Affiliations 

  • 1 National Neuroscience Institute, Singapore
  • 2 Singapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Singapore
  • 3 Epidemiology and Disease Control Division, Ministry of Health, Singapore
  • 4 Communicable Disease Centre, Institute of Infectious Disease and Epidemiology, Tan Tock Seng Hospital, Singapore
J Peripher Nerv Syst, 2018 09;23(3):197-201.
PMID: 30070025 DOI: 10.1111/jns.12284

Abstract

Although individuals with Zika virus (ZIKV) antibodies were reported in Malaya in mid-1950s, entomological and human surveillance in Singapore did not identify autochthonous transmission until the outbreak of August-November, 2016. A total of 455 cases from 15 separate clusters were identified. We asked if this ZIKV outbreak increased the incidence of Guillain-Barré syndrome (GBS) and aimed to characterize these cases. Eleven GBS cases, consecutively enrolled into our prospective GBS database from onset to 4 weeks after outbreak, and six controls, comprising three GBS patients enrolled before outbreak and three non-GBS patients, were examined for evidence of recent ZIKV infection. We performed serum, urine ZIKV RT-PCR, ZIKV serology, and virus neutralization assays, accounting for cross-reaction and co-infection with dengue (DENV). We found five GBS cases with only serological evidence of recent ZIKV infection (including one ZIKV-DENV co-infection). A temporal relationship with ZIKV outbreak was unlikely as two cases were GBS controls enrolled 3 months before outbreak. None reported symptoms of ZIKV infection. In addition, compared to last 10 years the national number of GBS hospitalizations did not increase during and immediately after outbreak. We conclude the 2016 Singapore ZIKV outbreak did not cause a change in GBS epidemiology.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.