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Infection and Immunity, September 2003, p. 5202-5209, Vol. 71, No. 9
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.9.5202-5209.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Influence of Pregnancy on the Pathogenesis of Listeriosis in Mice Inoculated Intragastrically

Terri S. Hamrick,{dagger} John R. Horton, Patricia A. Spears, Edward A. Havell, Ida W. Smoak, and Paul E. Orndorff*

College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606

Received 5 February 2003/ Returned for modification 30 April 2003/ Accepted 17 June 2003

Pregnancy increases the risk of listeriosis, a systemic disease caused by Listeria monocytogenes. However, there is incomplete agreement on the reasons for this increased risk. We examined two features of listeriosis in gravid and nongravid female mice following intragastric (gavage) inoculation, namely, (i) disease severity (measured by lethality) and (ii) listerial infectivity (measured by liver and spleen colonization levels up to 120 h postinoculation). Two listerial strains of differing serotype (1/2a and 4nonb) were initially employed. Neither strain produced a lethal infection in nonpregnant female mice (dose range, 106 to 109 CFU/mouse), and only the 4nonb strain produced lethalities in pregnant mice (dose range, 106 to 108 CFU/mouse). The 4nonb strain also produced a higher level of liver and spleen colonization than the 1/2a strain following gavage administration. (The two strains showed similar levels of colonization if parenterally administered.) Both strains were equally capable of binding to and forming plaques upon cultured mouse enterocytes. The ability of the 4nonb strain to produce a lethal infection in pregnant animals did not correlate with an increased incidence or level of liver and spleen colonization over that in nonpregnant females. However, the lethality rate did correlate well with the rate at which embryos and their surrounding decidual covering became infected, suggesting that intrauterine infection could be responsible for the increased disease severity in the gravid females.

* Corresponding author. Mailing address: College of Veterinary Medicine, 4700 Hillsborough St., Raleigh, NC 27606. Phone: (919) 513-6207. Fax: (919) 513-6455. E-mail: paul_orndorff{at}ncsu.edu.

Editor: J. T. Barbieri

{dagger} Present address: Department of Pharmaceutical Sciences, Campbell University School of Pharmacy, Buies Creek, NC 27506.

Infection and Immunity, September 2003, p. 5202-5209, Vol. 71, No. 9
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.9.5202-5209.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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