Pseudomonas And Acinetobacter From Drug Resistance To Pathogenesis

Pseudomonas aeruginosa and Acinetobacter baumannii are among the most common non-lactose-fermenting Gram-negative pathogens responsible for hospital-acquired infections, especially in intensive care units (ICUs). The treatment of infections caused by these bacteria is complicated due to the emergence of multi-drug resistance as the two species are noted for their intrinsic resistance to antimicrobial agents and their ability to acquire genetic elements that encode for resistance determinants. In both species, resistance to multiple classes of antimicrobial agents can seriously compromise the ability to treat infected patients, especially the immunocompromised. Consequently, very few antimicrobials remain as treatment options. Mechanisms of resistance in both of these pathogens include the production of β-lactamases and aminoglycoside-modifying enzymes as well as reduced or lack of expression of outer membrane proteins, mutations in topoisomerases, and up-regulation of efflux pumps. To that purpose, the findings of the studies included in this book deal with the prevalence of resistant isolates to various antimicrobial agents in both P. aeruginosa and A. baumannii, their underlying mechanisms of resistance, their virulence factors, their pathogenesis, and prospective treatment options. Special thanks are due to Mr. Bassam El-Hafi for facilitating procedures involved in this publication.

This book covers the wide set of well-regulated virulence factors and defense mechanisms of Pseudomonas aeruginosa focusing on stress responses and the evolution of this opportunistic human pathogen. Pseudomonas aeruginosa is responsible for one out of ten hospital infections. Additionally, this Gram-negative bacterium is accountable for persistent infections in immunocompromised individuals and the leading cause of chronic lung infections in cystic fibrosis patients. This book provides insight on the metabolic versatility of Pseudomonas aeruginosa and its mechanisms for biofilm formation that make this organism highly efficient in causing infections. The book invites the readers to learn more about the intrinsic ability of Pseudomonas aeruginosa to resist a wide variety of antimicrobial agents due to the concerted action of multidrug efflux pumps, antibiotic-degrading enzymes, and the low permeability of bacterial cellular envelopes. Particular focus is put on the evolutionary role of different types of protein-secretion systems in pathogenesis, flagella and their role in chemotaxis and surface sensing, and host-pathogen interactions. This book is a useful introduction to the field for junior scientists interested in the biology and pathogenesis of Pseudomonas aeruginosa. It is also an interesting read for advanced scientists and medical specialists working within this field, providing a broader view of the topic beyond their specific area of specialization.

Pseudomonas aeruginosa is known as a persistent bacterial pathogen. Antibiotics are currently the most common bacterial treatment for related infections but cases of microbial resistance are on the rise. Toxin-Antitoxin Systems in Pseudomonas aeruginosa describes one of the most important antimicrobial targets in the bacterium species. The contributors have compiled comprehensive information on the subject. The reference initially acquaints the reader with key topics about P. aeruginosa infection including virulence factors, pathogenicity, epidemiology, laboratory diagnosis and antibiotic resistance. This is followed by detailed chapters on toxin-antitoxin systems which explain their role in the bacterial pathogenesis with reference to P. aeruginosa. The comprehensive information on the subject makes this an ideal reference for newcomers to the field of bacteriology and target discovery. Students of medical microbiology and medical professionals who are interested in the finer details of P. aeruginosa pathogenicity will also be equipped with sufficient information to join the discussion on this topic with fellow researchers.

This ? rst edition of Antimicrobial Drug Resistance grew out of a desire by the editors and authors to have a comprehensive resource of information on antimicrobial drug resistance that encompassed the current information available for bacteria, fungi, protozoa and viruses. We believe that this information will be of value to clinicians, epidemiologists, microbiologists, virologists, parasitologists, public health authorities, medical students and fellows in training. We have endeavored to provide this information in a style which would be accessible to the broad community of persons who are concerned with the impact of drug resistance in our cl- ics and across the broader global communities. Antimicrobial Drug Resistance is divided into Volume 1 which has sections covering a general overview of drug resistance and mechanisms of drug resistance ? rst for classes of drugs and then by individual microbial agents including bacteria, fungi, protozoa and viruses. Volume 2 addresses clinical, epidemiologic and public health aspects of drug resistance along with an overview of the conduct and interpretation of speci? c drug resistance assays. Together, these two volumes offer a comprehensive source of information on drug resistance issues by the experts in each topic.

In the past two decades, great progress has been made in the understanding of copper as a bioelement. The book summarizes the current knowledge of copper toxicity, homeostasis and resistance in bacteria, in which proteins like copper ATPases, copper chaperones and copper-responsive regulators of gene expression play major roles. The author also discusses the metallation of cuproenzymes. The evolution of the use of copper by cells and of copper-homeostatic proteins are is also considered in this Brief.

Bacterial toxin-antitoxin (TA) systems, which are ubiquitously present in bacterial genomes, are not essential for normal cell proliferation. The TA systems regulate fundamental cellular processes, facilitate survival under stress conditions, have essential roles in virulence and represent potential therapeutic targets. These genetic TA loci are also shown to be involved in the maintenance of successful multidrug-resistant mobile genetic elements. The TA systems are classified as types I to VI, according to the nature of the antitoxin and to the mode of toxin inhibition. Type II TA systems encode a labile antitoxin and its stable toxin; degradation of the antitoxin renders a free toxin, which is bacteriostatic by nature. A free toxin generates a reversible state with low metabolic activity (quiescence) by affecting important functions of bacterial cells such as transcription, translation, DNA replication, replication and cell-wall synthesis, biofilm formation, phage predation, the regulation of nucleotide pool, etc., whereas antitoxins are toxin inhibitors. Under stress conditions, the TA systems might form networks. To understand the basis of the unique response of TA systems to stress, the prime causes of the emergence of drug-resistant strains, and their contribution to therapy failure and the development of chronic and recurrent infections, must be known in order to grasp how TA systems contribute to the mechanisms of phenotypic heterogeneity and pathogenesis that will enable the rational development of new treatments for infections caused by pathogens.

Antibiotics represent one of the most successful forms of therapy in medicine. But the efficiency of antibiotics is compromised by the growing number of antibiotic-resistant pathogens. Antibiotic resistance, which is implicated in elevated morbidity and mortality rates as well as in the increased treatment costs, is considered to be one of the major global public health threats (www.who.int/drugresistance/en/) and the magnitude of the problem recently prompted a number of international and national bodies to take actions to protect the public (http://ec.europa.eu/dgs/health_consumer/docs/road-map-amr_en.pdf: http://www.who.int/drugresistance/amr_global_action_plan/en/; http://www.whitehouse.gov/sites/default/files/docs/carb_national_strategy.pdf). Understanding the mechanisms by which bacteria successfully defend themselves against the antibiotic assault represent the main theme of this eBook published as a Research Topic in Frontiers in Microbiology, section of Antimicrobials, Resistance, and Chemotherapy. The articles in the eBook update the reader on various aspects and mechanisms of antibiotic resistance. A better understanding of these mechanisms should facilitate the development of means to potentiate the efficacy and increase the lifespan of antibiotics while minimizing the emergence of antibiotic resistance among pathogens.

This book provides essential insights into microbial pathogenesis, host-pathogen interactions, and the anti-microbial drug resistance of various human pathogens on the basis of various model organisms. The initial sections of the book introduce readers to the mechanisms of microbial pathogenesis, host-pathogen interactions, anti-microbial drug resistance, and the dynamics of biofilm formation. Due to the emergence of various microbial resistant strains, it is especially important to understand the prognosis for microbial infections, disease progression profiles, and mechanisms of resistance to antibiotic therapy in order to develop novel therapeutic strategies. In turn, the second part of the book presents a comparative analysis of various animal models to help readers understand microbial pathogenesis, host-pathogen interactions, anti-microbial drug discovery, anti-biofilm therapeutics, and treatment regimes. Given its scope, the book represents a valuable asset for microbiologists, biotechnologists, medical professionals, drug development researchers, and pharmacologists alike.