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Intrauterine Infection (intrauterine + infection)

Distribution by Scientific Domains

Medical Sciences	92%

Selected Abstracts

Maternal Death Following Cardiopulmonary Collapse After Delivery: Amniotic Fluid Embolism or Septic Shock Due to Intrauterine Infection?

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2010
Roberto Romero
Citation Romero R, Kadar N, Vaisbuch E, Hassan SS. Maternal death following cardiopulmonary collapse after delivery: amniotic fluid embolism or septic shock due to intrauterine infection? Am J Reprod Immunol 2010; 64: 113,125 Problem, The amniotic fluid embolism (AFE) syndrome is a catastrophic complication of pregnancy frequently associated with maternal death. The causes and mechanisms of disease responsible for this syndrome remain elusive. Method of study, We report two cases of maternal deaths attributed to AFE: (1) one woman presented with spontaneous labor at term, developed intrapartum fever, and after delivery had sudden cardiovascular collapse and disseminated intravascular coagulation (DIC), leading to death; (2) another woman presented with preterm labor and foul-smelling amniotic fluid, underwent a Cesarean section for fetal distress, and also had postpartum cardiovascular collapse and DIC, leading to death. Results, Of major importance is that in both cases, the maternal plasma concentration of tumor necrosis factor-, at the time of admission to the hospital and when patients had no clinical evidence of infection was in the lethal range (a lethal range is considered to be above 0.1 ng/mL). Conclusion, We propose that subclinical intraamniotic infection may be a cause of postpartum cardiovascular collapse and DIC and resemble AFE. Thus, some patients with the clinical diagnosis of AFE may have infection/systemic inflammation as a mechanism of disease. These observations have implications for the understanding of the mechanisms of disease of patients who develop cardiovascular collapse and DIC, frequently attributed to AFE. It may be possible to identify a subset of patients who have biochemical and immunological evidence of systemic inflammation at the time of admission, and before a catastrophic event occurs. [source]

Risk factors and mechanism of transplacental transmission of hepatitis B virus: A case-control study

JOURNAL OF MEDICAL VIROLOGY, Issue 1 2002
De-Zhong Xu
Abstract Intrauterine hepatitis B virus (HBV) infection has been suggested to be caused by transplacental transmission that cannot be blocked by hepatitis B vaccine. This would decrease the effectiveness of hepatitis B vaccine. This study examined the risk factors and mechanism of transplacental HBV transmission. A case-control study included 402 newborn infants from 402 HBsAg-positive pregnant women. Among these, 15 newborn infants infected with HBV by intrauterine transmission were selected as cases, and the rest as controls. A pathology study included 101 full-term placentas from the HBsAg-positive pregnant women above and 14 from HBsAg-negative pregnant women. Immunohistochemistry staining and HBV DNA in situ hybridization were used to estimate the association of intrauterine HBV infection and HBV infection in the placentas. HBeAg positivity in mothers' sera (OR,=,17.07, 95%CI 3.39,86.01) and threatened preterm labor (OR,=,5.44, 95%CI 1.15,25.67) were found to be associated with transplacental HBV transmission. The intrauterine infection rate increased linearly and significantly with maternal serum HBsAg titers (trend test P,=,0.0117) and HBV DNA concentration (trend test P,<,0.01). Results of the pathology study showed that HBV infection rates decreased gradually from the maternal side to the fetal side (trend test P,=,0.0009) in the placental cell layers. There was a significant association between intrauterine HBV transmission and HBV infection in villous capillary endothelial cells (VCEC) in the placenta (OR,=,18.46, P,=,0.0002). The main risk factors for intrauterine HBV infection are maternal serum HBeAg positivity, history of threatened preterm labor, and HBV in the placenta especially the villous capillary endothelial cells. Previous reports of transplacental leakage of maternal blood causing intrauterine infection are confirmed. In addition, there appears to be a "cellular transfer" of HBV from cell to cell in the placenta causing intrauterine infection. This latter hypothesis needs to be confirmed. J. Med. Virol. 67:20,26, 2002. © 2002 Wiley-Liss, Inc. [source]

Symptomatic infant characteristics of congenital cytomegalovirus disease in Australia

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 8 2005
Sian C Munro
Background: Human cytomegalovirus (CMV) is the most common cause of viral intrauterine infection. In utero transmission can occur during primary maternal infection, reactivation or reinfection of seropositive mothers. Objective: To describe the aetiology and clinical features of infants diagnosed with congenital CMV and to document maternal factors that were presented. Methods: Active national surveillance was initiated in 1999 in collaboration with the Australian Paediatric Surveillance Unit. Results: Monthly notifications resulted in 70 cases of congenital CMV being identified between 1999 and 2003. Nearly all of the cases were symptomatic with the most common clinical sequelae reported in infected infants being jaundice, thrombocytopaenia, hepatomegaly, petechiae, purpura and splenomegaly. Almost half (43.5%) of the infants had central nervous system (CNS) complications, such as microcephaly, chorioretinitis, sensorineural hearing loss, intracranial calcifications, developmental delay or seizures, with over half presenting two or more CNS abnormalities. Maternal febrile illness was noted in 54.8% of the cases. The majority of mothers were primiparous (46.4%) or secundiparous (39.3%), indicating two different population groups at risk of primary CMV infection. Conclusion: This study documents symptomatic congenital CMV cases in Australia. [source]

Periventricular leukomalacia, inflammation and white matter lesions within the developing nervous system

NEUROPATHOLOGY, Issue 3 2002
Payam Rezaie
Periventricular leukomalacia (PVL) occurring in premature infants, represents a major precursor for neurological and intellectual impairment, and cerebral palsy in later life. The disorder is characterized by multifocal areas of necrosis found deep in the cortical white matter, which are often symmetrical and occur adjacent to the lateral ventricles. There is no known cure for PVL. Factors predisposing to PVL include birth trauma, asphyxia and respiratory failure, cardiopulmonary defects, premature birth/low birthweight, associated immature cerebrovascular development and lack of appropriate autoregulation of cerebral blood flow in response to hypoxic-ischemic insults. The intrinsic vulnerability of oligodendrocyte precursors is considered as central to the pathogenesis of PVL. These cells are susceptible to a variety of injurious stimuli including free radicals and excitotoxicity induced by hypoxic-ischemic injury (resulting from cerebral hypoperfusion), lack of trophic stimuli, as well as secondary associated events involving microglial and astrocytic activation and the release of pro-inflammatory cytokines TNF-, and IL-6. It is yet unclear whether activated astrocytes and microglia act as principal participants in the development of PVL lesions, or whether they are representatives of an incidental pathological response directed towards repair of tissue injury in PVL. Nevertheless, the accumulated evidence points to a pathological contribution of microglia towards damage. The topography of lesions in PVL most likely reflects a combination of the relatively immature cerebrovasculature together with a failure in perfusion and/or hypoxia during the greatest period of vulnerability occurring around mid-to-late gestation. Mechanisms underlying the pathogenesis of PVL have so far been related to prenatal ischemic injury to the brain initiated within the third trimester, which result in global cognitive and developmental delay and motor disturbances. Over the past few years, several epidemiological and experimental studies have implicated intrauterine infection and chorioamnionitis as causative in the pathogenesis of PVL. In particular, recent investigations have shown that inflammatory responses in the fetus and neonate can contribute towards neonatal brain injury and development-related disabilities including cerebral palsy. This review presents current concepts on the pathogenesis of PVL and emphasizes the increasing evidence for an inflammatory pathogenic component to this disorder, either resulting from hypoxic-ischemic injury or from infection. These findings provide the basis for clinical approaches targeted at protecting the premature brain from inflammatory damage, which may prove beneficial for treating PVL, if identified early in pathogenesis. [source]

Lymphoid bronchiolitis presenting at birth in an immunocompetent child: Chronic interstitial lung disease of unknown aetiology

PEDIATRIC PULMONOLOGY, Issue 6 2009
Malcolm Brodlie MB ChB
Abstract A female infant presented at birth with respiratory distress, which was subsequently shown to be secondary to lymphoid bronchiolitis, an exceptionally rare condition in childhood. Over the following 13 years there has been a slow progressive deterioration in her respiratory status with forced expiratory volume in 1 sec currently 40% predicted. Tests for connective tissue disease, infection, or immunodeficiency have all been negative and in the absence of any other explanation we postulate that this severe problem may have occurred as a consequence of an unrecognized intrauterine infection. Pediatr Pulmonol. 2009; 44:622,624. © 2009 Wiley-Liss, Inc. [source]

Bacteriological Findings and Hormonal Profiles in the Postpartum Balady Goats

REPRODUCTION IN DOMESTIC ANIMALS, Issue 1 2006
M M Ababneh
Contents Twenty-six Balady goats categorized according to parity into primiparous and pluriparous goats were used to investigate bacterial flora of the genital tract and hormonal profiles during the postpartum (PP) period. Escherichia coli and Staphylococcus aureus were isolated in pure or mixed culture from the uterus. Arcanobacterium pyogenes was isolated from swabs obtained from the vagina and cervix of one primiparous goat. Uteri and cervices but not vaginas were free of bacterial contamination by day 10 PP except for one pluriparous goat with scanty E. coli contamination on day 25 PP. Fluctuating oestradiol 17, (E2) levels demonstrated resumption of follicular activity as early as day 13 PP in both parity groups. Progesterone (P4) levels remained low at basal levels throughout the study period. Higher concentrations of 15-keto-13,14-dihydroprostaglandin F2, (PGFM) were observed during the first week PP compared with the rest of the PP period. PGFM concentrations dropped to low basal level by day 10 PP and remained constantly low throughout the study period. P4, E2 and PGFM profiles were not different between the different parity groups. In conclusion, intrauterine infection is not common in goats with normal kidding. E. coli was the most common intrauterine bacterial isolate. E2 and P4 profiles were consistent with resumption of follicular growth but not ovulation. High PGFM concentrations coincided with the fast regression phase of uterine involution. Hormonal profile and bacterial contamination and clearance were similar to those reported in other related species and not related to parity. [source]

Maternal Death Following Cardiopulmonary Collapse After Delivery: Amniotic Fluid Embolism or Septic Shock Due to Intrauterine Infection?

Placental Lesions Caused by Experimental Infection of Sprague,Dawley Rats with Mycoplasma Pulmonis

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2003
Morgan R. Peltier
Problem: Sprague,Dawley (SD) rats infected during pregnancy with Mycoplasma pulmonis display adverse pregnancy outcomes that are similar to those observed in women with chorioamnionitis and may provide a good model system for this disease. The placental lesions caused by this microorganism, however, have not been thoroughly characterized. Method of study: Rats were infected with 107 colony-forming units (CFU) M. pulmonis or vehicle control on gestation day (gd) 14 and were euthanized on gd 16,18. Tissues were fixed in 10% neutral buffered formalin, embedded in paraffin, sectioned at 4 ,m, and stained with hematoxylin and eosin (H & E). The slides were coded and examined by a blinded pathologist using light microscopy. Results: Infection with M. pulmonis was associated with necrosis of trophoblast giant cells at gd 18. Significantly more neutrophils were observed in the decidual region of the apex of the placenta in M. pulmonis infected animals. The vast majority of neutrophils, however, were observed in the decidua in the lateral regions of the placenta and in the adjacent endometrium. Conclusions: Infection of SD rats with M. pulmonis resulted in histological placentitis similar to that described in deciduitis of humans and represents a good model system for investigations into the pathophysiology of intrauterine infection. The influx of neutrophils seems to migrate from the endometrium towards the lateral regions of the placenta near Reichert's membrane and the divergence of the parietal yolk sac. [source]

Fetal Endothelial Cells Express Vascular Cell Adhesion Molecule in the Setting of Chorioamnionitis

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2000
CATHERINE M. CRAVEN
PROBLEM: In intrauterine infection, inflammatory mediators may be released into the fetal circulation prior to fetal infection. We hypothesize that, in chorioamnionitis, inflammation alters fetal blood vessels. To test this, fetal endothelial cells were examined for vascular cell adhesion molecule (VCAM). METHOD OF STUDY: Umbilical cords (n=9) from placentas with chorioamnionitis were immunostained for VCAM. Controls from preterm preeclamptic pregnancies (n=7) without histologic inflammation were selected, and matched for gestational age and method of delivery. VCAM sections were reviewed by a pathologist blinded to clinical diagnoses. RESULTS: All endothelial cells from each of the nine cords from placentas with chorioamnionitis had strong VCAM staining. Two of nine samples also had acute cord vasculitis. No cord endothelial cells from preeclamptic placentas demonstrated similar VCAM staining (p<0.01). CONCLUSION: Histologic chorioamnionitis was associated with VCAM expression of the umbilical cord vessels. In chorioamnionitis, inflammatory mediators may have entered the fetal circulation to activate endothelial cells. Intrauterine inflammation was not restricted to the chorioamnion, but also involved the fetal circulation. [source]

Preterm premature rupture of membranes: diagnosis, evaluation and management strategies

BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 2005
Hyagriv N. Simhan
Preterm premature rupture of the membranes (PPROM) is responsible for one-third of all preterm births and affects 120,000 pregnancies in the United States each year. Effective treatment relies on accurate diagnosis and is gestational age dependent. The diagnosis of PPROM is made by a combination of clinical suspicion, patient history and some simple tests. PPROM is associated with significant maternal and neonatal morbidity and mortality from infection, umbilical cord compression, placental abruption and preterm birth. Subclinical intrauterine infection has been implicated as a major aetiological factor in the pathogenesis and subsequent maternal and neonatal morbidity associated with PPROM. The frequency of positive cultures obtained by transabdominal amniocentesis at the time of presentation with PPROM in the absence of labour is 25,40%. The majority of amniotic fluid infection in the setting of PPROM does not produce the signs and symptoms traditionally used as diagnostic criteria for clinical chorioamnionitis. Any evidence of infection by amniocentesis should be considered carefully as an indication for delivery. Documentation of amniotic fluid infection in women who present with PPROM enables us to triage our therapeutic decision making rationally. In PPROM, the optimal interval for delivery occurs when the risks of immaturity are outweighed by the risks of pregnancy prolongation (infection, abruption and cord accident). Lung maturity assessment may be a useful guide when planning delivery in the 32- to 34-week interval. A gestational age approach to therapy is important and should be adjusted for each hospital's neonatal intensive care unit. Antenatal antibiotics and corticosteroid therapies have clear benefits and should be offered to all women without contraindications. During conservative management, women should be monitored closely for placental abruption, infection, labour and a non-reassuring fetal status. Women with PPROM after 32 weeks of gestation should be considered for delivery, and after 34 weeks the benefits of delivery clearly outweigh the risks. [source]

Nifedipine trials: effectiveness and safety aspects

BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 2005
Herman P. van Geijn
Nifedipine (Adalat) is marketed as an anti-hypertensive agent. Nifedipine inhibits voltage-dependent L-type calcium channels, which leads to vascular (and other) smooth muscle relaxation and negative inotropic and chronotropic effects on the heart. Vasodilation, followed by a baroreceptor-mediated increase in sympathetic tone then results in indirect cardiostimulation. Nifedipine was introduced as a tocolytic agent at a time when ,-agonists and magnesium sulphate dominated the arena for the prevention of preterm birth. The oral administration route, the availability of immediate and slow-release preparations, the low incidence of (mild) side effects, and its limited costs explain the attraction to this medication from the obstetric field and its rapid and widespread distribution. Currently, over 40 studies have been published on nifedipine's tocolytic effectiveness, including seven meta-analyses. The quality of the studies suffers particularly from performance bias because the majority of them failed to ensure adequate blinding to treatment both for providers and patients. Concerns about other methodological flaws include measurements, outcome assessment and attrition bias. In particular, the safety aspects of nifedipine for tocolysis have been underassessed. Conclusions from the meta-analyses, favouring the use of nifedipine as a tocolytic agent, are not supported by close examination of the data. The tocolytic effectiveness and ,safety' of nifedipine has been studied primarily in normal pregnancies. Based on its pharmacological properties, one should be cautious to administer nifedipine when the maternal cardiovascular condition is compromised, such as with intrauterine infection, twin pregnancy, maternal hypertension, cardiac disease, etc. Life-threatening pulmonary oedema and/or cardiac failure are definite risks and have been reported. Under such circumstances, the baroreceptor-mediated increase in sympathetic tone may not balance the cardiac-depressant activity of nifedipine. [source]

The role of infection in preterm labour

BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 2003
Klaus Friese
Although there are many maternal characteristics associated with preterm birth, the aetiology in most cases is poorly understood. Our research demonstrates that multiple risk factors, such as maternal age and especially infection, are associated with preterm birth. Bacterial vaginosis and intrauterine infection are now believed to be an important risk factor for preterm delivery. [source]

Subacute sclerosing panencephalitis after intrauterine infection

ACTA PAEDIATRICA, Issue 9 2004
M Dasopoulou
Subacute sclerosing panencephalitis (SSPE), in the majority of cases, is caused by the wild measles virus, although there are some reports relating SSPE to vaccination. This paper presents an inborn that was infected during pregnancy by the measles virus and developed SSPE within the first year of life after a short incubation period. He progressed rapidly after a mild arrest with treatment. Subacute sclerosing panencephalitis is a fatal degenerative disease and, although it had largely disappeared because of nearly universal measles vaccination, it still remains a serious infection among children affected by human immunodeficiency virus (HIV). The lack of newer cases of SSPE occurring among normal children nowadays should not wane alertness by obstetricians and paediatricians, to recognize the risk with measles during pregnancy and the need for prevention and recognition of SSPE at an early stage. Although some references exist which report on SSPE cases related to vaccination, new work weakens the possible links between measles vaccine and SSPE. Conclusion: This report would like to stress the importance and success of reducing the SSPE problem with the aid of general measles vaccination with high coverage. [source]

Effect of maternal antibiotic treatment on fetal periventricular white matter cell death in a rabbit intrauterine infection model

ACTA PAEDIATRICA, Issue 1 2003
T Debillon
Aim: To evaluate the effects of maternal antibiotic treatment on fetal brain cell death in a rabbit intrauterine infection model. Methods: After Escherichia coli uterine-horn inoculation in 22 pregnant rabbits, followed at various times by ceftriaxone and caesarean section, cell death in white matter (histology and fragmented DNA staining) from fetuses killed at extraction was compared across groups using the Mantel-Haenszel test and Fisher's exact test for small numbers. Results: White matter cell death was consistently present at 48 h, with ceftriaxone initiation at 24 h (group 1), detectable at 84 but not 60 h, with ceftriaxone initiation at 12 h, and significantly reduced at 84 h with ceftriaxone initiation at 6 h (60% vs 100% in group 1, p < 0.001, Fisher's exact test). Conclusion: Early maternal antibiotic therapy delays white matter cell death in rabbit fetuses exposed to intrauterine infection. This may provide a window for preventing white matter damage. [source]