A 65-year-old man of Scottish-American descent presented to the emergency department (ED) in late summer 2008 complaining of fever, cough, and decreased oral intake for the past seven days. His symptoms were associated with blurry vision, nausea, and weakness. Past medical history included diabetes and hypertension. He was a former smoker (quit 4 years ago) and denied travel history or sick contacts.
In the ED, he was noted to be alert, conversant, and oriented. His temperature was 100.8 F, blood pressure was 133/76 mmHg, and heart rate was 104 bpm. Physical examination was unremarkable. The eyes were normal to inspection with normal visual acuity, extra-ocular movements were intact, with no evidence of scleral icterus or conjunctival erythema. Admission labs were notable for a sodium level of 125.2 mEq/L (reference range 135-146 mEq/L) and creatinine of 1.6 mg/dL (reference range 0.7-1.5 mg/dL). The WBC count was 7.6 × 103/μL (reference range 4.8-10.8 × 103/μL). Chest roentgenogram demonstrated no acute infiltrates. Electrocardiogram (EKG) showed normal sinus rhythm at a rate of 83. Blood cultures were drawn and the patient was started on intravenous ceftriaxone and azithromycin.
On day 1, the patient became slightly confused and disoriented at times. He still complained of blurry vision and was noted to have a fever of 103.4 F. Antibiotics were changed to ceftriaxone, vancomycin, and the antiviral acyclovir was also added.
On day 2, computed tomography of the head showed chronic inflammatory changes with no acute bleed, mass effect, or shift. Lumbar puncture was conducted and revealed colorless cerebrospinal fluid (CSF), 4 RBCs/mm3, 29 WBC/mm3 (68% lymphocytes, 31% neutrophils, 1% monocytes), glucose of 115 mg/dL (serum level, 219), and a protein of 195 mg/dL. Bacterial and fungal stains were negative. Herpes simplex virus (HSV) polymerase chain reaction (PCR) of the CSF was negative. Serum Lyme antibodies were negative. Blood cultures were negative. Vancomycin was stopped, while ceftriaxone and acyclovir were continued. A transthoracic echocardiogram revealed ejection fraction of 50-55% with abnormal left ventricular relaxation and a dilated left atrium. The serum sodium level was noted to be 128 mEq/L.
On day 3, the patient was noted to be lethargic and disoriented with a fever of 104.5 F. An electroencephalogram demonstrated abnormal moderate generalized background slowing consistent with diffuse encephalopathy. Antimicrobials were continued.
On day 4, during morning rounds, the patient was his usual self, but continued to be lethargic, yet arousable and responsive to questions, with no new complaints. Ten minutes later, he was found unresponsive and pulseless. The electrocardiogram revealed asystole. As the patient was not on telemetry monitoring nor was a routine electrocardiogram ordered for that morning, there was no other electrocardiogram to compare, besides the admission EKG. Cardio-pulmonary resuscitation was unsuccessful.
Subsequently, the CSF that had been sent to the Board of Health, was reported to be positive for West Nile Virus (WNV) genome by PCR. IgM antibodies for WNV were also reported positive in the CSF. Serum IgM antibodies for WNV were not carried out. An autopsy was conducted. The central nervous system examination revealed microglial nodules, sparse perivascular lymphocytic infiltrate, and focal leptomeningeal monovascular infiltrate consistent with viral meningoencephalitis. West Nile Virus genome was also detected in the brain tissue by PCR. The cardiovascular examination demonstrated focal left ventricular scarring with lymphocytes and histiocytes consistent with myocarditis. West Nile Virus genome was not detected in the myocardium by PCR. The autopsy revealed no evidence for pulmonary embolism or acute myocardial infarction.