BACKGROUND: Preterm birth from intrauterine infection is a leading cause of neonatal neurologic morbidity. Likewise, maternal obesity is associated with intra-amniotic infection and inflammation. Whether maternal obesity is a risk factor for fetal brain injury that occurs with premature birth remains unknown. This study hypothesized that maternal obesity intensifies fetal neuroinflammation in the setting of premature delivery.
OBJECTIVE: This study aimed to examine the influence of maternal obesity on perinatal neuroinflammatory responses that arise with preterm birth using a murine model.
METHODS: Dams with obesity were generated via a high-fat diet that was maintained throughout pregnancy. In parallel, dams without obesity (normal) received a control diet. All dams were paired with males on normal diet. Pregnant dams were randomized to receive an intrauterine administration of bacterial endotoxin (lipopolysaccharide) or the vehicle (phosphate-buffered saline) on embryo day 15.5 of what is typically a 19- to 21-day gestation. Fetal brains were harvested 6 hours after intrauterine administrations, and the expressions of key inflammatory cytokines (Il1b, Il6, and Tnf) and panels of metabolic, immune, and inflammatory genes were analyzed.
RESULTS: With the phosphate-buffered saline, there was no difference in gene expression related to maternal obesity. There were substantial differences in Il6 and immune/inflammatory expression profiles in fetal brains from dams with obesity vs normal dams that received lipopolysaccharide. Few differences were observed among the metabolic genes examined under these conditions. The gene expression pattern associated with maternal obesity correlated with pathways related to white matter injury.
CONCLUSIONS: The expression of neuroinflammatory markers instigated by bacterial endotoxin via intrauterine lipopolysaccharide was greater in embryo brains obtained from dams with obesity. Expression profiles suggest that in combination with intrauterine inflammation, maternal obesity may increase the risk of fetal white matter injury. Further investigation is warranted to understand the relationship between maternal health and neurologic outcomes associated with prematurity.

Pyometra is a very uncommon condition in postmenopausal women that rarely improves with standard antibiotic treatments. It is usually overlooked as the patient presents with vague symptoms. Our case presented a postmenopausal woman with sepsis due to a huge pyometra. Swabs for sensitivity, tubercular gene testing, and basic blood workup were done, and the patient was started on intravenous antibiotic therapy. Pyometra drainage could not be done due to thin, friable uterine walls. When the patient had improved, a clinically total abdominal hysterectomy was done after ruling out malignant causes. Delay in the diagnosis of this condition may lead to perforation, which may, in turn, cause peritonitis, which may gravely affect the patient.

BACKGROUND: Previous studies had found that the mechanical methods were as effective as pharmacological methods in achieving vaginal delivery. However, whether balloon catheter induction is suitable for women with severe cervical immaturity and whether it will increase the related risks still need to be further explored.
OBJECTIVE: To evaluate the efficacy and safety of Foley catheter balloon for labor induction at term in primiparas with different cervical scores.
METHODS: A total of 688 primiparas who received cervical ripening with a Foley catheter balloon were recruited in this study. They were divided into 2 groups: Group 1 (Bishop score ≤ 3) and Group 2 (3 < Bishop score < 7). Detailed medical data before and after using of balloon were faithfully recorded.
RESULTS: The cervical Bishop scores of the two groups after catheter placement were all significantly higher than those before (Group 1: 5.49 ± 1.31 VS 2.83 ± 0.39, P<0.05; Group 2: 6.09 ± 1.00 VS 4.45 ± 0.59, P<0.05). The success rate of labor induction in group 2 was higher than that in group 1 (P<0.05). The incidence of intrauterine infection in Group 1 was higher than that in Group 2 (18.3% VS 11.3%, P<0.05).
CONCLUSIONS: The success rates of induction of labor by Foley catheter balloon were different in primiparas with different cervical conditions, the failure rate of induction of labor and the incidence of intrauterine infection were higher in primiparas with severe cervical immaturity.

OBJECTIVE: Cardiopulmonary and infectious complications are more common in preterm newborns after preterm premature rupture of membranes (pPROM). Fetal echocardiography may be helpful in predicting neonatal condition. Our aim was to assess the cardiovascular changes in fetuses from pregnancies complicated by pPROM and possible utility in predicting the intrauterine or neonatal infection, and neonatal heart failure (HF).
METHODS: It was a prospective study enrolling 46 women with singleton pregnancies complicated by pPROM between 18+0 and 33+6 weeks of gestation and followed until delivery. 46 women with uncomplicated pregnancies served as a control group. Fetal echocardiographic examinations with the assessment of cardiac structure and function (including pulmonary circulation) were performed in all patients.
RESULTS: Mean gestational age of pPROM patients was 26 weeks. Parameters suggesting impaired cardiac function in fetuses from pPROM were: higher right ventricle Tei index (0.48 vs. 0.42 p<0.001), lower blood flow velocity in Ao z-score (0.14 vs. 0.84 p=0.005), lower cardiovascular profile score (CVPS), higher rate of tricuspid regurgitation (18.2 % vs. 4.4 % p=0.04) and pericardial effusion (32.6 vs. 0 %). Intrauterine infection was diagnosed in 18 patients (39 %). 4 (8.7 %) newborns met the criteria of early onset sepsis (EOS). HF was diagnosed in 9 newborns. In fetal echocardiographic examination HF group had shorter mitral valve inflow time and higher left ventricle Tei index (0.58 vs. 0.49 p=0.007).
CONCLUSIONS: Worse cardiac function was observed in fetuses from pPROM compared to fetuses from uncomplicated pregnancies.

An intrauterine infection during the first trimester of pregnancy can rapidly lead to bacteremia, with severe consequences for the patient. While these infections are mainly found after a miscarriage or an abortion, the diagnosis is sometimes made while the pregnancy is still in progress. The clinical history and symptoms reported by the patient lead to the suspicion of such a complication. Treatment must be rapid and based on a broad-spectrum antibiotic regimen covering Gram-negative, Gram-positive, aerobic and anaerobic bacteria. As soon as the treatment has been initiated, uterine curettage should be performed to remove the infected material, whether or not foetal cardiac activity is present at the time of diagnosis.
Une infection intra-utérine durant le premier trimestre de la grossesse peut rapidement mener à une bactériémie et avoir des conséquences sévères pour la patiente. Alors que ces infections sont principalement retrouvées après une fausse couche ou une interruption volontaire de grossesse, le diagnostic est parfois posé alors que la grossesse est évolutive. L’histoire clinique et les symptômes rapportés par la patiente permettent de suspecter une telle complication. La prise en charge doit être rapide et repose sur un traitement antibiotique à large spectre couvrant les bactéries Gram négatif, Gram positif, les aérobies et les anaérobies. Dès le traitement instauré, un curetage utérin devra être réalisé afin d’éliminer le matériel infecté, que l’activité cardiaque fœtale soit présente ou non au moment du diagnostic.

Parvovirus B19, a member of the Parvoviridae family, is a human pathogenic virus. It can be transmitted by respiratory secretions, hand-to-mouth contact, blood transfusion, or transplacental transmission. Most patients are asymptomatic or present with mild symptoms such as erythema infectiosum, especially in children. In rare cases, moderate-to-severe symptoms may occur, affecting blood cells and other systems, resulting in anemia, thrombocytopenia, and neutropenia. Non-immune pregnant women are at risk for fetal infection by parvovirus B19, with greater complications if transmission occurs in the first or second trimester. Infected fetuses may not show any abnormalities in most cases, but in more severe cases, there may be severe fetal anemia, hydrops, and even pregnancy loss. Maternal diagnosis of intrauterine parvovirus B19 infection includes IgG and IgM antibody testing. For fetal diagnosis, PCR is performed through amniocentesis. In addition to diagnosing the infection, it is important to monitor the peak of systolic velocity of the middle cerebral artery (PVS-MCA) Doppler to assess the presence of fetal anemia. There is no vaccine for parvovirus B19, and fetal management focuses on detecting moderate/severe anemia by fetal PVS-MCA Doppler, which, if diagnosed, should be treated with intrauterine transfusion by cordocentesis. Prevention focuses on reducing exposure in high-risk populations, particularly pregnant women.

Intrauterine infection is a significant cause of neonatal morbidity and mortality. Ureaplasma parvum is a microorganism commonly isolated from cases of preterm birth and preterm premature rupture of membranes (pPROM). However, the mechanisms of early stage ascending reproductive tract infection remain poorly understood. To examine inflammation in fetal (chorioamnionic) membranes we utilized a non-human primate (NHP) model of choriodecidual U. parvum infection. Eight chronically catheterized pregnant rhesus macaques underwent maternal-fetal catheterization surgery at ~105-112 days gestation and choriodecidual inoculation with U. parvum (105 CFU/mL, n =4) or sterile media (controls; n = 4) starting at 115-119 days, repeated at 5-day intervals until C-section at 136-140 days (term=167 days). The average inoculation to delivery interval was 21 days, and Ureaplasma infection of the amniotic fluid (AF) was undetectable in all animals. Choriodecidual Ureaplasma infection resulted in increased fetal membrane expression of MMP-9 and PTGS2, but did not result in preterm labor or increased concentrations of AF pro-inflammatory cytokines. However, membrane expression of inflammasome sensors, NLRP3, NLRC4, AIM2, and NOD2, and adaptor ASC (PYCARD) gene expression were significantly increased. Gene expression of IL-1β, IL-18, IL-18R1  , CASPASE-1, and pro-CASPASE-1 protein increased with Ureaplasma infection. Downstream inflammatory genes MYD88 and NFκB (Nuclear factor kappa-light-chain-enhancer of activated B cells) were also significantly upregulated. These results demonstrate that choriodecidual Ureaplasma infection, can cause activation of inflammasome complexes and pathways associated with pPROM and preterm labor prior to microbes being detectable in the AF.

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Bronchopulmonary dysplasia (BPD) is associated with poor survival in preterm infants. Intrauterine infection can aggravate the degree of obstruction of alveolar development in premature infants; however, the pathogenic mechanism remains unclear. In this study, we sought to determine whether pyroptosis could be inhibited by downregulating mammalian target of rapamycin (mTOR) activation and inducing autophagy in BPD-affected lung tissue.
We established a neonatal rat model of BPD induced by intrauterine infection via intraperitoneally injecting pregnant rats with lipopolysaccharide (LPS). Subsequently, mTOR levels and pyroptosis were evaluated using immunohistochemistry, immunofluorescence, TUNEL staining, and western blotting. The Shapiro-Wilk test was employed to assess the normality of the experimental data. Unpaired t-tests were used to compare the means between two groups, and comparisons between multiple groups were performed using analysis of variance.
Pyroptosis of lung epithelial cells increased in BPD lung tissues. After administering an mTOR phosphorylation inhibitor (rapamycin) to neonatal rats with BPD, the level of autophagy increased, while the expression of autophagy cargo adaptors, LC3 and p62, did not differ. Following rapamycin treatment, NLRP3, Pro-caspase-1, caspase-1, pro-IL-1β, IL-1β, IL-18/Pro-IL-18, N-GSDMD/GSDMD, Pro-caspase-11, and caspase-11 were negatively regulated in BPD lung tissues. The opposite results were observed after treatment with the autophagy inhibitor MHY1485, showing an increase in pyroptosis and a significant decrease in the number of alveoli in BPD.
Rapamycin reduces pyroptosis in neonatal rats with LPS-induced BPD by inhibiting mTOR phosphorylation and inducing autophagy; hence, it may represent a potential therapeutic for treating BPD.

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