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1 June 2005

Volume 191, Number 11
The Journal of Infectious Diseases 2005;191:1889–1897
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19111-0016$15.00
DOI: 10.1086/430090
MAJOR ARTICLE

Growth of Listeria monocytogenes in the Guinea Pig Placenta and Role of Cell‐to‐Cell Spread in Fetal Infection

Anna I. Bakardjiev,1

Brian A. Stacy,3,a and

Daniel A. Portnoy1,2

1Department of Molecular and Cell Biology and 2School of Public Health, University of California, Berkeley, and 3Anatomic Pathology Service, Veterinary Medical Teaching Hospital, University of California, Davis

Listeria monocytogenes causes foodborne outbreaks that lead to infection in human and other mammalian fetuses. To elucidate the molecular and cellular mechanisms involved in transplacental transmission, we characterized placental‐fetal infection in pregnant guinea pigs inoculated with wild‐type (wt) or mutant L. monocytogenes strains. The wt strain increased in number in the placenta by >1000‐fold during the first 24 h after inoculation—an increase that was unparalleled in other maternal organs. The ActA− mutant, which is impaired in cell‐to‐cell spread and attenuated in maternal organs, increased in the placenta by a similar amount, although, in fetal infection, the number of ActA− mutant bacteria was 100‐fold lower, compared with that of the wt strain. Furthermore, a mutant impaired in vacuolar escape was rapidly eliminated from maternal organs but persisted in the placenta. We concluded that cell‐to‐cell spread facilitates maternal‐to‐fetal transmission. Furthermore, the placenta provides a protective niche for growth of L. monocytogenes.

Received 11 November 2004; accepted 15 January 2005; electronically published 26 April 2005.

Reprints or correspondence: Dr. Anna I. Bakardjiev, Dept. of Molecular and Cell Biology, 510 Barker Hall, University of California, Berkeley, CA 94720‐3202 ().

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  • Presented in part: Gordon Research Conference on Microbial Toxins and Pathogenicity, Andover, New Hampshire, 18–23 July 2004; 42nd annual meeting of the Infectious Diseases Society of America, Boston, 30 September–3 October 2004 (abstract 109).

    Financial support: National Institutes of Health (grants RO1 AI27655 and R37 AI29619 to D.A.P.); Pediatric Scientist Development Program, National Institute of Child Health and Human Development (grant K‐12 HD00850 to A.I.B.); Biology of Infectious Diseases Training Program, National Institute of Allergy and Infectious Diseases (grant T32 AI07641 to A.I.B.).

  • Present affiliation: Small Animal Clinical Sciences, University of Florida, College of Veterinary Medicine, Gainesville.

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