Severe Ebola Virus Infection With Encephalopathy: Evidence for Direct Virus Involvement

To the Editor—Major neurological signs are infrequent in Ebola virus (EV) disease. When present, they consist mainly of meningitis, encephalopathy, and seizures [1, 2]. The physiopathology of brain impairment in EV disease is not well understood. Here, we report the case of an EV disease patient with encephalitis and meningitis from whom cerebrospinal fluid (CSF) was obtained. A 21-year-old man without any remarkable medical history was referred to our Ebola healthcare center with a 5-day history of severe febrile gastroenteritis and headache. At admission, the patient complained of diarrhea, vomiting, and abdominal pain and had signs of dehydration without neurological impairment or hemorrhagic symptoms. Throughout his stay, the patient's core body temperature was ≤38°C and his systolic blood pressure was >100 mmHg. He tested positive for EV (blood subjected to polymerase chain reaction; cycle threshold, 14.4); an immunochromatographic rapid test for malaria was negative. A routine blood panel revealed an elevated partial thromboplastin time (PTT) that was 4.4-fold the upper limit of normal values (ULN), an international normalized ratio (INR) of 1.9, a serum creatinine level of 173 µmol/L, and a high aspartate aminotransferase level (23-fold ULN). Twenty-four hours after being admitted, the patient worsened, exhibiting signs of hemorrhagic syndrome onset (ie, including hematuria, hemoptysis, and bleeding gums) and demonstrating an INR that had increased to 2.9. He was given 4 units of French lyophilized plasma. The next day, the patient was stuporous with nuchal stiffness and seizures but remained without focal neurologic signs. A lumbar puncture performed to test for bacterial meningitis revealed sterile CSF with no red or white blood cells. The patient's viral load was 105 copies/mL CSF and 6 × 109 copies/mL blood. His blood and CSF glucose levels were both 3.7 mmol/L. Proteinorachia could not be assessed due to the lack of an appropriate device. The patient died within 24 hours of the lumbar puncture. A few hours before the patient died, biologic analyses disclosed coagulopathy with a normal platelet count (PTT, 7.2-fold ULN; INR, 6.2), renal impairment (high serum creatinine [234 µmol/L] and urea [10.1 mmol/L]), and hyponatremia (130 mmol/L).

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