L isteria monocytogenes is an environmentally ubiquitous bacterium that causes foodborne illness. While infection in healthy individuals is generally not associated with signiﬁcant disease, it poses a substantial risk for speciﬁc populations, including immunocompromised, elderly, or pregnant individuals. Listeriosis during pregnancy is generally associated with a spectrum of adverse outcomes during the third trimester, including miscarriage, preterm labor, stillbirth, and neonatal infection (1). Inﬂammation of fetal membranes and placental villitis are noted in these cases (2), but the actual course of events at the maternal-fetal interface that cause fetal demise are poorly understood. In the clinic, human placental tissues generally are not available until after an adverse outcome, at which point fetal infection has progressed for an indeterminate period of time. In vitro studies with tissue explants from human ﬁrst (3) or third (4) trimester placentas concluded that either extravillous trophoblasts (3) or syncytiotro- phoblasts (4) are likely the primary route of placental infection. However, in vitro studies are limited in reproducing the physiological and immunological complexity at the maternal-fetal interface, and it is unclear how infection proceeds in vivo. Growing recognition of the impact of microbial infections on fetal well-being (e.g., Zika virus or TORCH [toxoplasmosis, other, rubella, cytomegalovirus, and herpes] infections) (5, 6) underscores the importance of gaining a better mechanistic understanding of such events. The aim of this study was to establish a nonhuman primate model to map the outcome of infection with L. monocytogenes during early pregnancy. Like humans, macaques and other nonhuman primates have villous hemochorial placentas and invasive extravillous fetal trophoblasts that actively remodel maternal spiral arteries in the decidua. Their similar endocrine, reproductive, and immune systems make nonhu- man primates a highly relevant model for examining the interplay of maternal and fetal responses to infection during pregnancy. Remarkably, ﬁrst trimester inoculation of cynomolgus macaques consistently resulted in maternal and fetal infection followed by fetal death within 7 to 13 days postinoculation. This contrasts with the general assumption that listeriosis is of greatest concern during the third trimester of preg- nancy. Microbial analysis of collected tissues revealed that the decidua basalis and placental bed as well as the placenta had signiﬁcant bacterial burden. These ﬁndings suggest that maternal infection affects both the placenta—the presumptive target of listeriosis during human pregnancy—and the maternal reproductive tract.
10 Read more
The true impact of recurrent maternal infection on both the incidence of congenital CMV infection and the long-term neurologic deficits in children with this intrauterine infection is not known, and prospec- tive population-based studies are needed to define this issue. A major limitation of the present study is our inability to categorize the type of maternal infec- tion in more than half of the children with symptom- atic congenital CMV infection born during the study period. It is possible, and perhaps likely, that the vast majority of symptomatic infections occur after a pri- mary CMV infection during pregnancy. It is also possible that categorization of most maternal infec- tions will lead to identification of an increased pro- portion of children who were born to mothers with preexisting immunity among infants with symptom- atic congenital CMV infection. The definition of the importance of recurrent maternal infection in neona- tal morbidity and long-term outcome is crucial be- cause of the considerable interest in the development of a safe and effective vaccine for the prevention of sequelae associated with congenital CMV infection. Knowledge of the mechanisms of transplacental transmission of CMV in women with preexisting immunity could provide important information about the protective role of virus-specific immune responses. Furthermore, studies in this population could shed more light on the issue of reinfection and strain-specific immune responses against CMV.
importantly, the breadth of protective immunity in HCMV-immune women that may reduce the risk of reinfection with new strains of virus, are unknown. Thus, direct comparison of rates of HCMV intrauterine transmission between women with nonpri- mary infections and HCMV-nonimmune women will likely be noninformative. To more fully illustrate the potential fallacies in estimates of the importance of adaptive immu- nity in limiting intrauterine transmission of HCMV in pregnant women undergoing nonprimary infections, I compared the rates of intrauterine transmission of HCMV in 1,000 women undergoing primary and nonprimary HCMV infection that would yield the expected number of congenitally infected infants born to these populations based on the prevalence of congenital HCMV in different populations (Fig. 1) (2). As can be seen, 1,000 nonimmune women are uniformly susceptible to infection, and approx- imately 3% will acquire HCMV during pregnancy, resulting in 30 maternal infections. Assuming the consistently reported 30% transmission rate, 9 infants (9/1,000) will be FIG 1 Estimated rates of HCMV intrauterine transmission as a function of maternal infection (serocon- version) in nonimmune women (primary infections) and reinfection (seroconversions) in immune women (nonprimary infections). Several possible seroconversion rates in immune women are shown, with transmission rates calculated based on the prevalence of congenitally infected infants from seroimmune maternal populations.
In the present study out of a data set of consecutive children infected with CMV, only infants born after a maternal infection having unquestionably occurred dur- ing pregnancy were retained for analysis, and cases for which the timing of the infection was doubtful were excluded. This approach has the disadvantage that a number of infections occurring very early in pregnancy (ie, before the initial blood sample was taken) were not included. This is reflected by the distribution of the infections in our study population, where a lower num- ber of primary infections occurring in the first trimester of pregnancy were noted.
ultrasound (of which 25 underwent an MRI as well), and 3 children underwent an MRI without a brain ultrasound. In Table 4, the results of brain imaging are shown. Chances of developing SNHL in the case of a normal imaging result (ultrasound and/or MRI) are 6.6%. In the case of an abnormal result (21 children), the risk of SNHL is 42.9% ( P , .001). The sensitivity in detecting SNHL was 52.9% in the case of an abnormal imaging result, and the speci ﬁ city was 90%. The risk of developing late- onset hearing loss after an abnormal imaging test was higher than in the case of a normal test result (14.3% vs 2.3%). Also, progression of SNHL occurred more often in the case of abnormal ultrasound and/or MRI results (28.6% vs 1.7%). Because of small numbers, a signiﬁcance was not obtained. Ultrasound examination was found to be a good predictor of the risk of having SNHL. Brain imaging results were abnormal in 60%, 0%, and 5.3% of the children with a maternal infection in the ﬁrst, second, and third trimester of pregnancy, respectively.
Factor known to alter early fetal brain development and in- crease the risk for ASD is maternal infection during pregnancy ,[,,,,,, Specifically cases of autism following congenital cytomegalovirus, perinatal herpes sim- plex virus, and congenital rubella infections have been report- ed ,,,. Gestational exposure to measles, rubella, and mumps and postnatal exposure to mumps and varicella were associated with higher autism risk in a large epidemio- logic study . Fever is the main presenting symptoms for these infections, and such fever during pregnancy is suppos- edly linked to ASD, most recent studies stated that maternal fever during pregnancy has been linked to increased risk of ASD .
We report a case of vertically transmitted molluscum contagiosum viral infection in which the maternal infection was clinically docu- mented before vaginal delivery. The aim of this report is to make prac- titioners aware that molluscum infections in neonates are likely verti- cally transmitted. Pediatrics 2010;125:e423–e425
early neonatal death. These cases were described during the same summer of 1979 in Milwaukee . Soudée and al.  studied the clinical, biological and demo- graphic characteristics of newborns hospitalized for en- terovirus infection in France in 2012. Data was retrieved from the database of the National Reference Center for Enterovirus Infections in Lyon. Among a total of 120 cases, 34 cases (28%) were diagnosed within the first 8 days of life. The clinical signs were respiratory and liver disease, includ- ing 11 severe cases (32%) defined by hepatitis (23%), myo- carditis (12%), and encephalitis (15%) or multi-organ failure (32%) leading to death in 3 cases. Yen and al. reported the case of a premature born at 35 weeks deceased at 2 months of age from liver failure. The newborn presented shortly after birth with jaundice and altered consciousness. Five days before delivery by caesarean section, a foot-hand- mouth syndrome was reported in the mother. Echovirus-6 and 71 were found in newborn cultures (rectum, blood) . Kao and al. reported a case of fatal neonatal Coxsack- ievirus B5 infection, confirmed by RT-PCR in the newborn and its mother . The mother had fever for a week, 9 days before delivery, and a decrease in active fetal move- ments had been observed. The newborn developed fever immediately after birth and died on day one of life. This case is also suggestive of transplacental enterovirus trans- mission. Verboon-Maciolek and al reported six cases of se- vere enterovirus meningoencephalitis with severe white matter damage and clinical sequelae .
The study from , reported that mothers with pneumonia were more likely to deliver prematurely, and have infants of lower birth weight. It is quite possible that the cascade of mediators released by the active host inflammatory response to infection exerts distant effects on the uterus, leading to a high rate of preterm labor during the course of pneumonia. Literatures had equally reported low birth weight among infants as risk factor for ARI in young children; this implies that exposure to pre-existing maternal pneumonia may increase the potential for ARI in infancy from an epidemiological point of view, whose principle and theoretical concepts form the basis for this research work. Our focus in this study was infant exposure to maternal/caregiver respiratory secretions and or droplets by way of nursing care or proximity.
12 Read more
Alcohol consumption was quoted as light (less than 1 litre but more than 30 cl/day) or heavy (more than 1 l/day) [3-5] and no counseling was initiated for drinkers. Maternal characteristics included age, parity, gestity, body mass index (BMI calculated as [weight (kg)/height (m)2]), and fat mass according to impedancimetry (with an OMRON BF 300 impedance meter). Risk factors for GDM were also registered: obesity (BMI > 25), family- history of diabetes (grandparents, parents, brothers, sis- ters), or of arterial hypertension (HTA), previous history of polyhydramnios, infant’s birth weight ≥ 3800 g (>
Pregnant women are vulnerable to viral respiratory in- fections [3, 4] and are considered to be at high risk for influenza  and its complications [6–8]. Preventing in- fluenza in mothers leads to increase in birth weights  and reduced infections in newborns [10, 11]. While the impact of influenza during pregnancy on newborns is now better understood [7, 8, 12, 13], the importance of other respiratory infections has not been studied. In order to improve maternal and neonatal outcomes and to develop appropriate preventive and treatment strat- egies, the association between common maternal illness and newborn’ s health needs to be studied. Therefore, we conducted this study to identify the association between maternal respiratory illnesses and infant birth weight in an urban slum of Pakistan.
under-reporting of maternal mortality. Maternal deaths have generally been classified as directly or indirectly as- sociated with pregnancy (e.g. medical causes not brought on or exacerbated by the pregnancy or trauma) . Ob- stetric conditions directly associated with maternal death include hypertensive diseases of pregnancy (preeclampsia/ eclampsia), obstetric hemorrhage (ante- or postpartum, with or without severe anemia), sepsis/infection and thromboembolism. Obstructed labor may be associated with maternal death, leading to either hemorrhage or se- vere infection but the primary cause of death in the current World Health Organization (WHO) international classifi- cation system (ICD-10) would be infection or hemorrhage, not obstructed labor. Deaths associated with ruptured uterus are presumed to be secondary to hemorrhage. Con- versely, abortion related deaths result from infection or hemorrhage, but deaths occurring at less than 20 weeks gestational age, including from ectopic pregnancy, are clas- sified as abortion related. Indirect causes of maternal death include trauma or medical conditions such as cardiac dis- ease, cancer, or diabetes.
11 Read more
In this 11 years retrospective study, 102 pregnant women were found seropositive with prevalence of 0.3%. Mean age in this study was 25.2 years which is comparable to study done by Prameela et al 16 in which mean age was 23 years, while mean age was 30 years in study done by Ezechi et al 2 . 67.6% women belonged to rural area similar to study done by Prameela et al (68.6%) 16 . In this study 55.9% husbands were HIV positive while in study done by Malik et al 17 and Prameela et al 16 , 44% and 44.3% spouses were found positive. Heterosexual contact was found main route of transmission of infection (92.2%). In discordant couple sexual promiscuity (73.3%) among women was main cause. In contrast study done by Malik et al 17 , heterosexual contact contributed 52% risk factor for transmission.
cidence of neonatal sepsis in our study population, including among the high- est reported incidence rates of GBS sepsis from any developing country, maternal HIV infection does not appear to increase the risk of either early- or late-onset neonatal sepsis, except among new- borns with HIV infection and possibly among newborns of severely immuno- compromized mothers. Consequently, we do not predict the HIV prevention roll-out in sub-Saharan Africa will result in im- portant reductions in neonatal sepsis in this region, and sepsis-speci ﬁ c inter- ventions such as GBS vaccines may hold most promise in reducing neonatal infection-associated mortality.
12 Read more
C linical and epidemiological studies have demonstrated an as- sociation of malnutrition, dietary deficiency, and infection (1, 2). Infections are more frequent and can be more chronic in pri- mary malnourished individuals (2, 3), with evidence suggesting that infection further weakens the host by reducing nutrient up- take and impeding the ability to mount an effective immune response (4–6). However, relatively little is known about the phys- iological and immunological signatures linking general malnutri- tion or specific dietary deficiencies to infection susceptibility.
10 Read more
DOI: 10.4236/ojog.2019.99119 1222 Open Journal of Obstetrics and Gynecology duced by a variety of stimuli or conditions, including immunosuppressant ad- ministration, HIV infection and septic shock . Therefore, maternal HIV in- fection is already described as a risk factor for cCMV  because of a higher risk of CMV reactivation. To the better of our knowledge, no case has been reported in the literature concerning cCMV infection following a maternal varicella dur- ing pregnancy.
According to the 2002 guidelines of the Centers for Disease Control and Prevention (CDC), United States of America, all pregnant women should be screened for GBS at 35-37 weeks of pregnancy. The health care provider is to take a swab from the vagina and rectum and send the sample to a laboratory for a culture to test for the presence of GBS. The results are usually available in 24- 48 hours. If a pregnant woman is found to carry GBS, she should be treated with intravenous antibiotics during labour and delivery. A recent CDC study showed that this approach may prevent nearly 90% of Early-onset GBS infections. Taking oral antibiotics prior to labour is not recommended as it is not effective in preventing GBS infection in the newborn.
107 Read more
efficacy of maternal vaccination. In contrast, neutralization titers could be detected 7 weeks after birth in pups of which mothers received two immuniza- tions and these pups were subsequently protected from lethal influenza challenge. In addition to neutralizing antibodies not detected by the HAI assay due to a lack in sensitivity, non-neutralizing antibodies could poten- tially also play a role in mediating protection via anti- body effector mechanisms such as ADCC . Our results show that vaccination of dams confers protection to offspring against lethal influenza challenge when ma- ternal antibodies were detectable by the sensitive H1 IgG HA ELISA assay. In addition, no HA-specific IgA binding antibodies were detected in serum of the off- spring 1 day after birth, nor in the serum of their dams after three immunizations with a seasonal vaccine (data not shown). We hypothesize that because the dams were immunized intramuscularly the immune response will be mainly dominated by IgG antibodies. In contrast, influenza vaccines given orally will induce higher levels of mucosal immunity and IgA. In view of the absence of detectable IgA in our system, anti-influenza IgA is unlikely to explain the observed effects.
12 Read more
After stratified by antiretroviral drugs use before or during pregnancy, we found that HAART or other regi- mens of antiretroviral therapy (ART) had no obvious effect on the associations between maternal HIV infec- tion and LBW/PTD. It is suggested that intrauterine ARVs exposure did not decrease or increase the risk of LBW or PTD in HIV infected women. And this is con- sistent with the findings reported by van der Merwe et al. and Townsend et al. [3, 4]. However, Papp et al.  suggested that Protease Inhibitor (PI)-based ART could increase the risk of adverse pregnancy outcomes mainly due to lower level of progesterone, which was signifi- cantly associated with fetal weight. Sibude et al.  also found that ARVs and, particularly, with the initiation of ritonavir-boosted PI therapy during pregnancy were correlated with PTD in HIV infected women. Though we did not found such effect of ARVs on the association between maternal HIV infection and LBW/PTD, no details of information for AVRs and therapy regimens may contribute to this. We found that studies during 2005–2015 were at slightly higher risk for both LBW
11 Read more
ABSTRACT Mother-to-child transmission (MTCT) of HIV provides a setting for studying immune correlates of protection. Neutralizing antibodies (NAbs) are suggested to contribute to a viral bottleneck during MTCT, but their role in blocking trans- mission is unclear, as studies comparing the NAb sensitivities of maternal viruses have yielded disparate results. We sought to determine whether transmitting mothers differ from nontransmitting mothers in the ability to neutralize individual autologous virus variants present at transmission. Ten transmitting and 10 nontransmitting HIV-infected mothers at high risk of MTCT were included in this study. Full-length HIV envelope genes (n ⴝ 100) were cloned from peripheral blood mononuclear cells obtained near transmission from transmitting mothers and at similar time points from nontransmitting mothers. Envelope clones were tested as pseudoviruses against contemporaneous, autologous maternal plasma in neutralization assays. The associ- ation between transmission and the log 2 50% inhibitory concentration (IC 50 ) for multiple virus variants per mother was esti-