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Transplacental Transmission (transplacental + transmission)
Selected AbstractsDetection of cytomegalovirus, parvovirus B19 and herpes simplex viruses in cases of intrauterine fetal death: Association with pathological findingsJOURNAL OF MEDICAL VIROLOGY, Issue 10 2008Garyfallia Syridou Abstract There are previous indications that transplacental transmission of cytomegalovirus (CMV), parvovirus B19 (PB19) and herpes simplex virus types 1 and 2 (HSV-1/2) cause fetal infections, which may lead to fetal death. In a prospective case,control study we examined the incidence of these viruses in intrauterine fetal death and their association with fetal and placenta pathological findings. Molecular assays were performed on placenta tissue extracts of 62 fetal deaths and 35 controls for the detection of CMV, PB19 and HSV-1/2 genomes. Formalin-fixed, paraffin-embedded liver, spleen and placenta tissues of fetal death cases were evaluated histologically. Thirty-four percent of placental specimens taken from intrauterine fetal deaths were positive for any of the three viruses (16%, 13%, and 5% positive for CMV, PB19, and HSV-1/2, respectively), whereas only 6% of those taken from full term newborns were positive (P,=,0.0017). No dual infection was observed. This difference was also observed when fetal deaths with a gestational age <20 weeks or a gestational age >20 weeks were compared with the controls (P,=,0.025 and P,=,0.0012, respectively). Intrauterine death and the control groups differed in the detection rate of CMV DNA (16% and 3%, respectively; P,=,0.047), which was more pronounced in a gestational age >20 weeks (P,=,0.03). Examination of the pathological findings among the PCR-positive and PCR-negative fetal deaths revealed that hydrops fetalis and chronic villitis were more common among the former group (P,=,0.0003 and P,=,0.0005, respectively). In conclusion, an association was detected between viral infection and fetal death, which was more pronounced in the advanced gestational age. Fetal hydrops and chronic villitis were evidently associated with viral DNA detection in cases of intrauterine death. J. Med. Virol. 80:1776,1782, 2008. © 2008 Wiley-Liss, Inc. [source] Risk factors and mechanism of transplacental transmission of hepatitis B virus: A case-control studyJOURNAL OF MEDICAL VIROLOGY, Issue 1 2002De-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] Protecting babies: vaccine strategies to prevent foetopathy in Neospora caninum -infected cattlePARASITE IMMUNOLOGY, Issue 3 2006Review Article SUMMARY Neospora caninum is an apicomplexan protozoan parasite that is a significant infectious abortifacient agent in cattle. Despite the fact that it is a member of a well described taxonomic group, it is a relatively newly discovered parasite and its biology is not yet fully understood. Cattle become infected either congenitally via transplacental transmission or post-natally by ingesting oocysts derived from the definitive host; dogs and coyotes are the only definitive hosts that have been described to date. It is not known which of these two forms of transmission occurs most frequently and which is the most likely to result in abortion; there are no drugs available to treat infected cattle, so current control strategies rely on prevention of infection by management methods and strict hygiene; an effective vaccine would be a great advantage in its control. Neospora caninum is an economically important veterinary pathogen, but we can also draw analogies between its foetopathic effects and those of human pathogens such as Toxoplasma gondii, Chlamydophila abortus and Plasmodium falciparum. Understanding the immune response and the materno,foetal relationship in N. caninum -infected cattle may help us to design vaccination strategies, not only for neosporosis but also for other foetopathic agents. [source] Immunological response to cytomegalovirus in congenitally infected neonatesCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2007J. Hassan Summary Cytomegalovirus (CMV) is the most common cause of congenital infection worldwide and occurs as a result of transplacental transmission of the virus. The human neonate is highly susceptible to infection due to a combination of immaturity of the immune system and antigenic inexperience. This study uses the in vivo model of congenital CMV to examine both the humoral and cell-mediated immune responses in vertically infected neonates and their mothers. Ten pairs of matched neonates and their mothers were evaluated for specific IgM responses to three immunodominant CMV antigens: pp38 (pUL80a), pp52 (pUL44) and pp150 (pUL32). In contrast to conventional enzyme immunoassay (EIA) testing for CMV-specific IgM, which found five of the mothers and four of the neonates to be positive, Western immunoblotting showed all 10 adults and nine newborns to be positive. Eight mothers and nine newborns had serological evidence of primary infection. All neonates showed a response to pp38, an assembly protein, nine responded to the pp52 immediate early antigen but only four had reactivity to the pp150 tegument associated protein. Of the mothers, eight had pp38 reactivity, 10 showed a response to the pp52 antigen and seven to the pp150 antigen. T cell-mediated immunity was assessed by measuring cytokines using a multiplex microarray assay. Levels of interferon (IFN)-, were high in both groups [mean ± standard error of the mean (s.e.m.): neonates = 657 ± 238 pg/ml, mothers = 1072 ± 677 pg/ml, pNS]; however, neonates had significantly higher levels of interleukin (IL)-8 (316 ± 136 pg/ml versus 48 ± 28 pg/ml, P < 0·005). Similar levels of IL-2, IL-7, IL-10 and IL-12 were measured in both groups, but levels of IL-1,, IL-1,, IL-4, IL-6 and tumour necrosis factor (TNF)-, were either absent or low. In response to CMV, neonates and adults mount a predominant T helper 1 (Th1) response, as evidenced by the presence of IL-2, IL-8, IL-12 and IFN-, with concomitant lack of IL-4. These findings suggest that the neonate, when presented with infection in utero, is capable of mounting an individual response; however, the lower IFN-, and higher IL-8 levels suggest reduced immune responsiveness when compared to their adult counterparts. [source] | ||||||||||