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Infection and Immunity, December 2009, p. 5640-5650, Vol. 77, No. 12
0019-9567/09/$08.00+0     doi:10.1128/IAI.00851-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Coxiella burnetii Isolates Cause Genogroup-Specific Virulence in Mouse and Guinea Pig Models of Acute Q Fever{triangledown} ,{dagger}

K. E. Russell-Lodrigue,1,3,{ddagger} M. Andoh,1,{ddagger} M. W. J. Poels,1,2 H. R. Shive,3 B. R. Weeks,3 G. Q. Zhang,1 C. Tersteeg,1,2 T. Masegi,4 A. Hotta,5 T. Yamaguchi,5 H. Fukushi,5 K. Hirai,5 D. N. McMurray,1 and J. E. Samuel1*

Department of Microbial and Molecular Pathogenesis, Texas A&M Health Science Center, College Station, Texas,1 Institute of Life Sciences and Chemistry, Utrecht, The Netherlands,2 Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas,3 and Department of Pathogenetic Veterinary Science,4 Department of Applied Veterinary Science, United Graduate School of Veterinary Sciences, Gifu University, Gifu, Japan5

Received 28 July 2009/ Returned for modification 13 August 2009/ Accepted 18 September 2009

Q fever is a zoonotic disease of worldwide significance caused by the obligate intracellular bacterium Coxiella burnetii. Humans with Q fever may experience an acute flu-like illness and pneumonia and/or chronic hepatitis or endocarditis. Various markers demonstrate significant phylogenetic separation between and clustering among isolates from acute and chronic human disease. The clinical and pathological responses to infection with phase I C. burnetii isolates from the following four genomic groups were evaluated in immunocompetent and immunocompromised mice and in guinea pig infection models: group I (Nine Mile, African, and Ohio), group IV (Priscilla and P), group V (G and S), and group VI (Dugway). Isolates from all of the groups produced disease in the SCID mouse model, and genogroup-consistent trends were noted in cytokine production in response to infection in the immunocompetent-mouse model. Guinea pigs developed severe acute disease when aerosol challenged with group I isolates, mild to moderate acute disease in response to group V isolates, and no acute disease when infected with group IV and VI isolates. C. burnetii isolates have a range of disease potentials; isolates within the same genomic group cause similar pathological responses, and there is a clear distinction in strain virulence between these genomic groups.

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

{triangledown} Published ahead of print on 28 September 2009.

{dagger} Supplemental material for this article may be found at http://iai.asm.org/.

Editor: R. P. Morrison

{ddagger} K.E.R.-L. and M.A. contributed equally to this work.

Infection and Immunity, December 2009, p. 5640-5650, Vol. 77, No. 12
0019-9567/09/$08.00+0     doi:10.1128/IAI.00851-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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