8 resultados para congenital infection
em Repositório Institucional UNESP - Universidade Estadual Paulista "Julio de Mesquita Filho"
Resumo:
Two studies, of a natural infection and an experimental infection, were performed in order to study congenital transmission of Toxoplasma gondii in cattle. In the first study, 50 fetuses were harvested from gestating cows that were eutanasied at a municipal slaughterhouse in Jaboticabal, São Paulo state, Brazil. In the second study, 11 gestating cows were divided into four groups for inoculation with T. gondii: GI consisted of three cows inoculated with 1.0 x 10(5) oocysts during their first trimester of gestation; GII consisted of three cows inoculated with 1.0 x 10(5) oocysts during their second trimester of gestation; GIII consisted of three cows inoculated with 1.0 x 10(5) oocysts during their last trimester of gestation; and GIV consisted of two control cows, one during its first and the other during its second trimester of gestation. In both studies, the presence of T. gondii was confirmed both indirectly by immunofluorescence assay (IFAT). In the natural infection experiment, 18% (9/50) of the gestating cows were confirmed to have specific antibodies (IFAT - 1:64) against T. gondii. The bioassay was able to diagnose the presence of T. gondii in the tissue samples from three calves. In the second experiment, the nine cows from groups I, II and III presented with specific antibodies (IFAT) against T. gondii. In contrast, T. gondii could not be detected by IFAT, histopathological examination or the bioassay in any of the nine calves born to cows experimentally infected with T. gondii oocysts. Based on the results from both studies, we conclude that congenital infection of T. gondii in cattle, while infrequent, does occur naturally. The pathogenicity of the strain of T. gondii may influence the likelihood of this route of transmission. (C) 2010 Elsevier B.V. All rights reserved.
Resumo:
Three Toxoplasma gondii free bitches (No, 3-5) were fed 15 000 sporulated T. gondii oocysts at 56, 40 and 32 day of gestation and the outcome of the pregnancy was monitored. Two of the three dogs infected during pregnancy showed evidence of congenital infection and one aborted. Two control bitches not fed oocysts delivered eight uninfected healthy pups. This study demonstrated that I gondii can be congenitally transmitted in dogs when bitches are infected during pregnancy. (C) 1999 Elsevier B.V. B.V. All rights reserved.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Resumo:
The aim of this study was to evaluate the incidence of and mortality due to meningitis and compare data according to microbiological diagnosis. This was a ten-year retrospective study conducted at a neonatal intensive care unit (NICU). Newborns with meningitis confirmed by positive CSF culture were included; those with congenital infection or malformations that made lumbar puncture impossible were excluded. The variables investigated were birth weight, gestational and postnatal age, procedures, hematological and CSF parameters, and complications. Parametric and non-parametric tests were used (statistical value p<0.05). The incidence of meningitis was 0.6% and mortality was 27%. of the 22 cases, 59% involved Gram-negative bacteria; 36% Gram-positive and 5% fungi. The groups did not differ in relation to birth weight, gestational and postnatal age, procedures or hematological and CSF parameters. Sepsis, convulsions and deaths were frequent in both groups, without statistical difference. Gram-negative cases showed abscesses and higher frequency of ventriculitis and hydrocephaly. Meningitis was infrequent, but presented high mortality and frequent complications.
Resumo:
Aicardi-Goutières syndrome (AGS) is a genetic encephalopathy whose clinical features mimic those of acquired in utero viral infection. AGS exhibits locus heterogeneity, with mutations identified in genes encoding the 3′→5′ exonuclease TREX1 and the three subunits of the RNASEH2 endonuclease complex. To define the molecular spectrum of AGS, we performed mutation screening in patients, from 127 pedigrees, with a clinical diagnosis of the disease. Biallelic mutations in TREX1, RNASEH2A, RNASEH2B, and RNASEH2C were observed in 31, 3, 47, and 18 families, respectively. In five families, we identified an RNASEH2A or RNASEH2B mutation on one allele only. In one child, the disease occurred because of a de novo heterozygous TREX1 mutation. In 22 families, no mutations were found. Null mutations were common in TREX1, although a specific missense mutation was observed frequently in patients from northern Europe. Almost all mutations in RNASEH2A, RNASEH2B, and RNASEH2C were missense. We identified an RNASEH2C founder mutation in 13 Pakistani families. We also collected clinical data from 123 mutation-positive patients. Two clinical presentations could be delineated: an early-onset neonatal form, highly reminiscent of congenital infection seen particularly with TREX1 mutations, and a later-onset presentation, sometimes occurring after several months of normal development and occasionally associated with remarkably preserved neurological function, most frequently due to RNASEH2B mutations. Mortality was correlated with genotype; 34.3% of patients with TREX1, RNASEH2A, and RNASEH2C mutations versus 8.0% RNASEH2B mutation-positive patients were known to have died (P = .001). Our analysis defines the phenotypic spectrum of AGS and suggests a coherent mutation-screening strategy in this heterogeneous disorder. Additionally, our data indicate that at least one further AGS-causing gene remains to be identified. © 2007 by The American Society of Human Genetics. All rights reserved.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Resumo:
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)