Q fever is a worldwide zoonosis caused by Coxiella burnetii. Domestic ruminants are considered to be the main reservoir. Sheep, in particular, may frequently cause outbreaks in humans. Because within-flock circulation data are essential to implementing optimal management strategies, we performed a follow-up study of a naturally infected flock of dairy sheep. We aimed to (i) describe C. burnetii shedding dynamics by sampling vaginal mucus, feces, and milk, (ii) assess circulating strain diversity, and (iii) quantify barn environmental contamination. For 8 months, we sampled vaginal mucus and feces every 3 weeks from aborting and nonaborting ewes (n ؍ 11 and n ؍ 26, respectively); for lactating females, milk was obtained as well. We also sampled vaginal mucus from nine ewe lambs. Dust and air samples were collected every 3 and 6 weeks, respectively. All samples were screened using real-time PCR, and strongly positive samples were further analyzed using quantitative PCR. Vaginal and fecal samples with sufficient bacterial burdens were then genotyped by multiple-locus variable-number tandem-repeat analysis (MLVA) using 17 markers. C. burnetii burdens were higher in vaginal mucus and feces than in milk, and they peaked in the first 3 weeks postabortion or postpartum. Primiparous females and aborting females tended to shed C. burnetii longer and have higher bacterial burdens than nonaborting and multiparous females. Six genotype clusters were identified; they were independent of abortion status, and within-individual genotype diversity was observed. C. burnetii was also detected in air and dust samples. Further studies should determine whether the within-flock circulation dynamics observed here are generalizable.Q fever is a widespread zoonosis caused by Coxiella burnetii, a Gram-negative intracellular bacterium that has been reported in a broad range of host species. Livestock, especially small ruminants, are the main sources of human infections (1-3). In domestic ruminants, Q fever's major clinical manifestations are abortions and stillbirths, whose occurrence may translate into significant economic losses (1, 3). In humans, C. burnetii infections range from asymptomatic to severe. Acute forms of the disease may result in high fevers and severe pneumonia or hepatitis, and chronic forms are strongly debilitating and may be fatal when endocarditis develops in patients with underlying heart disease (4-6).Animals and humans become infected essentially through the inhalation of airborne particles contaminated with C. burnetii (3,7,8). Contaminated dust particles may remain infectious for long periods of time due to the capacity of the bacterium to differentiate into highly resistant spore-like forms (9, 10). Consequently, knowledge of C. burnetii's sources and shedding dynamics is essential to assessing the risks of disease transmission and pathogen persistence. On livestock farms, C. burnetii DNA has been found in various environmental matrices, such as dust (11-13) and aerosols (14-16). However, studies that examin...