Publications by authors named "William Bachman"

Article Synopsis
  • - The study focused on KPC-Kp bloodstream infections, which are deadly, and aimed to understand how these bacteria resist a key defense mechanism in our blood, called complement.
  • - Researchers tested various KPC-Kp isolates from patients, discovering that 27% of them resisted killing by human serum; a specific gene mutation (wcaJ) linked to capsule production contributed to this resistance.
  • - This mutation resulted in less capsule presence, paradoxically increasing the bacteria's ability to bind complement proteins while also improving their survival against immune responses, potentially allowing them to thrive in the bloodstream without being overly virulent in tissues.
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β-Lactamases can accumulate stepwise mutations that increase their resistance profiles to the latest β-lactam agents. CMY-185 is a CMY-2-like β-lactamase and was identified in an clinical strain isolated from a patient who underwent treatment with ceftazidime-avibactam. CMY-185, possessing four amino acid substitutions of A114E, Q120K, V211S, and N346Y relative to CMY-2, confers high-level ceftazidime-avibactam resistance, and accumulation of the substitutions incrementally enhances the level of resistance to this agent.

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Article Synopsis
  • - This study investigated a variant of the blaCMY gene linked to resistance against the antibiotic combination ceftazidime/avibactam in a series of E. coli isolates from a patient with an intra-abdominal infection.
  • - Whole-genome sequencing showed the resistant E. coli strain, identified as ST410, carried a new CMY β-lactamase gene called blaCMY-185, which had specific amino acid changes that contributed to its resistance.
  • - The research concluded that the CMY-185 variant requires multiple amino acid mutations to effectively confer resistance, marking a significant differentiation from other similar enzymes when it comes to resisting ceftazidime/avibactam treatments.
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Article Synopsis
  • *Researchers found that 27% of KPC-Kp isolates showed increased resistance to human serum, linked to a mutation that reduces capsule content and helps the bacteria evade immune responses.
  • *The mutation allows KPC-Kp to survive better in the bloodstream while being less virulent in tissues, highlighting a complex interaction that aids the bacteria's persistence in the host.
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Objectives: To characterize a variant associated with ceftazidime-avibactam (CZA) resistance from a serially collected isolate.

Methods: A patient with an intra-abdominal infection due to recurrent was treated with CZA. On day 48 of CZA therapy, with a CZA MIC of >256 mg/L was identified from abdominal drainage.

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A common adverse response to the clinical use of glucocorticoids (GCs) is elevated intraocular pressure (IOP) which is a major risk factor for glaucoma. Elevated IOP arises due to impaired outflow of aqueous humor (AH) through the trabecular meshwork (TM). Although GC-induced changes in actin cytoskeletal dynamics, contractile characteristics, and cell adhesive interactions of TM cells are believed to influence AH outflow and IOP, the molecular mechanisms mediating changes in these cellular characteristics are poorly understood.

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Understanding cell behaviors can provide new knowledge on the development of different pathologies. Focal adhesion (FA) sites are important sub-cellular structures that are involved in these processes. To better facilitate the study of FA sites, deep learning (DL) can be used to predict FA site morphology based on limited microscopic datasets (e.

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Clinical use of glucocorticoids is associated with increased intraocular pressure (IOP), a major risk factor for glaucoma. Glucocorticoids have been reported to induce changes in actin cytoskeletal organization, cell adhesion, extracellular matrix, fibrogenic activity, and mechanical properties of trabecular meshwork (TM) tissue, which plays a crucial role in aqueous humor dynamics and IOP homeostasis. However, we have a limited understanding of the molecular underpinnings regulating these myriad processes in TM cells.

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One hundred forty-nine carbapenem-resistant Enterobacterales from clinical samples obtained between April 2014 and November 2017 were subjected to whole genome sequencing and multi-locus sequence typing. Klebsiella pneumoniae (81, 54.4%) and Escherichia coli (38, 25.

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Background: Carbapenem-resistant Enterobacteriaceae (CRE) is an urgent public health threat globally. Limited data are available regarding the epidemiology of CRE in South Florida. We describe the epidemiology of CRE within a large public healthcare system in Miami, FL, the experience with an internal registry, active surveillance testing, and the impact of infection prevention practices.

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