/µL) Glucose (mg/dL) Protein (mg/dL) Microbiology
Bacterial meningitis 200-300 100-5000; >80% PMNs < 40 >100 Specific pathogen demonstrated in 60% of Gram stains and 80% of cultures
Viral meningitis 90-200 10-300; lymphocytes Normal, reduced in LCM and mumps Normal but may be slightly elevated Viral isolation, PCR assays
Tuberculous meningitis 180-300 100-500; lymphocytes Reduced, < 40 Elevated, >100 Acid-fast bacillus stain, culture, PCR
Cryptococcal meningitis 180-300 10-200; lymphocytes Reduced 50-200 India ink, cryptococcal antigen, culture
Aseptic meningitis 90-200 10-300; lymphocytes Normal Normal but may be slightly elevated Negative findings on workup
Normal values 80-200 0-5; lymphocytes 50-75 15-40 Negative findings on workup
LCM = lymphocytic choriomeningitis; PCR = polymerase chain reaction; PMN = polymorphonuclear leukocyte; WBC = white blood cell.
Table 6. Comparison of CSF Findings by Type of Organism
Normal Finding Bacterial Meningitis Viral Meningitis* Fungal Meningitis**
Pressure (mm H2 O)



50-150



Increased Normal or mildly increased Normal or mildly increased in tuberculous meningitis; may be increased in fungal; AIDS patients with cryptococcal meningitis have increased risk of blindness and death unless kept below 300 mm H2 O
Cell count (mononuclear cells/µL)



Preterm: 0-25



Term: 0-22



>6 months: 0-5



No cell count result can exclude bacterial meningitis; PMN count typically in 1000s but may be less dramatic or even normal (classically, in very early meningococcal meningitis and in extremely ill neonates); lymphocytosis with normal CSF chemistries seen in 15-25%, especially when cell counts < 1000 or with partial treatment; ~90% of patients with ventriculoperitoneal shunts who have CSF WBC count >100 are infected; CSF glucose is usually normal, and organisms are less pathogenic; cell count and chemistries normalize slowly (over days) with antibiotics Cell count usually < 500, nearly 100% mononuclear; up to 48 hours, significant PMN pleocytosis may be indistinguishable from early bacterial meningitis; this is particularly true with eastern equine encephalitis; presence of nontraumatic RBCs in 80% of HSV meningoencephalitis, though 10% have normal CSF results Hundreds of mononuclear cells
Microscopy



No organisms



Gram stain 80% sensitive; inadequate decolorization may mistake Haemophilus influenzae for gram-positive cocci; pretreatment with antibiotics may affect stain uptake, causing gram-positive organisms to appear gram-negative and decrease culture yield by average of 20% No organism India ink is 50% sensitive for fungi; cryptococcal antigen is 95% sensitive; AFB stain is 40% sensitive for tuberculosis (increase yield by staining supernatant from at least 5 mL CSF)
Glucose



Euglycemia: >50% serum



Hyperglycemia: >30% serum



Wait 4 hr after glucose load



Decreased Normal Sometimes decreased; aside from fulminant bacterial meningitis, lowest levels of CSF glucose are seen in tuberculous meningitis, primary amebic meningoencephalitis, and neurocysticercosis
Protein (mg/dL)



Preterm: 65-150



Term: 20-170



>6 months: 15-45



Usually >150, may be >1000 Mildly increased Increased; >1000 with relatively benign clinical presentation suggestive of fungal disease
AFB = acid-fast bacillus; CSF = cerebrospinal fluid; HSV = herpes simplex virus; RBC = red blood cell; PMN = polymorphonuclear leukocyte.



*Some bacteria (eg, Mycoplasma, Listeria, Leptospira spp, Borrelia burgdorferi [Lyme], and spirochetes) produce spinal fluid alterations that resemble the viral profile. An aseptic profile also is typical of partially treated bacterial infections (>33% of patients have received antimicrobial treatment, especially children) and the 2 most common causes of encephalitis—the potentially curable HSV and arboviruses.



**In contrast, tuberculous meningitis and parasites resemble the fungal profile more closely.



Table 7. Recommended Empiric Antibiotics for Suspected Bacterial Meningitis, According to Age or Predisposing Factors [25]
Age or Predisposing Feature Antibiotics
Age 0-4 wk Ampicillin plus either cefotaxime or an aminoglycoside
Age 1 mo-50 y Vancomycin plus cefotaxime or ceftriaxone*
Age >50 y Vancomycin plus ampicillin plus ceftriaxone or cefotaxime plus vancomycin*
Impaired cellular immunity Vancomycin plus ampicillin plus either cefepime or meropenem
Recurrent meningitis Vancomycin plus cefotaxime or ceftriaxone
Basilar skull fracture Vancomycin plus cefotaxime or ceftriaxone
Head trauma, neurosurgery, or CSF shunt Vancomycin plus ceftazidime, cefepime, or meropenem
CSF = cerebrospinal fluid.



*Add ampicillin if Listeria monocytogenes is a suspected pathogen.



Table 8. Specific Antibiotics and Duration of Therapy for Acute Bacterial Meningitis
Bacteria Susceptibility Antibiotic(s) Duration (days)
Streptococcus pneumoniae Penicillin MIC ≤0.06 μg/mL Recommended: Penicillin G or ampicillin



Alternatives: Cefotaxime, ceftriaxone, chloramphenicol



10-14
Penicillin MIC ≥0.12 μg/mL



Cefotaxime or ceftriaxone MIC ≥0.12 μg/mL



Recommended: Cefotaxime or ceftriaxone



Alternatives: Cefepime, meropenem



Cefotaxime or ceftriaxone MIC ≥1.0 μg/mL Recommended: Vancomycin plus cefotaxime or ceftriaxone



Alternatives: Vancomycin plus moxifloxacin



Haemophilus influenzae Beta-lactamase−negative Recommended: Ampicillin



Alternatives: Cefotaxime, ceftriaxone, cefepime, chloramphenicol, aztreonam, a fluoroquinolone



7
Beta-lactamase−positive Recommended: Cefotaxime or ceftriaxone



Alternatives: Cefepime, chloramphenicol, aztreonam, a fluoroquinolone



Beta-lactamase−negative, ampicillin-resistant Recommended: Meropenem



Alternatives: Cefepime, chloramphenicol, aztreonam, a fluoroquinolone



Neisseria meningitidis Penicillin MIC < 0.1 μg/mL Recommended: Penicillin G or ampicillin



Alternatives: Cefotaxime, ceftriaxone, chloramphenicol



7
Penicillin MIC ≥0.1 μg/mL Recommended: Cefotaxime or ceftriaxone



Alternatives: Cefepime, chloramphenicol, a fluoroquinolone, meropenem



Listeria monocytogenes ... Recommended: Ampicillin or penicillin G



Alternative: TMP-SMX



14-21
Streptococcus agalactiae ... Recommended: Ampicillin or penicillin G



Alternatives: Cefotaxime, ceftriaxone, vancomycin



14-21
Enterobacteriaceae ... Recommended: Cefotaxime or ceftriaxone



Alternatives: Aztreonam, a fluoroquinolone, TMP-SMX, meropenem, ampicillin



21
Pseudomonas aeruginosa ... Recommended: Ceftazidime or cefepime



Alternatives: Aztreonam, meropenem, ciprofloxacin



21
Staphylococcus epidermidis   Recommended: Vancomycin



Alternative: Linezolid



Consider addition of rifampin



 
MIC= minimal inhibitory concentration; TMP-SMX = trimethoprim-sulfamethoxazole.
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.