The majority of birth defects have no known cause. Prenatal infection, which can occur without maternal symptoms, is likely responsible for many more of these newborn abnormalities than is currently suspected. Despite modern treatments such as antibiotics and antivirals, infection remains a serious problem during pregnancy. For example, a single pathogen, cytomegalovirus (CMV), is responsible for an alarming number of birth defects. According to the CDC, “Congenital (present at birth) CMV infection causes more long-term problems and childhood deaths than Down syndrome, fetal alcohol syndrome, and neural tube defects. About 1 in 750 children in the United States is born with or develops permanent problems due to congenital CMV infection."
This is but one example of a serious prenatal infection associated with lifelong repercussions to the infant. The wide range of prenatal infections and their many complications present a daunting problem to the physician. To address this issue, the Division of Neonatal and Developmental Medicine, supported in part by the March of Dimes Prematurity Research Center and the Chambers Family Fund for Excellence in Pediatric Research, is engaged in important basic research. The laboratory of Dr. Christopher Contag has developed a mouse model of prenatal infection that combines live animal imaging with molecular analysis, yielding data that identifies molecular causes of fetal pathology. Taking advantage of the Small Animal Imaging Facility at the Stanford Center for Innovation in In Vivo Imaging (SCI3), prenatal infection in mice is interrogated with bioluminescence, MRI, and ultrasound (see videos below). The experiments demonstrate that infection of the placenta can play a crucial role in causing birth defects, and that the fetus itself need not be infected for severe consequences to result. These studies are continually being expanded and developed to begin to understand the complexity of infection during pregnancy.
Fetal heartbeat of mouse infected with Listeria
Fetal heartbeat of uninfected mouse
These videos compare a fetus infected with Listeria to a normal, uninfected control from the same mother. Notice that the heartbeat of the infected fetus (left) is much slower than the control’s (right). Our research shows that fetal bradycardia is localized to infected fetuses and is not systemic or disseminated (Hardy et al., 2012).
Hardy, J., Kirkendoll, B., Zhao, H., Pisani, L., Luong, R., Switzer, A., . . . Contag, C. H. (2012). Infection of pregnant mice with Listeria monocytogenes induces fetal bradycardia. Pediatr Res, 71(5), 539-545.