Transmissibility: To be or not to be

Appraising SARS-CoV-2 virus under the taxonomy category of coronaviridae family, which has been responsible for more than two million fatalities across the globe. It not only jeopardizes the normal life, but also potentiating the evolutionary progress towards a more lethal form. The lethal form, albeit is a bit virulent, is likely to predominate, thereby causing cumulative damage in any cluster that cannot even combat the wide spectrum of genetic variation. The impact on the vertical COVID-19 transmissibility of antenatal population is still sketchy about “nosocomial transmission” and the measures crude. The paper has reviewed the placental pathological findings of pregnant women afflicted with SARS-CoV-2 including the information, gathered from the subsequent stages of gestational outcomes. The possibility of the vertical transmission of SARS-CoV-2 due to the probable placental barrier damage caused by the severe maternal hypoxia, Homo sapiens (human) angiotensin-converting enzyme-2 (hACE2) influenced transplacental migration of SARS-CoV-2 in advanced gestational age, the plausible presence of RNAemia (detection of SARS-CoV-2 in the blood) in hematogenous route was reviewed in this paper. Nevertheless, the probability of susceptible intrauterine or perinatal infection of fetus does not conclusively decide as chances of involving placental coexpression of hACE2 and transmembrane protease, serine 2 in cytoplasmic entry of SARS-CoV-2 remains insignificant, exhibiting the probable relative insensitivity to transplacental infection. The present paper will provide an important insight about the wider understanding of the SARS-CoV-2 pathogenesis in the placenta that canvassed across all trimesters of pregnancy in response to the indiscriminate spread across globe at the time of therapeutic interventions.

Intrauterine growth restriction predisposes to airway inflammation without disruption of epithelial integrity in postnatal male mice

Evidence from animal models demonstrate that intrauterine growth restriction (IUGR) alters airway structure and function which may affect susceptibility to disease. Airway inflammation and dysregulated epithelial barrier properties are features of asthma which have not been examined in the context of IUGR. This study used a maternal hypoxia-induced IUGR mouse model to assess lung-specific and systemic inflammation and airway epithelial tight junctions (TJs) protein expression. Pregnant BALB/c mice were housed under hypoxic conditions (10.5% O2) from gestational day (GD) 11 to 17.5 (IUGR group; term, GD 21). Following hypoxic exposure, mice were returned to a normoxic environment (21% O2). A Control group was housed under normoxic conditions throughout pregnancy. Offspring weights were recorded at 2 and 8 weeks of age and euthanized for bronchoalveolar lavage (BAL) and peritoneal cavity fluid collection for inflammatory cells counts. From a separate group of mice, right lungs were collected for Western blotting of TJs proteins. IUGR offspring had greater inflammatory cells in the BAL fluid but not in peritoneal fluid compared with Controls. At 8 weeks of age, interleukin (IL)-2, IL-13, and eotaxin concentrations were higher in male IUGR compared with male Control offspring but not in females. IUGR had no effect on TJs protein expression. Maternal hypoxia-induced IUGR increases inflammatory cells in the BAL fluid of IUGR offspring with no difference in TJs protein expression. Increased cytokine release, specific to the lungs of IUGR male offspring, indicates that both IUGR and sex can influence susceptibility to airway disease.

A Case of Fetal Tachycardia after Electroconvulsive Therapy: A Possible Effect of Maternal Hypoxia and Uterine Contractions

Electroconvulsive therapy (ECT) is considered to be an effective and safe treatment for depression in pregnant women in that it avoids the risk of psychotropic pharmacotherapy. However, clinicians should be cautious about the adverse effects in the fetus, such as fetal cardiac arrhythmia. Most of the previous studies have demonstrated a reduction in fetal heart rate associated with ECT. However, we encountered a case of fetal tachycardia after maternal ECT-induced convulsions. The patient was a woman who was 30 weeks’ pregnant and had severe depression; fetal tachycardia (180–200 bpm) occurred immediately after the electrical stimulation and lasted for more than 30 minutes. The fetal tachycardia might have been caused by maternal hypoxia and uterine contractions. To our knowledge, this is the first report of fetal tachycardia as an adverse effect of ECT. Prolonged fetal tachycardia may cause fetal heart failure. Therefore, oxygenation during convulsions and careful fetal cardiac monitoring are essential when administering ECT in pregnancy.

Preeclampsia link to gestational hypoxia

Complications of pregnancy remain key drivers of morbidity and mortality, affecting the health of both the mother and her offspring in the short and long term. There is lack of detailed understanding of the pathways involved in the pathology and pathogenesis of compromised pregnancy, as well as a shortfall of effective prognostic, diagnostic and treatment options. In many complications of pregnancy, such as in preeclampsia, there is an increase in uteroplacental vascular resistance. However, the cause and effect relationship between placental dysfunction and adverse outcomes in the mother and her offspring remains uncertain. In this review, we aim to highlight the value of gestational hypoxia-induced complications of pregnancy in elucidating underlying molecular pathways and in assessing candidate therapeutic options for these complex disorders. Chronic maternal hypoxia not only mimics the placental pathology associated with obstetric syndromes like gestational hypertension at morphological, molecular and functional levels, but also recapitulates key symptoms that occur as maternal and fetal clinical manifestations of these pregnancy disorders. We propose that gestational hypoxia provides a useful model to study the inter-relationship between placental dysfunction and adverse outcomes in the mother and her offspring in a wide array of examples of complicated pregnancy, such as in preeclampsia.

Fetal brain sparing in a mouse model of chronic maternal hypoxia

Hypoxic stress is a common occurrence during human pregnancy, yet little is known about its effects on the fetal brain. This study examined the fetal hemodynamic responses to chronic hypoxia in an experimental mouse model of chronic maternal hypoxia (11% O2 from E14.5 to E17.5). Using high-frequency Doppler ultrasound, we found fetal cerebral and ductus venosus blood flow were both elevated by 69% and pulmonary blood flow was decreased by 62% in the fetuses exposed to chronic hypoxia compared to controls. This demonstrates that brain sparing persists during chronic fetal hypoxia and is mediated by “streaming,” where highly oxygenated blood preferentially flows through the ductus venosus towards the cerebral circulation, bypassing the liver and the lungs. Consistent with these changes in blood flow, the fetal brain volume measured by MRI is preserved, while the liver and lung volumes decreased compared to controls. However, hypoxia exposed fetuses were rendered vulnerable to an acute hypoxic challenge (8% O2 for 3 min), demonstrating global blood flow decreases consistent with imminent fetal demise rather than elevated cerebral blood flow. Despite this vulnerability, there were no differences in adult brain morphology in the mice exposed to chronic maternal hypoxia compared to controls.