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The 2016 Singapore Zika virus outbreak did not cause a surge in Guillain‐Barré syndrome
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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: The 2016 Singapore Zika virus outbreak did not cause a surge in Guillain‐Barré syndrome
Description:
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.
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