The evolution of resistance to antibiotics is a major public health problem and an example of rapid adaptation under natural selection by antibiotics. The dynamics of antibiotic resistance within and between hosts can be understood in the light of mathematical models that describe the epidemiology and evolution of the bacterial population. "Between-host" models describe the spread of resistance in the host community, and in more specific settings such as hospitalized hosts (treated by antibiotics at a high rate), or farm animals. These models make predictions on the best strategies to limit the spread of resistance, such as reducing transmission or adapting the prescription of several antibiotics. Models can be fitted to epidemiological data in the context of intensive care units or hospitals to predict the impact of interventions on resistance. It has proven harder to explain the dynamics of resistance in the community at large, in particular because models often do not reproduce the observed coexistence of drug-sensitive and drug-resistant strains. "Within-host" models describe the evolution of resistance within the treated host. They show that the risk of resistance emergence is maximal at an intermediate antibiotic dose, and some models successfully explain experimental data. New models that include the complex host population structure, the interaction between resistance-determining loci and other loci, or integrating the within- and between-host levels will allow better interpretation of epidemiological and genomic data from common pathogens and better prediction of the evolution of resistance.
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http://dx.doi.org/10.1111/eva.12753 | DOI Listing |
Drugs
January 2025
Department of Chemical Biology, Helmholtz Centre for Infection Research, Inhoffenstraße 7, 38124, Braunschweig, Germany.
The rise of antimicrobial resistance represents a significant global health threat, driven by the diminishing efficacy of existing antibiotics, a lack of novel antibacterials entering the market, and an over- or misuse of existing antibiotics, which accelerates the evolution of resistant bacterial strains. This review focuses on innovative therapies by highlighting 19 novel antibacterials in clinical development as of June 2024. These selected compounds are characterized by new chemical scaffolds, novel molecular targets, and/or unique mechanisms of action, which render their potential to break antimicrobial resistance particularly high.
View Article and Find Full Text PDFMycoses
January 2025
Departamento Micología-Instituto Nacional de Enfermedades Infecciosas "Dr. Carlos G. Malbrán", Buenos Aires, Ciudad Autónoma de Buenos Aires, Argentina.
Background: Epidemiological surveillance of Candidozyma sp. has become important because many species of this new genus have been reported to be responsible for nosocomial outbreaks and to exhibit elevated minimal inhibitory concentrations (MIC) to one or more classes of antifungal drugs.
Objectives: To describe the genetic relationships among Argentinian clinical isolates belonging to the Candidozyma genus and to study the molecular mechanisms associated with antifungal resistance.
BMC Plant Biol
January 2025
Division of Plant Physiology, ICAR-Indian Agricultural Research Institute, New Delhi, 110012, India.
Background: The membrane transporters viz. multidrug and toxic compound extrusion (MATE) and aluminum-activated malate transporter (ALMT) are associated with aluminum (Al) tolerance by accelerating secretion of organic acids, which can influence nutrient availability and stress response. However, such transporter families have not yet been reported in lentil under Al stress condition.
View Article and Find Full Text PDFBMC Plant Biol
January 2025
College of Life Science, Jilin Agricultural University, Changchun, 13000, China.
Background: Thaumatin-like proteins (TLPs) are crucial pathogenesis-related proteins that significantly contribute to plant defense rection. Fusarium oxysporum f. sp.
View Article and Find Full Text PDFBMC Plant Biol
January 2025
Biosystematics Group, Wageningen University and Research, Droevendaalsesteeg 1, Wageningen, 6708 PB, The Netherlands.
Background: HOPZ-ACTIVATED RESISTANCE 1 (ZAR1) is a nucleotide-binding leucine-rich repeat (NLR) protein functioning as a recognition hub to initiate effector-triggered immunity against bacterial pathogens. To initiate defense, ZAR1 associates with different HOPZ-ETI-DEFICIENT 1 (ZED1)-Related Kinases (ZRKs) to form resistosomes to indirectly perceive effector-induced perturbations. Few studies have focused on the phylogenomic characteristics of ZAR1 and ZRK immune gene families and their evolutionary relationships.
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