Recommendations

Key Recommendations

The most important differential diagnoses for viral meningitis are encephalitis and bacterial meningitis.[3] Altered behavior suggests encephalitis and should prompt empiric treatment with acyclovir, along with further tests to try to establish the diagnosis and cause. Distinguishing viral meningitis from bacterial meningitis may be difficult. If the patient is very ill, is immunocompromised, or has received prior antibiotics, empiric antimicrobial therapy may be necessary. A lumbar puncture may confirm a diagnosis of viral meningitis and allow antibiotics to be stopped.[3] If the patient appears well it may be appropriate to observe without antibiotics while the cerebrospinal fluid is analyzed.

History

The symptoms of viral meningitis are similar to those of bacterial meningitis and accurately differentiating the two may be difficult.[13] Onset of symptoms in viral meningitis may be sudden or gradual. Patients usually complain of headache and may also describe photophobia, myalgia, or pharyngitis. Children are a common source, particularly of enteroviral infection, and so there may be a history of contact with children, either within the family or at work. The classic signs and symptoms of meningitis may not be present in older people, the very young, and immunocompromised people.[13] A careful travel history may identify a history of exposure to rodents, mosquitoes, or ticks. A sexual history may reveal risk factors for recent HIV infection or a recent episode of genital herpes. The vaccination history should be established to ensure immunity to mumps. Most people with mild illness usually recover within 1 week to 10 days.[4]

Examination

Examination findings in viral meningitis may be similar to those found in acute bacterial meningitis and it may be difficult to differentiate the two conditions. A diffuse maculopapular rash is often seen with enteroviral infection but may also be seen in meningococcal disease.[27] Conversely, petechiae similar to that seen with meningococcal sepsis may be seen in enteroviral meningitis.[28] The presence of genital herpetic lesions may suggest HSV-2 as the etiologic agent; however, the majority of patients with proven HSV-2 meningitis do not have genital lesions.[3][29]​​ Recent shingles is suggestive of varicella zoster viral meningitis. Kernig and Brudzinski signs are uncommon in viral meningitis.

Investigations

The most important investigation is examination of the cerebrospinal fluid (CSF), and this should be done in all patients with suspected meningitis.[3] If there is no history of immunocompromise, no focal neurologic deficit, and no decrease in consciousness, it is not necessary to perform a CT/MRI of the brain prior to carrying out a lumbar puncture.[3][30]​​ However, in the presence of these features, imaging may help rule out other causes such as cerebral abscess or encephalitis. EEG is not routinely performed but should be considered if the patient has signs of encephalitis (diffuse/focal neurologic deficit).

In viral meningitis the CSF pressure is usually normal or slightly elevated.[13] The CSF WBC count is usually 10 to 500 per mm³, but may be normal. In early infection there may be a neutrophil predominance, but this evolves to a more typical lymphocytic picture over the first 2 days of infection. In general, the CSF glucose and the CSF:plasma glucose ratio are normal but may be low.[13] CSF protein is usually slightly elevated.[13] Bacterial culture and Gram stain of the CSF should be negative. It may be difficult to distinguish viral meningitis from bacterial meningitis (including those caused by tuberculosis) on the basis of routine examination of the CSF. Isolation of virus from the CSF by cell culture is time-consuming and expensive, and so is not available in the majority of laboratories. Molecular testing of CSF, most commonly by using nucleic acid amplification test (NAAT), has largely replaced viral culture and is the gold standard for confirming the diagnosis of viral meningitis.[31]​ Polymerase chain reaction (PCR) methods are able to detect enteroviruses and herpes viruses in the CSF more rapidly than cell culture and with greater sensitivity and specificity.[3][16]​​​[32][33]​​​​ A negative PCR does not necessarily exclude viral meningitis; some people with viral meningitis won’t have a positive PCR test. Tests for lymphocytic choriomeningitis virus (LCMV) and many of the arboviruses are less widely available and often rely on serologic techniques as well as nucleic acid amplification.[31] Highly accurate rapid diagnostic viral PCR-based tests for specific organisms (e.g., enterovirus and tuberculosis) are widely available and can provide an accurate diagnosis within hours.[34][35]​​ Establishing a diagnosis of viral meningitis may allow earlier hospital discharge and cessation of unnecessary antibiotics.

Acute meningitis may occur in the early stages of HIV syndrome. Testing for HIV is recommended for all cases of meningitis. Diagnosis is based on typical CSF findings (a mild CSF lymphocytosis with a mildly elevated CSF protein level and normal glucose) combined with definitive evidence of recent HIV infection.[31]​ Although fourth-generation ELISAs have reduced the interval between infection and testing antibody-positive to under 1 month, it may be necessary to request viral load testing if HIV seroconversion is suspected and HIV serology is negative.

Emerging tests that may help eliminate the diagnosis of bacterial meningitis include serum and CSF procalcitonin and CSF C-reactive protein. A low CSF lactate (<35 mg/dL) is useful in distinguishing viral from bacterial meningitis, particularly if it is measured prior to antibiotics being administered. Sensitivity is reduced if antibiotics have been started.[36] A meta-analysis of 25 studies found that, as a single marker, CSF lactate concentration had better diagnostic accuracy in distinguishing bacterial from aseptic meningitis when compared with CSF glucose, CSF/plasma glucose quotient, CSF protein, and CSF total number of leukocytes.[3][37]​​

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