Importation of Zika Virus from Vietnam to Japan, November 2016

We report a case of Zika virus infection that was imported to Japan by a traveler returning from Vietnam. We detected Zika virus RNA in the patient’s saliva, urine, and whole blood. In the Zika virus strain isolated from the urine, we found clearly smaller plaques than in previous strains.

We report a case of Zika virus infection that was imported to Japan by a traveler returning from Vietnam. We detected Zika virus RNA in the patient's saliva, urine, and whole blood. In the Zika virus strain isolated from the urine, we found clearly smaller plaques than in previous strains.
Z ika virus has been documented in Southeast Asia since the 1940s; however, the prevalence and geographic extent of Zika virus disease in Asia remain unclear (1). In Vietnam, 219 cases of Zika virus infection were reported in 2016 and 13 new cases in 2017 (2). We report a case of Zika virus infection imported from Vietnam to Japan, diagnosed after PCR amplification of Zika virus RNA in the patient's saliva, urine, and whole blood.
A 40-year-old man came to the National Center for Global Health and Medicine in Tokyo, Japan, in the middle of November 2016 with fever and a rash. In early November 2016, he had traveled to Ho Chi Minh City, Vietnam, where he stayed for 10 days. During his return to Japan, he developed fever and a diffuse rash on his face, trunk, arms, and legs. He went to the hospital on the day after his return and reported having been bitten by mosquitoes in Ho Chi Minh City. Upon arrival at the hospital, he had no fever (temperature 36.8°C); physical examination revealed conjunctivitis and a maculopapular rash on his face, trunk, and extremities. Results of laboratory tests showed leukopenia (2,250 cells/µL; reference 3,500-8,500 cells/  (3) The phylogenetic tree that we constructed using the complete coding region of the Zika virus genome suggested that the sequence belonged to the Southeast Asian clade of the Asian lineage ( Figure). The plaque size of the isolated strain in Vero cells was obviously smaller than that of the Asian strain ZIKV/ Hu/S36/Chiba/2016 (Pacific clade) (online Technical Appendix, https://wwwnc.cdc.gov/EID/article/23/7/17-0519-Techapp1.pdf).
A previous study showed that Zika virus RNA could be detected more easily in urine than in serum a few days after disease onset (4). Other reports showed that Zika virus RNA could be detected for a longer period in whole blood than that in urine and serum (5) and that Zika virus RNA could be detected more easily in saliva than in plasma and urine during the first week after symptom onset (6). In the case we report, during RT-PCR analysis of the patient's serum, urine, saliva, whole blood, and semen samples, the urine sample showed the lowest C t , indicating that the urine sample had the highest concentration of Zika virus RNA. However, we could not detect the Zika virus genome in serum and semen samples.
Our phylogenetic analysis suggested that the Asian lineage can be divided into 3 clades (Southeast Asian, Pacific, and American), and the strain we isolated belonged to the Southeast Asian clade. A previous study indicated that a strain isolated in Singapore in 2016 (ZKA-16-291; GenBank accession no. KX827309) also belonged to the Southeast Asian branch, and it was distinct from the isolates obtained in the Americas (7). Therefore, it is possible that the isolate from the current case was the strain that is already circulating in Vietnam and was not imported from South America. Our isolate formed smaller plaques in Vero cells than those observed with the other Asian lineage ZIKV/Hu/S36/Chiba/2016 strain (Pacific clade). We also confirmed that the plaque sizes of the PRVABC59 (American clade) and MR766-NIID (African lineage) strains resemble that of ZIKV/Hu/Chiba/ S36/2016 (data not shown), suggesting that the Southeast Asian clade Zika virus strains might have a lower cytotoxicity and replicative ability than the American clade and African lineage.
In conclusion, the replicative ability of Zika virus might differ by region and thus influences endemic potential. Further studies are necessary to validate these findings. H uman African trypanosomiasis (HAT), known as African sleeping sickness, is a protozoal infection, the West African form of which is caused by Trypanosoma brucei gambiense. We report a case of imported T. brucei gambiense HAT, acquired in Nigeria, where no cases have been reported since 2012 (1).
The case-patient, a 58-year-old Nigerian woman, lived near Warri, in Delta State, Nigeria. She traveled infrequently to towns within Delta State, across the Niger River into Bayelsa State, and to larger cities in Nigeria, but never outside Nigeria. She reported no history of tsetse fly bites.
In January 2016, the patient experienced leg tremors and lethargy. These symptoms persisted until arrival in the United Kingdom in May 2016. Over the next 2 months, increasing malaise and unsteadiness in walking developed. In August 2016, the patient was admitted to a regional hospital with confusion and drowsiness. She was febrile at admission but had no lymphadenopathy; neurologic examination revealed no neck stiffness or photophobia, but did show poor coordination with slow cognitive processes.
Laboratory investigations revealed microcytic anemia with a C-reactive protein level of 13 mg/L (reference value <5 mg/L) and a total serum IgM of 13.7 g/L (reference range 0.5-2.0 g/L). A blood film was negative for malaria. Confirmatory assays after positive screening assay results for HIV and syphilis antibodies showed the original results to be false positive.
Cerebrospinal fluid (CSF) examination revealed 331 leukocytes/mm 3 , 99% lymphocytes; CSF protein level 0.82 g/L (reference range 0.23-0.38 g/L); and glucose level was >50% plasma glucose. Results of CSF PCR for herpesviruses, enterovirus, and JC virus were negative. Results of GeneXpert (Cepheid, Buckinghamshire, UK) tests of CSF and mycobacterial culture were negative. Magnetic resonance imaging of the brain showed, on T2 weighted and flair images, bilateral diffuse hyperintensities within white matter located in the periventricular regions, basal ganglia, cerebellum, and brainstem.
Treatment with ceftriaxone, acyclovir, antituberculous treatment and prednisolone was stopped at 14 days because of a lack of clinical improvement and drug-induced transaminitis.
The patient's lethargy, intermittent confusion, and periods of somnolence became more severe. Examination in August 2016 revealed intention tremor in all limbs and myoclonic jerks. Her case was discussed with the Imported Fever Service at Public Health England. A serum sample was sent to the Hospital of Tropical Diseases in London, UK for T. brucei gambiense indirect fluorescent antibody testing (IFAT), which showed a positive result (titer 1:400). The patient was transferred to this hospital.
Repeat CSF examination revealed a protein level of 1.14 g/L, CSF glucose level of 2.3 mmol/L (serum 5.5 mmol/L), and 1,140 leukocytes/mm 3 (90% mononuclear). No trypanosomes were seen in the buffy coat of peripheral blood or CSF. CSF total IgM of 1.98 mg/L (reference range 0-0.9 mg/L) and IgG of 306 mg/L (reference range 10-40 mg/L) were markedly raised (2).
T. brucei gambiense IFAT results for CSF (titer 1:4) and blood (titer 1:400) were positive. DNA extracted from CSF was positive for trypanosomes of the subgenus Trypanozoon by PCR (3) and confirmed as T. brucei gambiense group 1 by diagnostic PCR with TgsGP primers (4). The result of immune trypanolysis was negative