Pyometra is a gynecological condition characterized by pus accumulation in the endometrial cavity. It is a rare condition, and it should be included in the differential diagnosis of abdominal pain in postmenopausal women. We present a case of a 65-year-old postmenopausal woman with complaints of foul-smelling white discharge, itching in the perineal region, lower abdominal pain, and postmenopausal bleeding for two to three months. USG of the pelvis was done outside, which revealed heterogeneous ill-defined cervical growth with endometrial fluid collection and multiple uterine fibroids. CT and MRI of the pelvis were done in our hospital, which revealed an ill-defined heterogeneously enhancing growth in the cervix with multiple uterine fibroids and heterogeneous endometrial collection showing restricted diffusion in MRI suggestive of pyometra. Cervical biopsy revealed features suggestive of moderately differentiated squamous cell carcinoma.

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.

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.

Chorioamnionitis (CA) at term of pregnancy can have an infectious and/or inflammatory origin and is associated with adverse outcomes. Triple I (intrauterine inflammation, infection, or both, TI) has been proposed to reduce the overdiagnosis of infection and neonatal overtreatment. The aim of this study is to identify clinical and histological variables that could predict adverse outcomes when TI is suspected and/or confirmed. This retrospective cohort study included 404 pregnancies (gestational age ≥ 37 weeks) that were divided into 5 all-inclusive and mutually exclusive groups. TI was defined according to the NICHD definition of 2015, and it could be confirmed (TI+) or not confirmed (TI-) via histological examination. Signs of infection/inflammation that did not conform to the definition of TI were classified as \"clinical suspicion\" and could be supported (CS+) or not supported (CS-) by histology. Cases of histological chorioamnionitis (HCA) without clinical manifestation represented a fifth group. Whole placental involvement (WPLI) was defined as a histological inflammation involving the maternal and fetal sides. There were 113 TI+, 30 TI-, 186 CS+, 35 CS-, and 40 isolated HCA cases. WPLI was diagnosed in 133 cases (39.2%). Composite neonatal outcome (CNO) occurred in 114 cases (28.2%) while composite maternal outcome (CMO) occurred in 192 cases (47.5%). Compared with CS+, TI+ was more predictive of CNO (p = 0.001), CMO (p < 0.001), and WPLI (p = 0.005). WPLI was related both to CNO (p < 0.001) and to CMO (p = 0.046). TI+ and WPLI showed similar sensitivity but different specificity in predicting CNO. At logistic regression, CNO was independently predicted by TI+ (OR 2.21; p = 0.001) and by WPLI (OR 2.23; p = 0.001). Compared with CS, TI is a better predictor of CNO and can be useful for the identification of newborns at risk.

Intraamniotic infection is an infection resulting in the inflammation of any combination of the amniotic fluid, the placenta, the fetus itself, the fetal membranes, umbilical cord, or the decidua. In the past, an infection of the amnion and chorion or both was dubbed chorioamnionitis. In 2015, a proposal was made by an expert panel that, instead of clinical chorioamnionitis, the name intrauterine inflammation or infection or both be used, abbreviated as Triple I or simply IAI. However, the abbreviation IAI did not gain popularity, and this article uses the term chorioamnionitis. Chorioamnionitis may arise prior to, during, or following labor. It can present as a chronic, subacute, or acute infection. Its clinical presentation is generally referred to as acute chorioamnionitis. The treatment of chorioamnionitis varies widely across the world due to different bacterial causes and the absence of sufficient evidence to support a specific treatment regimen. There are limited randomized controlled trials that have evaluated the superiority of antibiotic regimens for treating amniotic infections during labor. This lack of evidence-based treatment suggests that the current choice of antibiotics is based on limitations in existing research, rather than absolute science. Chorioamnionitis cannot be cured by antibiotic therapy alone without delivery, and therefore it is necessary to make a decision according to the guidelines for induction of labor or acceleration of delivery. When a diagnosis is suspected or established, it is therefore necessary to apply broad-spectrum antibiotics according to the protocol used by each country, and to continue with them until delivery. A commonly recommended first-line treatment for chorioamnionitis is a simple regimen consisting of amoxicillin or ampicillin and once-daily gentamicin. Available information is not sufficient to indicate the best antimicrobial regimen to treat this obstetric condition. However, the evidence that is currently available suggests that patients with clinical chorioamnionitis, primarily women with a gestational age of 34 weeks or more and those in labor, should receive treatment with this regime. However, antibiotic preferences may vary based on local policy, clinician experience and knowledge, bacterial reasons for the infection, antimicrobial resistance patterns, maternal allergies, and drug availability.

OBJECTIVE: To investigate influencing factors of intrapartum fever during vaginal delivery and to construct a prediction model for infectious intrapartum fever.
METHODS: A total of 444 patients with intrapartum fever admitted in Ningbo Women and Children\'s Hospital from January 2020 to December 2021 were enrolled. The clinical data and laboratory findings were compared between patients with infectious intrapartum fever and non-infectious intrapartum fever, and the factors associated with intrapartum fever were analyzed with a multivariate logistic regression model. A prediction nomogram model was constructed based on the factors of intrapartum fever and its predictive efficiency was evaluated by correction curve and receiver operator characteristic curve.
RESULTS: In the 444 cases, 182 (41.0%) had definite intrauterine infection and 262 (59.0%) had no infectious intrapartum fever. Univariate analysis showed that the length of hospital stay before induced labor, the time of induced abortion, misoprostol administration, autoimmune diseases, white blood cell count (WBC) and hypersensitive C-reactive protein (hs-CRP) levels were significantly different between the two groups (all P<0.05). Multivariate analysis showed that misoprostol administration and autoimmune diseases were protective factors (OR=0.31 and 0.36, both P<0.05) for infectious intrapartum fever, while high WBC and hs-CRP were risk factors (OR=1.20 and 1.09, both P<0.05). The area under the curve of nomogram model for predicting infectious intrapartum fever was 0.823, and the calibration curve validation showed that the predicted and measured values were in general agreement.
CONCLUSIONS: Multiple factors cause intrapartum fever. The nomogram model constructed in this study has good predictive accuracy for infectious intrapartum fever.
目的: 研究阴道试产过程中产时发热的影响因素，并构建宫内感染所致产时发热的列线图预测模型。方法: 收集2020年1年—2021年12月宁波市妇女儿童医院收治的阴道试产过程中出现产时发热的444例产妇的资料。回顾性分析患者的临床资料、症状、体征及实验室检查结果，比较宫内感染所致产时发热与非宫内感染所致产时发热的临床特点及实验室指标差异，采用多因素logistic回归模型分析产时发热的相关因素。应用R4.1.0软件及rms和regplot程序包建立列线图模型，应用Bootstrap重采样法进行模型验证，绘制预测模型校准曲线及受试者操作特征曲线。结果: 444例产时发热产妇中，182例（41.0%）产后明确为宫内感染，262例（59.0%）为非宫内感染所致。单因素分析结果显示，引产前住院时间、引产时间、使用米索前列醇、妊娠合并免疫系统疾病、白细胞计数（WBC）及超敏C反应蛋白（hs-CRP）在宫内感染所致产时发热与非宫内感染所致产时发热组间差异有统计学意义（均P<0.05）；多因素logistic回归分析结果显示，妊娠合并免疫系统疾病和使用米索前列醇是宫内感染所致产时发热的保护因素（OR=0.31和0.36，均P<0.05），而WBC和hs-CRP增加是危险因素（OR=1.20和1.09，均P<0.05）。基于上述四项独立影响因素构建的列线图模型预测宫内感染所致产时发热的曲线下面积为0.823，校准曲线显示预测值与实测值基本一致。结论: 产时发热影响因素众多，本研究构建的列线图模型对于宫内感染所致产时发热具有较好的预测价值。.

Periodontitis is a chronic oral inflammatory disease with a high incidence in the global population. Periodontal pathogens can colonize and infect multiple human tissues and organs through blood transmission, which is an important risk factor of many systemic diseases. Recently, the correlation between periodontitis and adverse pregnancy outcomes (APOs) has attracted growing research interest. Herein, we systematically reviewed the research progress in the relationship between periodontitis and APOs and summarized reported findings on the pathways and mechanisms by which periodontitis contributes to APOs. We also clarified that intrauterine infection caused by oral pathogens transmitted through blood is an important pathway by which periodontitis interferes with pregnancy. In addition, further research focused on the discovery of more APOs-related oral pathogenic bacteria and their virulence factors, analysis of the interaction between pathogenic bacteria and placental tissue, and pathogenic pathways of oral bacterial invasion of the fetus will promote thorough analysis of the specific molecular mechanism of how periodontitis affects APOs. Furthermore, the validation of the results of human population-based studies through animal/cell experiments and the translation into effective intervention strategies are of great clinical significance to the prevention and control of the occurrence and development of APOs.