Encephalitis– An inflammation of the tissues of the brain and spinal cord that may result in altered neurologic function.

Causes and Incidence

The cause of primary encephalitis is usually direct invasion by one of several viruses (arbovirus, enterovirus, adenovirus, herpes virus, mumps virus). The mode of transmission is usually a mosquito bite, but ticks and amebae may also transmit the virus. Some forms of the virus (e.g., herpes virus) may be spread by direct contact with nasal excretions or open lesions. A rarer secondary encephalitis may occur as a complication of another primary viral infection such as measles, chicken pox, or rubella. Primary encephalitis occurs worldwide and may be sporadic or epidemic.

Disease Process

Within 24 hours of contact, the virus invades the bloodstream, lymph nodes, bone marrow, and most organs. Within 48 hours there is marked lymphocyte destruction and necrosis of lymph nodes. By day 4, macrophages have replaced the destroyed lymph nodes, bone marrow is depleted, and the cytoplasm and megakaryocyte nuclei are degenerating. The viral titer declines in peripheral tissues and increases in the brain. By day 6, there is extensive involvement of the meninges, brain, and spinal cord, with petechial hemorrhages, lymphocytic perivascular cuffing, gliosis, and neuronal necrosis, causing cerebral dysfunction.


Subclinical cases of encephalitis do occur and are largely asymptomatic or are accompanied by flulike symptoms such as fever and general fatigue. Common early signs of encephalitis are fever, severe frontal headache, nausea, and vomiting. If encephalitis is untreated, neurologic signs that may manifest 6 to 7 days after initial infection are nuchal rigidity, lethargy, confusion, stupor, coma, seizure activity, and extremity paralysis.

Potential Complications

The likelihood of complications is related to the etiologic agent and the person’s general premorbid condition. Complications include permanent neurologic damage and death.

Diagnostic Tests

Clinical evaluation
History of exposure; nuchal rigidity; positive Kernig’s sign; pathologic reflexes; muscle weakness; paralysis

Cerebrospinal fluid
Elevated pressure; WBCs, proteins slightly elevated; glucose normal; clear fluid; occasionally isolation of the virus (mobile amebae can be seen on wet mount)

Increase in antibody titer early in disease

Immunofluorescent stain of biopsy brain tissue
Positive for specific viruses



Antiinfective drugs for amebic infections: acylovir for herpes infections; sedatives for restlessness; anticonvulsants for seizure activity; mannitol and corticosteroids to reduce cerebral edema and inflammation.

Maintenance of fluid and electrolytes; maintenance of the airway: may need mechanical ventilation; oxygen to maintain blood gases; maintenance of nutritional status: may need nasogastric tube; seizure precautions; rest; neurologic assessments; secretion precautions to prevent transmission of some viral agents; prevention of spread through mosquito-ant-tick control.