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Influenza in Early Pregnancy and Fetal Demise | CDC EID

EID Journal Home > Volume 17, Number 1–January 2011
Volume 17, Number 1–January 2011
Seasonal Influenza A (H1N1) Infection in Early Pregnancy and Second Trimester Fetal Demise

Richard W. Lieberman, Comments to Author Natasha Bagdasarian, Dafydd Thomas, and Cosmas Van De Ven

Author affiliation: University of Michigan Health System, Ann Arbor, Michigan, USA

Suggested citation for this article

A second trimester fetal demise followed influenza-like illness in early pregnancy. Influenza A virus (H1N1) was identified in maternal and fetal tissue, confirming transplacental passage. These findings suggested a causal relationship between early exposure and fetal demise. Management of future influenza outbreaks should include evaluation of products of conception associated with fetal loss.

Increased maternal illness and death appeared in early reports of influenza A pandemic (H1N1) 2009. Three pregnancy-related complications associated with pandemic (H1N1) 2009 were reported in May 2009: 1 postpartum maternal death, 1 preterm birth, and 1 early second trimester (weeks 14–20) loss (1). In April 2010, a summary of pandemic (H1N1) 2009 among 788 pregnant women demonstrated a disproportionately high risk for death; the rate of spontaneous miscarriage was 1.4%, but details were not provided (2). Correlating influenza exposure to pregnancy loss is not straightforward because first trimester miscarriage is common, second trimester loss before 24 weeks is not well studied (3), and viral identification in products of conception has rarely been attempted. We report a second trimester fetal demise that occurred after exposure to seasonal influenza A virus (H1N1) early in pregnancy.

Influenza in Early Pregnancy and Fetal Demise | CDC EID

Suggested Citation for this Article

Lieberman RW, Bagdasarian N, Thomas D, Van De Ven C. Seasonal influenza A (H1N1) infection in early pregnancy and second trimester fetal demise. Emerg Infect Dis [serial on the Internet]. 2011 Jan [date cited].

DOI: 10.3201/eid1701.091895

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Richard W. Lieberman, Department of Pathology 4215, University of Michigan Medical School, 1301 Catherine Rd, Med Sci I, Ann Arbor, MI 48901, USA;

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