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Infection and Immunity, October 2007, p. 4754-4761, Vol. 75, No. 10
0019-9567/07/$08.00+0     doi:10.1128/IAI.00575-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Noncapsulated Toxinogenic Bacillus anthracis Presents a Specific Growth and Dissemination Pattern in Naive and Protective Antigen-Immune Mice{triangledown}

Ian J. Glomski, Jean-Philippe Corre, Michèle Mock, and Pierre L. Goossens*

Institut Pasteur, Unité des Toxines et Pathogénie Bactérienne, Paris F-75015, France, and CNRS, URA 2172, Paris F-75015, France

Received 20 April 2007/ Returned for modification 10 May 2007/ Accepted 9 July 2007

Bacillus anthracis is a spore-forming bacterium that causes anthrax. B. anthracis has three major virulence factors, namely, lethal toxin, edema toxin, and a poly-{gamma}-D-glutamic acid capsule. The toxins modulate host immune responses, and the capsule inhibits phagocytosis. With the goal of increasing safety, decreasing security concerns, and taking advantage of mammalian genetic tools and reagents, mouse models of B. anthracis infection have been developed using attenuated bacteria that produce toxins but no capsule. While these models have been useful in studying both toxinogenic infections and antitoxin vaccine efficacy, we questioned whether eliminating the capsule changed bacterial growth and dissemination characteristics. Thus, the progression of infection by toxinogenic noncapsulated B. anthracis was analyzed and compared to that by previously reported nontoxinogenic capsulated bacteria, using in vivo bioluminescence imaging. The influence of immunization with the toxin component protective antigen (PA) on the development of infection was also examined. The toxinogenic noncapsulated bacteria were initially confined to the cutaneous site of infection. Bacteria then progressed to the draining lymph nodes and, finally, late in the infection, to the lungs, kidneys, and frequently the gastrointestinal tract. There was minimal colonization of the spleen. PA immunization reduced bacterial growth from the outset and limited infection to the site of inoculation. These in vivo observations show that dissemination by toxinogenic noncapsulated strains differs markedly from that by nontoxinogenic capsulated strains. Additionally, PA immunization counters bacterial growth and dissemination in vivo from the onset of infection.

* Corresponding author. Mailing address: Unité des Toxines et Pathogénie Bactérienne, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris Cedex 15, France. Phone: 33 (0)1 45 68 82 49. Fax: 33 (0)1 45 68 89 54. E-mail: pierre.goossens{at}pasteur.fr

{triangledown} Published ahead of print on 16 July 2007.

Editor: V. J. DiRita

Infection and Immunity, October 2007, p. 4754-4761, Vol. 75, No. 10
0019-9567/07/$08.00+0     doi:10.1128/IAI.00575-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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