Pseudomonas Aeruginosa Biology Genetics And Host Pathogen Interactions

The opportunistic pathogen Pseudomonas aeruginosa offers a rich variety of biologically relevant topics to explore and serves as a model system to understand the interactions of Gram-negative bacteria with human hosts. The organism adapts readily to most environments. It has a large and variable genome with a great deal of metabolic potential. P. aeruginosa encodes a variety of regulatory systems to fine tune gene expression and integrate environmental signals. This organism can infect both plants and animals and produces a plethora of enzymes and factors that can overcome host defenses. Moreover, it has the ability to change between the states of a sedentary colonizer to an invasive and highly motile organism. Clinically, the bacterium is resistant to many antibiotics making it difficult to treat and impossible to eradicate from the lungs of patients with cystic fibrosis. Intrinsic antibiotic resistance combined with an armamentarium of tissue degradative enzymes makes it imperative to possess a comprehensive understanding of the biology, genetics and pathogenesis of this organism so that novel therapeutics based on virulence product neutralization can be designed and implemented. This Research Topics issue will be devoted to updating the current understanding of P. aeruginosa systems as they relate to its different lifestyles in different environments. The underlying theme is to provide broad overviews and to integrate protein structure-function and gene regulation as it relates to the biology of this bacterium.

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.

Despite not being a disease in and of itself, antibiotic resistance could be considered the global epidemic of modern times, since it produces the failure to prevent and treat many infectious diseases. This can ultimately lead to untreatable microbial infections becoming more widespread and this will significantly increase morbidity and mortality. This worldwide problem is estimated to cause millions of deaths per year and could become an even more significant menace to humanity than established illnesses, such as cancer. In February 2017, the World Health Organization (WHO) published a list of antibiotic-resistant “priority pathogens” – a catalogue of 12 families of bacteria which pose the greatest threat to human health - and Acinetobacter baumannii is leading the list. The most critical group includes multidrug-resistant bacteria, which pose a particular threat in hospitals, nursing homes, and among patients whose care requires devices such as ventilators and blood catheters. This group includes Acinetobacter, Pseudomonas, and various Enterobacteriaceae and they are often associated with deadly infections, such as bloodstream infections and pneumonia. Furthermore, these bacteria have become resistant to a large number of antibiotics, including carbapenems and third generation cephalosporins – the best available antibiotics for treating multidrug-resistant bacteria. A. baumannii is a particularly worrisome example and demands attention: This pathogen turned into a menace to humans during the late 70s, likely as a result of intense antibiotic use in hospital settings, and became one of the microorganisms that are challenging the antibiotic era. Its extreme genome plasticity, combined with mechanisms of horizontal genetic transfer, have played a key role in the evolution of this microorganism, as well as its adaptability to unfavorable environments. However, its pathophysiology, as well as the mechanisms leading to its success as a pathogen, are not that simple to unveil. However, what is clear is that the triad of host-pathogen-environment is crucial in selection and establishment of multidrug-resistant clones and outbreaks. Indeed, there are still many aspects of this pathogen that require a deeper understanding - not only regarding mechanisms of resistance but also its global pathophysiology. For example, basic understanding of transmission mechanisms; knowledge of ‘external’ factors modulating persistence of the pathogen; genetic effects on host susceptibility and infectiousness; mechanisms of pathogenicity and their dynamics; and genetic variation of the pathogen affecting virulence and transmissibility are some aspects that would require further study. Furthermore, the importance of other members of the genus as important nosocomial pathogens, such as Acinetobacter nosocomialis, has been increasingly recognized during the last few years.

Assembling the latest research by an international group of contributors, this volume covers the epidemiology, pathogenesis, clinical features, and control measures of this elusive microorganism. It will provide a deeper understanding of the pathogen to physicians and surgeons caring for patients infected, or at risk of becoming infected, with Pseudomonas Aeruginosa.

Plant diseases are destructive and threaten virtually any crop grown on a commercial scale. They are kept in check by plant breeding strategies that have introgressed disease resistance genes into many important crops, and by the deployment of costly control measures, such as antibiotics and fungicides. However, the capacity for the agents of plant disease - viruses, bacteria, fungi, and oomycetes - to adapt to new conditions, overcoming disease resistance and becoming resistant to pesticides, is very great. For these reasons, understanding the biology of plant diseases is essential for the development of durable control strategies. Plant-Pathogen Interactions provides and overview of our current knowledge of plant-pathogen interactions and the establishment of plant disease, drawing together fundamental new information on plant infection mechanisms and host responses. The role of molecular signals, gene regulation, and the physiology of pathogenic organisms are emphasized, but the role of the prevailing environment in the conditioning of disease is also discussed. Emphasizing the broader understanding that has emerged from the use of molecular genetics and genomics, Plant-Pathogen Interactions highlights those interactions that have been most widely studied and those in which genome information has provided a new level of understanding.

The development of antibiotic resistance within microbial communities, especially in clinical settings, is currently an important public health issue. Human activity, such as the clinical overuse of therapeutic antibiotics, as well as the spread of antibiotics in the environment by anthropogenic pollution, is mainly responsible for this observed rise in resistance. Furthermore, it is predicted that as antibiotic resistance increases in bacterial populations, as will virulence: the capacity of these microbes to infect. This is due to the selection of antibiotic resistance, through widespread antibiotic use, co-selecting for virulence via shared cellular mechanisms between the two factors. We investigated the proposed link between antibiotic resistance and virulence by utilizing larval zebrafish and Pseudomonas aeruginosa of varying degrees of antibiotic resistance as a host-pathogen model. We were successful in developing a novel method to test virulence via static immersion. Using this technique, we found that there was no significant correlation between antibiotic resistance and virulence in the P. aeruginosa strains that we tested. We conclude that the developed method of static immersion will prove useful in understanding host-pathogen interactions, and can be utilized in future studies moving forward. Lastly, we suggest that further P. aeruginosa strains should be tested, as the lack of correlation between antibiotic resistance and virulence could be due to the small sample size used in this study. Investigating the connection between antibiotic resistance and virulence is crucial in understanding the impacts and consequences of society's current antibiotic use, and potentially in remediating the human activity responsible for the rise of antibiotic resistance in microbial populations.