Publications by authors named "S J Pidot"

Specialized or secondary metabolites are small molecules of biological origin, often showing potent biological activities with applications in agriculture, engineering and medicine. Usually, the biosynthesis of these natural products is governed by sets of co-regulated and physically clustered genes known as biosynthetic gene clusters (BGCs). To share information about BGCs in a standardized and machine-readable way, the Minimum Information about a Biosynthetic Gene cluster (MIBiG) data standard and repository was initiated in 2015.

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Four Gram-stain-negative bacterial strains, CS20, AUT15.5, XENO-11, and CCN3.3, isolated from Steinernema entomopathogenic nematodes, were found to represent novel species within the genus Xenorhabdus (Gammaproteobacteria, Morganellaceae).

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Article Synopsis
  • Buruli ulcer (BU) is a skin disease caused by the bacterium Mycobacterium ulcerans, which is increasingly seen in Australia where possums serve as a reservoir for the infection.
  • In a study, six wild-caught possums that had never been exposed to MU were injected and all developed BU, with ulceration occurring between 49 and 77 days after infection.
  • The findings revealed systemic infection signs in most possums, indicating that this model can enhance understanding of how the bacterium spreads and can inform strategies to prevent further transmission and outbreaks.
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Reconstructing the evolutionary origins of Mycobacterium tuberculosis, the causative agent of human tuberculosis, has helped identify bacterial factors that have led to the tubercle bacillus becoming such a formidable human pathogen. Here we report the discovery and detailed characterization of an exceedingly slow growing mycobacterium that is closely related to M. tuberculosis for which we have proposed the species name Mycobacterium spongiae sp.

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Critical scientific questions remain regarding infection with Mycobacterium ulcerans, the organism responsible for the neglected tropical disease, Buruli ulcer (BU). A controlled human infection model has the potential to accelerate our knowledge of the immunological correlates of disease, to test prophylactic interventions and novel therapeutics. Here we present microbiological evidence supporting M.

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