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Infection and Immunity, November 2006, p. 6085-6091, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00763-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Clinical and Pathologic Changes in a Guinea Pig Aerosol Challenge Model of Acute Q Fever

K. E. Russell-Lodrigue,^1,2 G. Q. Zhang,² D. N. McMurray,² and J. E. Samuel^2*

Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas,¹ Department of Microbial and Molecular Pathogenesis, Texas A&M University System Health Science Center, College Station, Texas²

Received 12 May 2006/ Returned for modification 12 June 2006/ Accepted 26 July 2006

Acute Q fever is a zoonotic disease caused by the obligate intracellular bacterium Coxiella burnetii and can manifest as a flu-like illness, pneumonia, or hepatitis. A need exists in Q fever research for animal models mimicking both the typical route of infection (inhalation) and the clinical illness seen in human cases of Q fever. A guinea pig aerosol challenge model was developed using C. burnetii Nine Mile phase I (RSA 493), administered using a specialized chamber designed to deliver droplet nuclei directly to the alveolar spaces. Guinea pigs were given 10¹ to 10⁶ organisms and evaluated for 28 days postinfection. Clinical signs included fever, weight loss, respiratory difficulty, and death, with the degree and duration of response corresponding to the dose of organism delivered. Histopathologic evaluation of the lungs of animals infected with a high dose showed coalescing panleukocytic bronchointerstitial pneumonia at 7 days postinfection that resolved to multifocal lymphohistiocytic interstitial pneumonia by 28 days. Guinea pigs receiving a killed whole-cell vaccine prior to challenge with the highest dose of C. burnetii were protected against lethal infection and did not develop fever. Clinical signs and pathological changes noted for these guinea pigs were comparable to those seen in human acute Q fever, making this an accurate and valuable animal model of human disease.

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* Corresponding author. Mailing address: Department of Microbial and Molecular Pathogenesis, Texas A&M University System Health Science Center, College Station, TX 77843-1114. Phone: (979) 862-1684. Fax: (979) 845-3479. E-mail: jsamuel{at}medicine.tamhsc.edu.

Editor: R. P. Morrison

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Infection and Immunity, November 2006, p. 6085-6091, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00763-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

This article has been cited by other articles:

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