Viral meningitis

Viral meningitis characteristically presents with fever, headache and neck stiffness.[11] Fever is the result of cytokines released that affect the thermoregulatory neurons of the hypothalamus. Cytokines and increased intracranial pressure stimulate nociceptors in the brain that lead to headaches. Neck stiffness is the result of inflamed meninges stretching due to flexion of the spine.[12] In contrast to bacterial meningitis, symptoms are often less severe and do not progress as quickly.[11] Nausea, vomiting and photophobia (light sensitivity) also commonly occur, as do general signs of a viral infection, such as muscle aches and malaise.[11] Increased cranial pressure from viral meningitis stimulates the area postrema, which causes nausea and vomiting. Photophobia is due to meningeal irritation.[12] In severe cases, people may experience concomitant encephalitis (meningoencephalitis), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits.[13]

Babies with viral meningitis may only appear irritable, sleepy or have trouble eating.[7] In severe cases, people may experience concomitant encephalitis (meningoencephalitis), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits.[13] The pediatric population may show some additional signs and symptoms that include jaundice and bulging fontanelles.[12]

The most common causes of viral meningitis in the United States are non-polio enteroviruses. The viruses that cause meningitis are typically acquired from sick contacts. However, in most cases, people infected with viruses that may cause meningitis do not actually develop meningitis.[7]

Viruses that can cause meningitis include:[14]

Viral Meningitis is mostly caused by an infectious agent that has colonized somewhere in its host.[15] People who are already in an immunocompromised state are at the highest risk of pathogen entry.[12] Potential sites for this include the skin, respiratory tract, gastrointestinal tract, nasopharynx, and genitourinary tract. The organism invades the submucosa at these sites by invading host defenses, such as local immunity, physical barriers, and phagocytes or macrophages.[15] After pathogen invasion, the immune system is activated.[12] An infectious agent can enter the central nervous system and cause meningeal disease via invading the bloodstream, a retrograde neuronal pathway, or by direct contiguous spread.[16] Immune cells and damaged endothelial cells release matrix metalloproteinases (MMPs), cytokines, and nitric oxide. MMPs and NO induce vasodilation in the cerebral vasculature. Cytokines induce capillary wall changes in the blood brain barrier, which leads to expression of more leukocyte receptors, thus increasing white blood cell binding and extravasation.[12]

The barrier that the meninges create between the brain and the bloodstream are what normally protect the brain from the body's immune system. Damage to the meninges and endothelial cells increases cytotoxic reactive oxygen species production, which damages pathogens as well as nearby cells.[12] In meningitis, the barrier is disrupted, so once viruses have entered the brain, they are isolated from the immune system and can spread.[17] This leads to elevated intracranial pressure, cerebral edema, meningeal irritation, and neuronal death.[12]

The diagnosis of viral meningitis is made by clinical history, physical exam, and several diagnostic tests.[18] Most importantly, cerebrospinal fluid (CSF) is collected via lumbar puncture (also known as spinal tap). This fluid, which normally surrounds the brain and spinal cord, is then analyzed for signs of infection.[19] CSF findings that suggest a viral cause of meningitis include an elevated white blood cell count (usually 10-100 cells/µL) with a lymphocytic predominance in combination with a normal glucose level.[20] Increasingly, cerebrospinal fluid PCR tests have become especially useful for diagnosing viral meningitis, with an estimated sensitivity of 95-100%.[21] Additionally, samples from the stool, urine, blood and throat can also help to identify viral meningitis.[19]

In certain cases, a CT scan of the head should be done before a lumbar puncture such as in those with poor immune function or those with increased intracranial pressure.[1]

Aciclovir

Treatment is generally supportive. Rest, hydration, antipyretics, and pain or anti-inflammatory medications may be given as needed.[22]

Herpes simplex virus, varicella zoster virus and cytomegalovirus have a specific antiviral therapy. For herpes the treatment of choice is aciclovir.[23]

Surgical management is indicated where there is extremely increased intracranial pressure, infection of an adjacent bony structure (e.g. mastoiditis), skull fracture, or abscess formation.[12]

The majority of people that have viral meningitis get better within 7–10 days.[24]

From 1988–1999, about 36,000 cases occurred each year.[25] While the disease can occur in both children and adults, it is more common in children.[1] During an outbreak in Romania and in Spain viral meningitis was more common among adults.[26] While, people aged younger than 15 made up 33.8% of cases.[26] In contrast in Finland in 1966 and in Cyprus in 1996, Gaza 1997, China 1998 and Taiwan 1998, the incidences of viral meningitis were more common among children.[27][28][29][30]

It has been proposed that viral meningitis might lead to inflammatory injury of the vertebral artery wall.[31]

The Meningitis Research Foundation is conducting a study to see if new genomic techniques can improve the speed, accuracy and cost of diagnosing meningitis in children in the UK. The research team will develop a new method to be used for the diagnosis of meningitis, analysing the genetic material of microorganisms found in CSF (cerebrospinal fluid). The new method will first be developed using CSF samples where the microorganism is known, but then will be applied to CSF samples where the microorganism is unknown (estimated at around 40%) to try and identify a cause.[32]