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Coxiella burnetii causes significant reproduction losses in livestock and the disease Q fever in humans. Transmission of C. burnetii is facilitated by the stability of the bacterium in the environment and the susceptibility of a variety of host species to infection. Consequently, inter‐species transmission occurs frequently through either direct or indirect contact. Wildlife may represent reservoirs of C. burnetii and could therefore be a source of infection for domestic animals. Understanding the prevalence of C. burnetii infections at the wildlife‐livestock interface is important for disease control. This study aimed to investigate the extent of C. burnetii exposure in wild deer in eastern Australia. Serum samples were obtained from 413 wild deer from seven regions in four eastern Australian states from 2017 to 2020. Antibodies were detected using a commercial Q fever antibody kit validated for ruminants. Seroprevalence of C. burnetii antibodies in deer was determined and true prevalence estimated, for each region. The overall seroprevalence of C. burnetii antibodies in wild deer was 3.4% (14 seropositive of 413 deer sampled) with true prevalence estimated to be 4.3% (95% credible interval: 0.6%, 10.9%). Seropositive deer were identified only in Queensland (7/108 seropositive) and northern New South Wales (7/120 seropositive). This geospatial distribution is consistent with seropositivity in other animal species and indicative of the level of C. burnetii in the environment. The low seroprevalence suggests that wild deer are unlikely to be a major reservoir species for C. burnetii in eastern Australia but may still be implicated in inter‐species transmission cycles. [ABSTRACT FROM AUTHOR]

This paper provides specific guidelines on the management of tuberculosis infection and disease, covering general principles, recommended drug regimens and discuss the evidence to support these. It also covers use of corticosteroids, intermittent therapy, directly observed therapy and an approach to the management of a patient with drug-resistant tuberculosis. [ABSTRACT FROM AUTHOR]

Objectives: The role Staphylococcus aureus antimicrobial resistance genes and toxins play in disease severity, management and outcome in childhood is an emerging field requiring further exploration., Methods: A prospective multisite study of Australian and New Zealand children hospitalised with S. aureus bacteraemia (SAB) occurred over 24 months (2017-2018). Whole genome sequencing (WGS) data were paired with clinical information from the ISAIAH cohort., Results: 353 SAB isolates were sequenced; 85% methicillin-susceptible S. aureus ([MSSA], 301/353) and 15% methicillin-resistant S. aureus ([MRSA], 52/353). There were 92 sequence types (STs), most commonly ST5 (18%) and ST30 (8%), grouped into 23 clonal complexes (CCs), most frequently CC5 (21%) and CC30 (12%). MSSA comprised the majority of healthcare-associated SAB (87%, 109/125), with principal clones CC15 (48%, 11/21) and CC8 (33%, 7/21). Panton-Valentine leukocidin (PVL)-positive SAB occurred in 22% (76/353); predominantly MSSA (59%, 45/76), community-onset (92%, 70/76) infections. For community-onset SAB, the only microbiological independent predictor of poor outcomes was PVL positivity (aOR 2.6 [CI 1.0-6.2])., Conclusion: From this WGS paediatric SAB data, we demonstrate the previously under-recognized role MSSA has in harbouring genetic virulence and causing healthcare-associated infections. PVL positivity was the only molecular independent predictor of poor outcomes in children. These findings underscore the need for further research to define the potential implications PVL-producing strains may have on approaches to S. aureus clinical management., Competing Interests: Declaration of Competing Interest P.A.B. reports grants from National Health and Medical Research Council, Medical Research Futures Fund and Murdoch Children's Research Institute outside the submitted work and travel funds from the Royal Children's Hospital. S.O. has acted on an advisory board for CSL-Behring. All remaining authors have no reported conflicts of interest., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)