Brain abnormalities on neuroimaging in Children with Congenital Zika Syndrome in Salvador, Brazil, and its possible implications on neuropsychological development

Araújo

et al. 2022

IJERPH

Self Cite

This article describes the Salvador Primary Care Longitudinal Study of Child Development (CohortDICa). The exposed group was defined by confirmation of Congenital Zika Syndrome (CZS) diagnosed through computed tomography, magnetic resonance or transfontanellar ultrasound. A random selection of the 169 exposed children led to a subgroup of 120 children who were paired with children from the Live Birth Information System, according to birthdate, residence in the same street or neighborhood, and gestational age, resulting in 115 subjects in the non-exposed group. Following recruitment and before the participants completed 42 months, three measures were applied to assess cognitive, motor, and language performance, corresponding to three home visits. Social characteristics of the families and children, and the neurocognitive development of the children will be compared across the CZS exposed group (n = 147), the typical children with no exposure to CZS (n = 115) and the STORCH exposed group (Syphilis, Toxoplasma gondii, Rubella, Cytomegalovirus, and Herpes simplex) (n = 20). Primary Health Care (PHC) should include long-term care strategies for the care of children and family members, and might benefit from the research, teaching, and extension activities provided in this study. In the face of the consequences of the Zika virus epidemic, an opportunity arose to intervene in the integrated care of child development within PHC, including, on an equal basis, typical children and those with delays or disabilities in the first six years of life.

Section: Methodsmentioning

confidence: 99%

The Salvador Primary Care Longitudinal Study of Child Development (CohortDICa) Following the Zika Epidemic: Study Protocol

Araújo

et al. 2022

IJERPH

Self Cite

Current Opinion in Infectious Diseases

“…The differential diagnosis and testing should be driven by a combination of epidemiological risk factors, exposure history, as well as clinical and radiological features. Fetal–neonatal features and potential treatments for CMV [6 ▪▪ ,7 ▪ ,16–18,19 ▪▪ ,20 ▪ ], Toxoplasmosis [21–23,24 ▪ ], lymphocytic choriomeningitis virus (LCMV) [25,26], ZIKV [9,19 ▪▪ ,27 ▪ ,28–33], rubella [19 ▪▪ ,34 ▪▪ ], and syphilis [5,10 ▪ ,35] are summarized in Table 1.…”

Section: Clinical and Radiological Features Of Congenital Infectionsmentioning

confidence: 99%

Neurodevelopmental outcomes in congenital and perinatal infections

Fortin

Mulkey

2023

Purpose of review Congenital infections are a major cause of childhood multidomain neurodevelopmental disabilities. They contribute to a range of structural brain abnormalities that can cause severe neurodevelopmental impairment, cerebral palsy, epilepsy, and neurosensory impairments. New congenital infections and global viral pandemics have emerged, with some affecting the developing brain and causing neurodevelopmental concerns. This review aims to provide current understanding of fetal infections and their impact on neurodevelopment. Recent findings There are a growing list of congenital infections causing neurodevelopmental issues, including cytomegalovirus, Zika virus, syphilis, rubella, lymphocytic choriomeningitis virus, and toxoplasmosis. Fetal exposure to maternal SARS-CoV-2 may also pose risk to the developing brain and impact neurodevelopmental outcomes, although studies have conflicting results. As Zika virus was a recently identified congenital infection, there are several new reports on child neurodevelopment in the Caribbean and Central and South America. For many congenital infections, children with in-utero exposure, even if asymptomatic at birth, may have neurodevelopmental concerns manifest over time. Summary Congenital infections should be considered in the differential diagnosis of a child with neurodevelopmental impairments. Detailed pregnancy history, exposure risk, and testing should guide diagnosis and multidisciplinary evaluation. Children with congenital infections should have long-term follow-up to assess for neurodevelopmental delays and other neurosensory impairments. Children with confirmed delays or high-risk should be referred for rehabilitation therapies.

“…Zika virus (ZikV) is an emerging flavivirus that can be vertically transmitted to the fetus from an infected pregnant mother, leading to congenital Zika syndrome (CZS), which encompasses a range of fetal malformations including hearing loss, ocular manifestations, intrauterine growth restriction, and microcephaly 1–4 , as well as miscarriage 5–7 . CZS persists post-partum and imposes major complications to childhood development, now manifested across ZikV-endemic regions 8,9 . While the mechanism of microcephaly in CZS is thought to be related to ZikV infection and death of neural progenitor cells leading to decreased neurogenesis 10–12 , the pathogenesis of neurodevelopmental delay in CZS displaying normal brain development, termed “normocephalic”, is poorly understood.…”

Section: Mainmentioning

confidence: 99%

Section: Mainmentioning

confidence: 99%

Disruption of myelin structure and oligodendrocyte maturation in a pigtail macaque model of congenital Zika infection

Tisoncik-Go,

Stokes,

Whitmore

et al. 2023

Preprint

Zika virus (ZikV) infection during pregnancy can cause congenital Zika syndrome (CZS) and neurodevelopmental delay in non-microcephalic infants, of which the pathogenesis remains poorly understood. We utilized an established pigtail macaque maternal-to-fetal ZikV infection/exposure model to study fetal brain pathophysiology of CZS manifesting from ZikV exposure in utero. We found prenatal ZikV exposure led to profound disruption of fetal myelin, with extensive downregulation in gene expression for key components of oligodendrocyte maturation and myelin production. Immunohistochemical analyses revealed marked decreases in myelin basic protein intensity and myelinated fiber density in ZikV-exposed animals. At the ultrastructural level, the myelin sheath in ZikV-exposed animals showed multi-focal decompaction consistent with perturbation or remodeling of previously formed myelin, occurring concomitant with dysregulation of oligodendrocyte gene expression and maturation. These findings define fetal neuropathological profiles of ZikV-linked brain injury underlying CZS resulting from ZikV exposure in utero. Because myelin is critical for cortical development, ZikV-related perturbations in oligodendrocyte function may have long-term consequences on childhood neurodevelopment, even in the absence of overt microcephaly.