Placental infection with Chlamydia pneumoniae and intrauterine growth restriction.
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BACKGROUND: The concept that low birth weight infants are more predisposed to coronary artery disease (CAD) in adulthood has been studied extensively. Although many infectious agents have been associated with intrauterine growth restriction (IUGR), Chlamydia pneumoniae an organism implicated in CAD has not been investigated. It was our aim to assess whether C. pneumoniae DNA is present in placental tissue and whether its detection is associated with IUGR. METHODS: Fifty-nine pregnant women were studied: 32 women had an uncomplicated pregnancy with no antenatal or post-natal evidence of IUGR. Twenty-seven women had pregnancies with ultrasonographically demonstrated IUGR, defined as foetal abdominal circumference measuring less than 2 S.D.s from the mean for gestational age. At the time of delivery, maternal blood and placental tissue samples were obtained. Placental samples were taken from four sites centrally and peripherally on the maternal and foetal side of the placentas and tested by nested polymerase chain reaction for C. pneumoniae DNA. IgG antibodies to C. pneumoniae were measured using microimmunfluorescence. RESULTS: C. pneumoniae DNA was detected in 44% of the placental tissue but there was no difference in the prevalence of bacterial DNA between the control and the low birth weight group (P=0.58). Additionally C. pneumoniae seropositivity did not differ between the index and control groups (78 vs. 70%, P=0.44). CONCLUSIONS: C. pneumoniae is present in placental tissue. Its presence however does not correlate with IUGR. Similarly, maternal C. pneumoniae seropositivity is not related to low birth weight. Thus C. pneumoniae infection is unlikely to play a role in the pathogenesis of IUGR. (+info)
Abortive potency of Chlamydophila abortus in pregnant mice is not directly correlated with placental and fetal colonization levels.
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Abortion, placental and fetal colonization, and levels of gamma interferon were analyzed for four Chlamydophila abortus strains presenting antigenic variations in a mouse model. Expression of virulence of these strains varied and indicated that abortion was not directly related to the number of bacteria in the placenta, and thus, other factors may have an important role in activating the abortion process. (+info)
Placental malaria and perinatal transmission of human immunodeficiency virus type 1.
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Prevalence of placental malaria in human immunodeficiency virus (HIV) type 1-infected and -uninfected women and the effect of placental malaria on genital shedding and perinatal transmission of HIV-1 were examined. Genital samples for HIV-1 DNA RNA were collected during labor. Infants were tested for HIV-1 at 1 day and 6 weeks postpartum. Placental malaria was diagnosed by histopathological examination: 372 placentas of HIV-1-infected women and 277 of HIV-1-uninfected women were processed. A higher prevalence of placental malaria was seen in HIV-1-infected women. No association was found between placental malaria and either maternal virus load, genital HIV-1 DNA, or HIV-1 RNA. Placental malaria did not correlate with in utero or peripartal transmission of HIV-1. (+info)
Clumsiness and disturbed cerebellar development: insights from animal experiments.
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Cerebellar functioning has been implied in the fine adjustments of muscle tone, in the coordination and the feed-forward control of movements and posture, as well as in the establishment and performance of motor skills. The cerebellar cortex in mammals develops late in neuro-ontogeny and an extrapolation from experimental results indicates that in the human the proliferation of the granule cells and the development of circuitry in the cerebellar cortex starts only in the last trimester of pregnancy and lasts until beyond the first birthday. This late development makes the cerebellar development particularly vulnerable to situations like an insufficient supply of nutrients, which may follow placental dysfunction, or to side effects of pharmacological treatments like the administration of corticosteroids in the postnatal period. We studied whether such situations might also lead to motor impairments. In rats, the effects of undernutrition during the brain growth spurt were investigated as well as those of corticosteroids administered in a period that is analogous to the 7th to 8th month of pregnancy in the human. Both these interferences affect cerebellar development and our results in rats indicate that they also lead to retardations in the emergence of certain reflexes, as well as to longer lasting motor impairments during locomotion. Extrapolation of these results strongly suggests that a disturbed cerebellar development should be considered as an important etiological factor in clumsiness in human children. (+info)
Human cytomegalovirus transmission from the uterus to the placenta correlates with the presence of pathogenic bacteria and maternal immunity.
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Prenatal cytomegalovirus infection may cause pregnancy complications such as intrauterine growth restriction and birth defects. How virus from the mother traverses the placenta is unknown. PCR analysis of biopsy specimens of the maternal-fetal interface revealed that DNA sequences from cytomegalovirus were commonly found with those of herpes simplex viruses and pathogenic bacteria. Cytomegalovirus DNA and infected cell proteins were found more often in the decidua than in the placenta, suggesting that the uterus functions as a reservoir for infection. In women with low neutralizing titers, cytomegalovirus replicated in diverse decidual cells and placental trophoblasts and capillaries. In women with intermediate to high neutralizing titers, decidual infection was suppressed and the placenta was spared. Overall, cytomegalovirus virions and maternal immunoglobulin G were detected in syncytiotrophoblasts, villus core macrophages, and dendritic cells. These results suggest that the outcome of cytomegalovirus infection depends on the presence of other pathogens and coordinated immune responses to viral replication at the maternal-fetal interface. (+info)
Antibodies to variant surface antigens of Plasmodium falciparum-infected erythrocytes and adhesion inhibitory antibodies are associated with placental malaria and have overlapping and distinct targets.
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We measured antibodies to chondroitin sulfate A (CSA)-binding and placental Plasmodium falciparum-infected red blood cells (PRBCs) among pregnant women with or without placental malaria. Immunoglobulin G to PRBC surface antigens was rare in uninfected primigravidae (3.7%), more prevalent in infected primigravidae (70%; P<.001), and common in infected (77%) and uninfected (83%) multigravidae. Similar patterns were seen for agglutinating antibodies, and antibodies were similar among women with past or active placental infection. PRBC adhesion to CSA was inhibited 60% by serum from infected primigravidae but 24% by serum from uninfected primigravidae (P=.025), whereas infection did not alter adhesion inhibition by multigravidae (77% inhibition)[corrected]. There was substantial heterogeneity in antibody type and levels. Antibodies did not correlate with parasite density or pregnancy outcome. Comparisons between antibodies suggest that adhesion-inhibitory antibodies and those to PRBC variant antigens have distinct and overlapping epitopes, may be acquired independently, and have different roles in immunity. (+info)
Clinical management of thrombophilia-related placental vascular complications.
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Pregnancy is a hypercoagulable state with an increased thrombotic risk throughout gestation and the postpartum period. Women with thrombophilia may have a further increased risk of placental vascular complications, including pregnancy loss, preeclampsia, intrauterine growth restriction, and placental abruption. Preliminary data suggest that maternal antithrombotic prophylaxis may result in improved gestational outcome. Randomized trials are under way and hopefully will optimize maternal and neonatal outcome. (+info)
Vasa previa diagnosis and management.
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INTRODUCTION: Vasa previa is an uncommon obstetrical complication that poses a high risk of fetal demise if not recognized before rupture of membranes. It is vital that providers recognize risk factors for vasa previa and diagnose this condition before the onset of labor so that fetal shock or demise is prevented. METHODS: We report a patient with a bilobed placenta and perinatal hemorrhage caused by vasa previa that was not detected with antepartum ultrasound. A review of the literature published between January 1965 and August 2002 was conducted using a MEDLINE-assisted search using the key words "vasa previa," "bilobed placenta," and "succenturiate." RESULTS: Risk factors for vasa previa have been identified. Advances in ultrasound have led to improved ability to diagnose this condition. Evaluation of patients in high-risk groups with transvaginal color flow Doppler ultrasound should be considered. The accuracy of this technique for diagnosing vasa previa is not known, nor is the true incidence of this condition. Antepartum diagnosis is associated with improved outcomes but does not eliminate morbidity and mortality. CONCLUSIONS: A high index of suspicion for vasa previa at the time of amniotomy is required, because all cases cannot be diagnosed before the onset of labor. (+info)