Underreporting of #Fatal #Congenital #Zika #Syndrome, #Mexico, 2016–2017 (Emerg Infect Dis., abstract)

[Source: US Centers for Disease Control and Prevention (CDC), Emerging Infectious Diseases Journal, full page: (LINK). Abstract, edited.]

Volume 25, Number 8—August 2019 / Dispatch

Underreporting of Fatal Congenital Zika Syndrome, Mexico, 2016–2017

Victor M. Cardenas  , Angel Jose Paternina-Caicedo, and Ernesto Benito Salvatierra

Author affiliations: University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA (V.M. Cardenas); Universidad Nacional de Colombia, Bogota, Colombia (A.J. Paternina-Caicedo); Unidad San Cristóbal, Chiapas, Mexico (E.B. Salvatierra)



To determine completeness of fatal congenital Zika syndrome reporting in Mexico, we examined data from the Mexican National Institute of Statistics and Geography. We found that an estimated 50% more infants died from microcephaly attributable to congenital Zika syndrome during 2016–2017 than were reported by the existing surveillance system.

Keywords: Zika Virus; Microcephaly; Zika Congenital Syndrome; Mexico.



Alterations in #visual acuity and visual #development in #infants 1-24 months old either exposed to or infected by #Zika virus during #gestation, with and without #microcephaly (J AAPOS., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

J AAPOS. 2019 Jun 20. pii: S1091-8531(19)30137-5. doi: 10.1016/j.jaapos.2019.03.005. [Epub ahead of print]

Alterations in visual acuity and visual development in infants 1-24 months old either exposed to or infected by Zika virus during gestation, with and without microcephaly.

Baran LCP1, da Costa MF2, Vidal KS2, Damico FM3, Barboni MTS4, da S Lima D2, de C R de M França V5, Martins CMG2, Tabares HS2, Dias SL5, Silva LA2, Decleva D2, Hamer RD6, Zatz M7, Bertozzi APAP8, Gazeta RE8, Passos SD8, Ventura DF2.

Author information: 1 Department of Experimental Psychology, University of São Paulo Institute of Psychology, São Paulo, SP, Brazil; Nucleus of Neurosciences and Behavior, University of São Paulo, São Paulo, SP, Brazil. Electronic address: baranejbio@gmail.com. 2 Department of Experimental Psychology, University of São Paulo Institute of Psychology, São Paulo, SP, Brazil; Nucleus of Neurosciences and Behavior, University of São Paulo, São Paulo, SP, Brazil. 3 Department of Ophthalmology, University of São Paulo College of Medicine, São Paulo, SP, Brazil. 4 Department of Experimental Psychology, University of São Paulo Institute of Psychology, São Paulo, SP, Brazil; Nucleus of Neurosciences and Behavior, University of São Paulo, São Paulo, SP, Brazil; Department of Ophthalmology, Semmelweis University, Budapest, Hungary. 5 Department of Experimental Psychology, University of São Paulo Institute of Psychology, São Paulo, SP, Brazil. 6 Department of Experimental Psychology, University of São Paulo Institute of Psychology, São Paulo, SP, Brazil; Nucleus of Neurosciences and Behavior, University of São Paulo, São Paulo, SP, Brazil; Department of Psychology, Florida Atlantic University, Boca Raton, Florida. 7 Human Genome and Stem Cells Center, Bioscience Institute, University of São Paulo. 8 University of Jundiai Medical School, Jundiai, São Paulo, SP, Brazil.




To evaluate visual acuity and visual acuity development in children from the state of São Paulo, Brazil, who were exposed to the Zika virus (ZIKV) gestationally.


Children who had been exposed to ZIKV during gestation and age-matched control subjects received visual acuity and funduscopic examination. ZIKV exposure was confirmed by maternal quantitative polymerase chain reaction testing or serology assay. The ZIKV group was divided into two subgroups: Zika-exposed (ZE), with only the mother having confirmed ZIKV-infection, and Zika-infected (ZI), with confirmed infection. Visual acuity development was compared with prior norms and quantified by measuring visual acuity correlation with age.


A total of 110 children were included: 47 who had been exposed to ZIKV (ZE, 23; ZI, 24) and 63 controls. Abnormal visual acuity was found in 5 of 24 ZI children. Of the 4 children with microcephaly, only 2 had visual acuity loss (only 1 also had abnormal funduscopic findings). There was significant correlation between age and visual acuity in both the control group (R2 = 0.8; P < 0.0000) and the ZE subgroup (R2 = 0.6; P < 0.0000). However, visual acuity did not correlate with age in the ZI subgroup (R2 = 0.04; P = 0.38). Furthermore, the increment in octaves/month was much lower in the ZI subgroup.


Our data indicates that visual acuity losses only occur in infants who suffered gestational-infection, not simply exposure. Lack of correlation between age and visual acuity in the ZI subgroup suggests a slowing of visual development even in the absence of microcephaly. This result may have broad implications for the deleterious effects of ZIKV on the central nervous system.

Copyright © 2019 American Association for Pediatric Ophthalmology and Strabismus. Published by Elsevier Inc. All rights reserved.

PMID: 31229606 DOI: 10.1016/j.jaapos.2019.03.005

Keywords: Zika Virus; Zika Congenital Infection; Zika Congenital Syndrome; Microcephaly; Pediatrics; Ophthalmology; Neurology.


#Understanding the #relation between #Zika virus #infection during #pregnancy and adverse #fetal, #infant and #child #outcomes: a protocol … (BMJ Open., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

BMJ Open. 2019 Jun 18;9(6):e026092. doi: 10.1136/bmjopen-2018-026092.

Understanding the relation between Zika virus infection during pregnancy and adverse fetal, infant and child outcomes: a protocol for a systematic review and individual participant data meta-analysis of longitudinal studies of pregnant women and their infants and children.

Wilder-Smith A1, Wei Y2, Araújo TVB3, VanKerkhove M4, Turchi Martelli CM5, Turchi MD6, Teixeira M7, Tami A8, Souza J9, Sousa P10, Soriano-Arandes A11, Soria-Segarra C12, Sanchez Clemente N13, Rosenberger KD14, Reveiz L15, Prata-Barbosa A16, Pomar L17, Pelá Rosado LE18, Perez F19, Passos SD20, Nogueira M21, Noel TP22, Moura da Silva A23, Moreira ME24, Morales I14, Miranda Montoya MC25, Miranda-Filho DB26, Maxwell L27,28, Macpherson CNL22, Low N29, Lan Z30, LaBeaud AD31, Koopmans M32, Kim C33, João E34, Jaenisch T14, Hofer CB35, Gustafson P36, Gérardin P37,38, Ganz JS39, Dias ACF7, Elias V40, Duarte G41, Debray TPA42, Cafferata ML43, Buekens P44, Broutet N33, Brickley EB45, Brasil P46, Brant F7, Bethencourt S47, Benedetti A48, Avelino-Silva VL49, Ximenes RAA50, Alves da Cunha A51, Alger J52; Zika Virus Individual Participant Data Consortium.

Collaborators (33): Abreu de Carvalho LM, Batista R, Bertozzi AP, Carles G, Cotrim D, Damasceno L, Dimitrakis L, Duarte Rodrigues MM, Estofolete CF, Fragoso da Silveira Gouvêa MI, Fumadó-Pérez V, Gazeta RE, Kaydos-Daniels N, Gilboa S, Krystosik A, Lambert V, López-Hortelano MG, Mussi-Pinhata MM, Nelson C, Nielsen K, Oliani DM, Rabello R, Ribeiro M, Rockx B, Rodrigues LC, Salgado S, Silveira K, Sulleiro E, Tong V, Valencia D, De Souza WV, Villar Centeno LA, Zin A.

Author information: 1 Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore. 2 Centre for Mathematical Sciences, University of Plymouth, Plymouth, UK. 3 Department of Social Medicine, Universidade Federal de Pernambuco, Recife, Brazil. 4 Health Emergencies Programme, Organisation mondiale de la Sante, Geneve, Switzerland. 5 Department of Collective Health, Institute Aggeu Magalhães (CPqAM), Oswaldo Cruz Foundation, Recife, Brazil. 6 Institute of Tropical Pathology and Public Health, Federal University of Goias, Goiânia, Brazil. 7 Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. 8 Department of Medical Microbiology, University Medical Center Groningen, Groningen, The Netherlands. 9 Department of Social Medicine, University of São Paulo, São Paulo, Brazil. 10 Reference Center for Neurodevelopment, Assistance, and Rehabilitation of Children, State Department of Health of Maranhão, Sao Luís, Brazil. 11 Department of Pediatrics, University Hospital Vall d’Hebron, Barcelona, Spain. 12 SOSECALI C. Ltda, Guayaquil, Ecuador. 13 Department of Epidemiology, University of São Paulo, São Paulo, Brazil. 14 Department of Infectious Diseases, Section Clinical Tropical Medicine, UniversitatsKlinikum Heidelberg, Heidelberg, Germany. 15 Evidence and Intelligence for Action in Health, Pan American Health Organization, Washington, District of Columbia, USA. 16 Department of Pediatrics, D’Or Institute for Research & Education, Rio de Janeiro, Brazil. 17 Department of Obstetrics and Gynecology, Centre Hospitalier de l’Ouest Guyanais, Saint-Laurent du Maroni, French Guiana. 18 Hospital Materno Infantil de Goiânia, Goiânia State Health Secretary, Goiás, Brazil. 19 Communicable Diseases and Environmental Determinants of Health Department, Pan American Health Organization, Washington, District of Columbia, USA. 20 Department of Pediatrics, FMJ, São Paulo, Brazil. 21 Faculdade de Medicina de Sao Jose do Rio Preto, Department of Dermatologic Diseases, São José do Rio Preto, Brazil. 22 Windward Islands Research and Education Foundation, St. George’s University, True Blue Point, Grenada. 23 Department of Public Health, Universidade Federal do Maranhão – São Luís, São Luís, Brazil. 24 Department of Neonatology, Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil. 25 Facultad de Salud, Universidad Industrial de Santander, Bucaramanga, Colombia. 26 Faculty of Medical Sciences, University of Pernambuco, Recife, Brazil. 27 Reproductive Health and Research, World Health Organization, Geneva, Switzerland. 28 Hubert Department of Global Health, Emory University, Atlanta, Georgia, USA. 29 Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland. 30 McGill University Health Centre, McGill University, Montréal, Canada. 31 Pediatric Infectious Diseases, Stanford Hospital, Palo Alto, California, USA. 32 Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands. 33 Department of Reproductive Health and Research, World Health Organization, Geneva, Switzerland. 34 Department of Infectious Diseases, Hospital Federal dos Servidores do Estado, Rio de Janeiro, Brazil. 35 Instituto de Puericultura e Pediatria Martagão Gesteira, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. 36 Statistics, University of British Columbia, British Columbia, Vancouver, Canada. 37 INSERM CIC1410 Clinical Epidemiology, CHU La Réunion, Saint Pierre, Réunion. 38 UM 134 PIMIT (CNRS 9192, INSERM U1187, IRD 249, Université de la Réunion), Universite de la Reunion, Sainte Clotilde, Réunion. 39 Children’s Hospital Juvencio Matos, São Luís, Brazil. 40 Sustainable Development and Environmental Health, Pan American Health Organization, Washington, District of Columbia, USA. 41 Department of Gynecology and Obstetrics, University of São Paulo, São Paulo, Brazil. 42 Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. 43 Mother and Children Health Research Department, Instituto de Efectividad Clinica y Sanitaria, Buenos Aires, Argentina. 44 School of Public Health and Tropical Medicine, Tulane University, New Orleans, USA. 45 Department of Infectious Disease Epidemiology, London School of Hygiene and Tropical Medicine, London, UK. 46 Instituto de pesquisa Clínica Evandro Chagas, Fundacao Oswaldo Cruz, Rio de Janeiro, Brazil. 47 Facultad de Ciencias de la Salud, Universidad de Carabobo, Valencia, Carabobo, Bolivarian Republic of Venezuela. 48 Departments of Medicine and of Epidemiology, Biostatistics & Occupational Health, McGill University, Montreal, Quebec, Canada. 49 Department of Infectious and Parasitic Diseases, Faculdade de Medicina da Universidade de Sao Paulo, São Paulo, Brazil. 50 Department of Tropical Medicine, Federal University of Pernambuco, Recife, Brazil. 51 Department of Pediatrics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. 52 Facultad de Ciencias Médicas, Universidad Nacional Autónoma de Honduras, Tegucigalpa, Honduras.




Zika virus (ZIKV) infection during pregnancy is a known cause of microcephaly and other congenital and developmental anomalies. In the absence of a ZIKV vaccine or prophylactics, principal investigators (PIs) and international leaders in ZIKV research have formed the ZIKV Individual Participant Data (IPD) Consortium to identify, collect and synthesise IPD from longitudinal studies of pregnant women that measure ZIKV infection during pregnancy and fetal, infant or child outcomes.


We will identify eligible studies through the ZIKV IPD Consortium membership and a systematic review and invite study PIs to participate in the IPD meta-analysis (IPD-MA). We will use the combined dataset to estimate the relative and absolute risk of congenital Zika syndrome (CZS), including microcephaly and late symptomatic congenital infections; identify and explore sources of heterogeneity in those estimates and develop and validate a risk prediction model to identify the pregnancies at the highest risk of CZS or adverse developmental outcomes. The variable accuracy of diagnostic assays and differences in exposure and outcome definitions means that included studies will have a higher level of systematic variability, a component of measurement error, than an IPD-MA of studies of an established pathogen. We will use expert testimony, existing internal and external diagnostic accuracy validation studies and laboratory external quality assessments to inform the distribution of measurement error in our models. We will apply both Bayesian and frequentist methods to directly account for these and other sources of uncertainty.


The IPD-MA was deemed exempt from ethical review. We will convene a group of patient advocates to evaluate the ethical implications and utility of the risk stratification tool. Findings from these analyses will be shared via national and international conferences and through publication in open access, peer-reviewed journals.


PROSPERO International prospective register of systematic reviews (CRD42017068915).

© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY. Published by BMJ.

KEYWORDS: Microcephaly; Zika Virus; congenital Zika syndrome; individual participant data meta-analysisis; prognosis; risk prediction model

PMID: 31217315 DOI: 10.1136/bmjopen-2018-026092

Keywords: Zika Virus; Microcephaly; Pregnancy; Zika Congenital Infection; Zika Congenital Syndrome.


Development of Secondary #Microcephaly After #Delivery: Possible Consequence of #Mother- #Baby #Transmission of #Zika Virus in #Breast #Milk (Am J Case Rep., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Am J Case Rep. 2019 May 21;20:723-725. doi: 10.12659/AJCR.915726.

Development of Secondary Microcephaly After Delivery: Possible Consequence of Mother-Baby Transmission of Zika Virus in Breast Milk.

Siqueira Mello A1, Pascalicchio Bertozzi APA2, Rodrigues MMD2, Gazeta RE2, Moron AF3, Soriano-Arandes A4, Sarmento SGP3, Vedovello D1, Silva ACB1, Grillo Fajardo TC1, Witkin SS5, Passos SD2,1.

Author information: 1 Laboratory of Pediatric Infectology, Department of Pediatrics, Jundiaí School of Medicine, São Paulo, SP, Brazil. 2 Department of Pediatrics, Jundiaí School of Medicine, São Paulo, SP, Brazil. 3 Department of Obstetrics, Federal University of São Paulo (UNIFESP) – Paulista School of Medicine and Paulista Center for Fetal Medicine, São Paulo, SP, Brazil. 4 Paediatric Infectious Diseases and Immunodeficiencies Unit, Hospital Universitari Vall d’Hebron, Barcelona, Spain. 5 Department of Obstetrics and Gynecology, Weill Cornell Medicine, New York City, NY, USA.




The Zika virus is an arbovirus that has as main source of transmission the bite of infected insects of the genus Aedes and has been associated with cases of congenital malformation and microcephaly in neonates. However, other sources of transmission have been identified since the emergence of this virus in the world population, such as vertical transmission by semen and possibly other body fluids such as vaginal secretion and breast milk.


An infant, born to a mother whose previous delivery was a baby with severe microcephaly, was normal and was negative for Zika virus at birth but developed secondary microcephaly 1 month later, that persisted. The baby was exclusively breast-fed and Zika virus was present in the mother’s milk.


We report the detection of Zika virus exclusively in the breast milk of a woman after her second delivery of an infant, who later developed microcephaly. This case is consistent with possible vertical transmission.

PMID: 31110169 DOI: 10.12659/AJCR.915726

Keywords: Zika Virus; Pregnancy; Microcephaly.


The #challenge of the #laboratory #diagnosis in a confirmed #congenital #Zika virus #syndrome in #utero: A case report (Medicine (Baltimore), abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Medicine (Baltimore). 2019 May;98(20):e15532. doi: 10.1097/MD.0000000000015532.

The challenge of the laboratory diagnosis in a confirmed congenital Zika virus syndrome in utero: A case report.

Sulleiro E1,2, Frick MA1,2, Rodó C1,2, Espasa M1, Thorne C2,3, Espiau M1,2, Martín-Nalda A1,2, Suy A1,2, Giaquinto C2,4, Melendo S1, Rando A1, Alarcón A2,5, Martinón-Torres F2,6, Pumarola T1, Soler-Palacín P1, Soriano-Arandes A1,2.

Author information: 1 Hospital Universitari Vall d’Hebron, Barcelona, Spain. 2 ZIKAction Consortium, European Union’s Horizon 2020 Research and Innovation Programme under Grant Agreement No 734857. 3 University College London, London, United Kingdom. 4 University of Padova, PENTA Foundation, Padova, Italy. 5 Hospital Sant Joan de Déu, Esplugues de Llobregat, Barcelona, Spain. 6 Hospital Clínico Universitario, Santiago de Compostela, Spain.




Zika virus (ZIKV) has caused one of the most challenging global infectious epidemics in recent years because of its causal association with severe microcephaly and other congenital malformations. The diagnosis of viral infections usually relies on the detection of virus proteins or genetic material in clinical samples as well as on the infected host immune responses. Serial serologic testing is required for the diagnosis of congenital infection when diagnostic molecular biology is not possible.


A 2-year-old girl, born to a mother with confirmed ZIKV infection during pregnancy, with a confirmed ZIKV infection in utero, showed at birth a severe microcephaly and clinical characteristics of fetal brain disruption sequence compatible with a congenital ZIKV syndrome (CZS).


ZIKV-RNA and ZIKV-IgM serological response performed at birth and during the follow-up time tested always negative. Serial serologic ZIKV-IgG tests were performed to assess the laboratory ZIKV diagnosis, ZIKV-IgG seroreversion was observed at 21 months of age. ZIKV diagnosis of this baby had to be relied on her clinical and radiological characteristics that were compatible with a CZS.


The patient was followed-up as per protocol at approximately 1, 4, 9, 12, 18-21, and 24 months of age. Neurological, radiological, audiological, and ophthalmological assessment were performed during this period of time. Prompt rehabilitation was initiated to prevent potential adverse long-term neurological outcomes.


The growth of this girl showed a great restriction at 24 months of age with a weight of 8.5 kg (-2.5 z-score) and a head circumference of 40.5 cm (-4.8 z-score). She also had a great neurodevelopmental delay at the time of this report.


We presume that as a consequence of prenatal ZIKV infection, the fetal brain and other organs are damaged before birth through direct injury. Following this, active infection ends during intrauterine life, and as a consequence the immune system of the infant is unable to build up a consistent immune response thereafter. Further understanding of the mechanisms taking part in the pathogenesis of ZIKV congenital infection is needed. This finding might change our paradigm regarding serological response in the ZIKV congenital infection.

PMID: 31096455 DOI: 10.1097/MD.0000000000015532

Keywords: Zika Virus; Zika Congenital Syndrome; Microcephaly; Serology.


Reporting of #birth #defects from the #Zika #outbreak in #Colombia, 2015-2017 (Rev Panam Salud Publica, abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Rev Panam Salud Publica. 2019 May 3;43:e38. doi: 10.26633/RPSP.2019.38. eCollection 2019.

[Reporting of birth defects from the Zika outbreak in Colombia, 2015-2017]

Notificação de defeitos congênitos associados ao surto de vírus zika na Colômbia, 2015-2017].

[Article in Spanish]

Mendivelso Duarte FO1, Robayo García A2, Rodríguez Bedoya M3, Suárez Rángel G2.

Author information: 1 Centro de Medicina Basada en la Evidencia Keralty Centro de Medicina Basada en la Evidencia Keralty Bogotá Colombia Centro de Medicina Basada en la Evidencia Keralty, Bogotá, Colombia. 2 Programa de Entrenamiento en Epidemiología de Campo (FETP) del Instituto Nacional de Salud de Colombia Programa de Entrenamiento en Epidemiología de Campo (FETP) del Instituto Nacional de Salud de Colombia Colombia Colombia Programa de Entrenamiento en Epidemiología de Campo (FETP) del Instituto Nacional de Salud de Colombia, Colombia. 3 Fundación Universitaria Sanitas Fundación Universitaria Sanitas Bogotá Colombia Fundación Universitaria Sanitas, Bogotá, Colombia.


Abstract in English, Portuguese


The Zika outbreak affected several tropical countries in 2015 and 2016, requiring the creation of intensified surveillance strategies for microcephaly and other neurological syndromes. The effect of the Zika outbreak on the reporting of birth defects in Colombia was evaluated from the perspective of the national surveillance system.


National reporting of newborns with different birth defects was analyzed; variations in reporting attributed to the epidemic were determined through difference in differences (DID), a semiparametric model.


During the period of study, 18,234 cases of birth defects were reported in Colombia. The majority were congenital malformations (91.9%), and 82.3% was confirmed by clinical diagnosis or epidemiological link. In the case of microcephaly, eight new cases per epidemiological week were reported (coefficient of case reporting [D] = 8.8; P = 0.000) and 32 cases from other congenital anatomical malformations (D = 32.0; P = 0.000). The absolute value of the difference in differences estimator attributed to the Zika outbreak increased weekly case reporting of microcephaly (DID = |-5.0|; P = 0.008) and congenital malformations (DID = |-12.0|; P = 0.111).


The Zika outbreak increased reporting of newborns with microcephaly, but caused no significant variation in reporting of other malformations and functional birth defects of sensory or metabolic origin in the surveillance system.

KEYWORDS: Colombia; Zika virus; congenital abnormalities; health surveillance; public health

PMID: 31093262 PMCID: PMC6499088 DOI: 10.26633/RPSP.2019.38

Keywords: Zika Virus; Zika Congenital Syndrome; Microcephaly; Colombia.


#Congenital #Zika Syndrome: The Main Cause of #Death and Correspondence Between #Brain #CT and Postmortem #Histological Section Findings From the Same Individuals (Top Magn Reson Imaging, abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Top Magn Reson Imaging. 2019 Feb;28(1):29-33. doi: 10.1097/RMR.0000000000000194.

Congenital Zika Syndrome: The Main Cause of Death and Correspondence Between Brain CT and Postmortem Histological Section Findings From the Same Individuals.

de Fatima Viana Vasco Aragão M1,2, van der Linden V3, Petribu NC3, Valenca MM4, Parizel PM5,6, de Mello RJV4.

Author information: 1 Multimagem, Recife, Brazil. 2 Catholic University of Pernambuco, Recife, Brazil. 3 Barão de Lucena Hospital, Recife, Brazil. 4 Federal University of Pernambuco, Recife, Brazil. 5 Royal Perth Hospital (RPH), Perth, WA, Australia. 6 University of Western Australia (UWA) Medical School, Perth, WA, Australia.



In the present case series, the cause of death of infants diagnosed with congenital Zika syndrome (CZS) was lung disease (pneumonia and sepsis with massive pulmonary aspiration), probably secondary to dysphagia and reflux. The main findings in infants with a confirmed diagnosis of CZS who died were as follows: (1) calcification and hypoplasia of the lentiform nuclei, hypoplasia of the caudate nuclei, and calcification at the cortical-subcortical junction was noted in all cases (100%) and calcification of the caudate nuclei was noted in 66.7% of cases; (2) calcification in the brainstem and along the lateral wall of the lateral ventricles was noted in only the case with arthrogryposis (33.3%); and (3) lesions in the posterior fossa (hypoplasia of the brainstem and cerebellum) were noted in two cases (66.7%), including the case with arthrogryposis. The findings concerning calcifications and brain malformations obtained from non-contrast computed tomography (CT) demonstrated good agreement with findings obtained from the postmortem pathological analysis; however, CT failed to detect discontinuity of the pia mater with heterotopia, invasion of the cerebral tissue into the subarachnoid space, and discontinuity of the ependyma in the lateral ventricles with gliosis; this last feature was only imaged in the most severe case of extreme microcephaly with a simplified gyral pattern. Only histopathology showed grouped calcifications associated with scattered calcifications suggestive of the neuron morphology.

PMID: 30817678 DOI: 10.1097/RMR.0000000000000194 [Indexed for MEDLINE]

Keywords: Congenital Zika Syndrome; Zika Virus; Microcephaly; Histopathology; Neurology; Neuroimaging.