Encephalitis is an acute inflammation of the brain parenchyma and is usually caused by direct viral invasion. Concomitant meningitis occurring with encephalitis is known as meningoencephalitis, and the cellular infiltrate present in the CSF is typically lymphocytic rather than polymorphonuclear cells.

The host response to these CNS infections can differ somewhat from those associated with purulent or aseptic meningitis. Early in the course of viral encephalitis, or when considerable tissue damage occurs as a part of encephalitis, the nature of the inflammatory cells found in the CSF may be no different from that associated with bacterial meningitis; cell counts, however, are typically much lower.

Viral.

Viral encephalitis, which cannot always be distinguished clinically from meningitis, is common in the warmer months. The primary agents are enteroviruses (coxsackie viruses A and B, echoviruses), mumps virus, herpes simplex virus, and arboviruses (West Nile virus, togavirus, bunyavirus, equine encephalitis, St. Louis encephalitis, and other encephalitis viruses). Other viruses—such as measles, cytomegalovirus, lymphocytic choriomeningitis, Epstein-Barr virus, hepatitis, varicella-zoster virus, rabies virus, myxoviruses, and paramyxoviruses—are less commonly encountered. Any preceding viral illness and exposure history are important considerations in establishing a cause by clinical means. Since 1999, with the first debut of West Nile in the United States, the West Nile virus has been an important consideration in the diagnosis of viral encephalitis. The Centers for Disease Control and Prevention (CDC) reports that the incidence of West Nile infection peaked in 2003 with 9862 cases of West Nile infection; 2860 were reported cases of meningitis and encephalitis, resulting in 264 deaths. Since then the rates of infection have dropped: human cases reported to the CDC in 2010 were significantly lower with 1021 total reported cases of West Nile; 629 were neuroinvasive cases resulting in 57 deaths; a state by-state breakdown of the disease incidence is outlined in Table 1. In 2012, a deadly resurgence of West Nile virus occurred, including neuroinvasive and non-neuro invasive, for a total of 4531 cases through mid-October, according to the CDC.

Table1. Final 2010 West Nile Virus Human Infections in the United States *

Neuroinvasive infection with West Nile presents with symptoms of headache, fever, and a change in conscious ness along with altered mental status. The examination of the CSF shows an increase in leukocytes with a marked increase in lymphocytes. Chemistries demonstrate an elevated protein count and normal glucose levels. Definitive diagnosis requires testing for the presence of the IgM antibody to West Nile in the serum or CSF, and because IgM does not cross the blood-brain barrier, presence of IgM antibody to West Nile in the CSF is a strong indicator for CNS infection. Polymerase chain reaction (PCR) can also be used to test for West Nile infection, but because West Nile infections have a transient and low viremia, results must be interpreted with caution. A negative result does not necessarily rule out West Nile infection.

Involvement of the nervous system in patients who are infected with the human immunodeficiency virus (HIV) is common. HIV is a neurotropic (attracted to nerve cells) virus capable of entering the CNS by macro phage transport and the cause of various neurologic syndromes. As HIV-infected individuals become progressively more immunosuppressed, the CNS becomes a target for opportunistic pathogens, such as cytomegalovirus, BK virus, and JC (John Cunningham) virus, which can produce meningitis or encephalitis. BK virus is named after the initials of the first renal transplant patient where the virus was identified in association with clinical disease.

Parasitic

Parasites can cause meningoencephalitis, brain abscess (see the following discussion), or other CNS infection via two routes. A rare but devastating meningoencephalitis is caused by the free-living amebae, Naegleria fowleri and Acanthamoeba spp., which invade the brain via direct extension from the nasal mucosa. These organisms are acquired during swimming or diving in natural, stagnating freshwater ponds and lakes.

Other parasites reach the brain via hematogenous spread. Toxoplasmosis, caused by an intracellular para site that destroys brain parenchyma, is a common CNS affliction in HIV-infected patients with acquired immunodeficiency syndrome (AIDS). Entamoeba histolytica and Strongyloides stercoralis have been identified in brain tissue, and the larval form of Taenia solium (the pork tapeworm), called a cysticercus, can travel to the brain via the blood stream and encyst within the brain tissue. Amebic brain infection and cysticercosis cause changes in the CSF similar to meningitis.

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