Time Lags between Exanthematous Illness Attributed to Zika Virus, Guillain-Barré Syndrome, and Microcephaly, Salvador, Brazil

Paploski, Igor Adolfo Dexheimer; Prates, Ana Paula Pitanga Barbuda; Cardoso, Cristiane Wanderley; Kikuti, Mariana; Silva, Monaíse M. O.; Waller, Lance A.; Reis, Mitermayer Galvão dos; Kitron, Uriel; Ribeiro, Guilherme S.

doi:10.3201/eid2208.160496

Cited by 107 publications

(105 citation statements)

References 30 publications

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“…However, additional confirmation of these reports may show these numbers to be excessive. A clear temporal relationship between the peak of Zika virus infection in a susceptible population and a peak of GBS incidence 5 to 9 weeks later has been demonstrated, consistent with an autoimmune-mediated (rather than direct viral infectious neuropathy) pathologic mechanism [53]. Interim analysis of an ongoing prospective case study of ZIKV-infected pregnancies indicates a birth defect rate of circa 29% [38].…”

mentioning

confidence: 93%

Zika Fetal Neuropathogenesis: Etiology of a Viral Syndrome

et al. 2016

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The ongoing Zika virus epidemic in the Americas and the observed association with both fetal abnormalities (primary microcephaly) and adult autoimmune pathology (Guillain–Barré syndrome) has brought attention to this neglected pathogen. While initial case studies generated significant interest in the Zika virus outbreak, larger prospective epidemiology and basic virology studies examining the mechanisms of Zika viral infection and associated pathophysiology are only now starting to be published. In this review, we analyze Zika fetal neuropathogenesis from a comparative pathology perspective, using the historic metaphor of “TORCH” viral pathogenesis to provide context. By drawing parallels to other viral infections of the fetus, we identify common themes and mechanisms that may illuminate the observed pathology. The existing data on the susceptibility of various cells to both Zika and other flavivirus infections are summarized. Finally, we highlight relevant aspects of the known molecular mechanisms of flavivirus replication.

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confidence: 93%

Zika Fetal Neuropathogenesis: Etiology of a Viral Syndrome

et al. 2016

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“…A maculopapular rash (sometimes pruritic) was the most common symptom affecting 44%-93% of cases, followed by conjunctivitis (36%-58%), myalgia/arthralgia (39%-64%), headache (53%-62%) and lymphadenopathy (about 40%). (18,21,28,30) During pregnancy, there does not appear to be an increased risk of developing the rarer complications of myelitis and GBS, (32,33) with only one single case of GBS reported in pregnancy so far. (34) …”

Section: Is the Clinical Course Of Zikv Infection Different In Pregnamentioning

confidence: 99%

A review of Zika virus infections in pregnancy and implications for antenatal care in Singapore

Lin

Tambyah

Yong

et al. 2017

smedj

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Given the consensus that there is a causal relationship between Zika virus (ZIKV) infection in pregnancy and congenital Zika syndrome (CZS), clinicians must be prepared to manage affected patients despite the numerous gaps in current knowledge. The clinical course in pregnancy appears similar to that in non-pregnant women, although viraemia may be prolonged. ZIKV infection can be diagnosed by serum and urine reverse transcription-polymerase chain reaction, but commercially available serological tests are currently unreliable in dengue-endemic regions. Although vertical transmission can occur at any time during gestation, first-and second-trimester infections have the highest risk of developing central nervous system anomalies. Aberrant fetal growth and pregnancy loss may also occur. Serial ultrasonography should be conducted for infected cases. Without a vaccine, pregnant women should be advised to minimise mosquito bites and reduce sexual transmission risk. Overall, the absolute risk of CZS arising amid a ZIKV outbreak appears relatively low.

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“…This corresponds to a time of potential infection during the first trimester, and these findings support association of Guillain–Barré syndrome and microcephaly with Zika virus infection. 86 As well as Guillain–Barré syndrome, Zika virus has also been detected in CSF from patients with encephalopathy 87 and meningoencephalitis. 88 …”

Section: Neurological Sequelae Of Zika Virus: Microcephaly/guillain–bmentioning

confidence: 99%

Zika virus: An emergent neuropathological agent

White

Wollebo

Beckham

et al. 2016

Annals of Neurology

109

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The emergence of Zika virus in the Americas has followed a pattern that is familiar from earlier epidemics of other viruses, where a new disease is introduced into a human population and then spreads rapidly with important public health consequences. In the case of Zika virus, an accumulating body of recent evidence implicates the virus in the etiology of serious pathologies of the human nervous system, that is, the occurrence of microcephaly in neonates and Guillain–Barré syndrome in adults. Zika virus is an arbovirus (arthropod-borne virus) and a member of the family Flaviviridae, genus Flavivirus. Zika virions are enveloped and icosahedral, and contain a nonsegmented, single-stranded, positive-sense RNA genome, which encodes 3 structural and 7 nonstructural proteins that are expressed as a single polyprotein that undergoes cleavage. Zika genomic RNA replicates in the cytoplasm of infected host cells. Zika virus was first detected in 1947 in the blood of a febrile monkey in Uganda’s Zika Forest and in crushed suspensions of the Aedes mosquito, which is one of the vectors for Zika virus. The virus remained obscure, with a few human cases confined to Africa and Asia. There are two lineages of the Zika virus, African and Asian, with the Asian strain causing outbreaks in Micronesia in 2007 and French Polynesia in 2013–2014. From here, the virus spread to Brazil with the first report of autochthonous Zika transmission in the Americas in March 2015. The rapid advance of the virus in the Americas and its likely association with microcephaly and Guillain–Barré syndrome make Zika an urgent public health concern.

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Time Lags between Exanthematous Illness Attributed to Zika Virus, Guillain-Barré Syndrome, and Microcephaly, Salvador, Brazil

Abstract: There is strong evidence of a temporal relationship between virus infection in pregnant women and birth outcome.

Cited by 107 publications

References 30 publications

Zika Fetal Neuropathogenesis: Etiology of a Viral Syndrome

Zika Fetal Neuropathogenesis: Etiology of a Viral Syndrome

A review of Zika virus infections in pregnancy and implications for antenatal care in Singapore

Zika virus: An emergent neuropathological agent

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