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Journal articles on the topic 'Fetal intrauterine infection'

Author: Grafiati

Published: 28 May 2022

Last updated: 29 May 2022

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1

Silingardi, Enrico, Anna Laura Santunione, Francesco Rivasi, Bernard Gasser, Silvia Zago, and Lorella Garagnani. "Unexpected Intrauterine Fetal Death in Parvovirus B19 Fetal Infection." American Journal of Forensic Medicine and Pathology 30, no. 4 (December 2009): 394–97. http://dx.doi.org/10.1097/paf.0b013e3181c17b2e.

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2

Jawor, Paulina, John F. Mee, and Tadeusz Stefaniak. "Role of Infection and Immunity in Bovine Perinatal Mortality: Part 2. Fetomaternal Response to Infection and Novel Diagnostic Perspectives." Animals 11, no. 7 (July 15, 2021): 2102. http://dx.doi.org/10.3390/ani11072102.

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Bovine perinatal mortality due to infection may result either from the direct effects of intrauterine infection and/or the fetal response to such infection, leading to the fetal inflammatory response syndrome (FIRS). Both intrauterine infection and FIRS, which causes multi-organ damage and involution of immune organs, compromise fetal survivability, sometimes fatally. Organ injury associated with FIRS may, in addition to causing fetal mortality, irreversibly compromise extrauterine adaptation of the neonate, a recognized problem in human fetuses. Diagnosis of intrauterine infection and of FIRS requires related, but independent analytical approaches. In addition to detection of pathogens, the immune and inflammatory responses of the bovine fetus may be utilized to diagnose intrauterine infection. This can be done by detection of specific changes in internal organs and the measurement of antibodies and/or elements of the acute phase reaction. Currently our ability to diagnose FIRS in bovine fetuses and neonates is limited to research studies. This review focuses on both the fetomaternal response to infection and diagnostic methods which rely on the response of the fetus to infection and inflammatory changes, as well other methods which may improve diagnosis of intrauterine infection in cases of bovine perinatal mortality.

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3

Watson, William J., Sami Awadallah, and Mary Jo Jaqua. "Intrauterine Infection With Coxsackievirus: Is it a Cause of Congenital Cardiac Malformations?" Infectious Diseases in Obstetrics and Gynecology 3, no. 2 (1995): 79–81. http://dx.doi.org/10.1155/s1064744995000366.

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Background: Although maternal infections with coxsackievirus during pregnancy are relatively common, fetal infections are quite rare. Coxsackievirus infection in utero has been associated with myocarditis, but has not been proven a teratogen.Case: A patient whose fetus had structural cardiac anomalies and hydrops was found to have an intrauterine infection with Coxsackie B-1 virus, proven by virus isolation from the amniotic fluid. This infection led to increasing intrauterine hydrops and subsequent neonatal death. Conclusion: This interesting association of intrauterine infection with Coxsackie B virus and structural cardiac anomalies in the fetus warrants further investigation.

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4

Válková, Andrea, and Petr Hubka. "Covid-19 as a possible risk factor of intrauterine fetal death." Česká gynekologie 86, no. 6 (December 21, 2021): 410–13. http://dx.doi.org/10.48095/cccg2021410.

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Objective: To summarize information about possible effects of covid-19 on intrauterine fetal death and present three cases of intrauterine fetal death in women with recent covid-19 infection. Methods: Review of available information about pregnancy with covid-19 and comparison with own observation of cases during spring 2021. Conclusion: Covid-19 influences risk of intrauterine fetal death, preeclampsia/eclampsia or HELLP syndrome. Coagulation changes and drop of platelets is considered as one of the causes of intrauterine fetaldeath due to fetal vascular malperfusion. Key words: covid-19 – intrauterine fetal death – obstetrics

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5

Schwartz, David A., and Amareen Dhaliwal. "Infections in Pregnancy With COVID-19 and Other Respiratory RNA Virus Diseases Are Rarely, If Ever, Transmitted to the Fetus: Experiences With Coronaviruses, Parainfluenza, Metapneumovirus Respiratory Syncytial Virus, and Influenza." Archives of Pathology & Laboratory Medicine 144, no. 8 (April 27, 2020): 920–28. http://dx.doi.org/10.5858/arpa.2020-0211-sa.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the agent of coronavirus disease 2019 (COVID-19), is similar to 2 other coronaviruses, SARS-CoV and Middle East respiratory syndrome coronavirus (MERS-CoV), in causing life-threatening maternal respiratory infections and systemic complications. Because of global concern for potential intrauterine transmission of SARS-CoV-2 from pregnant women to their infants, this report analyzes the effects on pregnancy of infections caused by SARS-CoV-2 and other respiratory RNA viruses, and examines the frequency of maternal-fetal transmission with SARS-CoV-2, severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), influenza, respiratory syncytial virus (RSV), parainfluenza (HPIV), and metapneumovirus (hMPV). There have been no confirmed cases of intrauterine transmission reported with SARS-CoV-2 or any other coronaviruses—SARS and MERS. Influenza virus, despite causing approximately 1 billion annual infections globally, has only a few cases of confirmed or suspected intrauterine fetal infections reported. Respiratory syncytial virus is an unusual cause of illness among pregnant women, and with the exception of 1 premature infant with congenital pneumonia, no other cases of maternal-fetal infection are described. Parainfluenza virus and hMPV can produce symptomatic maternal infections but do not cause intrauterine fetal infection. In summary, it appears that the absence thus far of maternal-fetal transmission of the SARS-CoV-2 virus during the COVID-19 pandemic is similar to other coronaviruses, and is also consistent with the extreme rarity of suggested or confirmed cases of intrauterine transmission of other respiratory RNA viruses. This observation has important consequences for pregnant women because it appears that if intrauterine transmission of SARS-CoV-2 does eventually occur, it will be a rare event. Potential mechanisms of fetal protection from maternal viral infections are also discussed.

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6

BRADY, WILLIAM KIM, and ALFRED PURDON. "Intrauterine Fetal Demise Associated With Enterovirus Infection." Southern Medical Journal 79, no. 6 (June 1986): 770–72. http://dx.doi.org/10.1097/00007611-198606000-00032.

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7

Schild, R. L., R. Bald, H. Plath, A. M. Eis-Hübinger, G. Enders, and M. Hansmann. "Intrauterine management of fetal parvovirus B19 infection." Ultrasound in Obstetrics and Gynecology 13, no. 3 (March 1999): 161–66. http://dx.doi.org/10.1046/j.1469-0705.1999.13030161.x.

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8

Hichijo, Atsuko, and Mikio Morine. "A Case of Fetal Parvovirus B19 Myocarditis That Caused Terminal Heart Failure." Case Reports in Obstetrics and Gynecology 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/463571.

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Parvovirus B19 is a well-established cause of fetal anemia and nonimmune fetal hydrops in pregnancy. Fetal parvovirus infection can cause severe destruction of erythroid progenitor cells, resulting in fetal anemia, hydrops, and intrauterine death. However, viral myocarditis with subsequent heart failure is another possible mechanism for hydrops formation as viral infection of fetal myocardial cells has been reported in postmortem examinations. We herein report a case of fetal cardiomegaly and massive pericardial effusion secondary to myocarditis as a result of parvovirus B19 infection. The case developed hydrops as consequence of severe anemia and experienced terminal heart failure, which led to the fetus dying an intrauterine death at 22 weeks of gestation. This case demonstrates that there may be an association between myocarditis caused by intrauterine parvovirus B19 infection and a poor outcome. The presence of viral myocarditis may be the determining prognostic factor in that situation.

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9

Agra, Isabela, Antonio Amorim Filho, Lawrence Lin, Sckarlet Biancolin, Rossana Francisco, and Maria Brizot. "Parameters Associated with Adverse Fetal Outcomes in Parvovirus B19 Congenital Infection." Revista Brasileira de Ginecologia e Obstetrícia / RBGO Gynecology and Obstetrics 39, no. 11 (September 25, 2017): 596–601. http://dx.doi.org/10.1055/s-0037-1606859.

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Objective To investigate the clinical and sonographic parameters associated with adverse fetal outcomes in patients with congenital parvovirus B19 infection managed by intrauterine transfusion. Methods This was a single-center retrospective study conducted from January 2005 to December 2016 that assessed patients with singleton pregnancies with fetal parvovirus infection confirmed by a polymerase chain reaction of the amniotic fluid or fetal blood samples who underwent at least one intrauterine transfusion. The maternal characteristics, sonographic findings and parameters related to intrauterine transfusion were compared between the two groups (recovery/non-recovery), who were categorized based on fetal response after in-utero transfusions. Progression to fetal death or delivery without fetal recovery after the transfusions was considered non-recovery and categorized as an adverse outcome. Results The final analysis included ten singleton pregnancies: seven of which were categorized into the recovery group and three of which into the non-recovery group. The baseline characteristics were similar between the groups. All fetuses were hydropic at the time of diagnosis. No significant differences related to sonographic or intrauterine transfusion parameters were identified between the groups; however, the non-recovery group tended to have an increased number of sonographic markers and lower fetal hemoglobin and platelet levels before the transfusion. Conclusion We were unable to firmly establish the clinical or sonographic parameters associated with adverse fetal outcomes in patients with parvovirus infection managed with intrauterine transfusions; however, edema, placental thickening and oligohydramnios may indicate greater fetal compromise and, subsequently, adverse outcomes. However, further studies are necessary, mainly due to the small number of cases analyzed in the present study.

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10

Torabi, Rozbeh, Svetlana Charnova, Rosanna G. Abellar, Halit Pinar, and Monique E. De Paepe. "Intrauterine Infection with Klebsiella Pneumoniae: Report of a Case and Literature Review." Pediatric and Developmental Pathology 11, no. 2 (March 2008): 152–55. http://dx.doi.org/10.2350/07-09-0337.1.

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We report a case of intrauterine Klebsiella pneumoniae infection that resulted in premature rupture of membranes and fetal demise at 20 weeks' gestation in a pregnancy achieved by in vitro fertilization. Postmortem findings included massive panlobar pneumonia, the presence of abundant gram-negative, rod-shaped bacteria within the pulmonary air spaces and the lumen of the gastrointestinal tract, and fetal lung and blood cultures positive for Klebsiella pneumoniae. The placenta showed severe acute chorioamnionitis associated with a brisk fetal inflammatory response (umbilical cord and chorionic plate vasculitis). Marked pancreatic fibrosis was noted, indicative of a preceding necrotizing pancreatitis. In spite of this fulminant histopathologic evidence of intrauterine infection, the infection was clinically silent. This represents, to our knowledge, the 1st reported case of fatal intrauterine Klebsiella pneumoniae infection fully supported by conclusive fetal and placental histopathological evidence.

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11

Rutkovskiy, A. "Intrauterine fetal disease with ophthalmoblenorrhea." Journal of obstetrics and women's diseases 7, no. 4 (September 10, 2020): 350. http://dx.doi.org/10.17816/jowd74350.

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The most likely time of infection of the fetus with ophthalmoblenorrhea is when the face of the fetus during childbirth is most closely in contact with the stretched walls of the uterus and vagina, and therefore this disease is most often expressed 3-4 days after childbirth (3-4 days of the incubation period). Much more rare are those cases where the child is already born with a clearly expressed disease.

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12

Shadeeva, Yu A., V. A. Guryeva, M. G. Nikolaeva, and N. V. Evtushenko. "Predicting intrauterine fetal infection risk in extremely preterm and early preterm births induced by rupture of the amniotic membranes." Obstetrics, Gynecology and Reproduction 14, no. 4 (October 14, 2020): 490–501. http://dx.doi.org/10.17749/2313-7347/ob.gyn.rep.2020.110.

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Aim: developing a prognostic model for intrauterine fetal infection risk in extremely preterm and early preterm births induced by rupture of the amniotic membranes.Materials and Methods. A single-center prospective cohort study was conducted aimed at studying features of pregnancy and childbirth in 160 patients with extremely preterm and early preterm births induced by rupture of the amniotic membranes as well as neonatal period of 160 neonates. Two groups were distinguished: the main group – 37 patients with intrauterine neonatal infection and the comparison group – 123 women without signs of neonatal infection. Along with examination regulated by the order of the Ministry of Health of the Russian Federation No. 572 n, serum level of highly sensitive C-reactive protein, pro-inflammatory cytokines interleukin-6, tumor necrosis factor-α and anti-inflammatory cytokine interleukin-10 were assessed in patients. Risk factors (predictors) of intrauterine infection were assessed by analyzing anamnesis data, echography and laboratory assay data.Results. Multivariate logistic regression analysis allowed us to identify 10 predictors of intrauterine fetal infection based on which a mathematical model was developed that allowed to predict a risk of intrauterine fetal infection in 95.7 % of cases.Conclusion. Using a model for predicting intrauterine infection based on a comprehensive predictor assessment, it may allow to accomplish a personalized approach to justify adequate obstetric care and reduce adverse infection-associated perinatal outcomes.

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13

Miranda, Roberto N., Kenan Omurtag, William J. Castellani, Luis E. De Las Casas, Norma M. Quintanilla, and Emad Kaabipour. "Myelopoiesis in the Liver of Stillborns With Evidence of Intrauterine Infection." Archives of Pathology & Laboratory Medicine 130, no. 12 (December 1, 2006): 1786–91. http://dx.doi.org/10.5858/2006-130-1786-mitlos.

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Abstract Context.—Chorioamnionitis is the maternal and fetal response to an ascending intrauterine infection. The fetal response is manifested by funisitis and chorionic vasculitis, or as neutrophils within pulmonary spaces. Human hematopoiesis occurs in the liver primarily during the 6th to 22nd weeks of gestation. Objective.—To establish the relationship between the presence of an intrauterine infection and the degree of fetal hepatic myelopoiesis in second- and third-trimester fetuses. Design.—Liver and lungs from 49 fetal autopsies, 20 to 41 weeks of gestational age, and their associated placentas and membranes were analyzed for evidence of intrauterine infection and hepatic myelopoiesis. Hematoxylin-eosin– stained sections from fixed tissues were evaluated for the presence of amnionic fluid infection, defined by the presence of acute chorioamnionitis or funisitis. The degree of portal hematopoiesis, myelopoiesis and intra-alveolar neutrophils was assessed semiquantitatively with hematoxylin-eosin–stained sections and immunohistochemically with antimyeloperoxidase. The Kruskal-Wallis 1-way analysis of variance and the Wilcoxon-Mann-Whitney test were used to determine the significance of any observed difference. Results.—The degree of portal and lobular myelopoiesis was significantly greater with the presence of inflammation in both the membranes and umbilical cord, and correlated with the presence of intra-alveolar neutrophils (P < .001). A high correlation between the hematoxylin-eosin and immunohistochemistry assessment of myeloid cells was noted. Conclusions.—There is increased portal and lobular myelopoiesis in 20-week to 41-week gestational age fetal livers that is associated with intrauterine ascending infection. The presence of increased portal or lobular myelopoiesis suggests the presence of an active fetal response to an intrauterine ascending infection.

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14

Bondarenko, N. P., V. P. Lakatosh, Ya M. Vitovsky, T. T. Narytnyk, and P. V. Lakatosh. "Modern methods of treatment of intrauterinenon-immune fetal hydropsinduced by parvovirus infection." HEALTH OF WOMAN, no. 5-6(151-152) (July 30, 2020): 43–47. http://dx.doi.org/10.15574/hw.2020.151-152.43.

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During ultrasonography examinationfetuses infected by parvovirus B19, we have established 36/129 (27.9%) cases of non-immune hydrops in the different periods of pregnancy.The hyperdynamic type of blood flow in fetal middle cerebral arterial was observed in fetuses at the second trimester. Measurement of fetal middle cerebral arteria peak systolic velocity was started at 18 weeks of gestationonce a week in pregnant women who were infected by parvovirus B19. During our study were found 17 cases of severe fetal anemia which manifested after 18 weeks of gestation.Intrauterine transfusions were performed for 11 pregnant women with parvovirus induced fetal hydrops whose gestation age were between 22.4 -25.7 (average 24.0±0.2). After cordocentesis11 cases of severe fetal anemia were confirmed.In the last 6 cases fetuses were diagnosed terminal condition due to women`s refusal of intrauterine transfusion or untimely admission to the hospital. Taking to account the results of study, the efficacy of treatment non-immune hydrops infected by parvovirus B19 with severe fetal anemia and outcomes were evaluated and analyzed. Successful treatment of parvovirus-induced fetal non-immune hydrops in the second trimester of pregnancy has been found in 72.7% cases (OR=95%) after intrauterine transfusion compared to 100% lethal rate in fetuses with non-immune hydrops and severe anemia who were not treated. Criteria for effectiveness of intrauterine transfusion are in time diagnosis of severe fetal anemia in infected fetus with non-immune hydrops, determine the optimal gestation age for intrauterine transfusion, indicators of viremia in umbilical cord blood, the compensatory capacity of the fetus based on Doppler metric indicator of middle cerebral arterial peak systolic velocity and changes blood flow in ductus venous of the fetus. It helps to reduce perinatal loss. Keywords: parvovirus infection, non-immune hydrops fetalis, intrauterine transfusion.

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15

McDuffie, Robert S., Mirjam Kunze, Jane Barr, Douglas Wolf, Chun-I. Sze, Robert Shikes, Michael Sherman, and Ronald S. Gibbs. "Chronic intrauterine and fetal infection with Gardnerella vaginalis." American Journal of Obstetrics and Gynecology 187, no. 5 (November 2002): 1263–66. http://dx.doi.org/10.1067/mob.2002.127129.

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16

Thilaganathan, Baskaran, Steve G. Carroll, Nicholas Plachouras, George Makrydimas, and Kypros H. Nicolaides. "Fetal immunological and haematological changes in intrauterine infection." BJOG: An International Journal of Obstetrics and Gynaecology 101, no. 5 (May 1994): 418–21. http://dx.doi.org/10.1111/j.1471-0528.1994.tb11915.x.

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17

Michie, C. A., and D. Harvey. "Fetal immunological and haematological changes in intrauterine infection." BJOG: An International Journal of Obstetrics and Gynaecology 102, no. 1 (January 1995): 79. http://dx.doi.org/10.1111/j.1471-0528.1995.tb09041.x.

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18

Licci, Stefano. "Intrauterine fetal death due to congenital cytomegalovirus infection." Brazilian Journal of Infectious Diseases 21, no. 5 (September 2017): 567–68. http://dx.doi.org/10.1016/j.bjid.2017.03.022.

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19

Geng, Xiao-li, Ya-xuan Zhang, and Qi-zhi Ren. "Effects of intrauterine infection in different periods on the placenta and endometrial blood vessel formation of pregnant mice and the growth and development of fetal rats." Discussion of Clinical Cases 8, no. 2 (August 22, 2021): 18. http://dx.doi.org/10.5430/dcc.v8n2p18.

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Objective: To investigate the effects of intrauterine infection in different periods on the placenta and endometrial blood vessel formation of pregnant rats and the growth and development of fetal rats.Methods: According to the random number table method, 32 pregnant rats were divided into the early infection group, the mid-term infection group, the late infection group and the control group, with 8 rats in each group. On the 3rd, 9th and 15th day of pregnancy, lipopolysaccharide was injected intraperitoneally to construct intrauterine infection models. The pregnant rats in the control group were intraperitoneally injected with the same dose of 0.9% sodium chloride solution. On the 18th day of pregnancy, the inflammatory factors [interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α)], the blood vessel density of placenta and endometrium in the placental tissues of pregnant rats, dead fetus + absorbed fetus, the inflammatory factors IL-6, TNF-α and oxidation reaction indicators [malondialdehyde (MDA) and myeloperoxidase (MPO)] in the fetal rat lung and brain tissues were detected.Results: The changing trend of IL-6 and TNF-α levels in the placental tissues of pregnant rats with intrauterine infection in different periods was: the control group < the late infection group < the mid-term infection group < the early infection group, the differences were statistically significant (p <.05). The changing trend of fetal rat weight, placental weight and placental coefficient in the intrauterine infection groups in different periods was: the control group > the late infection group > the mid-term infection group > the early infection group, the differences were statistically significant (p < .05). The blood vessel density of placenta and endometrium, the mean number of fetuses, brain coefficient and lung coefficient in the late infection group were significantly increased in comparison with the early infection group and the mid-term infection group. The total number and the ratio of dead fetus + absorbed fetus, the levels of IL-6, TNF-α, MDA and MPO in brain and lung tissues were significantly reduced, and the differences were statistically significant (p < .05). The blood vessel density of placenta and endometrium, brain coefficient and lung coefficient of pregnant rats in the mid-term infection group were significantly increased in comparison with the early infection group, and the differences were statistically significant (p < .05). There was no statistically significant difference in the other indicators between the two groups (p > .05).Conclusions: Intrauterine infection in different periods can inhibit placental and endometrial angiogenesis, and affect the survival rate of fetal rats and the growth and development of brain and lung. The reason may be related to the aggravation of fetal inflammatory responses and oxidative stress. The earlier the intrauterine infection occurs, the severer the adverse effects on the fetal rats will be.

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Nikitina, Irуna M., Svitlana A. Smiian, Kateryna O. Kondratiuk, Natalia V. Kalashnyk, and Anzhelika A. Shevel. "CONDITIONS OF MICROELEMENTS EXCHANGE PROCESSES IN WOMEN’S PLACENTS IN INTRAUTERINE INFECTION OF THE FETUS." Wiadomości Lekarskie 73, no. 7 (2020): 1434–37. http://dx.doi.org/10.36740/wlek202007123.

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The aim: to study the content of trace elements (Fe, Cu, Zn, Co, Cr, Ni, Pb) in the placenta of pregnant healthy women and with signs of intrauterine infection of the fetus, features of transplacental transmission of infectious process from mother to fetus and to investigate the role of the placenta in trace element supply of the fetus. Materials and methods. 43 pregnant women between the aged 16 to 40 years were monitored, including 12 with physiological pregnancy (group 1) and 31 with signs of STI (group 2). All pregnant women underwent standard comprehensive examination, evaluation of fetal cardiac output and non-stress testing using cardio-toсography (CTG) in the third trimester. The group of pregnant women with signs of fetal ulcers included women whose pregnancy was complicated by chronic fetoplacental dysfunction (FPD), infectious lesions of the fetoplacental complex, which were diagnosed on the basis of ultrasound signs of placenta, syndrome of infectious and surrounding infections. Results: The content of essential trace elements in the placenta of the main group was significantly lower than in the placenta of the control group. There was a decrease in the concentration of iron by 32%, zinc – by 46%, nickel – by 44%, copper more than tripled, chromium – 4 times. Deficiency of essential trace elements (iron, zinc, copper, chromium, nickel) and elevated lead content in the placenta leads to the formation of conditions for the development of placental dysfunction, the progression of which leads to fetal distress, developmental delay syndrome and antenatal fetal death. Conclusions: 1. One of the links in the pathogenesis of intrauterine infection in the fetus is the imbalance of essential trace elements in the system «mother – placenta – fetus». 2. Pregnant women with signs of intrauterine infection are characterized by a deficiency of serum Fe, Cu, Zn, Ni and an increased content of Pb, Cr and Co compared with pregnant women with physiological pregnancy. 3. Umbilical cord blood of women with evidence of fetal fetal infection also has a reduced content of iron, copper, zinc and high levels of lead, cobalt and chromium. 4. Disruption of placental function in intrauterine infection of the fetus is caused by reduced content of iron, zinc, copper, nickel and lead accumulation.

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Shea, Stephanie, Alberto Paniz-Mondolfi, Emilia Sordillo, Michael Nowak, and Fumiko Dekio. "Florid Bacillus cereus Infection of the Placenta Associated With Intrauterine Fetal Demise." Pediatric and Developmental Pathology 24, no. 4 (March 17, 2021): 361–65. http://dx.doi.org/10.1177/1093526621999026.

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Bacillus cereus is a gram-positive, rod-shaped bacterium that is commonly implicated in foodborne illness but has also become increasingly recognized as a source of serious non-gastrointestinal infections, including sepsis, meningitis, and pneumonia. Non-gastrointestinal B. cereus infections have been identified in children, especially in neonates; however, there are no previously described cases of fetal demise associated with B. cereus placental infection. We present a case of acute chorioamnionitis-related intrauterine fetal demise of twin A at 17 weeks gestation, noted two days after selective termination of twin B. Histological examination revealed numerous gram-positive bacilli in placental tissue, as well as fetal vasculature, in the setting of severe acute necrotizing chorioamnionitis and subchorionitis, intervillous abscesses, acute villitis, and peripheral acute funisitis. Cultures of maternal blood and placental tissue both yielded growth of B. cereus. This case underscores the importance of B. cereus as a human pathogen, and specifically demonstrates its potential as an agent of severe intraamniotic and placental infection with poor outcomes for the fetus.

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Bondarenko, N. P., W. P. Lakatoch, O. J. Kostenko, and P. W. Lakatoch. "Features of diagnosis of parvovirus infection during pregnancy." HEALTH OF WOMAN, no. 8(124) (October 30, 2017): 27–31. http://dx.doi.org/10.15574/hw.2017.124.27.

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Clinical and diagnostic data of 129 cases of parvovirus B19 infection during pregnancy are presented. Serological and virological results ofparvovirus infection examination of pregnant women and fetuses were evaluated. In 50.4% of cases, the main factor ofdiseasetransmissionis physical contact of pregnant woman with children who had infectious erythema. Parvovirus infection is diagnosed in 27% of casespregnant women at a risk of intrauterine infection during pregnancy. In 38% of pregnant women, the infection is asymptomatic and can be accidentally detected by the method of determining antibodies to parvovirus B19. In 62%cases maternal and fetal symptoms manifest in parvovirus infection during pregnancy. In 70% of maternal symptoms correlates with fetus symptoms. Diagnosis of transplacental transmission of parvovirus B19 with symptomatic manifestations of infection occurs in 36.4%. The main clinical symptom of fetal parvovirus infection is the development of non-immune hydrop. In the structure of echographic diagnosis of intrauterine anomalies of fetal development, parvovirus infection occurs in 4.7%. Key words: parvovirus infection, pregnancy, symptomatology, diagnostics.

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23

Rose, Carl, Christian Briery, Chad Klauser, William Bennett, Josephine Wyatt-Ashmead, Kathy Cockrell, John Morrison, James Martin, and Joey Granger. "Timing of biochemical fetal brain injury following intrauterine infection." American Journal of Obstetrics and Gynecology 191, no. 6 (December 2004): S55. http://dx.doi.org/10.1016/j.ajog.2004.10.071.

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24

Kishikawa, Tadao, Tatsuhiko Kawarabayashi, Jun Hayasegawa, Hajime Sugimori, and Tatsuro Shimokama. "Intrauterine Cytomegalovirus Infection Associated with Fetal Ascites and Oligohydramnios." Asia-Oceania Journal of Obstetrics and Gynaecology 13, no. 3 (May 24, 2010): 297–300. http://dx.doi.org/10.1111/j.1447-0756.1987.tb00268.x.

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25

Ranucci-Weiss, Denise, Boonchai Uerpairojkit, Neil Bowles, Jeffrey A. Towbin, and Linda Chan. "Intrauterine adenoviral infection associated with fetal non-immune hydrops." Prenatal Diagnosis 18, no. 2 (February 1998): 182–85. http://dx.doi.org/10.1002/(sici)1097-0223(199802)18:2<182::aid-pd225>3.0.co;2-e.

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26

Marelli, Guido, Andrea Mariani, Luigi Frigerio, Eugenio Leone, and Augusto Ferrari. "Fetal Candida infection associated with an intrauterine contraceptive device." European Journal of Obstetrics & Gynecology and Reproductive Biology 68 (September 1996): 209–12. http://dx.doi.org/10.1016/0301-2115(96)02471-2.

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27

Semeniak, A. V., O. A. Andriyets, Nitsovych Nitsovych, S. V. Koliandretska, and N. S. Voloshynovych. "INTRAUTERINE FETAL INFECTION - THE REALITIES OF DIAGNOSIS AND TREATMENT." Neonatology, surgery and perinatal medicine 11, no. 2(40) (October 19, 2021): 27–32. http://dx.doi.org/10.24061/2413-4260.xi.2.40.2021.5.

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Іntroduction. Intrauterine infection of the fetus is oneof the most important problems in obstetrics. The absenceof adequate treatment leads to a number of complicationsthat develop during pregnancy, childbirth, and postpartumperiod. There are often situations when the consequences ofthe invasion of microorganisms are more important than thepresence of an infectious agent itself.The aim is to analyze the indicators of microcytosis ofthe vagina, cervical canal, the peculiarities of pregnancywith infection of the fetus, and the effectiveness of varioustreatment regimens.Material and methods. 20 healthy women withphysiological course of pregnancy (the control group) and62 pregnant women with signs of fetal infection (the maingroup) were examined using clinical, microbiological,bacteriological, serological methods, statistical analysis,and fetal ultrasound.Results. Depending on the trimester, pregnant womenof the main group were divided into two subgroups: thefirst subgroup - at 18-24 weeks (50 pregnant women), thesecond - at 28-34 weeks (12 pregnant women).The statistical analysis of changes in vaginalmicrocynosis was conducted depending on the term. Thesignificant difference regarding the effect of gram negativediplococci, morphologically similar to gonococcus,Streptococcus agalactiae in the third trimester was found outalong with Ureaplasma urealyticum, Chlamidia trahomatisin the second trimester and Trichomonas vaginalis andMycoplasma hominis regardless of trimester.Ultrasound in the first subgroup revealed a syndromeof fetal growth retardation in 20 % of women, an abnormalamount of amniotic fluid in 24 %, changes in the structureof the placenta in 14 %, enlargement of the pelvic system ofthe kidneys in 52 %, intestinal hyperechogenicity in 60 %,and hepatomegaly in 4 % of cases. In the second subgroup,the abnormal amount of amniotic fluid was found in 16.7 %of pregnant women, changes in the structure of the placentain 83,3 %, and progressive shortening of the cervix in 33.3% of cases.Pregnant women of the main group were offered acourse of specific antibacterial therapy.In case of positive dynamics within three days (reductionof pathological secretions, polyhydramnios and otherultrasound signs of fetal infection), treatment is continued.In case of negative dynamics or no effect within three daysantibacterial agent must be changed. If symptoms reoccur,a repeat course with a new antibacterial agent is prescribed.Conclusions. Disorders of vaginal microcynosis andcervical canal were found in 80.6% of pregnant women,the rest of them were diagnosed with the ultrasound signsof infection of the fetus without changes in vagina andcervical canal.The proposed regimens of antibacterial therapy areeffective in the second trimester of pregnancy, indicatingthe necessity of examination and treatment during thisperiod, and in case of structural changes in the cervix causedby gram-negative diplococci, morphologically similarto gonococcus and Trichomonas vaginalis. Antibacterialtherapy is not effective enough in case of the developmentof placental dysfunction, and the threat of premature birthin the third trimester.

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Franckeviča, Ivanda, Liene Rucka, Santa Smilga, and Agnese Anna Jaunākā. "Infection as the cause of perinatal mortality in Latvia." Papers on Anthropology 26, no. 2 (September 18, 2017): 95. http://dx.doi.org/10.12697/poa.2017.26.2.10.

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Infection is one of the leading causes of perinatal mortality worldwide – accounting for 36% of cases. Perinatal mortality in Latvia is slowly decreasing: from 7.3 per 1000 live births in 2013 to 6.7 per 1000 live births in 2015. Intrauterine infection still is a global problem and a significant factor that affects morbidity and mortality of the mother and the child.This study includes data about the cause of death, including infections, from 417 autopsy protocols of all fetuses and neonates between 22 weeks of gestation and < 7 days postpartum from 2013 to 2015.The main cause of perinatal mortality was antenatal fetal asphyxia in 50% (n=210), followed by infections – 39% (n=163), including cases of chorioamnionitis. The highest mortality rate was found in the 22nd–27th+6 (i.e. 27 full weeks and 6 days) gestational weeks – 32% of cases (n=135). Intrauterine pneumonia accounted for 24% (n=39) of all the infection caused deaths, meconium aspiration pneumonia – 0.04% (n=6), early neonatal sepsis – 0.03% (n=4) and specific infections like syphilis and cytomegalovirus – 0.02% (n=3). Histological examination of the placenta, the placental cord and fetal membranes was made in 61% (n=255) of cases, and 19.6% (n=50) of them had an infection.

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Матейко, Г. Б., and М. В. Матвисив. "Predicting Intrauterine Fetal Infection in Pregnant Women with Chronic Hepatitis C." Клиническая инфектология и паразитология, no. 3 (November 4, 2021): 291–96. http://dx.doi.org/10.34883/pi.2021.10.3.023.

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Работа посвящена изучению факторов риска внутриутробного инфицирования плода у беременных женщин с хроническим гепатитом С на основе анализа клинико-лабораторных данных, занесенных в прогностическую карту с целью прогнозирования риска внутриутробного инфицирования плода. The work is dedicated to the study of risk factors for intrauterine infection of the fetus in pregnant women with chronic hepatitis C based on the analysis of clinical and laboratory data entered in the prognostic chart in order to predict the risk of intrauterine infection of the fetus.

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Gravett, Michael G., and Miles J. Novy. "Endocrine-Immune Interactions in Pregnant Non-Human Primates With Intrauterine Infection." Infectious Diseases in Obstetrics and Gynecology 5, no. 2 (1997): 142–53. http://dx.doi.org/10.1155/s1064744997000227.

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Preterm birth remains the most common cause of perinatal mortality. Although the causes of preterm labor are multifactorial and vary according to gestational age, preterm labor and term labor share common cellular and molecular mechanisms, including stimulation of the fetal hypothalamic-pituitary-adrenal (HPA) axis and endocrine/immune system interactions. We have developed a non-human primate experimental model for intrauterine infection and preterm labor using chronically instrumented rhesus monkeys (Macaca mulatta) with timed gestations. We have documented the temporal and quantitative relationships among intrauterine infection, the synthesis and release of proinflammatory cytokines, prostaglandins, and fetal-placental steroid biosynthesis in this model. Infection-induced preterm parturition is characterized by significant elevations in amniotic fluid proinflammatory cytokines and by increases in fetal adrenal steroid biosynthesis, but not by corresponding increases in placental estrogen biosynthesis characteristic of spontaneous parturition. This suggests that activation of the fetal HPA axis by the stress of infection is accompanied by placental dysfunction and also that infection-induced preterm parturition is not dependent upon the increased estrogen biosynthesis observed in spontaneous parturition. These different endocrine and immune responses have important diagnostic and therapeutic implications in the management of preterm labor.

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Ohno, Yasumasa, Masahide Kasugai, Osamu Kurauchi, Shigehiko Mizutani, and Yutaka Tomoda. "Effect of interleukin 2 on the production of progesterone and prostaglandin E2 in human fetal membranes and its consequences for preterm uterine contractions." European Journal of Endocrinology 130, no. 5 (May 1994): 478–84. http://dx.doi.org/10.1530/eje.0.1300478.

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Ohno Y, Kasugai M, Kurauchi O, Mizutani S, Tomoda Y. Effect of interleukin 2 on the production of progesterone and prostaglandin E2 in human fetal membranes and its consequences for preterm uterine contractions. Eur J Endocrinol 1994;130:478–84. ISSN 0804–4643 Our objective was to clarify the mechanism of uterine contraction induced in pregnant women by intrauterine bacterial infection. The concentration of interleukin 2 (IL-2) was measured in amniotic fluids that had been obtained by amniocentesis, transvaginal amniotomy or by transuterine amniocentesis performed at cesarean section in 50 pregnant women. The concentration of IL-2 in those cases with intrauterine infection was significantly higher than that of those without intrauterine infection at preterm. The same tendency was found at term. Scatchard analysis demonstrated the presence of an IL-2 receptor in the fetal membranes. We collected the fetal membranes aseptically for the measurement of progesterone and prostaglandin E2 by radioimmunoassay following incubation with various concentrations of Interleukin I (IL-1) and IL-2 at 37°C for 16 h. The production of progesterone was inhibited significantly by 10 pmol/l IL-2 but not by 10 pmol/l IL-1. The production of prostaglandin E2 was accelerated significantly by either IL-1 or IL-2 at a dose of 10 pmol/l. The inhibitory effect of IL-2 on the production of progesterone was unaffected by indomethacin, which inhibits the production of arachidonate cycloxygenase metabolites such as prostaglandin E2. Our present data suggest that the presence of intrauterine bacterial infection may stimulate the intrauterine production of IL-2, and that the stimulation of IL-2 and the reduction of progesterone caused by IL-2 may in part explain the mechanism of uterine contraction associated with intrauterine infection during pregnancy. Yasumasa Ohno, Department of Obstetrics and Gynecology, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466, Japan

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Petrova, K. K. "Relative Risk Assessment of Intrauterine Infection of the Fetus During Cytomegalovirus Infection in Early Pregnancy." Acta Biomedica Scientifica 4, no. 3 (July 17, 2019): 45–51. http://dx.doi.org/10.29413/abs.2019-4.3.6.

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Background. Intrauterine fetal infection (IUI), the common cause of which is the cytomegalovirus (CMV), occupies one of the first places in the structure of perinatal morbidity and mortality. There are no data on the relative risk assessment of IUI at the exacerbation of CMV infection and its delitescent course in first trimester of pregnancy in the literature.Aim: to calculate the relative risks of fetal IUI in pregnant women with exacerbation of CMV infection in the first trimester of pregnancy.Methods. A retrospective review of the labor and delivery medical records and prenatal records of 104 CMV-seropositive women was carried out. Fifty of these women had an exacerbation of CMV infection in the first trimester of pregnancy – main group and 54 of them were with delitescent course of the disease (comparison group).Results. A comparative analysis of ultrasound and morphological markers of IUI with risk assessment depending on the course of CMV infection in the first trimester of pregnancy has been carried out. A high risk of placental structure abnormalities, as well as amniotic fluid and fetal membranes, fetal and placental blood flow pathology, onset of choroid plexus cyst and fetal growth restriction was found, with a statistically significant difference in the group of pregnant women with exacerbation of CMV infection in the first trimester of pregnancy.Conclusion. The findings suggest that the exacerbation of CMV infection in early pregnancy is a risk factor for IUI.

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Panah, E., B. Zelman, and K. Gvozdjan. "Echogenic Intestine: a Case of Intrauterine Fetal Demise at Term." American Journal of Clinical Pathology 156, Supplement_1 (October 1, 2021): S24—S25. http://dx.doi.org/10.1093/ajcp/aqab191.046.

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Abstract Introduction/Objective Parvovirus B19 is a non-enveloped, single-stranded DNA virus that preferentially infects early erythroids, and is commonly associated with second trimester hydrops fetalis. Third trimester non-hydropic intrauterine fetal demise due to parvovirus B19 infection with associated pathologic changes has rarely been described, particularly in the context of IgG seroconverted mother. Methods/Case Report We present a case of a 37 weeks’ gestation stillborn female fetus born to a 29 year-old mother who presented with lack of fetal movement for one day. Fetal ultrasound demonstrated diffuse intestinal echogenicity. Maternal parvovirus B19 IgG level was high (5.48, reference: <=0.90 Index). Postmortem examination revealed a non-dysmorphic fetus. Gross examination was unremarkable. Microscopic examination of small intestine revealed mucosal inflammation and multifocal calcifications. Prominent extramedullary hematopoiesis was present in the liver. Viral cytopathic effect was noted microscopically within nucleated red blood cells present intravascularly within chorionic villi, small intestine, liver, and spleen. Parvovirus B19 infection was confirmed by immunohistochemistry. Results (if a Case Study enter NA) NA Conclusion The cause of clinically puzzling intrauterine fetal demise at term with prominent intestinal echogenicity on ultrasound was determined to be parvovirus B19 infection on postmortem examination. We emphasize the possibility of this diagnostic differential in non-hydropic, third trimester fetal demise in presence of maternal IgG seroconversion and lack of signs of active infection.

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Kurland, Yonatan, Ranjit I. Kylat, Drew C. Johnson, Brent J. Barber, Alan D. Bedrick, and Mohammad Y. Bader. "Intravenous Immunoglobulin for Congenital Parvovirus Myocarditis." Journal of Pediatric Infectious Diseases 15, no. 01 (January 18, 2018): 053–56. http://dx.doi.org/10.1055/s-0037-1620249.

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AbstractCongenital parvovirus infection has a diverse presentation ranging from asymptomatic infants to intrauterine demise secondary to red cell aplasia or myocarditis. Treatment is aimed at correcting anemia with intrauterine and postnatal transfusions. We report a case of fetal hydrops with severe atrioventricular regurgitation and myocardial dysfunction secondary to parvovirus infection in a preterm infant. Myocarditis and myocardial dysfunction responded to immunoglobulin administration.

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Matvisiv, M. V. "Risk assessment of intrauterine infection in pregnant women with chronic hepatitis B." UKRAINIAN JOURNAL OF PERINATOLOGY AND PEDIATRICS, no. 3(87) (September 29, 2021): 12–16. http://dx.doi.org/10.15574/pp.2021.87.12.

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Purpose — to develop a method for predicting intrauterine fetal infection in pregnant women with CHB, infected and uninfected HIV, which provides the high accuracy of prognosis, is simple and accessible in practice and is achieved by analyzing multiple risk factors for mother-to-fetus transmission. Materials and methods. The course and consequences of pregnancy were analyzed in 211 women with chronic hepatitis B (CHB), not infected with HIV and in 18 — with CHB infected with HIV. The replicative activity of the virus and the activity of the inflammatory process in the liver were evaluated. We studied the dynamics of indicators depending on the trimester of pregnancy, the degree of immunosuppression caused by HIV. The frequency of risk factors was determined by «case-control» studies, and the frequency of identified risk factors was calculated in the groups of mothers in whom CHB was transmitted to the child and in those in which it did not occur. The degree of influence of individual risk factors was determined by the value of relative risk (RR), determined by their 95% confidence interval (95% CI), the reliability of the results (p) according to the Student's t-test. Differences at p<0.05 were considered probable. Results. It is established that risk factors that contribute to intrauterine infection of the fetus are: maternal — viral load HBV >105 copies/ml in the third trimester, HIV infection, immunosuppression caused by HIV (CD4+ Т-lymphocytes <500 cells/μL), low adherence to antiretroviral therapy, maternal bad habits; fetal — intrauterine growth restriction, fetal distress; obstetric — premature placental abruption, preterm delivery, placental dysfunction, prolonged anhydrous interval, prelabor rupture of membranes. In pregnant women with CHB, each risk factor was assessed in points depending on the RR: those factors whose relative risk was highest — 5 points, those whose score was lower — 4 and 3 points, respectively, and those whose score was the lowest — in 2 points. In order to predict the risk of fetal infection, a working prognostic chart with a score from 2 to 5 was developed. It was found that the risk of HBV infection in women with HIV-negative status is high with a score of 19–34, moderate — at 18–11, low — <10 points. In women with HIV-positive status — high risk of fetal intrauterine infection at a score of 24–46, moderate — at 13–23, low — <12 points. Conclusions. The use of the proposed prognostic map in the practice of medical institutions with a score of total risk factors for each pregnant woman will facilitate early prediction of fetal infection in pregnant women with CHB, taking into account their HIV status, which will allow to diagnose timely congenital infections and provides outpatient observation for these children. The research was carried out in accordance with the principles of the Helsinki declaration. The study protocol was approved by the Local ethics committee of all participating institution. The informed consent of the patient was obtained for conducting the studies. No conflict of interest was declared by the authors. Key words: pregnant women, chronic hepatitis B, co-HIV infection, risk factors for intrauterine infection of the fetus.

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Schwartz, David A. "Autopsy and Postmortem Studies Are Concordant: Pathology of Zika Virus Infection Is Neurotropic in Fetuses and Infants With Microcephaly Following Transplacental Transmission." Archives of Pathology & Laboratory Medicine 141, no. 1 (August 24, 2016): 68–72. http://dx.doi.org/10.5858/arpa.2016-0343-oa.

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Context.—Pathology studies have been important in concluding that Zika virus infection occurring in pregnant women can result in vertical transmission of the agent from mother to fetus. Fetal and infant autopsies have provided crucial direct evidence that Zika virus can infect an unborn child, resulting in microcephaly, other malformations, and, in some cases, death. Objective.—To better understand the etiologic role and mechanism(s) of Zika virus in causing birth defects such as microcephaly, this communication analyzes the spectrum of clinical and autopsy studies reported from fetuses and infants who developed intrauterine Zika virus infection, and compares these findings with experimental data related to Zika virus infection. Design.—Retrospective analysis of reported clinical, autopsy, pathology, and related postmortem studies from 9 fetuses and infants with intrauterine Zika virus infection and microcephaly. Results.—All fetuses and infants examined demonstrated an overlapping spectrum of gross and microscopic neuropathologic abnormalities. Direct cytopathic effects of infection by the Zika virus were confined to the brain; in cases where other organs were evaluated, no direct viral effects were identified. Conclusions.—There is concordance of the spectrum of brain damage, reinforcing previous data indicating that the Zika virus has a strong predilection for cells of the fetal central nervous system following vertical transmission. The occurrence of additional congenital abnormalities suggests that intrauterine brain damage from Zika virus interferes with normal fetal development, resulting in fetal akinesia. Experimental in vitro and in vivo studies of Zika virus infection corroborate the human autopsy findings of neural specificity.

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Heider, Amer. "Fetal Vascular Malperfusion." Archives of Pathology & Laboratory Medicine 141, no. 11 (November 1, 2017): 1484–89. http://dx.doi.org/10.5858/arpa.2017-0212-ra.

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Context.— Fetal vascular malperfusion, also known as fetal thrombotic vasculopathy, remains an underrecognized pathologic finding and should be noted during placental evaluation. Objective.— To review histologic findings, gain familiarity with the updated terminology, and to recognize important clinical associations with this entity. Data Sources.— University of Michigan cases, PubMed search, multiple review articles including recent placental workshop group consensus statement, and selected book chapters. Conclusions.— Multiple histologic patterns of fetal vascular malperfusion have been described including thrombosis, avascular villi, villous stromal-vascular karyorrhexis, intramural fibrin thrombi, and stem villous vascular obliteration. Various underlying etiologies can be involved in fetal vascular malperfusion. Cord lesions including abnormal insertion, length, and coiling are important causes. Maternal vascular malperfusion such as preeclampsia, hypercoagulable states, lupus anticoagulant, and sometimes diabetes have been associated with this condition. Fetal cardiac dysfunction/malformations and severe fetal inflammatory response in the setting of ascending intrauterine infection have also been attributed to this important finding. Fetal vascular malperfusion has been implicated in several significant and sometimes devastating clinical associations; these include intrauterine growth restriction, poor perinatal outcome, fetal demise, and neurodevelopmental sequelae. A diagnostic challenge may be encountered in cases with prior intrauterine fetal death, since degenerative changes post demise result in a similar histomorphologic picture. The diffuse versus the focal nature of the lesions may help in the distinction.

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Romero, R., and T. Chaiworapongsa. "Preterm Labor, Intrauterine Infection, and the Fetal Inflammatory Response Syndrome." NeoReviews 3, no. 5 (May 1, 2002): 73e—85. http://dx.doi.org/10.1542/neo.3-5-e73.

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Tolfvenstam, Thomas, Nikos Papadogiannakis, Oscar Norbeck, Karin Petersson, and Kristina Broliden. "Frequency of human parvovirus B19 infection in intrauterine fetal death." Lancet 357, no. 9267 (May 2001): 1494–97. http://dx.doi.org/10.1016/s0140-6736(00)04647-x.

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Huang, Qi-tao, Li-lin Hang, Mei Zhong, Yun-fei Gao, Man-ling Luo, and Yan-hong Yu. "Maternal HCV infection is associated with intrauterine fetal growth disturbance." Medicine 95, no. 35 (August 2016): e4777. http://dx.doi.org/10.1097/md.0000000000004777.

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Payne, Matthew S., Matthew W. Kemp, Suhas G. Kallapur, Paranthaman Senthamarai Kannan, Masatoshi Saito, Yuichiro Miura, John P. Newnham, et al. "Intrauterine Candida albicans infection elicits severe inflammation in fetal sheep." Pediatric Research 75, no. 6 (March 14, 2014): 716–22. http://dx.doi.org/10.1038/pr.2014.35.

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Maneenil, Gunlawadee, Matthew S. Payne, Paranthaman Senthamarai Kannan, Suhas G. Kallapur, Boris W. Kramer, John P. Newnham, Yuichiro Miura, Alan H. Jobe, and Matthew W. Kemp. "Fluconazole treatment of intrauterine Candida albicans infection in fetal sheep." Pediatric Research 77, no. 6 (March 11, 2015): 740–48. http://dx.doi.org/10.1038/pr.2015.48.

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43

Lockridge, Kristen. "Developmental susceptibility of fetal brain to intrauterine rhesus CMV infection." Journal of Clinical Virology 12, no. 2 (April 1999): 161. http://dx.doi.org/10.1016/s1386-6532(99)90520-6.

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McDuffie, R., M. Kunze, J. Barr, D. Wolf, C. Sze, R. Shikes, M. Sherman, and R. Gibbs. "409 Chronic intrauterine and fetal infection with G. vaginalis(GV)." American Journal of Obstetrics and Gynecology 185, no. 6 (December 2001): S192. http://dx.doi.org/10.1016/s0002-9378(01)80441-5.

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Wright, C., S. A. Hinchliffe, and C. Taylor. "Fetal pathology in intrauterine death due to parvovirus B19 infection." BJOG: An International Journal of Obstetrics and Gynaecology 103, no. 2 (February 1996): 133–36. http://dx.doi.org/10.1111/j.1471-0528.1996.tb09664.x.

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Leung, Wai-Ching. "Parvovirus B19 infection: association with third-trimester intrauterine fetal death." BJOG: An International Journal of Obstetrics and Gynaecology 107, no. 10 (October 2000): 1324. http://dx.doi.org/10.1111/j.1471-0528.2000.tb11634.x.

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Skjoldebrand-Sparre, Lottie, Thomas Tolfvenstam, Nikos Papadogiannakis, Britta Wahren, Kristina Broliden, and Margareta Nyman. "Parvovirus B19 infection: association with third-trimester intrauterine fetal death." BJOG: An International Journal of Obstetrics and Gynaecology 107, no. 4 (April 2000): 476–80. http://dx.doi.org/10.1111/j.1471-0528.2000.tb13265.x.

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Westover, Alana J., and Timothy JM Moss. "Effects of intrauterine infection or inflammation on fetal lung development." Clinical and Experimental Pharmacology and Physiology 39, no. 9 (August 28, 2012): 824–30. http://dx.doi.org/10.1111/j.1440-1681.2012.05742.x.

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von Chamier, Maria, Leticia Reyes, Linda F. Hayward, and Mary B. Brown. "Nicotine Induces Maternal and Fetal Inflammatory Responses Which Predispose Intrauterine Infection Risk in a Rat Model." Nicotine & Tobacco Research 23, no. 10 (April 24, 2021): 1763–70. http://dx.doi.org/10.1093/ntr/ntab080.

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Abstract Introduction Both smoking and infection adversely impact pregnancy. Previously, our group identified in a rodent model that 6 mg/kg/d nicotine increased the risk of fetal infection at gestation day (GD) 18. Here, we investigate lower nicotine doses. Methods Pregnant Sprague-Dawley rats received nicotine infusion at 0, 1, or 3 mg/kg/d (no, low-, and mid-dose nicotine, respectively) from GD 6, with intravenous inoculation with Mycoplasma pulmonis (MP) at 107 CFU (N = 20) or sterile broth (sham) (N = 11) on GD 14. Uterus and fetuses were retrieved on GD 18 for MP culture and histopathologic evaluation of maternal and fetal inflammatory responses (MIR and FIR). Results At 1 mg/kg/d nicotine, MP colonization rates were decreased, from 100% (9 of 9) to 40% (2 of 5) of MP-inoculated dams (p = .03), and 59% (66 of 111) to 39% (24 of 62) of fetuses (p = .01), versus no nicotine. Low-dose nicotine resulted in increased MIR and FIR in the sham-inoculated group; in the MP-inoculated group, this resulted in reduced relative risk (RR) for placental colonization (RR, 95% CI with high MIR = 0.14, 0.02 to 0.65; FIR = 0.38, 0.12 to 0.93). In contrast, 3 mg/kg/d nicotine treatment did not alter colonization rates; furthermore, FIR was completely suppressed, even in the face of placental or amniotic fluid colonization. Conclusion The 1 mg/kg/d nicotine dose decreased risk of intrauterine infection, with increased MIR and FIR. The 3 mg/kg/d nicotine dose inhibited FIR, and increased risk for intrauterine infection. Nicotine alterations of the intrauterine environment were markedly dose-dependent. Implications Nicotine exposure alters intrauterine infection and inflammation in a dose-dependent manner, potentially impacting fetal development and programming. Previous work in a rodent model showed that high-dose nicotine (6 mg/kg/d) exposure exacerbated intrauterine infection during pregnancy. The current study found that low-dose nicotine (1 mg/kg/d) exposure reduced colonization of placenta and amniotic fluid; this decrease was associated with increased intrauterine inflammation. Exposure to mid-dose nicotine (3 mg/kg/d) suppressed fetal inflammation. Elucidation of underlying mechanisms of these phenomena will inform public health and clinical care decisions, particularly in the context of risk assessment of nicotine replacement therapy during pregnancy for smoking cessation.

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Oshiro, Bryan T., Jack M. Graham, Jorge D. Blanco, Ibrahim M. Seraj, and Karen D. Bishop. "Pregnancy Outcome in Swiss-Webster Mice Infected WithChlamydia trachomatis." Infectious Diseases in Obstetrics and Gynecology 1, no. 5 (1994): 242–45. http://dx.doi.org/10.1155/s1064744994000165.

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Objective:The objective of this study was to observe pregnancy outcomes in mice infected transvaginally withChlamydia trachomatis.Methods:Pregnant mice were inoculated transvaginally with eitherC. trachomatis(CT) or sterile calf serum (CON) on pregnancy day 4. Pregnancy outcomes as well as genital tract histology and culture were compared. Statistical analysis was performed using Fisher's exact test and Student's t-test.Results:Twenty-four of 26 CT mice had positive uterine cultures forC. trachomatis.Inflammation occurred in 9 (34.6%) (P= 0.002, 95% confidence interval = 1.7–3.5) and intrauterine fetal demise occurred in 5 (19.2%) (P= 0.05, 95% confidence interval = 1.6–2.9) of CT mice. No mice in the CON group (0/24) had positive uterine cultures, developed inflammation, or experienced intrauterine fetal demise.Conclusions:Lower genital tract chlamydial infection is associated with intrauterine fetal demise in Swiss-Webster mice.

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