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Although most clinicians are aware of the problem of antimicrobial resistance, most also underestimate its significance in their own hospital. The incorrect and inappropriate use of antibiotics and other antimicrobials, as well as poor prevention and poor control of infections, are contributing to the development of such resistance. Appropriate use of antibiotics and compliance with infection prevention and control measures should be integral aspects of good clinical practice and standards of care. However, these activities are often inadequate among clinicians, and there is a considerable gap between the best evidence and actual clinical practice. In hospitals, cultural determinants influence clinical practice, and improving behaviour in terms of infection prevention and antibiotics-prescribing practice remains a challenge. Despite evidence supporting the effectiveness of best practices, many clinicians fail to implement them, and evidence-based processes and practices that are known to optimize both the prevention and the treatment of infections tend to be underused. Addressing precisely this problem, this volume offers an essential toolkit for all surgeons and intensivists interested in improving their clinical practices.
Surgery. --- Emergency medicine. --- Anesthesiology. --- Critical care medicine. --- Infectious diseases. --- Medical microbiology. --- Emergency Medicine. --- Intensive / Critical Care Medicine. --- Infectious Diseases. --- Medical Microbiology. --- Intensive care --- Intensive medicine --- Medicine --- Emergency medicine --- Intensive care units --- Anaesthesiology --- Surgery --- Medicine, Emergency --- Critical care medicine --- Disaster medicine --- Medical emergencies --- Surgery, Primitive --- Surgical wound infections --- Prevention. --- Operative wound infections --- Postoperative wound infections --- Wound infections, Postoperative --- Wound infections, Surgical --- Nosocomial infections --- Wounds and injuries --- Complications --- Infections
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Although 30% of the healthy human population is colonized with various Staphylococcus species, some staphylococcal strains, referred to as opportunistic pathogens, can cause minor to life-threatening diseases. The pathogenicity of these bacteria depends on their virulence factors and the robustness of the regulatory networks expressing these virulence factors. Virulence factors of pathogenic Staphylococcus spp. consist of numerous toxins, enterotoxins (some of which act as superantigens), enzymes, and proteins (cytoplasmic, extracellular, and surface) that are regulated by two-component (TC) and quorum-sensing (QS) regulatory networks. To enter this niche, some other Staphylococcus species, such as Staphylococcus simulans, produce a potent endopeptidase called lysostaphin, which can inhibit the growth of pathogenic S. aureus. Some other Staphylococcus species produce autolysins and cationic peptides to win the intra- and inter-species competition. The outcome of this microbial invasion depends not only on pathogenic factors but also on the host’s internal and external defense mechanisms, including a healthy skin microbiome. A healthy skin microbiome population can prevent colonization by other major pathogens. As normal host microflora, these commensals establish a complex relationship with the host as well as the surrounding microbial communities. This Special Issue of Microorganisms is focused on studies and recent advancements in our understanding of staphylococcal virulence mechanisms that enable Staphylococcus spp. either to successfully establish themselves as a colonizer or to overcome the host’s defense system to cause infection along with our effort to make an anti-staphylococcal vaccine.
biofilm --- MRSA --- silver ion --- silver sulfadiazine --- wound infections --- Staphylococcus aureus --- methicillin resistance --- human infection --- CC130 --- biomaterials --- medical devices --- HL-60 cells --- PMNs --- endotracheal tube --- titanium --- implantable devices --- nosocomial diseases --- Staphylococcus lugdunensis --- sortase A --- surface proteins --- LPXTG --- small colony variants --- influenza virus --- super-infection --- pro-inflammatory response --- rural Ghana --- molecular epidemiology --- chronic wounds --- invasive disease --- surgery-associated infection --- sepsis --- SA4Ag vaccine --- conjugated polysaccharide --- ClfA --- MntC --- protection --- animal models --- phase variation --- Staphylococcus epidermidis --- microbiota --- multidrug resistance --- genome sequencing --- phylogenetic analyses --- arthroplasty surgery --- methicillin-resistant Staphylococcus aureus (MRSA) --- community-associated MRSA (CA-MRSA) --- CA-MRSA strain USA300 --- murine skin infection model --- dermatopathology --- dermonecrosis --- neutrophil --- host antibacterial response --- cytokine --- chemokine --- physiology --- metabolism --- carbon catabolite repression --- CcpA --- HPr --- colonization --- mouse --- JSNZ --- aurintricarboxylic acid --- ATA --- adhesion inhibitor --- mupirocin --- nose --- superantigen --- mastitis --- food intoxication --- regulation --- sec variants --- CM lipids --- daptomycin resistance --- resensitization --- n/a
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Although 30% of the healthy human population is colonized with various Staphylococcus species, some staphylococcal strains, referred to as opportunistic pathogens, can cause minor to life-threatening diseases. The pathogenicity of these bacteria depends on their virulence factors and the robustness of the regulatory networks expressing these virulence factors. Virulence factors of pathogenic Staphylococcus spp. consist of numerous toxins, enterotoxins (some of which act as superantigens), enzymes, and proteins (cytoplasmic, extracellular, and surface) that are regulated by two-component (TC) and quorum-sensing (QS) regulatory networks. To enter this niche, some other Staphylococcus species, such as Staphylococcus simulans, produce a potent endopeptidase called lysostaphin, which can inhibit the growth of pathogenic S. aureus. Some other Staphylococcus species produce autolysins and cationic peptides to win the intra- and inter-species competition. The outcome of this microbial invasion depends not only on pathogenic factors but also on the host’s internal and external defense mechanisms, including a healthy skin microbiome. A healthy skin microbiome population can prevent colonization by other major pathogens. As normal host microflora, these commensals establish a complex relationship with the host as well as the surrounding microbial communities. This Special Issue of Microorganisms is focused on studies and recent advancements in our understanding of staphylococcal virulence mechanisms that enable Staphylococcus spp. either to successfully establish themselves as a colonizer or to overcome the host’s defense system to cause infection along with our effort to make an anti-staphylococcal vaccine.
Research & information: general --- Biology, life sciences --- biofilm --- MRSA --- silver ion --- silver sulfadiazine --- wound infections --- Staphylococcus aureus --- methicillin resistance --- human infection --- CC130 --- biomaterials --- medical devices --- HL-60 cells --- PMNs --- endotracheal tube --- titanium --- implantable devices --- nosocomial diseases --- Staphylococcus lugdunensis --- sortase A --- surface proteins --- LPXTG --- small colony variants --- influenza virus --- super-infection --- pro-inflammatory response --- rural Ghana --- molecular epidemiology --- chronic wounds --- invasive disease --- surgery-associated infection --- sepsis --- SA4Ag vaccine --- conjugated polysaccharide --- ClfA --- MntC --- protection --- animal models --- phase variation --- Staphylococcus epidermidis --- microbiota --- multidrug resistance --- genome sequencing --- phylogenetic analyses --- arthroplasty surgery --- methicillin-resistant Staphylococcus aureus (MRSA) --- community-associated MRSA (CA-MRSA) --- CA-MRSA strain USA300 --- murine skin infection model --- dermatopathology --- dermonecrosis --- neutrophil --- host antibacterial response --- cytokine --- chemokine --- physiology --- metabolism --- carbon catabolite repression --- CcpA --- HPr --- colonization --- mouse --- JSNZ --- aurintricarboxylic acid --- ATA --- adhesion inhibitor --- mupirocin --- nose --- superantigen --- mastitis --- food intoxication --- regulation --- sec variants --- CM lipids --- daptomycin resistance --- resensitization
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