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In this review, we highlight the variations of gut resistome studies, which may preclude comparisons and translational interpretations. Of 22 included studies, a range of 12 to 2000 antibiotic resistance (AR) genes were profiled. Overall, studies defined a healthy gut resistome as subjects who had not taken antibiotics in the last three to 12 months prior to sampling. In studies with de novo assembly, AR genes were identified based on variable nucleotide or amino acid sequence similarities. Different marker genes were used for defining resistance to a given antibiotic class. Validation of phenotypic resistance in the laboratory is frequently lacking. Cryptic resistance, collateral sensitivity and the interaction with repressors or promotors were not investigated. International consensus is needed for selecting marker genes to define resistance to a given antibiotic class in addition to uniformity in phenotypic validation and bioinformatics pipelines.

Hospital patients who are colonized with methicillin-resistant Staphylococcus aureus (MRSA), may transmit the bacteria to other patients. An agent-based simulation is designed to determine how the problem might be managed and the risk of transmission reduced. Most MRSA modeling studies have applied mathematical compartmental models or Monte Carlo simulations. In the agent-based model, each patient is identified on admission as being colonized or not, has a projected length of stay and may be more or less susceptible to colonization. Patient states represent colonization, detection, treatment, and location within the ward. MRSA transmission takes place between pairs of individuals in successive time slices. Various interventions designed to reduce MRSA transmission are embedded in the model including: admission and repeat screening tests, shorter test turnaround time, isolation, and decolonization treatment. These interventions can be systematically evaluated by model experimentation.

The use of successive generations of beta-lactams has selected successive generations of beta-lactamases including CTX-M ESBLs, AmpC beta-lactamases, and KPC carbapenamases in Enterobacteriaceae. Moreover, this cephalosporin resistance, along with rising resistance to fluoroquinolones, is now driving the use of carbapenems and unfortunately the carbapenem resistance has emerged markedly, especially in Acinetobacter spp. due to OXA- and metallo-carbapenemases. The industry responded to the challenge of rising resistance and recently developed some novel beta-lactams such as ceftobiprole, ceftaroline etc. and many beta-lactam compounds, including beta-lactamase-inhibitors, such as BMS-247243, S-3578, RWJ-54428, CS-023, SMP-601, NXL 104, BAL 30376, LK 157, and so on are under trials. This review provides the comprehensive accounts of the developments in penicillins, cephalosporins, carbapenems, and beta-lactamase-inhibitors, and the insight about medicinal chemistry, mechanism(s) of action and resistance, potential strategies to overcome resistance due to beta-lactamases, and also the recent advancements in the development of newer beta-lactam compounds; some of which are still under trials and yet to be classified. This review will fill the gap since previously published reviews and will serve as a comprehensive update on the current topic.

This review looks at the challenges facing the worldwide community with the increasing problem of methicillin resistance in Staphylococcus aureus. The epidemiology and natural history of community-associated methicillin-resistant Staphylococcus aureus and the challenge of control is discussed. Options for treatment and review of key antimicrobial agents acting against methicillin-resistant S. aureus, both currently in use and in development, are addressed. There are a number of new agents, the place of which in therapeutic regimens is yet to emerge. The review attempts to inform the reader of the probable position of these agents.