Approach Considerations
The challenges for emergency physicians when treating meningitis are as follows:
- Early identification and treatment of patients with acute bacterial meningitis
- Assessing whether a treatable CNS infection is present in those with suspected subacute or chronic meningitis
- Identifying the causative organism
Bacterial meningitis must be first and foremost in the differential diagnosis of patients with headache, neck stiffness, fever, and change in mental status. Acute bacterial meningitis is a medical emergency, and delays in instituting effective antimicrobial therapy result in increased morbidity and mortality.
The cornerstone in the diagnosis of meningitis is examination of the CSF. The diagnosis of bacterial meningitis is made by culture to isolate the bacteria in the CSF sample. Other laboratory tests, which may include other culture of blood specimens, 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.
In general, whenever the diagnosis of meningitis is strongly considered, a lumbar puncture should be promptly performed.
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 computed tomography (CT) scan of the brain may be performed prior to lumbar puncture in some patient groups with a higher risk of herniation. These groups include those made up of patients with the following risk factors:
- Newly onset seizures
- An immunocompromised state
- Signs suspicious for space-occupying lesions (such as papilledema and focal neurologic signs)
- Moderate to severe impairment in consciousness
Special studies, such as serology and nucleic acid amplification, may also be performed, depending on clinical suspicion of an offending organism.
In the absence of focal neurologic deficit, radiographic imaging of the head should not preclude performing a lumbar puncture.
Neurosurgical procedures are performed in consultation with a neurosurgical service in the presence of severe intracranial hypertension, evidence of paranasal and mastoid infection that requires surgical drainage, skull fractures, foreign body–associated infections (eg, ventriculoperitoneal shunts), or an associated abscess formation.
CBC Count with Differential
Complete blood cell (CBC) count with differential demonstrates polymorphonuclear leukocytosis with left shift in bacterial meningitis.
Comprehensive Metabolic Panel
The following should be obtained:
- Serum electrolytes, to determine dehydration or syndrome of inappropriate secretion of antidiuretic hormone [SIADH])
- Serum glucose (which is used in comparison with the CSF glucose)
- BUN and/or creatinine and liver profile, to assess organ functioning and adjust antibiotic dosing
The serum glucose may be low if glycogen stores are depleted, or they may be high in infected patients with diabetes.
Coagulation Profile
Coagulation profile and platelets are indicated in patients with chronic alcohol use or liver disease or if disseminated intravascular coagulation (DIC) is suspected. (Patients may require platelets or fresh frozen plasma [FFP] prior to lumbar puncture.)
Serum Test for Syphilis
Perform serologic tests to detect syphilis, such as the nontreponemal (ie, rapid plasma reagent [RPR] or VDRL test) and specific treponemal (ie, fluorescent treponemal antibody absorption [FTA-Abs], Treponema pallidum hemoagglutination [TPHA], microhemagglutination-Treponema pallidum [MHA-TP]) tests to support the diagnosis. These also guide the success of therapy. The titer of the nonspecific treponemal tests decreases and usually reverts back to negative or undetectable levels following treatment.
Serum Test for Procalcitonin
There is increasing data to suggest that serum procalcitonin (PCT) levels can be used as a guide to distinguish between bacterial and aseptic meningitis in children. The results yielded by a serum PCT, combined with other findings, could be helpful in making clinical decisions.[11]
In an analysis of retrospective, multicenter, hospital-based cohort studies, Dubos et al confirmed that measurement of the PCT level is the best biological marker to differentiate bacterial meningitis from aseptic meningitis in children in the ED. Sensitivity and specificity of the PCT level in distinguishing between bacterial and aseptic meningitis were 99% and 83%, respectively.[11]
Special Studies
Cultures prior to instituting antibiotics may be helpful if diagnosis is uncertain. 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 counter immunoelectrophoresis (CIE) of blood, urine, and CSF for specific bacterial antigens is recommended occasionally if diagnosis is challenging or in patients with partially treated meningitis.
Lumbar Puncture
Elevated opening pressure correlates with increased risk of morbidity and mortality in bacterial and fungal meningitis. In bacterial meningitis, elevated opening pressure (reference range is 80-200 mm water) suggests increased 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. The opening CSF pressure is usually elevated in tuberculous meningitis.
The CSF cell count varies depending on the offending pathogen. It is usually in the few hundreds (100-1000 cells/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.
Go to Lumbar Puncture for complete information on this topic.
See Table 5 "CSF Picture of Meningitis According to Etiologic Agent " and Table 6 "Comparison of CSF Findings by Type of Organism," below .
Table 5. CSF Picture of Meningitis According to Etiologic Agent (Open Table in a new window)
| Agent | Opening Pressure | WBC count per 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 |
| *Polymorphonuclear lymphocytes †Polymerase chain reaction | |||||
Table 6. Comparison of CSF Findings by Type of Organism (Open Table in a new window)
| Bacterial Meningitis | Viral Meningitis* | Fungal Meningitis** | |
| Pressure 5-15 cm H2 O | Increased | Normal or mildly increased | Normal or mildly increased in TB. May be increased in fungal. AIDS patients with cryptococcal meningitis have increased risk of blindness, death unless maintained at < 30 cm. |
| Cell count preterm: 0-25 term: 0-22 >6 months: 0-5 mononuclear cells/mm3 | No cell count result can exclude bacterial meningitis. Typically thousands of PMNs, 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 if partially treated. Approximately 90% of patients with ventriculoperitoneal shunts have CSF WBC count >100 cells/mm3 are infected; CSF glucose usually normal, and organisms are less pathogenic. Cell count and chemistries normalize slowly (over days) with antibiotics. | Usually < 500 cells, 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, although 10% have normal CSF results | Hundreds of mononuclear cells |
| Micro no organisms | Gram stain 80% sensitive. Inadequate decolorization may mistake H influenzae for gram-positive cocci. Pretreatment with antibiotics may affect stain uptake, causing gram-positive organisms to appear gram negative and decrease culture yield on average 20%. | No organism | India ink 80-90% sensitive for fungi; AFB stain 40% sensitive for TB (increase yield by staining supernate from at least 5 cc CSF) |
| Glucose euglycemia: >50% serum hyperglycemia: >30% serum wait 4 h after glucose load | Decreased | Normal | Sometimes decreased. Aside from fulminant bacterial meningitis, the lowest levels of CSF glucose are seen in TB, primary amebic meningoencephalitis, neurocysticercosis |
| Protein preterm: 65-150 term: 20-170 >6 months: 15-45 mg/dL | Usually >150, may be >1000 | Mildly increased | Increased; >1000 with relatively benign clinical presentation suggestive of fungal disease |
| *Some bacteria (eg, Mycoplasma, Listeria, Leptospira species, Borrelia burgdorferi [Lyme], spirochetes) produce spinal fluid alterations that resemble the viral profile. An aseptic profile also is typical of partially treated bacterial infections (more than 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. | |||
Take tube #1 to the chemistry lab for glucose and protein. Take tube #2 to the hematology lab for a cell count with differential. Take tube #3 to the microbiology and immunology lab for Gram stain, bacterial culture, acid-fast bacillus (AFB) stain and tuberculosis cultures, India ink stain, cryptococcal antigen testing, and fungal cultures, CIE, VDRL, and cryptococcal antigen, if indicated. Hold tube #4 for a repeat cell count with differential, if needed (or for other subsequent studies not initially ordered).
Research correlates CSF cytokines in children with bacterial meningitis.
According to Seupaul, the following 3 diagnostic tests have clinically useful likelihood ratios for the diagnosis of bacterial meningitis in adults:
- CSF/blood glucose - Ratio of 0.4 or less
- CSF white blood cell (WBC) count - Count of 500/L or more
- CSF lactate level – level of 31.53 or greater
CSF characteristics of acute bacterial meningitis
Examination of the CSF in patients with acute bacterial meningitis reveals the characteristic neutrophilic pleocytosis (usually hundreds to a few thousand, with >80% PMN cells). In some cases of L monocytogenes meningitis (25-30%), a lymphocytic predominance may occur. Low CSF WBC count (< 20 cells/µL) in the presence of a high bacterial load suggests a poor prognosis.
CSF characteristics of viral meningitis
In viral meningitis, the opening pressure is 90-200 mm H2 0, and the WBC count is 10-300 lymphocytes/µL. Although the glucose concentration is typically normal, in LCM, HSV, mumps, and polio, it can be below normal. 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 lymphocytes), a reduced glucose level, and an elevated protein level.
The CSF picture of other fungal meningitis is similar to the CSF picture 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, 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 is used in the diagnosis of many cases of fungal meningitis because isolating them from culture has been difficult (eg, presence of histoplasma antigen in the CSF). However, note that the serology for B dermatitidis is not accurate and a negative serology finding does not rule out the diagnosis.
CSF characteristics of eosinophilic/parasitic meningitis
PAM caused by N fowleri is characterized by a neutrophilic pleocytosis, low glucose levels, elevated protein levels, and red blood cells. Mononuclear pleocytosis may be observed in patients with subacute or chronic forms of PAM. Demonstration of the trophozoites, with the characteristic ameboid movement, using wet preparations of the CSF has been used for diagnosis. Alternatively, the ameba could be demonstrated in biopsy specimens.
Suspect meningitis caused by A cantonensis, G spinigerum, and B procyonis in the presence of exposure, profound peripheral blood eosinophilia, and characteristic eosinophilic pleocytosis. Demonstrating the larva antemortem is usually difficult, and diagnosis relies on clinical presentation and a compatible epidemiological history. Serologic tests may aid in the diagnosis. G spinigerum meningitis may mimic cerebrovascular disease because it may cause cerebral hemorrhage.
CSF characteristics of Lyme meningitis
The CSF in patients with Lyme meningitis 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 the serum is a helpful diagnostic test. A CSF-to-serum ratio of greater than 1 suggests intrathecal antibody production and neuroborreliosis.
CSF characteristics of tuberculous meningitis
The CSF of patients with tuberculous meningitis is characterized by a predominantly lymphocytic pleocytosis, usually in the hundreds.
Go to Tuberculous Meningitis for complete information on this topic.
CSF glucose study
In bacterial meningitis, the CSF glucose (reference range is 40-70 mg/dL) is less than 40 mg/dL in 60% of patients. Obtain a simultaneous blood glucose determination for comparison purposes. Some patients may have elevated blood glucose levels as a result of underlying diabetes mellitus, and the predictive value of the CSF and blood glucose ratio may not be accurate in these circumstances.
The CSF glucose level is usually within the reference range in viral meningitis, but some cases of LCM, HSV, mumps, and polio may cause low CSF glucose levels.
In tuberculous meningitis, a characteristic hypoglycorrhagia (glucose < 40 mg/dL) is present, and the protein level is usually elevated, especially if a CSF block is present.
CSF protein study
The CSF protein level (reference range is 20-50 mg/dL) is usually elevated in bacterial meningitis. In viral meningitis, these levels are also usually elevated, although 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 bacilli stain
CSF Gram stain 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 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 the acid-fast bacilli (eg, with auramine-rhodamine stain, Ziehl-Neelsen stain, Kinyoun stain) in the CSF is difficult and usually requires a large volume of CSF.
CSF culture and antigen testing
CSF bacterial cultures yield the bacterial cause in 70-85% of cases. The yield diminishes significantly 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 HIB, S pneumoniae, N meningitidis, E coli K1, and S agalactiae. Its theoretical advantage is the detection of the bacterial antigens even after microbial killing, as is observed following antibacterial therapy.
Others, however, have shown that the CSF bacterial antigen assay may not be better than the Gram stain. It is specific (a positive result indicates a diagnosis of bacterial meningitis), but a negative finding on the bacterial antigen test does not rule out meningitis (50-95% sensitivity).
C neoformans may be cultured from the CSF in cryptococcal meningitis. Other methods of identification have included 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 of greater than 90%. However, the CSF cryptococcal antigen determination is not universally available. In instances when the India ink results are negative but the 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.
Obtain blood cultures and serum cryptococcal antigen to determine if cryptococcal fungemia is present.
In syphilitic meningitis, isolating T pallidum from the CSF is extremely difficult and time consuming. The spirochete could be demonstrated 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 Venereal Disease Research Laboratory (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). Always take care to not contaminate the CSF with blood during spinal fluid collection (eg, traumatic tap).
The culture for B burgdorferi has a low yield. The recent availability of the CSF Lyme PCR assay offers a rapid, sensitive, and specific method of diagnosis. This assay is gaining popularity as the method of choice for diagnosis of Lyme meningitis.
The 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 advantage of a rapid, sensitive, and specific method of tuberculosis detection. The need for mycobacterial growth in cultures remains because this offers the advantage of performing drug susceptibility assays.
Viral isolation from the CSF
The isolation of viruses from the CSF has a sensitivity of 65-70% for enteroviruses. Alternatively, enterovirus isolation from throat and stool viral cultures may also be used to indirectly implicate it as the cause of the meningitis. Mumps viral culture from the CSF has a low sensitivity (30-50%). LCM virus may be cultured in blood early in the disease or later in the urine.
Blood cultures
Obtain blood cultures and appropriate cultures from possible sites of infection. Obtain these promptly and prior to the administration of an antibacterial agent. The utility of these cultures is most evident in cases in which the performance of a lumbar puncture is delayed by the need for head imaging (risk for herniation in a patient with focal neurologic deficit or coma) and when antimicrobial therapy is rightfully initiated before the lumbar puncture and neuroimaging tests.
Nucleic acid amplification
The use of nucleic acid amplification (eg, PCR) has revolutionized the diagnosis of herpes simplex 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 enterovirus 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.
Serology
The demonstration of a 4-fold rise in antibodies between acute and convalescent sera traditionally has been used to document meningeal infection in many viral pathogens.
Go to Lumbar Puncture for complete information on this topic.
Chest Radiography
As many as 50% of patients with pneumococcal meningitis also have evidence of pneumonia on initial chest radiograph.
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.
Go to Imaging in Bacterial Meningitis for complete information on this topic.
CT Scanning and MRI
CT scans 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.
The practice of obtaining CT scans of the head may lead to the unnecessary delay in the performance of diagnostic lumbar puncture and the initiation of antibiotic therapy. The delay in the institution of antimicrobial therapy may be detrimental to the total 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 happens within 24 hours following the lumbar puncture and should always be considered in the differential diagnosis if the patient's neurologic status deteriorates.
Presence of papilledema and inability to fully assess fundi or neurologic status are indications for CT scan prior to lumbar puncture. Obtain blood cultures and initiate treatment before imaging studies and lumbar puncture in patients with suspected bacterial meningitis. Results may be normal or demonstrate small ventricles, effacement of sulci, and contrast enhancement over convexities. Late findings include venous infarction and communicating hydrocephalus. Rule out brain abscess, sinus or mastoid infection, skull fracture, and congenital anomalies. Acute bacterial meningitis is shown in the CT and MRI scans (all from the same patient) below.
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). Neuroimaging is indicated in patients with prolonged fever, focal neurologic symptoms and signs, evidence of increased ICP, and suspected basilar fracture. It is also indicated for evaluation of the paranasal sinuses. These studies are helpful in the detection of CNS complications of bacterial meningitis, such as hydrocephalus, cerebral infarct, brain abscess, subdural empyema, and venous sinus thrombosis.
Go to Imaging in Bacterial Meningitis for complete information on this topic.
Meningeal Biopsy
Meningeal biopsy, with the demonstration of caseating granulomas and acid-fast bacilli on the smear, may prove useful, because it has a higher yield than does the CSF acid-fast bacilli smear.
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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.
Scheld WM, Koedel U, Nathan B, Pfister HW. Pathophysiology of bacterial meningitis: mechanism(s) of neuronal injury. J Infect Dis. Dec 1 2002;186 Suppl 2:S225-33. [Medline].
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.
Thigpen MC, Whitney CG, Messonnier NE, et al. Bacterial meningitis in the United States, 1998-2007. N Engl J Med. May 26 2011;364(21):2016-25. [Medline].
van de Beek D, de Gans J, Tunkel AR, Wijdicks EF. Community-acquired bacterial meningitis in adults. N Engl J Med. Jan 5 2006;354(1):44-53. [Medline].
Moses S. Meningitis: acute bacterial meningitis. Accessed February 8, 2011. Available at http://www.fpnotebook.com/neuro/ID/Mngts.htm.
Worsoe L, Caye-Thomasen P, Brandt CT, Thomsen J, Ostergaard C. Factors associated with the occurrence of hearing loss after pneumococcal meningitis. Clin Infect Dis. Oct 15 2010;51(8):917-24. [Medline].
[Best Evidence] 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. Dec 2008;162(12):1157-63. [Medline].
Gilbert DN, Moellering RC Jr, Sande MA. Antimicrobial Therapy. In: Sanford Guide to Antimicrobial Therapy. 33rd ed. March 15, 2003.
van de Beek D, de Gans J, McIntyre P, Prasad K. Steroids in adults with acute bacterial meningitis: a systematic review. Lancet Infect Dis. Mar 2004;4(3):139-43. [Medline].
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[Best Evidence] 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. Oct 8 2008;CD005647. [Medline].
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[Guideline] Centers for Disease Control and Prevention (CDC). Updated recommendations for use of meningococcal conjugate vaccines --- Advisory Committee on Immunization Practices (ACIP), 2010. MMWR Morb Mortal Wkly Rep. Jan 28 2011;60(3):72-6. [Medline]. [Full Text].
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- Table 1. Infectious Agents Causing Aseptic Meningitis Syndrome
- Table 2. Causes of Chronic Meningitis
- Table 3. Changing Epidemiology of Acute Bacterial Meningitis in the United States*
- Table 4. The Most Common Bacterial Pathogens Based on Age and Predisposing Risks
- Table 5. CSF Picture of Meningitis According to Etiologic Agent
- Table 6. Comparison of CSF Findings by Type of Organism
- Table 7. Recommended Empiric Antibiotics According to Predisposing Factors for Patients With Suspected Bacterial Meningitis
- Table 8. Recommended Empiric Antibiotics for Patients With Suspected Bacterial Meningitis and Known CSF Gram Stain Results
- Table 9. Specific Antibiotics and Duration of Therapy for Patients With Acute Bacterial Meningitis
| Category | Agent |
| Bacteria | Partially-treated bacterial meningitis L monocytogenes Brucella species Rickettsia rickettsii Ehrlichia species Mycoplasma pneumoniae Borrelia burgdorferi Treponema pallidum Leptospira species Mycobacterium tuberculosis Nocardia species |
| Parasites | N fowleri Acanthamoeba species Balamuthia species Angiostrongylus cantonensis G spinigerum Baylisascaris procyonis S stercoralis Taenia solium (cysticercosis) |
| Fungi | Cryptococcus neoformans C immitis Blastomyces dermatitidis H capsulatum Candida species Aspergillus species |
| Viruses | Enterovirus Poliovirus Echovirus Coxsackievirus A Coxsackievirus B Enterovirus 68-71 |
| Herpesvirus HSV-1 and HSV-2 Varicella-zoster virus EBV CMV HHV*-6 HHV-7 | |
| Paramyxovirus Mumps virus Measles virus | |
| Togavirus Rubella virus | |
| Flavivirus 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*** | |
| *Human herpes virus **Lymphocytic choriomeningitis ***Human immunodeficiency virus | |
| Category | Agent |
| Bacteria | M tuberculosis B burgdorferi T pallidum Brucella species Francisella tularensis Nocardia species Actinomyces species |
| Fungi | C neoformans C immitis B dermatitidis H capsulatum Candida albicans Aspergillus species Sporothrix schenckii |
| Parasites | Acanthamoeba species N fowleri Angiostrongylus cantonensis G spinigerum B procyonis Schistosoma species S stercoralis Echinococcus granulosus |
| Bacteria | 1978-1981 | 1986 | 1995 | 1998-2007 | |
| H influenzae | 48% | 45% | 7% | 6.7% | |
| Listeria monocytogenes | 2% | 3% | 8% | 3.4% | |
| N meningitidis | 20% | 14% | 25% | 13.9% | |
| S agalactiae | 3% | 6% | 12% | 18.1% | |
| S pneumoniae | 13% | 18% | 47% | 58% | |
| *Nosocomial meningitis is not included. These data include only the 5 major meningeal pathogens. | |||||
| Risk and/or Predisposing Factor | Bacterial Pathogen |
| Age 0-4 weeks | Streptococcus agalactiae (group B streptococci) E coli K1 Listeria monocytogenes |
| Age 4-12 weeks | S agalactiae E coli H influenzae S pneumoniae N meningitidis |
| Age 3 months to 18 years | N meningitidis S pneumoniae H influenzae |
| Age 18-50 years | S pneumoniae N meningitidis H influenzae |
| Age older than 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 P aeruginosa |
| Basilar skull fracture | S pneumoniae H influenzae Group A streptococci |
| CSF shunts | Coagulase-negative staphylococci S aureus Aerobic gram-negative bacilli Propionibacterium acnes |
| Agent | Opening Pressure | WBC count per 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 |
| *Polymorphonuclear lymphocytes †Polymerase chain reaction | |||||
| Bacterial Meningitis | Viral Meningitis* | Fungal Meningitis** | |
| Pressure 5-15 cm H2 O | Increased | Normal or mildly increased | Normal or mildly increased in TB. May be increased in fungal. AIDS patients with cryptococcal meningitis have increased risk of blindness, death unless maintained at < 30 cm. |
| Cell count preterm: 0-25 term: 0-22 >6 months: 0-5 mononuclear cells/mm3 | No cell count result can exclude bacterial meningitis. Typically thousands of PMNs, 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 if partially treated. Approximately 90% of patients with ventriculoperitoneal shunts have CSF WBC count >100 cells/mm3 are infected; CSF glucose usually normal, and organisms are less pathogenic. Cell count and chemistries normalize slowly (over days) with antibiotics. | Usually < 500 cells, 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, although 10% have normal CSF results | Hundreds of mononuclear cells |
| Micro no organisms | Gram stain 80% sensitive. Inadequate decolorization may mistake H influenzae for gram-positive cocci. Pretreatment with antibiotics may affect stain uptake, causing gram-positive organisms to appear gram negative and decrease culture yield on average 20%. | No organism | India ink 80-90% sensitive for fungi; AFB stain 40% sensitive for TB (increase yield by staining supernate from at least 5 cc CSF) |
| Glucose euglycemia: >50% serum hyperglycemia: >30% serum wait 4 h after glucose load | Decreased | Normal | Sometimes decreased. Aside from fulminant bacterial meningitis, the lowest levels of CSF glucose are seen in TB, primary amebic meningoencephalitis, neurocysticercosis |
| Protein preterm: 65-150 term: 20-170 >6 months: 15-45 mg/dL | Usually >150, may be >1000 | Mildly increased | Increased; >1000 with relatively benign clinical presentation suggestive of fungal disease |
| *Some bacteria (eg, Mycoplasma, Listeria, Leptospira species, Borrelia burgdorferi [Lyme], spirochetes) produce spinal fluid alterations that resemble the viral profile. An aseptic profile also is typical of partially treated bacterial infections (more than 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. | |||
| Predisposing Feature | Antibiotic(s) |
| Age 0-4 weeks | Ampicillin plus cefotaxime or an aminoglycoside |
| Age 1-3 months | Ampicillin plus cefotaxime plus vancomycin* |
| Age 3 months to 50 years | Ceftriaxone or cefotaxime plus vancomycin* |
| Older than 50 years | Ampicillin plus ceftriaxone or cefotaxime plus vancomycin* |
| Impaired cellular immunity | Ampicillin plus ceftazidime plus vancomycin* |
| Neurosurgery, head trauma, or CSF shunt | Vancomycin plus ceftazidime |
| *Vancomycin is added empirically to the initial regimen if the presence of penicillin-resistant S pneumoniae is suspected or if a high incidence of resistance is reported in the community. | |
| Gram Stain Morphology | Antibiotic(s) |
| Gram-positive cocci | Vancomycin plus ceftriaxone or cefotaxime |
| Gram-negative cocci | Penicillin G* |
| Gram-positive bacilli | Ampicillin plus an aminoglycoside |
| Gram-negative bacilli | Broad-spectrum cephalosporin† plus an aminoglycoside |
| *Use ceftriaxone if penicillin-resistant N meningitidis occurs in the community. †Ceftriaxone is preferred. Ceftazidime is used when Pseudomonas infection is likely (eg, neurosurgical procedures). | |
| Bacteria | Susceptibility | Antibiotic(s) | Duration (Days) |
| S pneumoniae | Penicillin MIC < 0.1 mg/L | Penicillin G | 10-14 |
| MIC 0.1-1 mg/L | Ceftriaxone or cefotaxime | ||
| MIC >2 mg/L | Ceftriaxone or cefotaxime | ||
| Ceftriaxone MIC >0.5 mg/L | Ceftriaxone or cefotaxime plus vancomycin or rifampin | ||
| H influenzae | Beta-lactamase-negative | Ampicillin | 7 |
| Beta-lactamase-positive | Ceftriaxone or cefotaxime | ||
| N meningitidis | ... | Penicillin G or ampicillin | 7 |
| L monocytogenes | ... | Ampicillin or penicillin G plus an aminoglycoside | 14-21 |
| S agalactiae | ... | Penicillin G plus an aminoglycoside, if warranted | 14-21 |
| Enterobacteriaceae | ... | Ceftriaxone or cefotaxime plus an aminoglycoside | 21 |
| P aeruginosa | ... | Ceftazidime plus an aminoglycoside | 21 |
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