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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]

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]

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

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]

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]

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.

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.

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.

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.

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.

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]

Background: Fetal 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., Methods: We 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., Result: High 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)., Conclusion: The 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., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Li, Ju, Xu, Jiang, Lu and Ju.)

Autism Spectrum Disorder (ASD) is the collective term for neurodevelopmental disorders characterised by qualitative impairments in social interaction and communication, and a restricted range of activities and interests. Many countries, including Australia, have reported a dramatic increase in the number of diagnoses over the past three decades, and recent reports suggest a prevalence of ASD of 1 in every 110 individuals (~1%). The potential role for an immune-mediated mechanism in ASD has been implicated by several studies, and some evidence suggests a potential link between prenatal infection-driven inflammation and subsequent development of ASD. Furthermore, contemporary studies have reported a markedly increased prevalence of ASD in children born preterm, who are at highest risk of exposure to perinatal inflammation. However, the mechanisms that underpin the susceptibility to infection-driven inflammation during pregnancy and risk of preterm birth, and how these intersect with the subsequent development of ASD in the offspring, is not understood. This review aims to summarise and evaluate the potential mechanisms and evidence for the role of prenatal infection on the central nervous system, and how it may increase the susceptibility for ASD pathogenesis in children born preterm.

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 synchronization 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. [ABSTRACT FROM AUTHOR]

Autism Spectrum Disorder (ASD) is the collective term for neurodevelopmental disorders characterized by qualitative impairments in social interaction, communication, and a restricted range of activities and interests. Many countries, including Australia, have reported a dramatic increase in the number of diagnoses over the past three decades, with current prevalence of ASD at 1 in every 110 individuals (~1%). The potential role for an immune-mediated mechanism in ASD has been implicated by several studies, and some evidence suggests a potential link between prenatal infection-driven inflammation and subsequent development of ASD. Furthermore, a modest number of contemporary studies have reported a markedly increased prevalence of ASD in children born preterm, who are at highest risk of exposure to perinatal inflammation. However, the mechanisms that underpin the susceptibility to infection-driven inflammation during pregnancy and risk of preterm birth, and how these intersect with the subsequent development of ASD in the offspring, is not understood. This review aims to summarize and discuss the potential mechanisms and evidence for the role of prenatal infection on the central nervous system, and how it may increase the susceptibility for ASD pathogenesis in children born preterm. [ABSTRACT FROM AUTHOR]

Fetal exposure to inflammatory mediators is associated with a greater risk of brain injury and may cause endothelial dysfunction; however, nearly all the evidence is derived from gram-negative bacteria. Intrapleural injections of OK-432, a killed Su-strain of Streptococcus pyogenes, has been used to treat fetal chylothorax. In this study, we evaluated the neural and cardiovascular effects of OK-432 in preterm fetal sheep (104 ± 1 days, term 147 days). OK-432 (0.1 mg, n 6) or saline vehicle (n = 7) was infused in the fetal pleura, and fetuses were monitored for 7 days. Blood samples were taken routinely for plasma nitrite measurement. Fetal brains were taken for histological assessment at the end of the experiment. Between 3 and 7 h postinjection, OK-432 administration was associated with transient suppression of fetal body and breathing movements and electtroencephalogram activity (P < 0.05), increased carotid and femoral vascular resistance (P < 0.05), but no change in blood pressure. Brain activity and behavior then returned to normal except in one fetus that developed seizures. OK-432 fetuses showed progressive, sustained vasodilatation (P < 0.05), with lower blood pressure after 4 days (P < 0.05), but normal heart rate. There were no changes in plasma nitrite levels. Histological studies showed bilateral infarction in the dorsal limb of the hippocampus of the fetus that developed seizures, but no injury in other fetuses. We conclude that a single low-dose injection of OK-432 can be associated with risk of focal cerebral injury in the preterm fetus and chronic central and peripheral vasodilatation that does not appear to be mediated by nitric oxide. [ABSTRACT FROM AUTHOR]

Maternal influenza during pregnancy is a controversial risk factor for schizophrenia in the child. We conducted a meta-analysis to examine whether birth during the 9-month period after the pandemic of 1957 was a risk factor for schizophrenia. Studies that compared the risk of schizophrenia among subjects born after the pandemic with that among those born in corresponding time periods in surrounding years were divided into those conducted in the United States, Europe, or Australia (type A studies, n = 8) and those from Japan, where the epidemic came in 2 waves (type B studies, n = 3). Other studies examined the risk among subjects born to mothers who were pregnant during the pandemic and reported having had influenza (type C studies, n = 2). Relative risks (RRs) were extracted or calculated for each month and/or trimester of possible exposure by 2 independent authors. All analyses were performed using a fixed-effects model. The weighted results of the type A studies did not indicate a significantly increased risk of schizophrenia among children exposed during any trimester or month of prenatal life. Not a single study found a significant first- or second-trimester effect. The mean weighted RR for subjects who were in their first, second, or third trimester of prenatal life during the pandemic (8 effect sizes) was 0.91 (95% confidence interval [CI]: 0.85–0.98), 1.00 (95% CI: 0.93–1.07), and 1.05 (95% CI: 0.98–1.12), respectively. The pooled results of the type B and type C studies were also negative. Given high infection rates during the pandemic (about 50%), these results do not support the maternal influenza hypothesis. [ABSTRACT FROM PUBLISHER]

Archived neonatal blood cards (Guthrie cards) from children who later contracted leukaemia and matched normal controls were assayed for adenovirus (AdV) C DNA content using two highly sensitive methods. In contrast to a previous report, AdV DNA was not detected at a higher frequency among neonates who later developed leukaemia, when compared with controls. [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. <75%) using logistic regression, adjusting for confounders. One-third of mothers were underweight (BMI < 18.5 kg/m2) 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. [ABSTRACT FROM AUTHOR]

Background: Temporal lobe T2 hyperintensity has been described in association with prenatal cytomegalovirus (CMV) infection on fetal MRI. However, these findings are often perplexing with high inter-observer variability. Our objective was to evaluate temporal lobe T2 signal quantitatively in prenatal CMV infection., Methods: In this retrospective study, 119 fetuses, of which 51 fetuses with suspected CMV exposure (29-36 weeks of gestation) based on maternal seroconversion and age-matched 68 normal controls, were included. Mean and maximal temporal lobe T2 signal were evaluated quantitatively by measuring the T2 signal in the temporal lobes relative to the amniotic fluid's signal. Intra-observer, inter-observer variability and diagnostic performance were assessed. The occurrence of neonatal sensorineural hearing loss (SNHL) was recorded., Results: Relative temporal lobe T2 signal did not change along with the examined gestational age. Of our suspected CMV cohort, 29 fetuses were positive for fetal CMV infection on polymerase chain reaction (PCR) analysis. There were no statistically significant differences in the relative mean or maximal temporal lobes T2 signal between CMV positive, CMV negative fetuses, or normal controls. No correlation was found between neonatal SNHL and temporal lobe T2 signal., Conclusions: When temporal lobe T2 signal is analyzed quantitatively, CMV infected fetuses do not present an increased signal than age-matched controls. Thus, reported subjective temporal T2 hyperintensities should be interpreted carefully and should have a limited effect on pregnancy management, especially as an isolated finding. Our study illustrates the importance of quantitative imaging in diagnostic neuroradiology., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/qims-21-22). The authors have no conflicts of interest to declare., (2021 Quantitative Imaging in Medicine and Surgery. All rights reserved.)

Maternal severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in the second and third trimesters of pregnancy may impact fetal development via vertical transmission, complications of coronavirus disease 2019 (COVID-19), or placental injury. However, potential associations between prenatal SARS-CoV-2 infection and fetal loss are not well understood. This case series of thirteen second and third trimester fetal losses reported by local public health departments to California's state public health surveillance included maternal clinical and demographic characteristics as well as placental pathology, fetal autopsy reports, and coroner report. There was no evidence that maternal COVID-19 disease severity, placental injury, or SARS-CoV-2 vertical transmission contributed to pregnancy loss. However, this case series is a limited sample; more research is needed to identify factors of prenatal SARS-CoV-2 that may contribute to fetal death in the second and third trimesters., Competing Interests: None., (Copyright © 2022 The Chinese Medical Association, published by Wolters Kluwer Health, Inc.)

Background: Infection with the parasite Toxoplasma gondii is a common infection in animals and humans worldwide. This infection can occur after ingestion of water or food contaminated with cat oocytes, ingestion of tissue cysts in mammalian and avian meat and congenitally. The prenatal infection can lead to Congenital Toxoplasmosis with miscarriage or stillbirth. After infection, laboratory tests are positive within 2-3 weeks and remain positive throughout life. However, testing for Toxoplasma infection during pregnancy is necessary in some countries, while in others it is not a mandatory "screening" test., Objective: The aim of this study was to review systematically the screening of toxoplasmosis in pregnancy in different countries worldwide., Methods: Cohorts, retrospective and cross-sectional studies were incorporated in our review, finally including 11 articles from an initial pool of 1532 related papers., Results: The seroprevalence of pregnant women varies from countries with low prevalence to regions with high prevalence and screening policies also differ. Most countries worldwide have control policies, while Germany and Mexico that do not have systematic screening for Toxoplasma during the prenatal period., Conclusion: Our results show that Congenital Toxoplasmosis is very rare in some countries and it is very difficult to find a balance between potential risk and benefit of a screening program. For this reason, some countries are limited to prenatal counseling to reduce CT. In addition, the reduction of major sources of contamination especially in developing countries is the most important prevention measure., Competing Interests: There are no conflicts of interest., (© 2021 Chrysa Voyiatzaki, Christos Orovas, Maria Trapali, Dimitrios I. Chaniotis, Anastasios G. Kriebardis, Apostolos Beloukas1, Nikolaos D. Thalassinos, Eirini Orovou, Georgios Iatrakis, Evangelia Antoniou.)