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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of pregnant women with Toxoplasma gondii places the developing fetus at risk for congenital infection. We report a prospective study of 43 documented cases of acute maternal Toxoplasma infections acquired during gestation in which the polymerase chain reaction (PCR) was evaluated for diagnosis of fetal infection and compared with the current standard methods. On the basis of direct lysis of pelleted amniotic fluid cells followed by amplification of a gene sequence specific for T. gondii, PCR correctly identified the presence of T. gondii in five of five samples of amniotic fluid from four proven cases of congenital infection. PCR also detected three of five positive cases from a nonprospective group. The two diagnostic methods of comparable speed, detection of specific immunoglobulin M from fetal blood and and inoculation of amniotic fluid into tissue culture, correctly identified only 3 and 4 of the 10 positive samples, respectively. The considerably more time-consuming methods of mouse inoculation of amniotic fluid and fetal blood both detected 7 of 10 positive samples. There were no false-positive diagnoses by any of the methods. Therefore, detection of T. gondii by PCR appears to be the most promising method for prenatal diagnosis of congenital Toxoplasma infection, since it is both extremely rapid and highly sensitive.
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PMID:Rapid prenatal diagnosis of congenital Toxoplasma infection by using polymerase chain reaction and amniotic fluid. 222 55

Transmission of mouse hepatitis virus (MHV) in utero following oronasal inoculation of pregnant mice was found to depend upon MHV strain and host genotype. Virulent, polytropic MHV-JHM was recovered from multiple maternal tissues, including liver and uterus, as well as placenta and fetus in susceptible BALB/cByJ mice. Fetuses were infected during all 3 trimesters of pregnancy. Low virulence, polytropic MHV-S infected fetuses in a low percentage of susceptible BALB/cByJ dams. Infection of resistant CD-1 mice with MHV-JHM was limited, with no fetal infection. Enterotropic MHV-Y was largely restricted to intestine of BALB/cByJ and CD-1 dams, with minimal dissemination and no fetal infection. Maternally-derived MHV IgG antibody was detectable in pup sera through 4 weeks of age. Antibody titers were generally lower in second litters of the same dam. Cross-fostering experiments showed that antibody was transferred via colostrum and not in utero, and that pups were capable of absorption through 2 weeks of age. Pups nursing immune dams were protected against MHV challenge at 1 and 2 weeks of age, compared to pups nursing naive dams. Immunity to MHV challenge was cross-protective against both antigenically homotypic and heterotypic strains of MHV.
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PMID:Mouse hepatitis virus and host determinants of vertical transmission and maternally-derived passive immunity in mice. 284 Aug 71

Fetal and neonatal infections can occur at different times during pregnancy, from conception to birth. Infections that take place near the time of conception often destroy the zygote or embryo and only rarely leave definitive evidence. The mother can transmit the infection to her fetus through several routes, but the most likely routes are through ascending infections and through the blood. The inability of most agents to infect the early embryo probably depends largely on local barriers to the infectious agent, such as the zona pellucida. Some viruses, however, because of their systems for gene regulation of expression, can infect only embryos of certain developmental stages. Certain retroviruses can infect embryos, integrate into cellular DNA, and become part of the germline. After implantation, most infectious agents reach the fetus hematogenously. Organisms circulating in the mother reach and infect the placenta. They then may breach the placenta, gain access to the fetal circulation, and disseminate through the fetal body. Agents with particular tropisms infect particular organs and cause particular symptom complexes. The damage done by the organisms depends largely on the gestational age of the fetus at the time of the infection. The ability of the agent to infect or damage the fetus at all often depends on whether the mother is experiencing a primary infection or has previously mounted an effective immune response. Agents harm the fetus through direct destruction of parenchymal cells, through destruction of blood vessels and resulting infarction, through continued replication in fetal and neonatal tissues, through altering the growth parameters of various fetal tissues, and through provoking autoimmune responses. Infections that begin in the perinatal period usually infect the fetus by direct inoculation from infected foci in the birth canal or through direct contact with large amounts of infected maternal body fluids. Direct tissue destruction of the immediate sequelae of invasive infections usually causes the fetal damage from these perinatally acquired agents. The clinical features of the disease that begin in this period provide an opportunity for effective therapeutic intervention. Understanding the routes of fetal infection and the mechanisms underlying fetal damage from infection will help in devising strategies for preventing and treating congenital infections.
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PMID:Mechanisms and pathways of congenital infections. 328 20

When infection with Toxoplasma gondii occurs during pregnancy, there is a risk that the parasite will cause severe congenital toxoplasmosis. We developed a method of diagnosing and treating congenital toxoplasmosis in utero. Diagnosis was based on the identification of maternal acute infection, followed by culture of fetal blood and amniotic fluid, testing of fetal blood for toxoplasma-specific IgM and nonspecific measures of infection, and ultrasound examination of the fetal brain. Treatment included the administration of antibiotics to all mothers with confirmed acute infection during pregnancy, with more intensive antibiotic treatment of those who had infected fetuses and who chose to continue the pregnancy. We report a prospective study of 746 documented cases of maternal toxoplasma infection, in which the infants were followed for at least three months. Infection was diagnosed antenatally in 39 of 42 fetuses. Twenty-four of the 39 pregnancies were terminated, and 15 were continued. All the mothers were treated with spiramycin throughout pregnancy; if fetal infection was demonstrated, pyrimethamine and either sulfadoxine or sulfadiazine were added to the regimen. Of the 15 fetuses with congenital toxoplasmosis who were carried to term, all but 2, who had chorioretinitis, remained clinically well during follow-up. We conclude that prenatal diagnosis of congenital toxoplasmosis is practical and that prenatal therapy in women who wish to continue their pregnancies reduces the severity of the manifestations of the disease.
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PMID:Prenatal management of 746 pregnancies at risk for congenital toxoplasmosis. 333 19

The results of prenatal diagnosis of fetal rubella infection by specific IgM antibody detection in fetal infection by specific IgM antibody detection in fetal blood obtained in the 21st to 23rd weeks of pregnancy of women with different types of rubella problems during pregnancy (categorised in four groups) showed that in 28 of 31 cases the diagnosis apparently assisted in the correct management of the pregnancy. However, in two cases with negative IgM findings in the fetal blood, children with rubella embryopathy were born, and in one case with positive IgM antibody findings, the child was infected but healthy. From this experience we recommend that in all cases of symptomatic rubella infection in the first 12 weeks, termination of pregnancy should be considered without prenatal diagnosis. Prenatal diagnosis, if considered at all, should be limited to "symptomless" acute rubella infection and reinfection in the first 12 weeks and to symptomatic rubella infection in the 12th to 17th weeks of pregnancy.
Infection
PMID:Prenatal diagnosis of intrauterine rubella. 361 Mar 20

Infection of pregnant mice with Ross River or Getah viruses after the establishment of a functional placenta resulted in fetal infection with these viruses. However, only with Ross River virus was there any significant fetal death. There was significant post-partum mortality in mice infected in utero with Ross River but not with Getah virus. In contrast, significant post-partum mortality occurred in Murray Valley encephalitis virus-infected mice despite the inability of the virus to cross the placenta. Infection of mice with Ross River, Getah, or Murray Valley encephalitis viruses before placentation had occurred (5th day post-conception) did not result in fetal infection although there was significant post-partum death in litters born to Ross River virus-infected mothers.
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PMID:Effect on mice of infection during pregnancy with three Australian arboviruses. 625 57

Akabane virus, an arthropod-borne Bunyavirus, is the major cause of epizootics of congenital malformations in ruminants in Australia, Japan, Korea, and Israel, and is suspected to be a cause of sporadic outbreaks elsewhere. Blood-sucking insects, such as biting midges, transmit the virus horizontally to vertebrates. Climatic factors influence the seasonal activity and geographic range of the vector population and, therefore, occurrence of related disease. Inoculated ruminants seroconvert rapidly after a short subclinical viremia. Infection is of consequence only if ruminants are pregnant and not protected by adequate specific neutralizing antibodies. In naive pregnant animals, virus may spread hematogenously to replicate and persist in trophoblastic cells of placental cotyledons and subsequently invade the fetus. A distinct tropism for immature rapidly dividing cells of the fetal central nervous system and skeletal muscle results in direct virus-induced necrotizing encephalomyelitis and polymyositis. If fetuses survive, such injury may manifest as arthrogryposis, hydranencephaly, porencephaly, microencephaly, hydrocephalus, or encephalomyelitis at term. The earlier in gestation that fetal infection occurs, the more severe the lesions, reflecting the large population of vulnerable cells and lack of fetal immunocompetency at earlier stages of pregnancy. Injury during the period of critical cell migration and differentiation in organogenesis may substantially disrupt structural development in target organs. Late gestational infections cause nonsuppurative inflammation in the brain and spinal cord, premature birth, or fetal death with stillbirth or abortion. Affected neonates are nonviable. Control is by vaccination but is not always justified economically. Akabane viral infections must be differentiated from infections with other teratogenic viruses (including related Bunyaviruses), inherited conditions, and maternal intoxications. Diagnosis is made by serology and viral isolation.
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PMID:Akabane virus. 772 35

Maternofetal infection occurs in 1 to 10 of every 1,000 newborns. Prognosis is poor and an extremely rapid the clinical course is sometimes observed. The situation suggests that widespread use of antibiotics and more than 90% of the newborns receiving antibiotics are not infected. A prospective study based on simple, recognized criteria predictive of maternal-fetal infection was conducted in 3,392 deliveries to evaluate the effect of an antibiotic prophylaxy protocol. Specificity, sensitivity, positive and negative predictive value were evaluated for each of the eleven criteria retained with the goal of increasing sensitivity and decrease the use of unnecessary antibiotics. Among the 3,392 infants delivered from January 1989 to December 1990, 286 (8.4%) newborns entered the study and were given mezlocillin (150 mg/kg/12 h). This treatment was stopped at 48 hours of life if the infant was not infected. RESULTS. Infection was confirmed in 48 of 3,392 infants (1.4%). All were in the risk group: 48/286 (16.7%). The germs the most often found were group B Streptococcus (n = 16), Escherichia coli (n = 8) and Listeria monocytogenes (n = 3). Nine criteria were well correlated with maternal-fetal infection. The two most important criteria were maternal pyrexia above 39 degrees C and Apgar score below 7 to 5 min (poor neonatal adaptation), with a 99% and 90% and a positive predictive value of 80% and 37% respectively. Inversely, Two criteria were poorly correlated with maternal-fetal infection: labour duration above 12 hours and instrumental extraction (positive predictive value from 10% to 17%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Validation trial of a neonatal prophylactic antibiotic protocol in the delivery room]. 778 94

Toxoplasmosis is a worldwide health problem. Infection of a pregnant woman can result in severe fetal morbidity or in subclinical neonatal infection; most subclinical cases will develop ocular and neurological sequelae. Fetal infection and clinical outcome is related to when in pregnancy toxoplasmosis was acquired. The risk of transmission increases from 14% in the first trimester to 29% in the second and 59% in the third. Conversely, clinical damage decreases from about 80% in the first to 10% in the third trimester, but up to 50% of patients with subclinical congenital toxoplasmosis will develop neurologic and ocular sequelae. Congenital toxoplasmosis can be prevented by identification of non immune women at the beginning of pregnancy, by giving information on how to avoid the infection and by a serological follow-up until the delivery. Serological follow-up is based on repeated testing for specific IgG and IgM, but other serologic methods are necessary to differentiate between acute and chronic infections and possibly on a single serum sample. Procedures to detect fetal infection are ultrasound examination, cordocentesis and amniocentesis; prenatal diagnosis relies on demonstration of toxoplasma in fetal blood or amniotic fluid by mouse inoculation. Very promising results have recently obtained by the PCR-method applied to amniotic fluid samples. All strongly suspected cases of acquired toxoplasmosis in pregnancy have to be treated.
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PMID:[Toxoplasmosis in pregnancy. Prevention, diagnosis, and therapy]. 818 79

Toxoplasmosis is caused by the protozoan organism, Toxoplasma gondii. Infection with this organism primarily results from contact with infected cats and from ingestion of improperly cooked meat. Most adults with toxoplasmosis are asymptomatic. When symptoms are present, they typically resemble a mononucleosis or flulike illness. The diagnosis of toxoplasmosis in the pregnant adult is best made using serological techniques to detect IgM antibody and to document significant changes in the IgG antibody titer. Congenital toxoplasmosis usually occurs as a result of primary maternal infection. The most useful tests for confirmation of fetal infection are ultrasound examination, cordocentesis for detection of IgM-specific antibody, and amniocentesis for detection of toxoplasma DNA in amniotic fluid. Congenital toxoplasmosis can be treated with reasonable success by administration of antibiotics (spiramycin, sulfadiazine, and pyrimethamine) to the mother. In an effort to prevent acquisition of infection, pregnant women should be counseled to avoid contact with cat litter and improperly cooked beef, pork, or lamb.
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PMID:Toxoplasmosis. 973 98


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