Prevalence of the SigB-Deficient Phenotype among Clinical Staphylococcus aureus Isolates Linked to Bovine Mastitis
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Published:2023-04-03
Issue:4
Volume:12
Page:699
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ISSN:2079-6382
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Container-title:Antibiotics
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language:en
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Short-container-title:Antibiotics
Author:
Walzl Anna1, Marbach Helene1, Belikova Darya2, Vogl Claus3, Ehling-Schulz Monika1ORCID, Heilbronner Simon2ORCID, Grunert Tom1ORCID
Affiliation:
1. Institute of Microbiology, Department of Pathobiology, University of Veterinary Medicine, A-1210 Vienna, Austria 2. Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, D-72076 Tübingen, Germany 3. Molecular Genetics, Institute of Animal Breeding and Genetics, Department of Biomedical Sciences, University of Veterinary Medicine, A-1210 Vienna, Austria
Abstract
Phenotypic adaptation has been associated with persistent, therapy-resistant Staphylococcus aureus infections. Recently, we described within-host evolution towards a Sigma factor B (SigB)-deficient phenotype in a non-human host, a naturally infected dairy cow with chronic, persistent mastitis. However, to our knowledge, the prevalence of SigB deficiency among clinical S. aureus isolates remains unknown. In this study, we screened a collection of bovine mastitis isolates for phenotypic traits typical for SigB deficiency: decreased carotenoid pigmentation, increased proteolysis, secretion of α-hemolysin and exoproteins. Overall, 8 out of 77 (10.4%) isolates of our bovine mastitis collection exhibited the SigB-deficient phenotype. These isolates were assigned to various clonal complexes (CC8, CC9, CC97, CC151, CC3666). We further demonstrated a strong positive correlation between asp23-expression (a marker of SigB activity) and carotenoid pigmentation (r = 0.6359, p = 0.0008), underlining the role of pigmentation as a valuable predictor of the functional status of SigB. Sequencing of the sigB operon (mazEF-rsbUVW-sigB) indicated the phosphatase domain of the RsbU protein as a primary target of mutations leading to SigB deficiency. Indeed, by exchanging single nucleotides in rsbU, we could either induce SigB deficiency or restore the SigB phenotype, demonstrating the pivotal role of RsbU for SigB functionality. The data presented highlight the clinical relevance of SigB deficiency, and future studies are needed to exploit its role in staphylococcal infections.
Funder
the Austrian Science Fund Deutsche Forschungsgemeinschaft German Center of Infection Research
Subject
Pharmacology (medical),Infectious Diseases,Microbiology (medical),General Pharmacology, Toxicology and Pharmaceutics,Biochemistry,Microbiology
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