The author would like to acknowledge the first edition authors Thomas A. Kurrus


and Martin G. Tauber.


Meningitis is a relatively rare inflammation of the membranes surrounding the brain and spinal cord. This inflammation results from locally produced cytokines (primarily interleukin [IL]-1, IL-6, and tumor necrosis factor [TNF]) and is most commonly caused by infectious agents such as viruses and bacteria ( Box 37.1 ). The antibiotic-induced lysis of bacteria produces additional inflammatory cytokines that complicate therapy. Meningeal inflammation may also result from parameningeal infective foci. Noninfectious causes of meningeal inflammation include reactions to medications, autoimmune diseases, vasculitis, and tumors. Untreated bacterial meningitis is usually fatal. Early antibiotic therapy has reduced but not eliminated the mortality and morbidity. Viral meningitis is often self-limited. Vaccines that reduce meningitis risks are available and in development.

BOX 37.1

  • Meningitis: Inflammation of the subarachnoid space and adjacent structures surrounding the brain and spinal cord. Typical clinical manifestations are fever, headache, nuchal rigidity, and altered mental status. The cerebrospinal fluid (CSF) is abnormal.

  • Encephalitis: Inflammation of the brain parenchyma with accompanying clinical evidence of abnormal brain function including altered mental status, motor or sensory deficits, altered behavior, or personality change. The CSF findings are variable. Meningoencephalitis represents a clinical syndrome in which inflammatory changes involve both the brain parenchyma and the subarachnoid space.

  • Community-acquired meningitis: Meningitis acquired in the community setting. There are multiple causes, including viral, bacterial, and fungal. The cause and frequency may be influenced by seasonality, geographic location, age, and immunologic status of the host.

  • Nosocomial meningitis: Meningitis acquired in a medical care setting, usually associated with neurosurgery or trauma. Other sources include hematogenous spread of bacteria from distant infections, indwelling devices and drains, and vascular access catheters.

  • Aseptic or viral meningitis: Clinical and laboratory signs of meningeal inflammation with negative routine cultures in a patient who has not received prior antibiotic therapy. Viral infection is the most common cause. Other causes include drug hypersensitivity, reaction to intrathecal medications, and some vasculitides.

  • Chronic meningitis: Evidence of meningeal inflammation lasting for 4 or more weeks.

  • Recurrent meningitis: Recurrent episodes of meningeal inflammation. This can occur in both community-acquired and nosocomial settings. Recurrent meningitis mandates evaluation for immunologic or anatomic host defects. Indwelling medical devices may be involved.

Clinical Vignette

A 50-year-old farmer is admitted with an unsteady gait, diplopia, headache, nausea, and vomiting. He had been in excellent health until fever, unsteady gait, and neck soreness started 7 days before admission and progressed to diplopia, dysarthria, dysphagia, headache, and a vague numbness in his right cheek. Nausea and vomiting started 3 days before admission. He lived on a farm in Vermont with his family, who were all healthy. He had many animal exposures but none that were unusual. He denied drinking unpasteurized milk, eating rare meat, or drinking excessive alcohol. In the past his medical health had been excellent. On physical exam his temperature was 37.5°C. He was markedly irritable and had diminished light touch sensation over his right cheek as well as a left sixth nerve palsy with right-eye nystagmus when he looked to the right. He was ataxic with a broad-based gait and no muscle weakness. Nuchal rigidity was absent and plantar reflexes were normal. Hemoglobin was 15.3 g/dL; white blood cells (WBCs) 11,400 with 72% polymorphonuclear leukocytes (PMNs), 11% bands, and 1 eosinophil. A comprehensive metabolic panel was normal. Lumbar puncture (LP) showed an opening pressure of 130 mm of fluid, 103 red blood cells (RBCs), 78 WBCs (4% PMNs, 90% lymphocytes, 6% monocytes), protein 91 mg/dL, glucose 59 mg/dL (140 mg/dL in blood). Gram smear was negative. Cryptococcal antigen (cerebrospinal fluid [CSF] and blood), syphilis, and HIV serologies were negative. A chest x-ray and cranial computed tomography (CT) scan were normal. On the third day his temperature was 38.5°C. Blood cultures were repeated. His laboratory data were unchanged. A second LP revealed clear fluid with 10 RBCs and 250 WBCs (22% PMNs, 53% lymphocytes, 25% monocytes). CSF glucose was now 40 mg/dL (120 mg/dL in blood), CSF protein had increased to 106 mg/dL. Gram stain was negative. Culture was sterile on no antibiotic. He became progressively obtunded. Four-drug tuberculosis (TB) therapy was started. On the fifth day his temperature was normal, he was more alert, and his headache had diminished. One of two blood cultures from day 3 was growing a small gram-positive bacillus identified as Listeria monocytogenes . His antituberculous therapy was switched to ampicillin 12 g/day for 3 weeks. At the end of therapy his mental status was normal, his ataxia and gaze palsies had resolved, and he had no neurologic sequelae.

This patient had rhombencephalic listeriosis. He lacked the more classic, abrupt onset of meningeal changes and demonstrated the value of repeat LPs and blood cultures. The rifampin in his TB regimen probably produced the initial improvement. Fortunately the blood culture result established the true cause. The lack of risk factors for TB and the farm animal exposures in this healthy 50-year-old were clues. A chronic meningitis presentation (usually more than 7 days) should be treated as TB initially, but a specific diagnosis must be established.

Anatomic and Physiologic Considerations

The meninges consist of three layers ( Fig. 37.1 ). The outer layer (dura mater) is a tough white fibrous connective tissue that forms the inner periosteum of the cranium and the inner meningeal layer protecting the brain. The middle layer (arachnoid) is a thin layer with numerous threadlike strands attaching it to the innermost layer, the pia mater. The pia mater is a thin, delicate membrane tightly bound to the surface of the brain and spinal cord. The subarachnoid space between the arachnoid and the pia is filled with CSF and traversed by the blood vessels of the brain.

Fig. 37.1, (A) Circulation of cerebrospinal fluid and (B) meninges and superficial cerebral veins.

Meningitis is an inflammation in the subarachnoid and ventricular spaces; it involves the adjacent meninges, the traversing blood vessels, and the brain structures. This inflammation occurs within a closed anatomic space that is devoid of significant defense mechanisms. Many presentations of meningitis include altered mentation due to brain inflammation and can be described as meningoencephalitis. Infection of the subdural space (empyema) usually stems from a sinus, middle ear, facial, or scalp infection. Except in infants, meningitis is a very rare cause of subdural empyema. The differential diagnosis of subdural infection is similar to that of meningitis, meningoencephalitis, brain abscess, epidural infection, subdural hematoma, and even thrombophlebitis of cerebral vessels, since headache, fever, neck stiffness, altered mental status, seizures, and focal neurologic signs can be seen in all of these entities. An epidural abscess from a contiguous infection or hematogenous spread may have a more gradual onset and feature local spine pain, myalgias, and minimal fever. Although brain abscess, subdural and epidural abscess, and encephalitis are often in the differential diagnosis of meningitis, the primary focus of this chapter is on meningitis.

CSF is produced by the choroid plexus in the lateral, third, and fourth ventricles. The choroid plexus consists of projections of vessels and pia mater into the ventricular cavities. Normally about 500 mL of CSF is produced per day by both filtration and active transport at a rate of about 20 mL/h. CSF circulates from the lateral ventricles into the third and fourth ventricles and then into the subarachnoid space over the surfaces of the brain and down the spinal cord. CSF is reabsorbed back into the bloodstream via the arachnoid villi located along the superior sagittal and intracranial venous sinuses and around the spinal nerve roots. The movement of CSF and cellular components across arachnoid villi occurs via transport within giant vesicles and functions as a one-way valve from CSF to peripheral blood (see Fig. 37.1 ). This description of the transport mechanism for CSF is overly simplistic, since brain lymphatic pathways have recently been discovered.

Two interfaces exist between the blood and the brain. The larger and better known is the blood-brain barrier (BBB). It functions to protect the interstitial fluid of the brain from changes in the blood levels of ions, amino acids, peptides, and other substances. Lipid-soluble molecules—including those of oxygen, carbon dioxide, anesthetics, and alcohol—can pass through the BBB and gain access to all parts of the brain depending on the rate of blood flow. The permeability of the BBB is primarily dependent on lipid solubility, molecular size, and protein binding of drugs. Drugs that are bound to plasma protein must be in a free form (unbound) to adequately penetrate the BBB. An example is ceftriaxone, a beta lactam, which is highly protein bound, hydrophilic rather than lipid soluble, and penetrates relatively poorly across the BBB. Fortunately the high antibacterial potency of ceftriaxone against Streptococcus pneumoniae , Neisseria meningitidis , and Haemophilus influenzae makes it a drug of choice in bacterial meningitis. (See resistance concerns further on regarding organisms with increasing minimal inhibitory concentrations [MICs] to beta-lactams.) The smaller, less direct interface between blood and brain is between the blood and the CSF (BcsfB). This interface controls the composition of the CSF, and its permeability is primarily dependent on meningeal inflammation and secretion in the choroid plexus. Both barrier interfaces have distinct pharmacokinetics and are important for the regulation of CSF hydrodynamics and the exchange of substances, including antibiotics between the blood and the CNS compartments.

Normal CSF is clear and colorless. CSF sampled from the lumbar spine area in adults contains 15 to 45 mg/dL of protein and 50 to 80 mg/dL of glucose, corresponding to two-thirds of the simultaneous blood glucose value. It may also contain up to five mononuclear cells and five RBCs per microliter. More than three PMNs per microliter is considered abnormal. Trauma, spinal anesthesia, stroke, and CNS malignancy may increase the PMN count in the absence of infection. The volume of CSF sampled is usually about 15 mL divided into four tubes. Higher amounts do not seem to add to the post-LP headache risk, but elderly patients with cerebral atrophy may have a higher risk of subdural bleed.

The normal pressure measured at the lumbar space by LP is 100 to 200 mm H 2 O with the patient in the lateral recumbent position. The reliability of LP pressure measurements when the patient is sitting is uncertain. During the pressure reading, the patient’s legs should be slightly straightened to avoid compression of the intra-abdominal cavity and artificially increasing cerebral venous blood pressure. Children may have normal CSF opening pressures to 280 mm H 2 O. High CSF pressure with normal CSF content can indicate cerebral vein or dural sinus thrombosis. Cerebral venous thrombosis can be acute, subacute, or chronic in onset and often presents with new severe headache that worsens with recumbency. The headache is not a “thunderclap” type headache but can mimic a subarachnoid hemorrhage. Cerebral venous thrombosis is rare and more likely seen in young women with increased coagulation risks, such those who are pregnant or taking oral contraceptives. Specific diagnosis requires brain MRI and MR venography. Additional manifestations of intracranial hypertension include focal neurologic deficits, seizures, and encephalopathy.

Accidental breach of a small vessel in the lumbar region at the time of spinal tap may allow peripheral blood to mix with CSF, thus increasing the number of both WBCs and RBCs. The color of CSF from a traumatic tap may vary from pink to red and often shows progressive clearing in sequentially gathered collection tubes. Correction of the WBC count when CSF is contaminated with peripheral blood is done by subtracting one WBC from the CSF count for every 1000 RBCs seen, provided that the peripheral WBC count is within the normal range.

The first and third tubes usually go for microscopy to distinguish cellular constituents. A culture and potentially molecular testing—for example, via the polymerase chain reaction (PCR)—is done on the third tube of CSF. Fungal and mycobacterial cultures require larger CSF volumes. Mycobacterium tuberculosis may take 4 weeks to grow. There are nucleic acid amplification assays for M. tuberculosis , but in the United States they are approved only for sputum specimens. The second CSF tube is sent for protein and glucose. The fourth CSF tube can be held for later testing (e.g., CSF antibodies, syphilis serology, and fungal serology, especially a cryptococcal antigen). The detection of CSF autoimmune disorders requires looking for anti– N -methyl- d -aspartate (NMDA) antibodies in some encephalitis settings and occasionally a CSF protein 14-3-3 biomarker of neurodegenerative disorders such as Creutzfeldt-Jakob disease.

Xanthochromia, a yellow to amber color of the CSF, results from the breakdown of RBCs and the release of hemoglobin components. Xanthochromia requires about 4 hours to develop and suggests a subarachnoid or intracerebral bleed. However, high CSF protein concentrations or high bilirubin levels can also produce xanthochromia. Subarachnoid hemorrhage as opposed to a traumatic bloody tap would produce many RBCs, which would not reduce in number from tube one to tube three. The classic “thunderclap” headache onset is seen in many subarachnoid hemorrhages, most of which are due to leaking or ruptured cerebral aneurysms. A prodromal sentinel headache is present in as many as 40% of patients with aneurysmal subarachnoid hemorrhages. A sudden, severe headache with nausea and vomiting would not be typical of meningitis. Brain CT is more reliable than xanthochromia for diagnosing subarachnoid hemorrhage in the emergency department.

LP should always be done using sterile technique. Meningitis produced by a nonsterile LP has been well documented. Hematoma and post-LP headache are potential complications. There are concerns for brain herniation as well. When should brain imaging precede an LP to reduce the risk of intracranial hypertension and possible brain herniation? There are no studies to guide a decision here; only case reports. Herniation may occur due to increased intracranial pressure produced by meningeal inflammation unrelated to the decreased CSF pressure resulting from an LP. The presence of a brain abscess is a major concern but is more commonly associated with focal neurologic findings and a longer symptom duration than seen in meningitis. Cranial CT scans do not rule out the possibility of a very high intracranial pressure. A retrospective study of the Swedish quality registry for acute community-acquired bacterial meningitis from 2005 to 2012 suggests that LP without imaging is safe in the setting of altered mental status and leads to earlier antibiotic treatment.

Skin or deep tissue infection at the site of LP or a significant coagulation problem is a contraindication to an LP. Some guiding principles are as follows: Never delay antibiotic therapy in suspected bacterial meningitis. If brain imaging (CT scan) is imperative or a difficult LP needs to be done by interventional radiology, blood cultures should immediately be collected and appropriate antibiotic therapy started beforehand. Concomitant dexamethasone therapy is usually indicated. Generally accepted reasons for brain imaging before LP include the following: altered mental status with strong suspicion of intracranial pressure, papilledema, focal neurologic deficits, new-onset seizures, a history of stroke or CNS mass, especially in persons over 60 years of age, and an immunocompromised host. Increased intracranial pressure heightens the risk of cerebral herniation and requires emergency measures, including neurosurgical assistance ( Table 37.1 ).

TABLE 37.1
Organisms That Cause Bacterial Meningitis
Organism Age Range/Frequency Pathogenesis Risk Factors Note
Streptococcus pneumoniae Most common cause, highest mortality in all ages. Hematogenous from nasopharyngeal colonization or contiguous otitis, sinusitis. Infants or elderly, HIV, head trauma, splenectomy, IgG deficiencies, immunosuppression. Decreased prevalence since introduction of pneumococcal vaccines.
Neisseria meningitidis Endemic worldwide, epidemic in sub-Saharan Africa, increased prevalence in youth. Hematogenous from nasopharyngeal colonization. Close contacts, HIV, terminal complement deficiencies. Fluoroquinolone resistance increasing. Prophylaxis and carriage eradication needed.
Droplet isolation day 1.
Haemophilus influenzae Any age.
H. influenzae non–type b since Hib vaccine used.
Hematogenous from nasopharyngeal colonization. Nonimmunized and Native American Indian population at increased risk. Vaccines since 1980s changed disease to nontypeable or non–type b.
Listeria monocytogenes All ages but highest in newborns and elderly.
Third or fourth most common meningitis.
Gastrointestinal tract, food outbreaks, placenta. Elderly, pregnancy, immunosuppression, but about 30% occur in normal hosts. Soft cheese, milk, processed meats as sources. Listeria is neurotropic.
Resistant to cephalosporins.
Coagulase-negative Staphylococcus All ages. Dermal sinus or CNS foreign body. Surgery, ventricular shunt (LPs done without mask). Difficult to diagnose.
Group B Streptococcus (GBS) Meningitis, early onset (within 6 days).
Late onset (7–90 days).
Acquired in utero or on passage through the birth canal. Vaginal colonization, premature membrane rupture, chorioamnionitis, lack of prenatal screening. Vaginal screening and therapy in pregnancy reduces early GBS but not late GBS meningitis. Universal GBS vaccine is needed.
Staphylococcus aureus All ages.
Rare cause of community-onset meningitis.
Bacteremia or contiguous infective focus. Neurosurgery, ventricular shunt, endocarditis. MRSA complicates therapy.
Gram-negative rods Most common in neonates, infants, or after neurosurgery. Bacteremia. Advanced age, severe comorbidities, neurosurgery. Multidrug resistance is a problem.
CNS, Central nervous system; Hib, H. influenzae type b; HIV, human immunodeficiency virus; LP, lumbar puncture; MRSA, methicillin-resistant Staphylococcus aureus .


The incidence of meningitis in the United States and the developed world has changed greatly over the past 30 years, in large part due to the development of vaccines for H. influenzae type b, S. pneumoniae , and N. meningitidis . The incidence of bacterial meningitis in the United States is about 0.8/100,000 persons per year (approximately 2700 bacterial meningitis cases per year). Most community-acquired bacterial meningitis is caused by S. pneumoniae , N. meningitidis , H. influenzae , and L. monocytogenes .

In the population older than 50 years of age, Pneumococcus is the predominant pathogen. In neonates, group B streptococcus (GBS) (Streptococcus agalactiae) and Escherichia coli predominate. GBS meningitis can manifest within the first 6 days of life or have a late onset within 90 days. Prenatal rectovaginal screening cultures for GBS at 35 to 37 weeks of gestation and, in the setting of premature onset of labor or rupture of membranes at less than 37 weeks of gestation, the use of targeted intrapartum antibiotic prophylaxis decreased the early postpartum incidence of neonatal infection. Unfortunately, the incidence of late-onset invasive GBS infection in infants has not changed. A multivalent vaccine to prevent vaginal colonization is in development. Of note, the incidence of invasive GBS disease among nonpregnant adults in the United States has increased, abetted by chronic diseases, diabetes, and obesity. Most of this GBS increase in nonpregnant adults does not involve CNS infection.

Before the introduction of Hemophilus influenzae type b (Hib) vaccines in the late 1980s, an average of 25,000 children developed Hib yearly in the United States, amounting to about 45% of all cases of bacterial meningitis. The conjugate Hib vaccine (1990) resulted in decreased nasopharyngeal colonization and a herd immunity in the unvaccinated population. However, the lack of vaccines for other serotypes or nontypeable H. influenzae has allowed the non–type b strains to increase, especially among the elderly. Pneumococcal and meningococcal meningitis are still much more common than meningitis due to H. influenzae .

The meningitis mortality rate decreased by 70% from 1980 (1.36 deaths per 100,000) to 2014 (0.41 deaths per 100,000). Mortality is driven by host defenses, organism virulence factors, and access to care. Faster diagnosis and treatment along with immunization programs reduced mortality rates, but there is still a significant geographic variation in the United States. S. pneumoniae accounts for the most common bacterial meningitis in the United States and has the highest mortality and morbidity. Increasing age and comorbidities are the major risks. Pneumococcal vaccines—pneumococcal polysaccharide vaccine (Pneumovax 23) in the 1980s and pneumococcal conjugate vaccines (Prevnar 7 and PCV13) in 2000 and 2010—have caused a significant reduction in pneumococcal invasive disease in most age groups, especially under the age of 2 years. However, a reduction in pneumococcal meningitis specifically due to vaccines is difficult to demonstrate. Any reduction in invasive disease is serotype specific and includes unvaccinated populations by “herd immunity.” Of note, the incidence of serotype 3 invasive pneumococcal disease in unvaccinated children has not significantly changed with PCV13 (containing serotype 3) infant immunization programs. An increase in mucosal carriage of non-vaccine serotypes (serotype replacement) with lower virulence has been noted.

Since 1980, antimicrobial resistance among S. pneumoniae isolates has dramatically increased worldwide. Beta-lactam resistance is associated with reduced enzyme binding site affinity and can be overcome with higher doses. However, the CNS is an area that is both difficult to penetrate with antibiotics and relatively lacking in immunologic defenses. Consequently antibiotic resistance definitions (MICs) of beta-lactams defining resistance are much lower for CNS infections than for other anatomic locations. A relatively low dose of a beta-lactam will treat a pneumonia or skin/soft tissue infection, whereas meningitis will call for much higher dosing.

N. meningitidis can cause epidemics; the most devastating occur in the sub-Saharan “meningitis belt.” In the United States, N. meningitidis is the second most common cause of meningitis, with serogroups B, C, and Y accounting for about two-thirds of the cases. The Centers for Disease Control and Prevention (CDC) reported a total of 350 meningococcal meningitis cases in 2017; 92% were sporadic, unrelated to an outbreak. Risk factors include close contact among cases (within households, in military barracks or college dorms), men who have sex with men, travelers to hyperendemic areas (e.g., the Hajj pilgrimage), and complement component deficiencies. Quadrivalent meningococcal polysaccharide conjugate vaccines (MenACWY-DT) in 2005 and (MenACWY-CRM) in 2010 reduced the risk, but serogroup B increased. Serogroup B recombinant protein meningococcal vaccines (MenB) were introduced in 2015. Ongoing studies suggest that they have benefits in reducing outbreaks and nasopharyngeal carriage, but herd immunity seems lacking. Mortality from meningococcal meningitis is still around 15%, and at least 20% of survivors develop major clinical sequelae.

Listeria monocytogenes meningitis is the third or fourth most common cause of bacterial meningitis. Approximately 30% of Listeria meningitis occurs in normal hosts; 60% is seen in compromised hosts, including alcoholics, diabetics, pregnant women, and the extremes of age. Outbreaks are often associated with foodborne sources. Rhombencephalitis or brain-stem involvement is rare and can present over days as headache, fever, and gastrointestinal complaints followed by cranial nerve deficits, cerebellar signs of tremor or ataxia, seizures, and obtundation. Brain-stem involvement may mimic herpes simplex encephalitis and a variety of other infective and noninfective brain-stem diseases. Listeria under the microscope is a tiny gram-positive rod that may be difficult to see on a CSF smear and may be misidentified as a diphtheroid or possible contaminant on culture. Of note, Listeria is intrinsically resistant to cephalosporins, and adjuvant steroid use in Listeria meningitis may be detrimental.

Nosocomial meningitis usually occurs as a complication of neurosurgery or head trauma. Postoperative CNS infection can manifest as meningitis, brain abscess, or subdural/epidural empyema. Depending on the virulence of the involved organisms, infection becomes clinically apparent within hours to days or even weeks after invasive procedures on the head or spine. Unlike community-acquired meningitis, the causative organisms differ significantly, with S. aureus , coagulase-negative staphylococci, Cutibacterium spp. ( Propionibacterium spp.), and gram-negative rods predominating. The incidence of nosocomial meningitis is approximately 1% following craniotomy procedures. In addition to recent neurosurgery, risk factors for infection include placement of CSF drainage tubes, head trauma within 1 month, and CSF leaks, which may cause recurrent meningitis.

Recurrent meningitis can arise in both the community and nosocomial settings and may have an incidence as high as 6% in the combined settings. Recurrent meningitis is also associated with deficiencies of one or more terminal complement components in the case of recurrent meningococcal infections or an immunoglobulin deficiency, a splenectomy, or a chronic CSF leak in the case of recurrent pneumococcal meningitis. Immunizations seem justified but are often overlooked. Of note, a case control study (2008 to 2017) from Kaiser Permanente Northern California found that a history of prior head injury or spine surgery well beyond the 30-day postoperative period was a potential risk for pneumococcal meningitis among adults.

The term “aseptic meningitis” has been applied to patients with clinical and laboratory signs of meningeal inflammation who have negative bacterial or fungal cultures. Viruses produce most cases of aseptic meningitis, which is much more common than bacterial meningitis. Other infective causes include partially treated bacterial meningitis, parameningeal infections, infections with mycobacteria, fungi, spirochetes (syphilis, neuroborreliosis, or leptospirosis), and parasites. Hypersensitivity reactions to medication (e.g., nonsteroidal antiinflammatory drugs [NSAIDs], sulfa drugs), malignancy, and immunologic disorders such as anti-NMDA-receptor encephalitis can produce meningeal inflammation. The extent of CSF inflammation and the cellular composition can vary widely and may be of limited diagnostic value. Predominantly lymphocytic CSF pleocytosis and mild chemical abnormalities are suggestive of viral meningitis, whereas other causes can result in mixed cellular inflammations (e.g., tuberculous meningitis or predominantly granulocytic inflammation resembling bacterial meningitis). Unfortunately the clinical and laboratory findings are not sensitive or specific. The clinical history (time of year, location, exposures, etc.) and the physical findings (rash, encephalopathy, seizures, etc.) are of some differential value but lack both sensitivity and specificity.

Most viral meningitis in adults and children is caused by enteroviruses and typically occurs from May through October in the Western Hemisphere. All members of the herpesvirus family can produce an aseptic meningitis syndrome year round. PCR testing has helped to define the cause of aseptic meningitis. Herpes simplex virus 2 (HSV-2) may be the second most common cause of aseptic meningitis in adults. A retrospective review of adults with HSV-2 in CSF found that most did not have concomitant genital lesions. It also found recurrent viral meningitis uncommon, although HSV-2 has been said to be a common cause of Mollaret syndrome, a recurrent benign lymphocytic meningitis. Other common causes of viral meningitis include mumps, varicella zoster virus, arthropod-borne viruses, lymphocytic choriomeningitis, and several adenovirus serotypes. A subset of patients with acute human immunodeficiency virus (HIV) infections will develop meningitis or meningoencephalitis manifested by headache and confusion as well as occasional focal neurologic deficits.

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