foetal malformations
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2021 ◽  
Vol 102 (9) ◽  
Author(s):  
Heiko D. Guggemos ◽  
Matthias Fendt ◽  
Kyra Hermanns ◽  
Christian Hieke ◽  
Verena Heyde ◽  
...  

The genus Orbivirus includes a variety of pathogenic viruses that are transmitted by biting midges, mosquitoes and ticks. Some of the economically most relevant orbiviruses are endemic to Namibia, like the livestock-pathogenic Bluetongue and African horse sickness viruses. Here, we assessed the diversity of orbiviruses circulating in the Zambezi region of north-eastern Namibia. A total of 10 250 biting midges and 10 206 mosquitoes were collected and screened for orbivirus infections. We identified Palyam virus (PALV) in a pool of biting midges (Culicoides sp.) sampled in the Wuparo Conservancy and three strains of Corriparta virus (CORV) in Culex sp. mosquitoes sampled in Mudumu National Park and the Mashi Conservancy. This is, to our knowledge, the first detection of PALV and CORV in Namibia. Both viruses infect vertebrates but only PALV has been reported to cause disease. PALV can cause foetal malformations and abortions in ruminants. Furthermore, a novel orbivirus, related to Kammavanpettai virus from India and Umatilla virus from North America, was discovered in biting midges (Culicoides sp.) originating from Mudumu National Park and tentatively named Mudumu virus (MUMUV). Complete genomes of PALV, CORV and MUMUV were sequenced and genetically characterized. The Namibian CORV strain showed 24.3 % nucleotide divergence in its subcore shell gene to CORV strains from Australia, indicating that African CORV variants vary widely from their Australian relatives. CORV was isolated in cell culture and replicated to high titres in mosquito and duck cells. No growth was found in rodent and primate cells. The data presented here show that diverse orbiviruses are endemic to the Zambezi region. Further studies are needed to assess their effects on wildlife and livestock.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Beatriz López-Escobar ◽  
Rut Fernández-Torres ◽  
Viviana Vargas-López ◽  
Mercedes Villar-Navarro ◽  
Tatyana Rybkina ◽  
...  
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2020 ◽  
Vol 91 ◽  
pp. 14-26 ◽  
Author(s):  
Vivi Flou Hjorth Jensen ◽  
Anne-Marie Mølck ◽  
Jens Lykkesfeldt ◽  
Johannes Josef Fels ◽  
Lene Andersen ◽  
...  

2019 ◽  
Vol 90 (e7) ◽  
pp. A3.1-A3
Author(s):  
Frank JE Vajda ◽  
Janet E Graham ◽  
Alison A Hitchcock ◽  
Cecilie M Lander ◽  
Terry J O’Brien ◽  
...  

BackgroundThe Australian Pregnancy Register (APR) established in 1998, collects data concerning the hazard of foetal malformations from intrauterine exposure to antiepileptic drugs.Methods4 telephone interviews, ethical approval, informed consent, observational study, statistical analyses.ResultsBy December 2017, the APR recorded 1879 pregnancies, followed prospectively. There had been 1766 live births (94.0%), 5 stillbirths (0.3%), 54 spontaneous abortions (2.9%), and 30 induced abortions (1.6%), while 24 pregnancies had an unknown outcome due to loss of contact with the women involved (1.3%). Foetal malformations had occurred in 71 of the live-born infants. Of the induced abortions, 15 had been for intrauterine foetal death, 10 for major foetal malformation (spina bifida, anencephaly and left heart underdevelopment), 2 for detected chromosome defects and 3 for maternal reasons (major illness in 2).By the end of the post-pregnancy year a further 99 pregnancies had become unavailable for follow-up (resulting in an 84.9% live-born infant final retention rate). An additional 33 pregnancies that had resulted in late recognised foetal malformations had been identified, nearly all in the first 6 months after birth. Intrauterine valproate exposure was involved in 447 of the 1731 antiepileptic drug treated pregnancies, a malformation-carrying pregnancy rate of 11.86%, as compared with a rate of 2.70% in the 148 drug-unexposed pregnancies (O.R. = 4.84; 95% C.I. 1.72, 13.62), used as comparators.ConclusionThis report confirms previous interpretations of the APR data, also providing insights into the pregnancies of women with epilepsy that did not result in live- born offspring.


2018 ◽  
Vol 139 (1) ◽  
pp. 42-48 ◽  
Author(s):  
Frank J. E. Vajda ◽  
Terence J. O'Brien ◽  
Janet E. Graham ◽  
Alison A. Hitchcock ◽  
Cecilie M. Lander ◽  
...  
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2018 ◽  
Vol 205 (5-6) ◽  
pp. 256-278 ◽  
Author(s):  
Alexander Rulle ◽  
Nikoloz Tsikolia ◽  
Bernadette de Bakker ◽  
Charis Drummer ◽  
Rüdiger Behr ◽  
...  

Existence and biomedical relevance of the neurenteric canal, a transient midline structure during early neurulation in the human embryo, have been controversially discussed for more than a century by embryologists and clinicians alike. In this study, the authors address the long-standing enigma by high-resolution histology and three-dimensional reconstruction using new and historic histological sections of 5 human 17- to 21-day-old embryos and of 2 marmoset monkey embryos of the species Callithrix jacchus at corresponding stages. The neurenteric canal presents itself as the classical vertical connection between the amniotic cavity and the yolk sac cavity and is lined (a) craniolaterally by a horseshoe-shaped “hinge of involuting notochordal cells” within Hensen’s node and (b) caudally by the receding primitive streak epiblast dorsally and by notochordal plate epithelium ventrally, the latter of which covered the (longitudinal) notochordal canal on its ventral side at the preceding stage. Furthermore, asymmetric parachordal nodal expression in Callithrix and morphological asymmetries within the nodes of the other specimens suggest an early non-cilium-dependent left-right symmetry breaking mode previously postulated for other mammals. We conclude that structure and position of the mammalian neurenteric canal support the notion of its homology with the reptilian blastopore as a whole and with a dorsal segment of the blastopore in amphibia. These new features of the neurenteric canal may further clarify the aetiology of foetal malformations such as junctional neurulation defects, neuroendodermal cysts, and the split notochord syndrome.


2016 ◽  
Vol 135 (3) ◽  
pp. 360-365 ◽  
Author(s):  
F. J. E. Vajda ◽  
T. J. O'Brien ◽  
J. E. Graham ◽  
A. A. Hitchcock ◽  
C. M. Lander ◽  
...  

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