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Background: Research exploring the relationship between prenatal infection and child behavioural outcomes would benefit from further studies utilising full‐population samples with the scale to investigate specific infections and to employ robust designs. We tested the association among several common infections requiring inpatient admission during and after pregnancy with a range of childhood behavioural outcomes, to determine whether any negative impact was specific to the period of foetal development. Methods: The sample included all mother–offspring pairs from the Australian state of New South Wales (NSW) for whom the child commenced their first year of full‐time schooling in 2009 (~age 5 years; n = 77,302 offspring), with records linked across four health administrative data sets including the NSW perinatal data collection (PDC), the NSW admitted patient data collection (APDC) and the NSW component of the 2009 Australian Early Development Census (AEDC). Multivariable linear regression was used to test associations between a number of infections requiring inpatient admission during and after pregnancy with a range of teacher assessed behavioural outcomes. Results: Associations specific to the prenatal period were only found for streptococcus A although this would need to be reproduced in external samples given the low prevalence. Otherwise, 12 out of 15 selected infections either showed no association prenatally or also demonstrated associations in the 12 months after pregnancy. For example, prenatal hepatitis C, influenza and urinary E. coli infections were associated with lower scores of several domains of childhood behaviour, but even stronger associations were found when these same maternal infections occurred after pregnancy. Conclusions: The prenatal infections we tested appeared not to impact childhood behaviour by altering foetal neurodevelopment. Rather, the strong associations we found among infections occurring during and after pregnancy point to either residual socioeconomic/lifestyle factors or a shared familial/genetic liability between infections and behavioural problems. [ABSTRACT FROM AUTHOR]

Cytomegalovirus (CMV) can cause serious complications in immunocompromised individuals and fetuses with congenital infections. These can include neurodevelopmental impairments and congenital abnormalities in newborns. This paper emphasizes the importance of concurrently evaluating ultrasonography findings and laboratory parameters in diagnosing congenital CMV infection. To examine the prenatal characteristics of CMV DNA-positive patients, we assessed serum and amniotic fluid from 141 pregnant women aged 19–45 years, each with fetal anomalies. ELISA and PCR tests, conducted in response to these amniocentesis findings, were performed at an average gestational age of 25 weeks. Serological tests revealed that all 141 women were CMV IgG-positive, and 2 (1.41%) had low-avidity CMV IgG, suggesting a recent infection. CMV DNA was detected in 17 (12.05%) amniotic fluid samples using quantitative PCR. Of these, 82% exhibited central nervous system abnormalities. Given that most infections in pregnant women are undetectable and indicators non-specific, diagnosing primary CMV in pregnant women using clinical findings alone is challenging. We contend that serological tests should not be the sole means of diagnosing congenital CMV infection during pregnancy. [ABSTRACT FROM AUTHOR]

Numerous studies reported an increase of postpartum mood symptoms during the COVID-19 pandemic. Yet, the link between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and perinatal mental health is less well understood. We investigated the associations between prenatal SARS-CoV-2 infection and postpartum depressive and anxiety symptoms, including examinations of infection timing and pandemic timeline. We included 595 participants from Generation C, a prospective pregnancy cohort in New York City (2020–2022). Prenatal SARS-CoV-2 infection was determined via laboratory or medical diagnosis. Depression and anxiety symptoms were measured 4–12 weeks postpartum using the Edinburgh Postnatal Depression Scale (EPDS) and Generalized Anxiety Disorder questionnaire (GAD), respectively. Quantile regressions were conducted with prenatal SARS-CoV-2 infection as exposure and continuously measured EPDS and GAD scores as outcomes. We reran the analyses in those with COVID-19-like symptoms in the trimester during which infection occurred. 120 (20.1%) participants had prenatal SARS-CoV-2 infection. After adjusting for socio-demographic, obstetric and other maternal health factors, prenatal SARS-CoV-2 infection was associated with higher median postpartum anxiety scores (b = 0.55, 95% CI = 0.15; 0.96). Late gestation infection (b = 1.15, 95% CI = 0.22; 2.09) and symptomatic infection (b = 1.15, 95% CI = 0.12; 2.18) were also associated with higher median postpartum anxiety scores. No associations were found with depressive symptoms. The associations were not moderated by time since the start of the pandemic. This study suggests that prenatal SARS-CoV-2 infection increases the risk of postpartum anxiety symptoms among participants reporting median anxiety symptoms. Given that this association was not affected by pandemic timing and that SARS-CoV-2 transmission continues, individuals infected with SARS-CoV-2 during pregnancy should be monitored for postpartum anxiety symptoms. • Prenatal SARS-CoV-2 infection is associated with increased postpartum anxiety symptoms. • Prenatal SARS-CoV-2 infection is not associated with postpartum depressive symptoms. • Time between start pandemic and birth did not affect the association between infection and postpartum mood symptoms. [ABSTRACT FROM AUTHOR]

Abstract Background Prenatal infection has been implicated in the development of neuropsychiatric disorders in children. We hypothesised that exposure to lipopolysaccharide during prenatal development could induce anxiety-like behaviour and sensorineural hearing loss in offspring, as well as disrupt neural differentiation during embryonic neural development. Methods We simulated prenatal infection in FVB mice and mouse embryonic stem cell (ESC) lines, specifically 46C and E14Tg2a, through lipopolysaccharide treatment. Gene expression profiling analyses and behavioural tests were utilized to study the effects of lipopolysaccharide on the offspring and alterations in toll-like receptor (TLR) 2-positive and TLR4-positive cells during neural differentiation in the ESCs. Results Exposure to lipopolysaccharide (25 µg/kg) on gestation day 9 resulted in anxiety-like behaviour specifically in male offspring, while no effects were detected in female offspring. We also found significant increases in the expression of GFAP and CNPase, as well as higher numbers of GFAP + astrocytes and O4+ oligodendrocytes in the prefrontal cortex of male offspring. Furthermore, increased scores for genes related to oligodendrocyte and lipid metabolism, particularly ApoE, were observed in the prefrontal cortex regions. Upon exposure to lipopolysaccharide during the ESC-to-neural stem cell (NSC) transition, Tuj1, Map2, Gfap, O4, and Oligo2 mRNA levels increased in the differentiated neural cells on day 14. In vitro experiments demonstrated that lipopolysaccharide exposure induced inflammatory responses, as evidenced by increased expression of IL1b and ApoB mRNA. Conclusions Our findings suggest that prenatal infection at different stages of neural differentiation may result in distinct disturbances in neural differentiation during ESC—NSC transitions. Furthermore, early prenatal challenges with lipopolysaccharide selectively induce anxiety-like behaviour in male offspring. This behaviour may be attributed to the abnormal differentiation of astrocytes and oligodendrocytes in the brain, potentially mediated by ApoB/E signalling pathways in response to inflammatory stimuli.

Cytomegalovirus (CMV) can cause serious complications in immunocompromised individuals and fetuses with congenital infections. These can include neurodevelopmental impairments and congenital abnormalities in newborns. This paper emphasizes the importance of concurrently evaluating ultrasonography findings and laboratory parameters in diagnosing congenital CMV infection. To examine the prenatal characteristics of CMV DNA-positive patients, we assessed serum and amniotic fluid from 141 pregnant women aged 19–45 years, each with fetal anomalies. ELISA and PCR tests, conducted in response to these amniocentesis findings, were performed at an average gestational age of 25 weeks. Serological tests revealed that all 141 women were CMV IgG-positive, and 2 (1.41%) had low-avidity CMV IgG, suggesting a recent infection. CMV DNA was detected in 17 (12.05%) amniotic fluid samples using quantitative PCR. Of these, 82% exhibited central nervous system abnormalities. Given that most infections in pregnant women are undetectable and indicators non-specific, diagnosing primary CMV in pregnant women using clinical findings alone is challenging. We contend that serological tests should not be the sole means of diagnosing congenital CMV infection during pregnancy.

Background: Prenatal infection has been implicated in the development of neuropsychiatric disorders in children. We hypothesised that exposure to lipopolysaccharide during prenatal development could induce anxiety-like behaviour and sensorineural hearing loss in offspring, as well as disrupt neural differentiation during embryonic neural development. Methods: We simulated prenatal infection in FVB mice and mouse embryonic stem cell (ESC) lines, specifically 46C and E14Tg2a, through lipopolysaccharide treatment. Gene expression profiling analyses and behavioural tests were utilized to study the effects of lipopolysaccharide on the offspring and alterations in toll-like receptor (TLR) 2-positive and TLR4-positive cells during neural differentiation in the ESCs. Results: Exposure to lipopolysaccharide (25 µg/kg) on gestation day 9 resulted in anxiety-like behaviour specifically in male offspring, while no effects were detected in female offspring. We also found significant increases in the expression of GFAP and CNPase, as well as higher numbers of GFAP + astrocytes and O4+ oligodendrocytes in the prefrontal cortex of male offspring. Furthermore, increased scores for genes related to oligodendrocyte and lipid metabolism, particularly ApoE, were observed in the prefrontal cortex regions. Upon exposure to lipopolysaccharide during the ESC-to-neural stem cell (NSC) transition, Tuj1, Map2, Gfap, O4, and Oligo2 mRNA levels increased in the differentiated neural cells on day 14. In vitro experiments demonstrated that lipopolysaccharide exposure induced inflammatory responses, as evidenced by increased expression of IL1b and ApoB mRNA. Conclusions: Our findings suggest that prenatal infection at different stages of neural differentiation may result in distinct disturbances in neural differentiation during ESC—NSC transitions. Furthermore, early prenatal challenges with lipopolysaccharide selectively induce anxiety-like behaviour in male offspring. This behaviour may be attributed to the abnormal differentiation of astrocytes and oligodendrocytes in the brain, potentially mediated by ApoB/E signalling pathways in response to inflammatory stimuli. [ABSTRACT FROM AUTHOR]

This systematic review explored the impact of maternal immune activation (MIA) on learning and memory behavior in offspring, with a particular focus on sexual dimorphism. We analyzed 20 experimental studies involving rodent models (rats and mice) exposed to either lipopolysaccharide (LPS) or POLY I:C during gestation following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Our findings reveal that most studies report a detrimental impact of MIA on the learning and memory performance of offspring, highlighting the significant role of prenatal environmental factors in neurodevelopment. Furthermore, this review underscores the complex effects of sex, with males often exhibiting more pronounced cognitive impairment compared to females. Notably, a small subset of studies report enhanced cognitive function following MIA, suggesting complex, context-dependent outcomes of prenatal immune challenges. This review also highlights sex differences caused by the effects of MIA in terms of cytokine responses, alterations in gene expression, and differences in microglial responses as factors that contribute to the cognitive outcomes observed. • Maternal immune activation (MIA) can impair offspring learning and memory. • MIA negatively impacts cognition in rodents. • Males are more susceptible to cognitive deficits. • Some studies show improved cognition after MIA. • Sex differences in immune responses may explain cognitive outcomes. [ABSTRACT FROM AUTHOR]

Milestones of brain development in mammals are completed before birth, which provide the prerequisite for cognitive and intellectual performances of the offspring. Prenatal challenges, such as maternal stress experience or infections, have been linked to impaired cognitive development, poor intellectual performances as well as neurodevelopmental and psychiatric disorders in the offspring later in life. Fetal microglial cells may be the target of such challenges and could be functionally modified by maternal markers. Maternal markers can cross the placenta and reach the fetus, a phenomenon commonly referred to as "vertical transfer." These maternal markers include hormones, such as glucocorticoids, and also maternal immune cells and cytokines, all of which can be altered in response to prenatal challenges. Whilst it is difficult to discriminate between the maternal or fetal origin of glucocorticoids and cytokines in the offspring, immune cells of maternal origin-although low in frequency-can be clearly set apart from offspring's cells in the fetal and adult brain. To date, insights into the functional role of these cells are limited, but it is emergingly recognized that these maternal microchimeric cells may affect fetal brain development, as well as post-natal cognitive performances and behavior. Moreover, the inheritance of vertically transferred cells across generations has been proposed, yielding to the presence of a microchiome in individuals. Hence, it will be one of the scientific challenges in the field of neuroimmunology to identify the functional role of maternal microchimeric cells as well as the brain microchiome. Maternal microchimeric cells, along with hormones and cytokines, may induce epigenetic changes in the fetal brain. Recent data underpin that brain development in response to prenatal stress challenges can be altered across several generations, independent of a genetic predisposition, supporting an epigenetic inheritance. We here discuss how fetal brain development and offspring's cognitive functions later in life is modulated in the turnstile of prenatal challenges by introducing novel and recently emerging pathway, involving maternal hormones and immune markers.

BackgroundFetal ventriculomegaly (VM) is one of the most common abnormalities of the central nervous system (CNS), which can be significantly identified by brain anomalies prenatally by magnetic resonance imaging (MRI). Aberrant white blood cells (WBCs) levels indicate that the maternal is suffering from the infection. Previous studies have confirmed that prenatal infection can affect fetal brain structure, but there is no research revealed the association between maternal blood parameters with fetal VM until now.MethodsWe measured the width of the lateral ventricle of 142 fetuses, which were divided into the fetal VM group (n = 70) and the normal lateral ventricle group (n = 72). We compared maternal blood cell levels between the two groups and investigate potential biomarkers of fetal VM.ResultHigh levels of maternal WBC and neutrophil (NE#) levels were observed in fetuses with VM (p < 0.001), while lymphocyte percentage, monocytes (MO#), neutrophil/lymphocyte ratio (NLR), and platelet were also increased in the fetal VM group (p = 0.033, 0.027, 0.034, and 0.025, respectively). receiver–operator curve (ROC) analysis suggested that WBC and NE# counts might be useful to distinguish fetuses with enlarged lateral ventricles (AUC = 0.688, 0.678, respectively).ConclusionThe current study emphasizes the importance of maternal infection for fetal brain growth, which could provide important information for prenatal diagnosis of CNS anomalies. Future research needs longitudinal analysis and exploration of the influence of maternal blood inflammatory marker levels on fetal brain development.

Human pegivirus (HPgV) is best known for persistent, presumably non-pathogenic, infection and a propensity to co-infect with human immunodeficiency virus or hepatitis C virus. However, unique attributes, such as the increased risk of malignancy or immune modulation, have been recently recognized for HPgV. We have identified a unique case of a woman with high levels HPgV infection in two pregnancies, which occurred 4 years apart and without evidence of human immunodeficiency virus or hepatitis C virus infection. The second pregnancy was complicated by congenital heart disease. A high level of HPgV infection was detected in the maternal blood from different trimesters by RT-PCR and identified as HPgV type 1 genotype 2 in both pregnancies. In the second pregnancy, the decidua and intervillous tissue of the placenta were positive for HPgV by PCR but not the chorion or cord blood (from both pregnancies), suggesting no vertical transmission despite high levels of viremia. The HPgV genome sequence was remarkably conserved over the 4 years. Using VirScan, sera antibodies for HPgV were detected in the first trimester of both pregnancies. We observed the same anti-HPgV antibodies against the non-structural NS5 protein in both pregnancies, suggesting a similar non-E2 protein humoral immune response over time. To the best of our knowledge, this is the first report of persistent HPgV infection involving placental tissues with no clear indication of vertical transmission. Our results reveal a more elaborate viral-host interaction than previously reported, expand our knowledge about tropism, and opens avenues for exploring the replication sites of this virus. [ABSTRACT FROM AUTHOR]

Prenatal infections that have been exhaustively studied help frame the current Severe Acute Respiratory Syndrome related coronavirus-2 (SARS-CoV-2) pandemic, with the caveat that asymptomatic SARS-CoV-2 infected patients are not tested, while those symptomatic are delivered and/or treated with drug(s) available on-site. Thus, management and therapy are still heterogeneous. SARSCoV-2 induced respiratory infection remains mostly local, unless severe, which lessens transplacental vertical transmission (VT). Vaccination prior to or during pregnancy significantly changes the prognosis for both the mother and newborn. The virus spread to the fetus can be binding to ACE2 and TMPRSS2 protein receptors. A recent study demonstrated ACE2 and TMPRSS2 fetal expression in the intestine from the second trimester. Most placental infections are subclinical unless severe villitis and apoptosis are observed. The placenta is rarely tested, and it is highly probable that most are positive for the virus, requiring sophisticated diagnostics to document. Other VT modalities, such as vaginal, rectal or through amniotic fluid contamination, are very rare. Therefore, vaginal delivery is preferable when clinically feasible. It has not yet been determined whether the placenta is a shield or if it transmits infection, while, on the other hand, recent data support fetal resilience, which is plausible due to themajor difference between the placental and fetal rates of infection: only 3%-5% of documentable VT compared with up to 100% expected placental exposure to viremia. Newborn Polymerase Chain Reaction (PCR) from nasal swab is more practical as an option for VT diagnosis compared to ocular or anal swab, with low yield. The maternal infection leads to antiviral IgG production of 100% in severe cases, which is transferred to the fetus and breast milk. Postpartum-documenting VT is difficult since horizontal viral transmission may be common and minimized by mother/staff/family-preventive measures. Breastfeeding is safe and encouraged because, beyond nutrition, it promotes protective antibody transfer and maternal bonding. Lessons learned from other Betacorona viruses (SARS-CoV and Middle East Respiratory Syndrome related coronavirus [MERS-CoV]) virulence are relevant since mutations can increase or decrease vulnerability. Overall, data support fetal/newborn resilience against SARS-CoV-2 VT. However, viremia monitoring by sensitive tests and assessment for delayed sequelae shown in adults is necessary. [ABSTRACT FROM AUTHOR]

Prenatal infections that have been exhaustively studied help frame the current Severe Acute Respiratory Syndrome related coronavirus-2 (SARS-CoV-2) pandemic, with the caveat that asymptomatic SARS-CoV-2 infected patients are not tested, while those symptomatic are delivered and/or treated with drug(s) available on-site. Thus, management and therapy are still heterogeneous. SARS-CoV-2 induced respiratory infection remains mostly local, unless severe, which lessens transplacental vertical transmission (VT). Vaccination prior to or during pregnancy significantly changes the prognosis for both the mother and newborn. The virus spread to the fetus can be binding to ACE2 and TMPRSS2 protein receptors. A recent study demonstrated ACE2 and TMPRSS2 fetal expression in the intestine from the second trimester. Most placental infections are subclinical unless severe villitis and apoptosis are observed. The placenta is rarely tested, and it is highly probable that most are positive for the virus, requiring sophisticated diagnostics to document. Other VT modalities, such as vaginal, rectal or through amniotic fluid contamination, are very rare. Therefore, vaginal delivery is preferable when clinically feasible. It has not yet been determined whether the placenta is a shield or if it transmits infection, while, on the other hand, recent data support fetal resilience, which is plausible due to the major difference between the placental and fetal rates of infection: only 3%–5% of documentable VT compared with up to 100% expected placental exposure to viremia. Newborn Polymerase Chain Reaction (PCR) from nasal swab is more practical as an option for VT diagnosis compared to ocular or anal swab, with low yield. The maternal infection leads to antiviral IgG production of 100% in severe cases, which is transferred to the fetus and breast milk. Postpartum-documenting VT is difficult since horizontal viral transmission may be common and minimized by mother/staff/family-preventive measures. Breastfeeding is safe and encouraged because, beyond nutrition, it promotes protective antibody transfer and maternal bonding. Lessons learned from other Betacorona viruses (SARS-CoV and Middle East Respiratory Syndrome related coronavirus [MERS-CoV]) virulence are relevant since mutations can increase or decrease vulnerability. Overall, data support fetal/newborn resilience against SARS-CoV-2 VT. However, viremia monitoring by sensitive tests and assessment for delayed sequelae shown in adults is necessary.

BackgroundChorioamnionitis is a risk factor for cerebral palsy. The relationship between extra-amniotic infections and cerebral palsy is less well studied. We examined maternal intra-amniotic and extra-amniotic infections and risk of cerebral palsy in the child.MethodsAmong a retrospective cohort of 6 million Californian births, 1991-2001, we analyzed administrative maternal and newborn hospital discharge abstracts linked to records of all children receiving services for cerebral palsy at the California Department of Developmental Services. We identified maternal hospital diagnoses of intra-amniotic (chorioamnionitis) and extra-amniotic (other genitourinary and respiratory) infections occurring up to 12 months before delivery. Using multivariable logistic regression, we determined the independent association between maternal infections and cerebral palsy, adjusting for infant sex, maternal age, race, education, socioeconomic status, and obesity.ResultsAbout 5.5% of mothers had a hospital discharge diagnosis of at least one of the following: chorioamnionitis (2.0%), other genitourinary (3.1%), and respiratory infection (0.6%). An infection diagnosis was more common in mothers of the 8473 infants with cerebral palsy than in mothers of unaffected children (13.7% vs 5.5%, P

To better understand the impact of prenatal severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on infants, this study sought to compare the risk of hospital visits and of postnatal SARS-CoV-2 infection between infants born to mothers with and without prenatal SARS-CoV-2 infection. In this retrospective observational cohort study of 6871 mothers and their infants, overall rates of emergency department (ED) visits and hospital admissions in the first 90 days of life were similar for infants born to mothers with and without prenatal SARS-CoV-2 infection. Infants born to negative mothers were more likely than infants of positive mothers to be hospitalized after ED visit (relative risk: 3.76; 95% confidence interval: 1.27-11.13, P =.003). Five infants tested positive; all were born to negative mothers, suggesting that maternal prenatal SARS-CoV-2 infection may protect infants from postnatal infection. The lower acuity ED visits for infants born to mothers with prenatal SARS-CoV-2 infection may reflect a heightened level of concern among these mothers. [ABSTRACT FROM AUTHOR]

Human pegivirus (HPgV) is best known for persistent, presumably non-pathogenic, infection and a propensity to co-infect with human immunodeficiency virus or hepatitis C virus. However, unique attributes, such as the increased risk of malignancy or immune modulation, have been recently recognized for HPgV. We have identified a unique case of a woman with high levels HPgV infection in two pregnancies, which occurred 4 years apart and without evidence of human immunodeficiency virus or hepatitis C virus infection. The second pregnancy was complicated by congenital heart disease. A high level of HPgV infection was detected in the maternal blood from different trimesters by RT-PCR and identified as HPgV type 1 genotype 2 in both pregnancies. In the second pregnancy, the decidua and intervillous tissue of the placenta were positive for HPgV by PCR but not the chorion or cord blood (from both pregnancies), suggesting no vertical transmission despite high levels of viremia. The HPgV genome sequence was remarkably conserved over the 4 years. Using VirScan, sera antibodies for HPgV were detected in the first trimester of both pregnancies. We observed the same anti-HPgV antibodies against the non-structural NS5 protein in both pregnancies, suggesting a similar non-E2 protein humoral immune response over time. To the best of our knowledge, this is the first report of persistent HPgV infection involving placental tissues with no clear indication of vertical transmission. Our results reveal a more elaborate viral-host interaction than previously reported, expand our knowledge about tropism, and opens avenues for exploring the replication sites of this virus.

Pregnant women have been carefully observed during the COVID-19 pandemic, as the pregnancy-specific immune adaptation is known to increase the risk for infections. Recent evidence indicates that even though most pregnant have a mild or asymptomatic course, a severe course of COVID-19 and a higher risk of progression to diseases have also been described, along with a heightened risk for pregnancy complications. Yet, vertical transmission of the virus is rare and the possibility of placental SARS-CoV-2 infection as a prerequisite for vertical transmission requires further studies. We here assessed the severity of COVID-19 and onset of neonatal infections in an observational study of women infected with SARS-CoV-2 during pregnancy. Our placental analyses showed a paucity of SARS-CoV-2 viral expression ex vivo in term placentae under acute infection. No viral placental expression was detectable in convalescent pregnant women. Inoculation of placental explants generated from placentas of non-infected women at birth with SARS-CoV-2 in vitro revealed inefficient SARS-CoV-2 replication in different types of placental tissues, which provides a rationale for the low ex vivo viral expression. We further detected specific SARS-CoV-2 T cell responses in pregnant women within a few days upon infection, which was undetectable in cord blood. Our present findings confirm that vertical transmission of SARS-CoV-2 is rare, likely due to the inefficient virus replication in placental tissues. Despite the predominantly benign course of infection in most mothers and negligible risk of vertical transmission, continuous vigilance on the consequences of COVID-19 during pregnancy is required, since the maternal immune activation in response to the SARS-CoV2 infection may have long-term consequences for children’s health.

Pregnant women have been carefully observed during the COVID-19 pandemic, as the pregnancy-specific immune adaptation is known to increase the risk for infections. Recent evidence indicates that even though most pregnant have a mild or asymptomatic course, a severe course of COVID-19 and a higher risk of progression to diseases have also been described, along with a heightened risk for pregnancy complications. Yet, vertical transmission of the virus is rare and the possibility of placental SARS-CoV-2 infection as a prerequisite for vertical transmission requires further studies. We here assessed the severity of COVID-19 and onset of neonatal infections in an observational study of women infected with SARS-CoV-2 during pregnancy. Our placental analyses showed a paucity of SARS-CoV-2 viral expression ex vivo in term placentae under acute infection. No viral placental expression was detectable in convalescent pregnant women. Inoculation of placental explants generated from placentas of non-infected women at birth with SARS-CoV-2 in vitro revealed inefficient SARS-CoV-2 replication in different types of placental tissues, which provides a rationale for the low ex vivo viral expression. We further detected specific SARS-CoV-2 T cell responses in pregnant women within a few days upon infection, which was undetectable in cord blood. Our present findings confirm that vertical transmission of SARS-CoV-2 is rare, likely due to the inefficient virus replication in placental tissues. Despite the predominantly benign course of infection in most mothers and negligible risk of vertical transmission, continuous vigilance on the consequences of COVID-19 during pregnancy is required, since the maternal immune activation in response to the SARS-CoV2 infection may have long-term consequences for children's health. [ABSTRACT FROM AUTHOR]

Objective: There is conflicting evidence in recent literature about whether the incidence of schizophrenia is increasing or decreasing. A role for prenatal and early childhood viral infections in the aetiology of schizophrenia has also been debated. We examined the incidence of schizophrenia and the catatonic subtype of schizophrenia over a 30‐year period in Finland. We also investigated whether the incidence rate of the catatonic subtype of schizophrenia was linked to changes in exposure to viral infection (polio and measles) during the prenatal or infant period. Methods: Persons with schizophrenia were identified from the Hospital Discharge Register. Cumulative incidence of schizophrenia from 1956 to 1989 in 4 age groups was calculated with follow‐up from 1972 to 2014. Annual rates of polio and measles were derived from nationwide registers. The association between log‐transformed polio and measles incidence and incidence of schizophrenia, and specifically catatonic schizophrenia, were analysed using linear models. Results: Cumulative incidence of schizophrenia among individuals born 1956–1989 decreased by 23% (from 13 to 10 cases per 1000 live births). The decline was the most prominent in those with onset of schizophrenia diagnosed 16–25 years of age (−41%). The incidence of catatonic schizophrenia declined by 90% over three decades, and there was a significant association between annual polio incidence during the birth year and incidence of catatonic schizophrenia. Conclusions: The results indicate that the incidence of schizophrenia in Finland has declined for individuals born between 1956 and 1989, and that the decline of catatonic schizophrenia may be partially attributable to eradication of polio. [ABSTRACT FROM AUTHOR]

Relevance. According to official statistics prenatal infections outweigh neonatal purulent-septic infections. The clinical picture of prenatal infections is not the specifics. Doctors put a newborn diagnosed based on the mother's medical history, additional studies are not carried out. This leads to incorrect treatment of newborns and incorrect assessment of the epidemiological situation in the matenityhospital. We need to study prenatal infections as a marker epidemic in the matenity hospital. Materials and methods. The study used data from official statistics and special form developed by researchers. Follow-up was 26 years (1991 to 2016). Total 26601 analyzed the case of newborn infections, including 6330 – prenatal infections. Results. Increasing the number of diagnoses prennatalnyh infections coincides with increasing neonatal sepsis diseases, respiratory tract infections, skin infections and intestinal infections. Growth for the prenatal infections correlates with lack midwife and their high production load, the increasing number of complications during childbirth. Conclusion. Prenatal neonatal infection is a mask of infections associated with medical care. The medical organization requires constant monitoring of the number of prenatal infections. Growth prenatal infections should be regarded as a marker to the complications of the epidemiological situation in the hospital.

No abstract available

Background: Although the aetiology of schizophrenia remains unknown, it has been suggested that it might occur in response to alterations in the gut-brain axis (GBA), the bi-directional communication system between the gut and the brain. The current study aimed to determine whether the “two-hit” animal model of neuropsychopathology (maternal immune activation combined with adolescent cannabinoid exposure), produced abnormalities in the GBA Method: Pregnant Wistar rats were administered the viral mimetic polyI:C on gestational day 19 and offspring were administered the synthetic cannabinoid HU210 from postnatal days 35–48. Evidence of GBA activation was assessed in the hypothalamus, colon and fecal samples from male and female offspring at adolescence and adulthood Results: Findings were sex-specific with adolescent female offspring exhibiting an increased hypothalamic inflammatory profile, increased hypothalamic CRHR1 mRNA, and decreased fecal expression of Bifidobacterium longum, however, no changes were detected in colonic inflammation or integrity. Conclusion: These results indicate that the rat two-hit model, documented to produce behavioural and neuroanatomical abnormalities, also produces hypothalamic and microbiota abnormalities. The results also demonstrate significant sex differences, suggesting that this model may be useful for investigating the role of the GBA in the aetiology of neurodevelopmental disorders such as schizophrenia.

Background: Cytomegalovirus (CMV) is a virus that belongs to the herpes viruses' family. It is a deoxyribonucleic acid (DNA) virus. Once the virus gets to access the fetus's body, it starts attacking the nervous system. This has been connected with earlypregnancy abortions or congenital defects while almost one-third demise. Objectives: Clinical practitioners fail to convey this knowledge to the public to improve their awareness. Therefore, in this paper, we will review the available literature discussing the classification, clinical features, and management of CMV infection to print a concise picture of this important disease that will provide practitioners with a clear picture of this issue. Methodology: We conducted the literature search within the PubMed database using the keywords: "Cytomegalovirus", "Prenatal infection", "Fetal infection", "Congenital infection", "Fetal diagnosis", "CMV prevention", and "CMV hyperimmune globulin" from 1990 to 2020. Review: The incidence of noncongenital CMV infection in the developed world reaches almost 3 in every 10 completed pregnancies. Almost one-fifth of a newborn with a congenital CMV infection are symptomatic at birth. The gold standard diagnostic test for congenital CMV is viral isolation in the bodily fluid (e.g. urine and/or saliva) within the first three weeks of life. There are no effective therapies for CMV infections. Conclusion: Clinicians need to be aware of the importance of educating pregnant women on the dangers of CMV infections and be actively vigilant for identifying CMV infection in fetuses and infants. [ABSTRACT FROM AUTHOR]

Parasites have evolved a diversity of lifestyles that exploit the biology of their hosts. Some nematodes that parasitize mammals pass via the placenta or milk from one host to another. Similar cases of vertical transmission have never been reported in avian and nonavian reptiles, suggesting that egg laying may constrain the means of parasite transmission. However, here we report the first incidence of transovarial transmission of a previously undescribed nematode in an egg-laying amniote, the common wall lizard (Podarcis muralis). Nematodes enter the developing brain from the female ovary early in embryonic development. Infected lizard embryos develop normally and hatch with nematodes residing in their braincase. We present a morphological and molecular phylogenetic characterization of the nematode and suggest that particular features of lizard biology that are absent from birds and turtles facilitated the evolutionary origin of this novel life history. [ABSTRACT FROM AUTHOR]

Background: Previous epidemiologic studies have reported adverse neurodevelopmental sequelae following prenatal infectious exposure, yet long-term effects estimated from these observational studies are often subject to biases due to confounding and loss to follow-up.Objectives: We demonstrate the joint use of inverse probability (IP) treatment and censoring weights when evaluating neurotoxic effects of prenatal bacterial infection.Methods: We applied IP weighting for both treatment and censoring to estimate the effects of maternal bacterial infection during pregnancy on mean intelligence quotient (IQ) scores measured at age 7 using the Wechsler Intelligence Scale for Children. Participants were members of a population-based pregnancy cohort recruited in the Boston and Providence sites of the Collaborative Perinatal Project between 1959 and 1966 (n = 11 984). We calculated average treatment effects (ATE) and average treatment effects on the treated (ATT) using IP weights estimated via generalized boosted models.Results: ATE- and ATT-weighted mean IQ scores were lowest among offspring exposed to multi-systemic bacterial infection during pregnancy and highest for those unexposed. The effects of prenatal bacterial infection were greater among male offspring, particularly on performance IQ scores. Offspring who were exposed to multi-systemic bacterial infection in the third trimester displayed the largest reduction in mean full-scale, verbal, and performance IQ scores at age 7 compared to those unexposed or exposed in earlier trimesters.Conclusions: We find that prenatal bacterial infection is associated with cognitive impairments at age 7. Associations are strongest for more severe infections, that occur in the third trimester, and among males. Public health intervention targeting bacterial infection in pregnant women may help enhance the cognitive development of offspring. [ABSTRACT FROM AUTHOR]

Inflammation may adversely affect early human brain development. We aimed to assess the role of maternal nutrition and infections on cord blood inflammation. In a pregnancy cohort in Sylhet, Bangladesh, we enrolled 251 consecutive pregnancies resulting in a term livebirth from July 2016–March 2017. Stillbirths, preterm births, and cases of neonatal encephalopathy were excluded. We prospectively collected data on maternal diet (food frequency questionnaire) and morbidity, and analyzed umbilical cord blood for interleukin (IL)-1α, IL-1β, IL-6, IL-8 and C-reactive protein. We determined associations between nutrition and infection exposures and cord cytokine elevation (≥75% vs. 2) at enrollment. Antenatal and intrapartum infections were observed among 4.8% and 15.9% of the sample, respectively. Low pregnancy intakes of B vitamins (B1, B2, B3, B6, B9 (folate)), fat-soluble vitamins (D, E), iron, zinc, and linoleic acid (lowest vs. middle tertile) were associated with higher risk of inflammation, particularly IL-8. There was a non-significant trend of increased risk of IL-8 and IL-6 elevation with history of ante-and intrapartum infections, respectively. In Bangladesh, improving micronutrient intake and preventing pregnancy infections are targets to reduce fetal systemic inflammation and associated adverse neurodevelopmental outcomes.

Maternal immune activation (MIA) during pregnancy represents an important environmental factor in the etiology of schizophrenia and autism spectrum disorders (ASD). Our goal was to investigate the impacts of MIA on the brain and behavior of adolescent and adult offspring, as a rat model of these neurodevelopmental disorders. We injected bacterial lipopolysaccharide (LPS, 1 mg/kg) to pregnant Wistar dams from gestational day 7, every other day, up to delivery. Behavior of the offspring was examined in a comprehensive battery of tasks at postnatal days P45 and P90. Several brain parameters were analyzed at P28. The results showed that prenatal immune activation caused social and communication impairments in the adult offspring of both sexes; males were affected already in adolescence. MIA also caused prepulse inhibition deficit in females and increased the startle reaction in males. Anxiety and hypolocomotion were apparent in LPS-affected males and females. In the 28-day-old LPS offspring, we found enlargement of the brain and decreased numbers of parvalbumin-positive interneurons in the frontal cortex in both sexes. To conclude, our data indicate that sex of the offspring plays a crucial role in the development of the MIA-induced behavioral alterations, whereas changes in the brain apparent in young animals are sex-independent.

Abstract There is strong evidence that immune activation from prenatal infection increases the risk for offspring to develop schizophrenia. The endocannabinoid (eCB) system has been implicated in the pathophysiology of schizophrenia while models of cortical dysfunction postulate an imbalance between neuronal excitation and inhibition in the disorder. The current study examined the impact of prenatal immune activation on eCB-mediated inhibitory mechanisms. We compared two forms of eCB-related plasticity of evoked inhibitory postsynaptic currents, namely depolarization-induced suppression of inhibition (DSI) and metabotropic glutamate receptor-induced long term depression (mGluR-iLTD), in both the dorsal and ventral hippocampus between adolescent offspring from rat dams that received either saline or bacterial lipopolysaccharide (LPS) during pregnancy. Compared to prenatal saline offspring, prenatal LPS offspring displayed prolonged DSI and stronger mGluR-iLTD in the dorsal and ventral hippocampus, respectively. The sensitivity of mGluR-iLTD to the CB1 receptor antagonist AM251 was also lower in the dorsal hippocampus of prenatal LPS compared to prenatal saline offspring. Testing whether changes in eCB receptor signaling or levels could contribute to these changes in inhibitory transmission, we found region specific increases in 2-arachidonoylglycerol-stimulated signaling and in basal and mGluR-induced levels of anandamide in prenatal LPS offspring when compared to prenatal saline offspring. Our findings indicate that prenatal immune activation can lead to long-term changes in eCB-related plasticity of hippocampal inhibitory synaptic transmission in adolescent rat offspring. Perturbation of the eCB system resulting from prenatal immune activation could represent a mechanism linking early life immune events to the development of psychopathology in adolescence. [ABSTRACT FROM AUTHOR]

Congenital cytomegalovirus infection is a major cause of central nervous system and sensory impairments that affect cognition, motor function, hearing, language development, vestibular function, and vision. Although the importance of congenital cytomegalovirus infection is readily evident, the vast majority of maternal and fetal infections are not identified, even in developed countries. Multiple studies of prenatal cytomegalovirus infections have produced a body of knowledge that can inform the clinical approach to suspected or proven maternal and fetal infection. Reliable diagnosis of cytomegalovirus infection during pregnancy and accurate diagnosis of fetal infection are a reality. Approaches to preventing the transmission of cytomegalovirus from mother to fetus and to the treatment of fetal infection are being studied. There is evidence that public health approaches based on hygiene can dramatically reduce the rate of primary maternal cytomegalovirus infections during pregnancy. This review will consider the epidemiology of congenital cytomegalovirus infection, the diagnosis and management of primary infection during pregnancy, and approaches to preventing maternal infection.

Milestones of brain development in mammals are completed before birth, which provide the prerequisite for cognitive and intellectual performances of the offspring. Prenatal challenges, such as maternal stress experience or infections, have been linked to impaired cognitive development, poor intellectual performances as well as neurodevelopmental and psychiatric disorders in the offspring later in life. Fetal microglial cells may be the target of such challenges and could be functionally modified by maternal markers. Maternal markers can cross the placenta and reach the fetus, a phenomenon commonly referred to as “vertical transfer.” These maternal markers include hormones, such as glucocorticoids, and also maternal immune cells and cytokines, all of which can be altered in response to prenatal challenges. Whilst it is difficult to discriminate between the maternal or fetal origin of glucocorticoids and cytokines in the offspring, immune cells of maternal origin—although low in frequency—can be clearly set apart from offspring's cells in the fetal and adult brain. To date, insights into the functional role of these cells are limited, but it is emergingly recognized that these maternal microchimeric cells may affect fetal brain development, as well as post-natal cognitive performances and behavior. Moreover, the inheritance of vertically transferred cells across generations has been proposed, yielding to the presence of a microchiome in individuals. Hence, it will be one of the scientific challenges in the field of neuroimmunology to identify the functional role of maternal microchimeric cells as well as the brain microchiome. Maternal microchimeric cells, along with hormones and cytokines, may induce epigenetic changes in the fetal brain. Recent data underpin that brain development in response to prenatal stress challenges can be altered across several generations, independent of a genetic predisposition, supporting an epigenetic inheritance. We here discuss how fetal brain development and offspring's cognitive functions later in life is modulated in the turnstile of prenatal challenges by introducing novel and recently emerging pathway, involving maternal hormones and immune markers.

Animal models of maternal immune activation study the effects of infection, an environmental risk factor for schizophrenia, on brain development. Microglia activation and cytokine upregulation may have key roles in schizophrenia neuropathology. We hypothesised that maternal immune activation induces changes in microglia and cytokines in the brains of the adult offspring. Maternal immune activation was induced by injecting polyriboinosinic:polyribocytidylic acid into pregnant rats on gestational day (GD) 10 or GD19, with brain tissue collected from the offspring at adulthood. We observed no change in Iba1, Gfap, IL1-β and TNF-α mRNA levels in the cingulate cortex (CC) in adult offspring exposed to maternal immune activation. Prenatal exposure to immune activation had a significant main effect on microglial IBA1-positive immunoreactive material (IBA1+IRM) in the corpus callosum; post-hoc analyses identified a significant increase in GD19 offspring, but not GD10. No change in was observed in the CC. In contrast, maternal immune activation had a significant main effect on GFAP+IRM in the CC at GD19 (not GD10); post-hoc analyses only identified a strong trend towards increased GFAP+IRM in the GD19 offspring, with no white matter changes. This suggests late gestation maternal immune activation causes subtle alterations to microglia and astrocytes in the adult offspring. [ABSTRACT FROM AUTHOR]

Rationale: Schizophrenia is associated with prenatal inflammation and/or postnatal stressors such as drug abuse, resulting in immune-redox dysfunction. Antioxidants may offer therapeutic benefits. Objectives: The objective of this study is to investigate N-acetyl cysteine (NAC) as a therapeutic antioxidant to reverse schizophrenia-like bio-behavioural changes in rats exposed to maternal immune activation (MIA), adolescent methamphetamine (MA) or a combination thereof. Methods: Sprague-Dawley offspring prenatally exposed to saline/lipopolysaccharide (LPS) received saline or MA (0.2-6 mg kg twice daily × 16 days) during adolescence and divided into LPS, MA and LPS + MA groups. Vehicle/NAC (150 mg kg × 14 days) was administered following MA/saline exposure on postnatal day 51-64. Social interaction, novel object recognition and prepulse inhibition (PPI) of startle, as well as regional brain monoamines, lipid peroxidation, plasma reactive oxygen species (ROS) and pro- and anti-inflammatory cytokines (TNF-α; IL-10), were assessed. Results: NAC reversed LPS, MA and LPS + MA-induced anxiety-like social withdrawal behaviours, as well as MA and LPS + MA-induced deficits in recognition memory. PPI deficits were evident in MA, LPS and LPS + MA models, with NAC reversing that following LPS + MA. NAC reversed LPS, MA and LPS + MA-induced frontal cortical dopamine (DA) and noradrenaline (NA) elevations, LPS and LPS + MA-induced frontal cortical 3,4-dihydroxyphenylacetic acid (DOPAC), serotonin (5-HT) and striatal NA deficits as well as LPS + MA-induced frontal cortical 5-HT turnover. Decreased IL-10 in the LPS, MA and LPS + MA animals, and increased TNF-α in the LPS and MA animals, was reversed with NAC. NAC also reversed elevated lipid peroxidation and ROS in the LPS and LPS + MA animals. Conclusions: Prenatal LPS, LPS + postnatal MA challenge during adolescence, and to a lesser extent MA alone, promotes schizophrenia-like bio-behavioural changes later in life that are reversed by NAC, emphasizing therapeutic potential for schizophrenia and MA-associated psychosis. The nature and timing of the dual-hit are critical. [ABSTRACT FROM AUTHOR]

Introduction: The middle ear ossicles form a semi rigid chain in the middle of the ear for conduction and amplification of sound waves from the tympanic membrane to the inner ear. Although, our knowledge of the ear ossicles dates back to the 15th century, and various studies have been carried out on their morphometry, morphology, anomalies, embryology, function and structure throughout the world, information about the morphology of middle ear ossicles is meagre in Indian subjects. Aim: To find out the morphological variations of middle ear ossicles of right and left sides. Materials and Methods: In the present study, the middle ear ossicles were bilaterally dissected out from the temporal bones obtained from 26 cadaveric heads from the Department of Anatomy under a surgical oto-microscope with micro instruments. Morphological variations were studied under the magnification of the operating microscope. Attempt was also made to evaluate the clinical implications related to such variants and compare the results with those observations made in other parts of India and abroad. Age variation was not considered as the ossicles reach their full size at birth. Results: It was observed that the stapes was the most variable and the incus as the most stable ossicle so far as morphological variations are concerned. Malleus presented variations in the free ends of manubrium, lateral process and anterior process. Variation in morphology of stapes did not follow any fixed pattern. Conclusion: It is expected that this work may also inspire many others to continue temporal bone dissection with a view to gather more ossicles which might be preserved in ossicular banks by following proper sterilization methods for future use as homografts in ossiculoplasty. These harvested ossicles may be used to replace eroded middle ear ossicles as an alternative to manufactured prosthesis.

Objective: to reveal and estimate dependence between a long waterless interval, infectious process at mother and pathology of newborn children. Material and Methods: Supervision and research have been carried out in Perinatal Center of Saratov region for the last 2 years. 167 women and 173 newborns were included in the research. The big group was composed by prematurely born children. Women were divided into 2 groups depending on infectious process of patrimonial ways and on duration of a waterless interval. Children were divided on gestation term. Results: fetoplacental insufficiency and threatened miscarriage are the main factors of extremely immature children birth. Under these conditions, prolongation of pregnancy and preparing a fetus to labor act are important factors for improving the adaptive capacity of a premature baby. One of the important factors of insolvency is membranes infection. It is a distinct disease or a result of complications of pregnancy prolongation in women with PROM, is a precursor of systemic inflammatory response and in the majority of newborns was realized in infectious process. Conclusion. Women with infectious pathology of birth canal should be thoroughly sanitized, preventive treatment should be carried out, it would prevent the implementation of fetus infection, reduce posthypoxic disorders and incidence of preterm birth and IUGR. Long PSU without infectious support contributes to a lesser extent implementation of infection in fetus and less effect on a child's neurological status.

Abstract. To improve diagnostics of prenatal infections the basic obstetrics indices in Omsk region in the period of 2000–2010 years have been analyzed. It was found that perinatal mortality reduced 2.5 times (from 14.5 till 5.7 per 1000 newborns) as well as neonatal mortality (from 6.5 till 0.9 per 1000 newborns). The laboratory testing of 187 newborns (85 pairs mother-newborn) revealed monoinfection in 24% of cases and mixed infection in 7% of cases with predomination of herpes viruses (HHV-6, CMV, EBV, HSV1,2). Newborns with manifested infections had increased number of cytotoxic T-cells, intensive expression of HLA-DR antigens on monocytes and IL-8 chemokine increased production.

Prenatal maternal infection and maternal iron deficiency during pregnancy are 2 early environmental insults associated with increased risk for schizophrenia in offspring. Substantial evidence suggests that abnormalities in inhibitory γ-ami nobutyric acid (GABA) interneuron function, especially in the parvalbumin subtype of GABA interneuron, both developmentally and in adulthood, may contribute mechanistically to cognitive deficits and psychotic symptoms in schizophrenia. This study used a rat model to test whether prenatal immune activation with lipopolysaccharide (LPS; at gestation days, GD, 15 and 16) or maternal iron deficiency (from GD2 to postnatal day P7) or the combination of both insults alters major subtypes of GABAergic interneurons (parvalbumin, somatostatin, cholecystokinin) in brain regions relevant to schizophrenia (medial and dorsolateral prefrontal cortex [PFC], hippocampal CA1 and dentate gyrus, ventral subiculum) in offspring at P14 or P28. Prenatal LPS treatment significantly increased the density of parvalbumin-immunoreactive neurons at P14 in the medial PFC, dorsolateral PFC, and ventral subiculum of offspring born from iron-sufficient but not iron-deficient dams. Prenatal LPS also increased cholecystokinin neuron density in the medial PFC at P28, under both iron-sufficient and iron-deficient conditions. We observed a large increase in parvalbumin neuron density from P14 to P28 in the medial PFC and subiculum across all birth groups, that was not observed in other brain regions, and significant decreases in somatostatin neuron density from P14 to P28 in all brain regions examined across all birth groups, indicating differential developmental trajectories for parvalbumin and somatostatin neurons in various brain regions during this early postnatal period. Thus, it appears that the medial PFC and ventral subiculum, brain regions involved in circuitry modulating ventral tegmental dopamine and nucleus accumbens activities, may be regions vulnerable to effects of prenatal LPS on specific subpopulations of interneurons. It is known that the timing of maturation and expansion of parvalbumin neurons in early development provides threshold levels of inhibition that trigger critical periods for cortical plasticity, leading to long-term circuit consolidation. Thus, our finding of increased parvalbumin neuron density at early developmental times might suggest a mechanism by which an acute prenatal insult like LPS exposure could produce long-term changes in prefrontal cortical or subicular function. [ABSTRACT FROM AUTHOR]

Group B Streptococcus (GBS) is a commensal bacterium present in the lower genital tract of 15-30% of healthy pregnant women. GBS is the leading cause of chorioamnionitis and cerebral injuries in newborns, occurring most often in the absence of maternofetal pathogen translocation. Despite GBS being the most frequent bacterium colonizing pregnant women, no preclinical studies have investigated the impact of end-gestational maternal GBS exposure on the offspring's brain development and its behavioral correlates. Our hypothesis is that GBS-induced gestational infection/inflammation has a deleterious neurodevelopmental impact on uninfected offspring. Our goal was to study the impact of maternal GBS infection on the placental and neurodevelopmental features in the offspring using a new preclinical rat model. GBS-exposed placentas exhibited chorioamnionitis characterized by the presence of Gram-positive cocci and polymorphonuclear cells, with the latter being significantly more prominent in the labyrinth of male offspring. GBS-exposed male offspring had reduced thickness of periventricular white matter. In addition, they exhibited autistic-like behaviors, such as abnormal social interaction and communication, impaired processing of sensory information and hyperactivity. Overall, these data show for the first time that gestational exposure to GBS plays an important role in the generation of neurodevelopmental abnormalities reminiscent of human autism spectrum disorders (ASD). These results provide new evidence in favor of the role of a common and modifiable infectious/inflammatory environmental factor in human ASD pathophysiology. Autism Res 2017, 10: 233-245. © 2016 International Society for Autism Research, Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Introduction: The middle ear ossicles form a semi rigid chain in the middle of the ear for conduction and amplification of sound waves from the tympanic membrane to the inner ear. Although, our knowledge of the ear ossicles dates back to the 15th century, and various studies have been carried out on their morphometry, morphology, anomalies, embryology, function and structure throughout the world, information about the morphology of middle ear ossicles is meagre in Indian subjects. Aim: To find out the morphological variations of middle ear ossicles of right and left sides. Materials and Methods: In the present study, the middle ear ossicles were bilaterally dissected out from the temporal bones obtained from 26 cadaveric heads from the Department of Anatomy under a surgical oto-microscope with micro instruments. Morphological variations were studied under the magnification of the operating microscope. Attempt was also made to evaluate the clinical implications related to such variants and compare the results with those observations made in other parts of India and abroad. Age variation was not considered as the ossicles reach their full size at birth. Results: It was observed that the stapes was the most variable and the incus as the most stable ossicle so far as morphological variations are concerned. Malleus presented variations in the free ends of manubrium, lateral process and anterior process. Variation in morphology of stapes did not follow any fixed pattern. Conclusion: It is expected that this work may also inspire many others to continue temporal bone dissection with a view to gather more ossicles which might be preserved in ossicular banks by following proper sterilization methods for future use as homografts in ossiculoplasty. These harvested ossicles may be used to replace eroded middle ear ossicles as an alternative to manufactured prosthesis. [ABSTRACT FROM AUTHOR]

The results of the research established determination of immunologic marker for prognosis of intranatal infection. The authors performed a comparative study of the immunity values of women in a risk group for prenatal infection. As it was shown when prenatal infection develops, there is an increase in the content of proinflammatory cytokines in the pregnant woman serum and activation of the ingestion rate. Account the results to devise an algorithm the pregnant woman care.

Objective To investigate the correlation between prenatal infection and premature rupture of membranes (PROM). Methods Eighty-three cases of PROM in People's Hospital of Chengmai County from July 2014 to July 2015 were selected as observation group， and 80 cases of normal pregnant women were randomly selected as control group．Prenatal genital tract infection， neonatal morbidity，maternal serum C reactive protein (CRP) and white blood cell count level， maternal amniotic fluid cell factor level were compared between two groups. Results The total incidence rate in the control group was 23.75% ，and the difference was statistically significant (P<0.05). The incidence of respiratory distress syndrome， pneumonia and high serum bilirubin in the observation group was significantly higher than those in the control group (P<0.05). The IL-6， IL-8 and TNF-α in the observation group were significantly higher than those in the control group (P<0.05). Conclusion Prenatal reproductive tract infection and PROM are closely related．Infection is a factor causing PROM， which increases the rate of neonatal morbidity. Through prenatal test of blood CRP， amniotic fluid IL-6， IL-8， and detection of TNF - levels， the risk of PROM can be predicted in advance so that measures can be taken to avoid PROM and PROM-related maternal and fetal complications can be taken. [ABSTRACT FROM AUTHOR]

Background: Chorioamnionitis is a risk factor for cerebral palsy. The relationship between extra-amniotic infections and cerebral palsy is less well studied. We examined maternal intra-amniotic and extra-amniotic infections and risk of cerebral palsy in the child.Methods: Among a retrospective cohort of 6 million Californian births, 1991-2001, we analyzed administrative maternal and newborn hospital discharge abstracts linked to records of all children receiving services for cerebral palsy at the California Department of Developmental Services. We identified maternal hospital diagnoses of intra-amniotic (chorioamnionitis) and extra-amniotic (other genitourinary and respiratory) infections occurring up to 12 months before delivery. Using multivariable logistic regression, we determined the independent association between maternal infections and cerebral palsy, adjusting for infant sex, maternal age, race, education, socioeconomic status, and obesity.Results: About 5.5% of mothers had a hospital discharge diagnosis of at least one of the following: chorioamnionitis (2.0%), other genitourinary (3.1%), and respiratory infection (0.6%). An infection diagnosis was more common in mothers of the 8473 infants with cerebral palsy than in mothers of unaffected children (13.7% vs 5.5%, P < 0.001). All three types of maternal infections (chorioamnionitis, odds ratio [OR] 3.1, 95% confidence interval [CI] 2.9-3.4; other genitourinary infection, OR 1.4, 95% CI 1.3-1.6; and respiratory infection, OR 1.9, 95% CI 1.5-2.2) were associated with cerebral palsy in multivariable analyses. Maternal extra-amniotic infections, whether diagnosed during prenatal or birth hospitalizations, conferred an increased risk of cerebral palsy.Conclusions: Maternal extra-amniotic infections diagnosed in the hospital during pregnancy are associated with a modestly increased risk of cerebral palsy in the child. [ABSTRACT FROM AUTHOR]

Maternal exposure to infection occurring mid-gestation produces a three-fold increase in the risk of schizophrenia in the offspring. The critical initiating factor appears to be the maternal immune activation (MIA) that follows infection. This process can be induced in rodents by exposure of pregnant dams to the viral mimic Poly I:C, which triggers an immune response that results in structural, functional, behavioral, and electrophysiological phenotypes in the adult offspring that model those seen in schizophrenia. We used this model to explore the role of synchronisation in brain neural networks, a process thought to be dysfunctional in schizophrenia and previously associated with positive, negative, and cognitive symptoms of schizophrenia. Exposure of pregnant dams to Poly I:C on GD15 produced an impairment in long-range neural synchrony in adult offspring between two regions implicated in schizophrenia pathology; the hippocampus and the medial prefrontal cortex (mPFC). This reduction in synchrony was ameliorated by acute doses of the antipsychotic clozapine. MIA animals have previously been shown to have impaired pre-pulse inhibition (PPI), a gold-standard measure of schizophrenia-like deficits in animal models. Our data showed that deficits in synchrony were positively correlated with the impairments in PPI. Subsequent analysis of LFP activity during the PPI response also showed that reduced coupling between the mPFC and the hippocampus following processing of the pre-pulse was associated with reduced PPI. The ability of the MIA intervention to model neurodevelopmental aspects of schizophrenia pathology provides a useful platform from which to investigate the ontogeny of aberrant synchronous processes. Further, the way in which the model expresses translatable deficits such as aberrant synchrony and reduced PPI will allow researchers to explore novel intervention strategies targeted to these changes.

Animal models and epidemiologic studies suggest that prenatal maternal infection, and sexually transmitted infection (STI) in particular, is associated with an increased risk of schizophrenia in the offspring. However, findings from prior research studies on common infections, including herpes simplex virus type 2 (HSV-2) and Chlamydia trachomatis ( C. trachomatis ) have been inconsistent. To investigate these associations, we conducted a case–control study nested in the population-based Finnish Prenatal Study of Schizophrenia. Using linked national registries, 963 cases with schizophrenia (ICD-10 F20) or schizoaffective disorder (ICD-10 F25), and 963 matched controls were identified from among all persons born between 1983 and 1998 in Finland. HSV-2 IgG antibody levels were quantified in archived maternal serum samples drawn during pregnancy. Mothers of 16.4% of cases versus 12.6% of controls were HSV-2 seropositive. Mean levels of maternal HSV-2 IgG were marginally higher among cases than controls (index values of 0.98 versus 0.86; p = 0.06). The unadjusted odds ratio (OR) of maternal HSV-2 IgG seropositivity was 1.33 (95% confidence interval (CI) = 1.03–1.72, p = 0.03). Following adjustment for covariates, the relationship was attenuated (OR = 1.22, CI = 0.93–1.60; p = 0.14). In an exploratory analysis of another STI, C. trachomatis antibodies were measured in a subsample of 207 case–control pairs drawn from the cohort. The proportions of subjects that were seropositive and the mean levels of C. trachomatis antibodies were similar for cases and controls. This study does not support a strong association of HSV-2 or C. trachomatis IgG antibodies in maternal serum during early to mid-gestation with the development of schizophrenia in the offspring. [ABSTRACT FROM AUTHOR]

Systemic maternal inflammation is implicated in preterm birth and bronchopulmonary dysplasia (BPD) and may induce morbidities including reduced pulmonary function, sleep-disordered breathing, and cardiovascular disorders. Here we test the hypothesis that antenatal maternal inflammation per se causes altered alveolar development and increased chemoreflex sensitivity that persists beyond infancy. Pregnant C57BL/6 mice were administered lipopolysaccharide (LPS) (150 µg/kg ip) to induce maternal inflammation or saline (SHAM) at embryonic day 16 (randomized). Pups were weighed daily. On days 7, 28, and 60 (D07, D28, and D60), unrestrained wholebody plethysmography quantified ventilation and chemoreflex responses to hypoxia (10%), hypercapnia (7%), and asphyxia (hypoxic hypercapnia). Lungs were harvested to quantify alveolar number, size, and septal thickness. LPS pups had reduced baseline ventilation per unit bodyweight (~40%, P < 0.001) vs. SHAM. LPS increased ventilatory responses to hypoxia (D07: 66% vs. 28% increase in ventilation; P < 0.001) hypercapnia (170% vs. 88%; P < 0.001), and asphyxia (249% vs. 154%; P < 0.001); hypersensitive hypoxic responsiveness persisted until D60 (P < 0.001). LPS also increased apnea frequency (P < 0.01). LPS caused thicker alveolar septae (D07, P < 0.001), diminished alveolar number (D28, P < 0.001) vs. SHAM, but effects were minimal by D60. Pups delivered from mothers exposed to antenatal inflammation exhibit deficits in lung structure and hypersensitive responses to respiratory stimuli that persist beyond the newborn period. Antenatal inflammation may contribute to impaired gas exchange and unstable breathing in newborn infants and adversely affect long-term health. [ABSTRACT FROM AUTHOR]