eMedicine Specialties > Neurology > Neurological Infections

Viral Meningitis

Author: Amir Vokshoor, MD, Staff Neurosurgeon, Department of Neurosurgery, Spine Surgeon, Diagnostic and Interventional Spinal Care, St John's Health Center
Coauthor(s): Cordia Wan, MD, Staff Neurologist, Beverly Hills Pain and Neurology Institute
Contributor Information and Disclosures

Updated: Oct 28, 2009

Introduction

Background

Viral meningitis is inflammation of the leptomeninges as a manifestation of CNS infection. Viral names the causative agent, and the term meningitis implies lack of parenchymal and spinal cord involvement (otherwise called encephalitis and myelitis, respectively). Viral meningitis is also often referred to as aseptic meningitis.


In uncomplicated viral meningitis, the clinical course is usually self-limited, with complete recovery in 7-10 days. However, when the viral pathogen causes a more involved meningoencephalitis or meningomyelitis, the course can be significantly more protracted.

Currently, more than 85% of viral meningitis cases are caused by nonpolio enteroviruses. Disease characteristics, clinical manifestations, and epidemiology generally mimic those of enteroviral infections.

Mumps, polio, and lymphocytic choriomeningitis viruses (LCMV) are now rare offenders in developed countries. However, polio remains a major cause of debilitating myelitis in some regions of the world.

For the clinician, consideration of other pathogens such as bacteria, mycoplasma, or fungi is crucial. Partially untreated bacterial meningitis in particular can present similarly to viral meningitis. These are treatable pathogens that can have devastating outcomes if misdiagnosed. The physician should also realize that the picture of aseptic meningitis is created not only by infectious agents, but also by chemical irritation (chemical meningitis), neoplasm (meningitis carcinomatous), granulomatous disorders, and any other inflammatory conditions. This discussion, however, will focus on meningitis by viral agents.

This rash consists of an enlarging annular plaque...

This rash consists of an enlarging annular plaque. Image courtesy of Lyme Disease Network (http://www.lymenet.org/).

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This rash consists of an enlarging annular plaque...

This rash consists of an enlarging annular plaque. Image courtesy of Lyme Disease Network (http://www.lymenet.org/).


Pathophysiology

Viral pathogens may gain access to the CNS via 2 main routes: hematogenous or neural. The hematogenous route is more common for penetration of most known viral pathogens. Neural penetration refers to spread along nerve roots and usually is limited to herpes viruses (HSV-1, HSV-2, and varicella zoster virus [VZV] B virus), and possibly some enteroviruses.

Multiple host defenses prevent viral inoculum from causing clinically significant infection. These include local and systemic immune responses, skin and mucosal barriers, and the blood-brain barrier (BBB).

The virus replicates in the initial organ system (ie, respiratory or gastrointestinal mucosa) and gains access to the bloodstream. Primary viremia introduces the virus to the reticuloendothelial organs (liver, spleen, and lymph nodes.) If the replication persists despite immunologic defenses, secondary viremia occurs, which is thought to be responsible for seeding of the CNS. Rapid viral replication likely plays a major role in overcoming the host defenses.

The actual mechanism of viral penetration into the CNS is not well understood. The virus may cross the BBB directly at the capillary endothelial level or through natural defects such as the area postrema and other sites that lack a BBB. The inflammatory response is seen in the form of pleocytosis; polymorphonuclear leukocytes (PMNs) lead the differential cell count in the first 24-48 hours, followed later by increasing numbers of monocytes and lymphocytes. The cerebrospinal fluid (CSF) lymphocytes have been recognized as T cells, although B cell immunity is also important in defending against some viruses.

Evidence exists that some viruses gain access to the CNS by retrograde transport along nerve roots. For example, the likely pathway for HSV-1 encephalitis is via the olfactory or trigeminal nerve roots, with the virus being transported by the olfactory fibers to the basal frontal and anterior temporal lobes.

Frequency

United States

More than 10,000 cases of viral meningitis are reported annually, but the actual incidence may be as high as 75,000. Lack of reporting is due to the uneventful clinical outcome of most cases and the inability of some viral agents to grow in culture. According to CDC reports, inpatient hospitalizations resulting from viral meningitis range from 25,000-50,000 each year. An incidence of 11 per 100,000 population per year has been estimated in some reports.

International

Obtaining accurate international prevalence and incidence of this clinically heterogenous and often benign disease is difficult. Worldwide causes of viral meningitis include enteroviruses, mumps virus, measles virus, VZV, and HIV. Meningitis symptoms may develop in as few as 1 in 3,000 cases of infection by these agents. Studies from Finland have estimated the incidence to be 19 per 100,000 population in children aged 1-4 years. This is in significant contrast to 219 cases per 100,000 population estimated for children younger than 1 year. Japanese B encephalitis virus, the most common pathogen in epidemic viral meningitis worldwide, accounts for more than 35,000 infections annually throughout Asia but is estimated to cause 200-300 times that number of subclinical infections.

The distribution and attack characteristics of some agents, such as arboviruses, which are transmitted by arthropod vectors, show strong geographic variability. Lack of effective vaccination policies in some Third World countries plays a role in the geographic discrepancy of other infectious agents.

Mortality/Morbidity

  • Excluding the neonatal period, the mortality rate associated with viral meningitis is less than 1%; the morbidity rate is also low.
  • Some controversy exists as to the long-term effects on children, with some studies attributing learning disabilities, neuromuscular impairments, and deafness to viral meningitis. Investigators believe that most of these cases must involve the CNS parenchyma, causing encephalitis or encephalomyelitis. Children may complain of irritability, incoordination, and inability to concentrate for several weeks or longer. Infants with enteroviral meningitis during the first few months of life may have an increased risk of altered language development.
  • Physicians must realize that viruses capable of causing meningitis also can cause more serious infections of the CNS as well as other organs. The World Health Organization (WHO) statistical reports from 1997 reported enteroviral meningitis with sepsis as the fifth most frequent cause of neonatal mortality. Complications such as brain edema, hydrocephalus, and seizures can occur in the acute period and are discussed later in this article.

Race

No specific racial predilection has been identified.

Sex

Depending on the type of viral pathogen, the ratio of affected males to females can vary. Enteroviruses are thought to affect males 1.3-1.5 times more often than females. Mumps virus is known to affect males 3 times more frequently than females. Most arboviruses have diverse attack characteristics, affecting both sexes but at different ages.

Age

  • The incidence of viral meningitis drops with age.
  • Neonates are at greatest risk and have the most significant risk of morbidity and mortality.
  • In neonates older than 7 days, enteroviruses are the most common cause of aseptic meningitis. Vaccination has greatly reduced the incidence of meningitis from mumps, polio, and measles viruses.
  • The incidence during the first year of life is 20 times higher than in older children and adults.
  • Some of the arboviruses strike at the extremes of age, with the elderly at greater risk of infection, while mumps and measles peak in the later teenage years.

Clinical

History

  • Upon presentation, most patients report fever, headache, irritability, nausea, vomiting, stiff neck, rash, or fatigue within the past 18-36 hours.
    • Headache is almost always present and often reported as severe. However, the classic description of abrupt onset of the "worst headache of my life," attributable to aneurysmal subarachnoid hemorrhage, is uncommon.
    • Constitutional symptoms of vomiting, diarrhea, cough, and myalgias appear in more than 50% of patients.
    • History of temperature elevation occurs in 76-100% of patients who come to medical attention. A common pattern is low-grade fever in the prodromal stage and higher temperature elevations at the onset of neurological signs.
    • Younger children may not report headache and may simply be irritable.
    • Newborns may present with poor feeding and lethargy.
  • Some viruses cause rapid onset of the above symptoms, while others manifest as nonspecific viral prodromes, such as malaise, myalgia, and upper respiratory symptoms. In many cases, symptoms have a biphasic pattern; the nonspecific flu-like symptoms and low-grade fever precede neurologic symptoms by approximately 48 hours. With the onset of neck stiffness and headache, the fever usually returns.
  • Meticulous history taking is essential and must include evaluation of exposure to ill contacts, mosquitoes, ticks, outdoor activity in areas of endemic Lyme disease, travel history with possible exposure to tuberculosis, as well as history of medication use, intravenous drug use, and sexually transmitted disease risk.
  • An important part of the history is prior antibiotic use, which may alter the clinical picture of bacterial meningitis.

Physical

General physical findings in viral meningitis are common to all causative agents, but some viruses produce unique clinical manifestations that help in focusing the diagnostic approach. The classically taught triad of meningitis consists of fever, nuchal rigidity, and altered mental status, but not all patients have all three symptoms, and almost all patients have headache. The examination reveals no focal neurological deficits in the majority of cases.

  • Fever is common (80-100% of cases) and usually ranges between 38ºC and 40ºC.
  • Nuchal rigidity or other signs of meningeal irritation (Brudzinski or Kernig sign) may be seen in more than half of patients but is generally less severe than in bacterial meningitis. Pediatric patients, especially neonates, tend not to exhibit nuchal rigidity on examination.
  • Irritability, disorientation, and altered mentation may be seen. Severe lethargy or bulging fontanelle in neonates are signs of increased intracranial pressure but may be absent in more than half of cases. The neonate may exhibit hypotonia, irritability, and poor feeding. The clinical picture can mimic neonatal bacterial septicemia accompanied by multiple organ system involvement.
  • Headache is common and is characteristically severe.
  • Photophobia is relatively common but may be mild. Phonophobia may also be present.
  • Seizures occur occasionally and are usually from the fever, although the involvement of brain parenchyma (encephalitis) should be considered. Global encephalopathy and focal neurological deficits are rare but can be present. Deep tendon reflexes are usually normal but may be brisk.
  • Other signs of specific viral infection can aid in diagnosis. These include the following:
    • Pharyngitis and pleurodynia in enteroviral infections
    • Skin manifestations, such as zoster eruption in VZV, maculopapular rash from measles and enteroviruses, vesicular eruption by herpes simplex, and herpangina in coxsackievirus A infections.
    • Pharyngitis, lymphadenopathy, and splenomegaly suggest Epstein-Barr virus (EBV) infection.
    • Immunodeficiency and pneumonia should suggest adenovirus, cytomegalovirus (CMV), or HIV as the causative agent.
    • Parotitis and orchitis can occur with mumps
    • Gastroenteritis and rash occur with most enteroviral infections.

Causes

Many viruses are capable of causing meningitis. This discussion attempts to simplify the microbiology of each viral family with emphasis on disease manifestations and risk factors. Note that in as many as one third of cases, no causative agents are identified. This number is improving with new testing methodologies.

  • Enteroviruses account for more than 85% of all cases of viral meningitis. They are part of the viral family Picornaviridae ("pico" for small, "rna" for ribonucleic acid), and include echoviruses, coxsackieviruses A and B, polioviruses, and the numbered enteroviruses. Nonpolio enteroviruses are common viruses, nearly as prevalent as rhinoviruses (which cause the common cold).
    • The overwhelming majority of meningitis cases are caused by serotypes of coxsackievirus and echovirus. Coxsackievirus B subgroups alone account for more than 60% of meningitis cases in children younger than 3 months.
    • Enteroviruses enter the human host usually via the oral-fecal route, but can also spread through the respiratory route.
    • Enteroviruses are ubiquitous in the summer and early fall; their propensity to cause infection during the warmer months is the major factor in the higher incidence of aseptic meningitis during that time.
    • The associated clinical findings in enteroviral infections may include pharyngitis, pleurodynia, rash, and pericarditis.
    • Expectant mothers infected with coxsackievirus B may remain minimally symptomatic, but their infants can acquire the infection perinatally and develop a potential fatal illness, with the infection targeted mainly toward the heart.
    • Enteroviruses 70 and 71, which exhibit strong neurotropism, are associated with meningoencephalitis, poliolike paralytic syndromes, and Guillain-Barre syndrome, as well as aseptic meningitis.
  • Arboviruses account for about 5% of cases in North America
    • Arboviruses consist of more than 500 viruses from different viral families, all given the common name of "ar-bo" for arthropod-borne disease. Blood-sucking arthropods, usually mosquitoes, serve as vectors for transmission.
    • Since exposure to mosquito or ticks is the risk factor for transmission, the number of infections is highest in summer and early fall, in concordance with high mosquito populations.
    • Some of the important arboviruses include the eastern and western equine encephalitis viruses in the Togavirus family; St. Louis encephalitis, West Nile, Japanese B, and Murray Valley viruses of the Flavivirus family; and California group and Jamestown Canyon viruses from the Bunyaviridae family. Colorado tick fever is caused by a coltivirus in the western regions of the United States.
    • The most common clinical manifestation is meningoencephalitis rather than pure meningitis
    • Seizures are more common with arboviral meningitis than any other group of viruses.
    • Some agents preferentially infect certain age groups, such as St. Louis encephalitis, which affects the extremes of age, and California virus, which infects young children.
      • Children with St. Louis or California group encephalitis viruses may not exhibit any neurological signs or altered mental status.
      • St. Louis encephalitis (SLE) virus is the most common cause of arboviral meningitis, and is also the most common overall mosquito-transmitted disease in the United States. Japanese B virus is the biggest offender of this group internationally.
  • Of the arboviruses, West Nile virus caused much recent attention as it was first recognized in the United States only in 1999 and quickly became an epidemic in 2002 with more than 4,000 reported cases. In 2008, 1,356 cases were reported.1
    • Infection with the West Nile virus is usually asymptomatic or manifests as mild symptoms of nonspecific fever, myalgia, fatigue.  However, 1 in 150 cases develop into severe disease involving the nervous system, with encephalitis reported more than meningitis. In 2008, 687 cases of West Nile neuroinvasive disease were reported to the CDC from all across the US.1
    • Neuroinvasive West Nile disease occurs more often in elderly persons.
  • Mumps: A member of the Paramyxovirus family, mumps virus was one of the first known causative agents of meningitis and meningoencephalitis.
    • The incidence of mumps in the vaccination era has decreased significantly to 1 per 100,000 population in the United States. Nonetheless, outbreaks have occurred in vaccinated populations, including a large epidemic in the United Kingdom that peaked in 2005, and several outbreaks in the American Midwest in 2006.2  In addition, mumps continues to cause 10-20% of meningitis and meningoencephalitis cases in parts of the world where vaccines are not readily accessible. 
    • Males 16-21 years of age are at highest risk of developing this infection, with a 3:1 male/female ratio.
    • Clusters of cases occur in schools and colleges in the winter months.
    • Concomitant parotitis is a helpful clinical tool but may be absent in as many as half of cases with CNS involvement.
    • A cohort study of 12,000 unvaccinated children from northern Finland revealed mumps meningoencephalitis accounting for 40.9% of all viral CNS infections. It also remains an important cause of aseptic meningitis in England and Japan.
    • in 2003, epidemics of aseptic meningitis following MMR vaccination campaigns in various nations (including Brazil and the UK) prompted the Global Advisory Committee on Vaccine Safety to conduct a review of vaccine-derived mumps meningitis.3  At the time, the committee stated that certain strains of the mumps vaccine (Urabe, Leningrad-Zagreb, and Leningrad-3 strains) were associated with higher incidences of postvaccination aseptic meningitis. Later in 2006, the committee determined that the international literature reviewed were actually inconclusive and further studies were needed.4  Even so, replacement mumps components were developed and vaccines reformulated worldwide.     
  • Herpes family viruses: HSV-1, HSV-2, VZV, EBV, CMV, and human herpesvirus 6 collectively cause approximately 4% of cases of viral meningitis, with HSV-2 being the most common offender.
    • They may attack any time of the year.
    • The disease is often self-limited. When associated with encephalitis, however, the mortality rate can be high. Early treatment with acyclovir can significantly reduce morbidity.
    • HSV-1 remains the most common cause of sporadic encephalitis, while HSV-2 infections of CNS mostly are restricted to aseptic meningitis.
    • HSV-2 genital infection may precede meningitis; sexual contact with actively infected individuals is one of the known risk factors. In one review, however, only 3 of 23 patients with HSV-2 meningitis had a history of prior genital herpes or had genital lesions noted at the time of presentation.5 Maternal-fetal transmission of HSV-2 can occur, leading to significant systemic sequelae including infantile septicemia and death.
    • EBV, HSV-1, and especially HSV-2 have been associated with Mollaret meningitis, a rare, benign, recurrent meningitis that resolves spontaneously.  Mollaret cells (activated monocytes with atypical appearance of enlarged, bilobed nuclei and amorphous cytoplasm) are found in the CSF usually on the first day of symptoms. Herpesvirus 6, EBV, and HIV have also been implicated.  These viruses are all known to remain latent within the nervous system.
    • CMV infections occur mostly in immunocompromised hosts. CMV may cause a subacute encephalitis in patients with AIDS. Congenital CMV, which is a much more serious form of infection, has significant associated morbidity and mortality. 
    • Childhood or adult chickenpox infections by VZV rarely are complicated by meningitis. Adult zoster involving any dermatome may lead to meningitis or meningoencephalitis.
  • Lymphocytic choriomeningitis virus: LCMV belongs to the family of arenaviruses. Now a rare cause of meningitis, the virus is transmitted to humans by contact with rodents (eg, hamster, rats, mice) or their excreta. Those at highest risk are laboratory workers, pet owners, or persons living in nonhygienic areas.
  • Adenovirus: Adenovirus is a rare cause of meningitis in immunocompetent individuals but a major cause in AIDS patients. The infection may occur simultaneously with an upper respiratory infection.
  • Measles: This Morbillivirus is another now  rare cause. The characteristic maculopapular rash aids in the diagnosis. Most cases occur in younger people in schools and colleges. Measles remains a worldwide health threat with the highest attack rate of any infection; eradication of measles is an important public health goal of the WHO.
  • HIV: HIV may be a cause of atypical meningitis characterized by chronicity and recurrence. About the time of seroconversion, patients may present with CSF pleocytosis, elevated protein level and, occasionally, high intracranial pressure. Reports have suggested that as many as 5-10% of HIV infections can be heralded by meningitis. Aside from the usual meningeal signs, HIV infections may also cause global encephalopathy, seizures, and focal neurologic deficits. Some patients develop chronically abnormal CSF findings with mild or no symptoms. HIV often can be isolated from the CSF.
  • Tuberculous, fungal, mycoplasmal, and other causes of nonbacterial meningitis are not included in this discussion since they are not viruses. However, they are important causes of aseptic meningitis and should be suspected in the appropriate clinical setting. For example, Lyme borreliosis causes a significant number of cases of aseptic meningitis in the Northeast and Mid-Atlantic states. The diagnosis is suggested by the history of tick bite or outdoor activity in these areas of endemic disease, and presence of erythema chronicum migrans at the site of tick bite is pathognomonic. Lyme meningitis has a predilection to cause focal cranial nerve palsies, with the seventh nerve most commonly affected.
  • Clinicians must consider partially treated bacterial meningitis as a possible etiology for the aseptic nature of their patient's disease; for example, patients with bacterial otitis and sinusitis who have been taking antibiotics may present with meningitis and CSF findings identical to viral meningitis.

More on Viral Meningitis

Overview: Viral Meningitis
Differential Diagnoses & Workup: Viral Meningitis
Treatment & Medication: Viral Meningitis
Follow-up: Viral Meningitis
Multimedia: Viral Meningitis
References
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References

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Further Reading

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Keywords

aseptic meningitis, serous meningitis, nonpyogenic leptomeningitis, abacterial meningitis, enterovirus, coxsackievirus, echovirus, viral meningitis, viral infection, herpes viruses, HSV-1, HSV-2, varicella zoster virus, VZV, B virus

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Contributor Information and Disclosures

Author

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.

Coauthor(s)

Cordia Wan, MD, Staff Neurologist, Beverly Hills Pain and Neurology Institute
Cordia Wan, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Medical Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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; Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Paraplegia Society, and National Multiple Sclerosis Society
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

 
 
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