James E. Samuel – författare

This volume contains the proceedings of the 5th International Conference on Rickettsiae and Rickettsial Diseases, in which an effort is made to address and clarify issues from clinical, diagnostic, epidemiologic, and molecular perspectives that have remained unsolved in the past. NOTE: Annals volumes are available for sale as individual books or as a journal. For information on institutional journal subscriptions, please visit www.blackwellpublishing.com/nyas.ACADEMY MEMBERS: Please contact the New York Academy of Sciences directly to place your order (www.nyas.org). Members of the New York Academy of Science receive full-text access to the Annals online and discounts on print volumes. Please visit http://www.nyas.org/MemberCenter/Join.aspx for more information about becoming a member.

Coxiella burnetii is the etiological agent of Q fever, a zoonotic disease found worldwide. The bacterium is a fascinating example of intracellular parasitism that has uniquely evolved to thrive in the most inhospitable of cellular compartments-the phagolysosome. Understanding how C. burnetii resists the degradative functions of this vacuole, and the host cell functions coopted for successful parasitism, are central to understanding Q fever pathogenesis. Recent achievements in glycomics and proteomics are guiding development of enhanced detection schemes for the bacterium in addition to shedding light on the host immune response to the pathogen. Several chapters survey immune functions that control or potentially exacerbate Coxiella infection and delve into correlates of protective immunity elicited by vaccination. Comparative genomics is also the foundation of chapters discussing diagnostic antigen discovery and molecular typing of the bacterium, with significance for development of new clinical, epidemiologic, and forensic tools.

Coxiella burnetii is the etiological agent of Q fever, a zoonotic disease found worldwide. The bacterium is a fascinating example of intracellular parasitism that has uniquely evolved to thrive in the most inhospitable of cellular compartments-the phagolysosome. Understanding how C. burnetii resists the degradative functions of this vacuole, and the host cell functions coopted for successful parasitism, are central to understanding Q fever pathogenesis. Recent achievements in glycomics and proteomics are guiding development of enhanced detection schemes for the bacterium in addition to shedding light on the host immune response to the pathogen. Several chapters survey immune functions that control or potentially exacerbate Coxiella infection and delve into correlates of protective immunity elicited by vaccination. Comparative genomics is also the foundation of chapters discussing diagnostic antigen discovery and molecular typing of the bacterium, with significance for development of new clinical, epidemiologic, and forensic tools.