Nature 2011, 477:596–600.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions PCYW and JLLT conceived the study. PCYW, JLLT and LX wrote the manuscript;
PCYW, JLLT, LX and SKPL participated in the design of the study; LX and JLLT performed the experiments. LX, JLLT and PCYW analyzed the data; RMW, BK and SKPL corrected the manuscript; all authors read and approved the final manuscript.”
“Background Coxiella burnetii, the etiological agent of Q fever and a category B biothreat agent, has the potential for rapid, BIBW2992 in vitro long distance dispersal. This obligate intracellular bacterium is easily aerosolized and has been known to cause infections downwind of a likely source [1, 2]. In humans, inhalation is a significant route of infection as 1 to 10 organisms can cause disease [3]. While most cases are relatively mild, some infections result in abortions, premature birth, pneumonia, endocarditis or death. selleck compound livestock contaminate the environment by shedding live C. burnetii
cells in feces, urine and milk; in sheep and goats, birthing tissues contain particularly high quantities of live cells. Viable C. burnetii cells can persist in the environment due to resistance to environmental degradation as a small cell variant, however their longevity is unknown. Mild effects of infections in most zoonotic Selleck AZD1390 reservoirs enable them to remain ambulatory and facilitate continued transmission; often, domestic and wild animal hosts suffer either no disease, or only mild forms
when infected [4]. With the possible exception of New Zealand, C. burnetii is found worldwide. Studies of prevalence in livestock have produced highly variable results due to different methodologies and study designs [5], similarly, PCR based detection studies also show variable levels of infection ranging from 20 to 100% of samples [6–10]. Due to the suspected importance of livestock in maintenance and transmission of C. burnetii, dairy products have been recently sampled and show high prevalence rates [8, 11–13]. Environmental sampling in the United States also shows highly variable but widespread CFTR modulator prevalence of C. burnetii[14]. In the Netherlands, environmental presence was correlated with incidences of Q fever in humans [15]. With few exceptions, the variability and relatedness among C. burnetii detected across the landscape is unknown. As such, we cannot determine the extent to which the current distribution is due to frequent, but isolated occurrences, or a single large outbreak. Despite its ubiquity and importance, genotyping efforts on C. burnetii have lagged behind those of other bacterial pathogens because of culturing difficulties and the reliance of genotyping technologies on good quantity/quality DNA obtained through culturing.