Eastern Equine Encephalitis (EEE) Clinical Presentation

Because of the lack of specific symptoms, eastern equine encephalitis (EEE) is difficult to diagnose. A rewarding diagnostic approach is to determine the extent of the patient’s illness and to determine whether central nervous system (CNS) infection is present. The prodromal phase is often short (average, 5-10 days) and consists of fever, headache, and some abdominal pain with diarrhea. Compared with other alphavirus infections, EEE progresses more rapidly to both CNS involvement and death. Once symptoms arise, the patient often deteriorates rapidly.

Neurologic symptoms include the following:

• Headache - Most prevalent symptom

• Nausea or vomiting - Present in both the prodromal and active stages of the infection

• Confusion

• Focal neurologic deficits - Sensory or motor loss (relatively low prevalence of focal deficits)

• Seizures – Reported in roughly 50% of patients (most often generalized tonic-clonic with occasional partial complex seizures)

• Somnolence

• Neck stiffness

• Malaise and weakness

• Cranial nerve palsies - Often developing either directly from the disease or secondary to elevated CSF pressure (nerves most commonly affected are VI, VII, and occasionally XII)

• Photophobia

• Autonomic disturbances (eg, sialorrhea)

Other associated symptoms include the following:

• Fever - Almost invariably present at some point

• Chills

• Abdominal pain

• Diarrhea

• Sore throat

• Arthralgia or myalgia

• Respiratory difficulty

The following are other important factors to consider in the patient’s history:

• Social history

• Recent travel to endemic areas

• Outdoor exposure history

• Work related to the care of horses or work located in marshes

• Recent insect bites

• Work or home in areas with high mosquito counts

The physical examination for EEE also is nonspecific, yielding findings similar to those seen with many other encephalitides.

Changes in vital signs may include the following:

• Fever

• Tachycardia

• Possible tachypnea

Neurologic findings may include the following:

• Bilateral papilledema

• Nuchal rigidity

• Focal sensory or motor deficit

• Depressed or hyperactive reflexes

• Tremors

• Fasciculations

• Seizure activity

• Spastic paralysis

Other findings may include the following:

• Cyanosis - With respiratory compromise

• Facial, periorbital, or generalized edema

• Lymphadenopathy - Not necessarily present

Possible pharyngeal erythema

The primary complication, other than death, is often a variable level of CNS impairment. Numerous factors, including location and specific inflammatory cell response, may determine the result.

Demyelination is a known by-product of this disease and can be radiologically detected. Often, these areas heal well, unless overlying fibrosis is present or cell death occurs.

Additional potential complications include the following:

• Mental retardation

• Behavioral changes

• Paralysis

• Permanent focal neurologic deficits

• Seizure disorders

• Emotional lability

• Adjustment disorders