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Volume 14, Issue 4, Pages 182-189 (August 2009)


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Infection and stillbirth

Elizabeth M. McClureaCorresponding Author Informationemail address, Robert L. Goldenbergb

published online 16 March 2009.

Summary 

Infection may cause stillbirth by several mechanisms, including direct infection, placental damage, and severe maternal illness. Various organisms have been associated with stillbirth, including many bacteria, viruses, and protozoa. In developed countries, between 10% and 25% of stillbirths may be caused by an infection, whereas in developing countries, which have much higher stillbirth rates, the contribution of infection is much greater. In developed countries, ascending bacterial infection, both before and after membrane rupture, with organisms such as Escherichia coli, group B streptococci, and Ureaplasma urealyticum is usually the most common infectious cause of stillbirth. However, in areas where syphilis is prevalent, up to half of all stillbirths may be caused by this infection alone. Malaria may be an important cause of stillbirth in women infected for the first time in pregnancy. The two most important viral causes of stillbirth are parvovirus and Coxsackie virus, although a number of other viral infections appear to be causal. Toxoplasma gondii, Listeria monocytogenes, and the organisms that cause leptospirosis, Q fever, and Lyme disease have all been implicated as etiologic for stillbirth. In certain developing countries, the stillbirth rate is high and the infection-related component so great that achieving a substantial reduction in stillbirth should be possible by reducing maternal infections. However, because infection-related stillbirth is uncommon in developed countries, and because those that do occur are caused by a wide variety of organisms, reducing this etiologic component of stillbirth much further will be difficult.

a Department of Epidemiology, UNC Global School of Public Health, Chapel Hill, North Carolina, USA

b Department of Obstetrics/Gynecology, Drexel University College of Medicine, 245 N. 15th Street, 17th Floor, Room 17113, Philadelphia, PA 19102, USA

Corresponding Author InformationCorresponding author.

PII: S1744-165X(09)00024-9

doi:10.1016/j.siny.2009.02.003


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