Eastern equine encephalitis.

We describe a patient who died from a fulminant presentation of encephalitis. After an exhaustive search, we found no treatable cause. Postmortem PCR analysis of brain tissue led to a diagnosis of eastern equine encephalitis. We have identified several clinical pearls that may assist others in making the diagnosis earlier in the disease course.

Eastern equine encephalitis: a classical case.

We present the case of a 40-year-old man with rapidly deteriorating acute meningoencephalitis, finally diagnosed as eastern equine encephalitis (EEE). The course and timing in this patient are quite characteristic. EEE is an arthropod borneviral illness in which the mosquito serves as the vector. It is amongst the most severe of the arbovirus encephalitides and has a high mortality and morbidity. In nonfatal cases, residual neurological deficits are often severe and permanent. North American lineage of EEE is mainly found in the northeast especially along the coastal areas. EEE is primarily found in horses and other domestic mammals that remain outdoors nocturnally. In humans, symptoms range from nonspecific constitutional features to catastrophic neurological sequelae including death. Hyponatremia and increased cerebrospinal fluid (CSF) white blood cell count are independent predictors of poor outcomes. Diagnosis is suggestive by demonstrating IgM antibody in blood or CSF samples and can be confirmed by other serologic assay including immunohistochemistry and polymerase chain reaction (PCR). Measures recommended by the Center for Disease Control (CDC) for prevention include using repellents, protective clothing, screens, and eradication of mosquito breeding areas. EEE remains without cure and prevention is the best medicine.

Eastern equine encephalitis virus infection and hemophagocytic lymphohistiocytosis in a 5-month-old infant.

Eastern equine encephalitis virus infection is a rare sporadic central nervous system infection transmitted by a mosquito vector. Hemophagocytic lymphohistiocytosis (HLH) is a rare life-threatening disease associated with the inability of an overactive immune system to effectively respond to infections. Many viruses are known to trigger primary, as well as secondary, HLH. We report a pediatric case of eastern equine encephalitis virus-associated HLH which caused severe neurologic injury and death.

Eastern equine encephalitis in a captive harbor seal (Phoca vitulina).

A 31-yr-old male, captive harbor seal (Phoca vitulina) was evaluated for a 48-hr period of anorexia followed by the onset of seizures. A prolonged seizure failed to respond to anticonvulsant therapy and the animal was euthanized. At necropsy, no significant gross lesions were identified. Reverse transcriptase-polymerase chain reaction testing of brain samples was positive for eastern equine encephalitis virus (EEEV) RNA, and serum was positive for anti-EEEV antibodies by plaque reduction neutralization. Histopathologic evaluation revealed severe and multifocal encephalitis with leptomeningitis, characterized by neutrophilic infiltrates in neuropil, neuronal necrosis, satellitosis, neuronophagia, and perivascular cuffs of lymphocytes, macrophages, and neutrophils. Additionally there was moderate, multifocal, adrenal cortical necrosis. Immunohistochemical staining for EEEV demonstrated viral antigen within necrotic neurons and glial cells. Virus was isolated from frozen brain tissue, sequenced for comparison to other strains, and determined to be a typical North American strain. EEEV should be included as a possible cause of neurologic disease in harbor seals with compatible signs located in geographic regions where vector transmission of EEEV is encountered.