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1.
Can J Infect Dis ; 13(5): 311-8, 2002 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-18159407

RESUMO

OBJECTIVE: To determine the demographic, clinical and microbiological characteristics of a representative Canadian obstetrical population. DESIGN: A one-year cohort study of all maternity patients who were followed to delivery, using detailed patient questionnaires containing more than 60 demographic and clinical variables, and three microbiological evaluations during gestation - first trimester, 26 to 30 weeks, and labour and delivery. Outcome measurements included birth weight and gestational age. SETTING: Labour and delivery suites of all office obstetrical practices affiliated with a single hospital. POPULATION STUDIED: A consecutive sample of pregnant women in the study practices during one year were eligible for enrolment; 2237 consecutive patients were approached for consent, 2047 enrolled and 1811 completed the study through delivery. RESULTS: The average patient was white, married and 29 years of age. Slightly more than half of the patients had postsecondary education, but 10% fell below the national poverty line for income. Frequency of factors linked to adverse pregnancy outcomes included cigarette smoking (19%), alcohol ingestion (18%), previously having had a premature infant (7%), and maternal diabetes (2%). Overall prevalence of genital microbes variously implicated in prematurity was 37% for ureaplasma, 11% for group B streptococcus and 4% for Mycoplasma hominis. Prevalence of bacterial vaginosis was 14%. The median gestational age for the cohort was 39 weeks, with 7% of infants born less than 37 weeks' gestation. Mean birth weight was 3415 g. CONCLUSIONS: The present clinical cohort represents demographic and medical characteristics of the Canadian obstetrical population. The birth outcomes are consistent with national data. This database provides valuable information about a general obstetrical population that is managed by a universal health care system.

2.
Microb Pathog ; 39(5-6): 197-204, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-16271847

RESUMO

We investigated the extent to which tobacco smoke could induce persistence of Chlamydia pneumoniae in human endothelial cells. Aortic and coronary artery endothelia were infected in the absence or presence of non-cytotoxic concentrations of tobacco smoke medium. Following exposure to smoke medium, chlamydial inclusions were smaller and demonstrated fewer genome copies as determined by real-time PCR. Enumeration of inclusion-forming units (IFU) established a significant smoke-mediated, dose-dependent inhibition of elementary bodies (EB). Host cell apoptosis did not contribute to the observed restriction of productive infection. Ultrastructure analysis demonstrated an arrest in chlamydial development following smoke-exposure, with a predominance of reticulate bodies (RB) observed inside inclusions. Recovery of viable IFU was achieved with removal of smoke-medium and addition of L-tryptophan. In the presence of smoke, C. pneumoniae infection demonstrated all the characteristics of persistence in human endothelia cells. This is the first time that primary human arterial endothelial cells have been shown to support chlamydial persistence. Tobacco smoke is a well-characterized risk factor for progression of atherosclerosis, but a novel means of inducing chlamydial persistence in vascular cells. Thus, smoking may additionally contribute to atherosclerotic disease by inducing a persistent chlamydial infection in arterial endothelium.


Assuntos
Chlamydophila pneumoniae/crescimento & desenvolvimento , Células Endoteliais/microbiologia , Nicotiana , Fumaça , Aorta , Apoptose , Aterosclerose/etiologia , Linhagem Celular , Chlamydophila pneumoniae/genética , Chlamydophila pneumoniae/ultraestrutura , Contagem de Colônia Microbiana , Vasos Coronários , Células Endoteliais/ultraestrutura , Dosagem de Genes , Humanos , Corpos de Inclusão , Reação em Cadeia da Polimerase
3.
CMAJ ; 171(6): 585-9, 2004 Sep 14.
Artigo em Inglês | MEDLINE | ID: mdl-15367460

RESUMO

BACKGROUND: Aboriginal women have been identified as having poorer pregnancy outcomes than other Canadian women, but information on risk factors and outcomes has been acquired mostly from retrospective databases. We compared prenatal risk factors and birth outcomes of First Nations and Métis women with those of other participants in a prospective study. METHODS: During the 12-month period from July 1994 to June 1995, we invited expectant mothers in all obstetric practices affiliated with a single teaching hospital in Edmonton to participate. Women were recruited at their first prenatal visit and followed through delivery. Sociodemographic and clinical data were obtained by means of a patient questionnaire, and microbiological data were collected at 3 points during gestation: in the first and second trimesters and during labour. Our primary outcomes of interest were low birth weight (birth weight less than 2500 g), prematurity (birth at less than 37 weeks' gestation) and macrosomia (birth weight greater than 4000 g). RESULTS: Of the 2047 women consecutively enrolled, 1811 completed the study through delivery. Aboriginal women accounted for 70 (3.9%) of the subjects who completed the study (45 First Nations women and 25 Métis women). Known risk factors for adverse pregnancy outcome were more common among Aboriginal than among non-Aboriginal women, including previous premature infant (21% v. 11%), smoking during the current pregnancy (41% v. 13%), presence of bacterial vaginosis in midgestation (33% v. 13%) and poor nutrition as measured by meal consumption. Although Aboriginal women were less likely than non-Aboriginal women to have babies of low birth weight (odds ratio [OR] 1.46, 95% confidence interval [CI] 0.52-4.15) or who were born prematurely (OR 1.45, 95% CI 0.57-3.72) and more likely to have babies with macrosomia (OR 2.04, 95% CI 1.03-4.03), these differences were lower and statistically nonsignificant after adjustment for smoking, cervicovaginal infection and income (adjusted OR for low birth weight 0.85, 95% CI 0.19-3.78; for prematurity 0.90, 95% CI 0.21-3.89; and for macrosomia 2.12, 95% CI 0.84-5.36). INTERPRETATION: After adjustment for potential confounding factors, we found no statistically significant relation between Aboriginal status and birth outcome.


Assuntos
Indígenas Norte-Americanos , Resultado da Gravidez/etnologia , Adulto , Canadá/epidemiologia , Diabetes Mellitus/etnologia , Feminino , Macrossomia Fetal/etnologia , Humanos , Recém-Nascido de Baixo Peso , Recém-Nascido , Recém-Nascido Prematuro , Estado Nutricional , Gravidez , Cuidado Pré-Natal , Estudos Prospectivos , Fatores de Risco , Fumar/epidemiologia , Fumar/etnologia , Fatores Socioeconômicos , Vaginose Bacteriana/etnologia
4.
Microb Pathog ; 37(3): 141-8, 2004 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-15351037

RESUMO

We examined tobacco smoke exposure and its effect on the life cycle of Chlamydophila pneumoniae (C. pneumoniae) in HEp-2, a human respiratory epithelial cell line. Using noncytotoxic concentrations of smoke medium, chlamydiae were grown in tissue culture and infectious particles were quantitated indirectly by immunocytometry of infected indicator cells. Chlamydial genome copy number was assessed with real-time polymerase chain reaction, and ultrastructure was examined by transmission electron microscopy. There was a significant reduction (56-64%; p<0.05) in the number of infectious elementary bodies following smoke exposure compared to untreated cultures. Under the same conditions, at late time points, smoke-exposed cultures showed significantly fewer chlamydial DNA copies (p<0.04). Moreover, smoke exposure induced large aberrant bodies that predominated within the inclusion. Following in vitro smoke exposure, alterations in the developmental cycle of C. pneumoniae included: inhibition of productive infection, reduced bacterial cell division, and formation of aberrant bodies. Thus, using this novel system, we were able to induce chlamydial persistence. Tobacco smoke exposure may represent a risk for establishment of a chronic reservoir of C. pneumoniae infection within respiratory epithelium.


Assuntos
Chlamydophila pneumoniae/crescimento & desenvolvimento , Chlamydophila pneumoniae/patogenicidade , Laringe/microbiologia , Nicotiana , Fumaça , Linhagem Celular Tumoral , Chlamydophila pneumoniae/genética , Meios de Cultura , Células Epiteliais/microbiologia , Células Epiteliais/patologia , Imunofluorescência , Humanos , Laringe/citologia , Laringe/patologia , Microscopia Eletrônica , Reação em Cadeia da Polimerase
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