By antibody and antigen tests at Rigshospitalet University Hospital, Department of Virology, Statens Serum Institut, Copenhagen, and Bernhard Nocht Institut, Hamburg, the patient was found negative for HSV, VZV, Enterovirus, Parechovirus, West Nile virus, Chicungunya virus, Rickettsia, Mycobacterium tuberculosis, tick borne encephalitis, Toxocara canis, malaria, and syphilis. Slightly elevated

Dengue virus immunoglobulin M (IgM) antibodies with identical titers were found in blood samples on days 8 and 19, but were interpreted as unspecific reactions. While blood and CSF samples drawn on day 1 of admission were negative for JE antibodies, blood samples drawn later were antibody positive: day 8 IgM 1 : 160 and immunoglobulin G (IgG) 1 : 1,280; day 19 IgM 1 : 320 and IgG 1 : 1,280; day 36 IgM negative and IgG 1 : 320. A CSF sample EPZ015666 manufacturer drawn on day 19 was antibody positive (IgM 1 : 10 and IgG 1 : 80). All samples were polymerase chain reaction negative for JE RNA (blood on days 8 and 19; CSF on days 1, 3, 8, 19, and 36). The patient gradually improved over the next couple of months although he was continuously lethargic with mild cognitive impairment and upper left extremity paresis. Four months after symptom debut he suddenly had a generalized seizure. On arrival at hospital, he went into cardiac arrest and Sirolimus supplier was declared dead. No autopsy was performed. A classical presentation

of symptomatic JE includes an incubation period of 5 to Liothyronine Sodium 15 days and 2 to 4 days of non-specific illness followed by headache, fever, rigor, gastrointestinal symptoms, and an encephalitis syndrome characterized by behavioral abnormality, alteration in sensorium, seizures, and neurological deficit in the form of hemiplegia, quadriplegia, or

cerebellar signs.1 The upper extremities are more commonly affected than the lower limbs. Bilateral thalamic lesions in encephalitis patients are highly indicative of JE.2,3 About 50% of survivors have severe neurological sequels in the form of cognitive impairment, behavioral abnormality, focal weakness, seizures, and a variety of movement disorders.1 JE virus cannot usually be isolated in primarily infected patients who instead mount an IgM antibody response. The patient’s symptoms, clinical findings, course of disease, and JE antibody response indicative of acute infection were perfectly compatible with such a classical JE presentation. The concerning thing about this case is that the patient was not at particular risk of JE. Although he had traveled to an endemic country (Cambodia), he had only been in Cambodia for 14 days, he had visited parts of Phnom Penh and Angkor Wat/Siem Reap, where pigs were not kept, and he had not had any contact with such animals. He had used mosquito repellent and had only to a lesser degree been bitten by mosquitoes. As far as we know this patient is the first JE patient among western travelers to Cambodia.