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Cardiovascular Research 2003 60(1):165-169; doi:10.1016/S0008-6363(03)00321-3
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Placental infection with Chlamydia pneumoniae and intrauterine growth restriction

Christina Babooniana, David A Smitha, David Shaplandb, Gavin Arnoa, Behnam Zala, Julius Akiyua and Juan Carlos Kaskia,*

aDepartment of Cardiological Sciences, St. George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK
bDepartment of Obstetrics and Gynaecology, Morecambe Bay Hospitals NHS Trust, Furness General Hospital, Dalton Lane, Barrow-in-Furness, Cumbria LA14 4LF, UK

*Corresponding author. Tel.: +44-20-8725-5901; fax: +44-20-8725-3328. Email address: jkaski{at}sghms.ac.uk

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.

KEYWORDS Atherosclerosis; Infection/inflammation; Congenital defects; Coronary circulation; Coronary disease

Time for primary review 35 days.


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