By Karim E. Hechemy (auth.), Rudolf Toman, Robert A. Heinzen, James E. Samuel, Jean-Louis Mege (eds.)
Coxiella burnetii is the etiological agent of Q fever, a zoonotic illness chanced on around the globe. The bacterium is an engaging instance of intracellular parasitism that has uniquely developed to thrive within the so much inhospitable of mobile compartments-the phagolysosome. figuring out how C. burnetii resists the degradative capabilities of this vacuole, and the host phone features coopted for profitable parasitism, are valuable to knowing Q fever pathogenesis. contemporary achievements in glycomics and proteomics are guiding improvement of better detection schemes for the bacterium as well as laying off gentle at the host immune reaction to the pathogen. a number of chapters survey immune capabilities that regulate or probably exacerbate Coxiella an infection and delve into correlates of protecting immunity elicited through vaccination. Comparative genomics can also be the root of chapters discussing diagnostic antigen discovery and molecular typing of the bacterium, with value for improvement of recent medical, epidemiologic, and forensic tools.
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Additional resources for Coxiella burnetii: Recent Advances and New Perspectives in Research of the Q Fever Bacterium
1; Campoy et al. 2010). Interaction with the ER may provide a source of membrane to produce the large PV necessary for C. burnetii replication, which 2 Phylogenetic Diversity, Virulence and Comparative Genomics 31 again supports the notion that this compartment is not static (Campoy et al. 2010). The PV membrane is enriched in cholesterol, which is unusual for a lysosomal-like compartment (Howe and Heinzen 2006). Furthermore, C. burnetii infection causes an up-regulation in expression of the genes involved in cholesterol production during mid-log phase of growth at which point the PV occupies most of the internal host cell volume (Howe and Heinzen 2006; Coleman et al.
Immunol Rev 168:199–215. 1999. x Campoy EM, Zoppino FCM, Colombo MI (2010) The early secretory pathway contributes to the growth of the Coxiella-replicative niche. Infect Immun. 00688-10. 00688-10v1 Capo C, Lindberg FP, Meconi S, Zaffran Y, Tardei G, Brown EJ, Raoult D, Mege J-L (1999) Subversion of monocyte functions by Coxiella burnetii: impairment of the cross-talk between avß3 integrin and CR3. J Immunol 163:6078–6085. org/content/163/11/6078. abstract Capo C, Moynault A, Collette Y, Olive D, Brown EJ, Raoult D, Mege J-L (2003) Coxiella burnetii avoids macrophage phagocytosis by interfering with spatial distribution of complement receptor 3.
The cytosolic pH of C. burnetii was maintained near neutrality by both passive and active mechanisms even in highly acidic solutions, suggesting that it behaves like acidophilic bacteria (Hackstadt 1983). The ability to maintain neutral pH during intracellular infections was proposed to energize nutrient transport using proton motive force (Hackstadt 1983). In the development of extracellular growth sustained metabolism for >24 h C. burnetii was achieved using CCM (complex Coxiella medium) a citrate based acidic medium with complex nutrient sources (Omsland et al.