Coxiella burnetii: Host and bacterial responses to infection

Coxiella-like Endosymbionts

“…All species in the genus Coxiella are intracellular bacteria (Raoult 1993 ;Waag 2007 ) . Coxiella -like bacteria share tick host and geographic distribution with C. burnetii (Parola and Raoult 2001 ;Childs and Paddock 2003 ) .…”

“…C. burnetii is an obligate intracellular bacterium (Maurin and Raoult 1999 ) and the aetiological agent of human Q fever, a zoonotic disease that is distributed world-wide and causes acute or chronic disease with symptoms including fever, hepatitis, and respiratory complications (Raoult 1993 ;Waag 2007 ) .…”

“…Studies of Coxiella have largely focused on pathogenic strains of C. burnetii , which have been identi fi ed in arthropods, birds, fi sh, mammals, and reptiles (Waag 2007 ;Angelakis and Raoult 2010 ) . Recently, many Coxiella -like bacteria have been reported in ticks.…”

Two rare manifestations of Q fever: splenic and hepatic abscesses and cerebral venous thrombosis, with literature reviewma non troppo

“…Macrophages are the main host for C burnetii , which lives inside acidic lysosomes; this fact is thought to have therapeutic implications 1 14 . C burnetii has the ability to change the properties of its lipopolysaccharide, resulting in a phase variation, being that phase I is highly infectious and is the natural phase found in infected animals, whereas phase II is less infectious and is obtained only in laboratory.…”

Assessment of Potential Long Term Health Effects on Army Human Test Subjects of Relevant Biological and Chemical Agents, Drugs, Medications and Substances

“…61 Decreases in timeout responses continued throughout the washout period, while other deficits corrected. 23 In a separate study, these researchers also found that rats treated with sub-clinical doses (dose range, 0.25-1.0 mg/kg every other day over the course of 30 days) of DFP had cognitive deficits in spatial learning and recall as well as recognition memory, and that such cognitive deficits may be related to persistent functional changes in brain neurotrophin and cholinergic pathways. 62 Additionally, a study on the mechanisms underlying the neurological deficits caused by organophosphates by Torres-Altoro and colleagues found that DFP alone or as part of a combination of neurotoxicants caused hyper-phosphorylation of Thr205 tau in mice.…”