Microbial Endocrinology: A Personal Journey.- Evolutionary Considerations of Neurotransmitters in Microbial, Plant, and Animal Cells.- Mechanisms by Which Catecholamines Induce Growth in Gram-Negative and Gram-Positive Human Pathogens.- Dietary Catechols and their Relationship to Microbial Endocrinology.- Interactions Between Bacteria and the Gut Mucosa: Do Enteric Neurotransmitters Acting on the Mucosal Epithelium Influence Intestinal Colonization or Infection?.- Modulation of the Interaction of Enteric Bacteria with Intestinal Mucosa by Stress-Related Catecholamines.- The Role of Microbial Endocrinology in Periodontal Disease.- Staphylococci, Catecholamine Inotropes and Hospital-Acquired Infections.- The Microbial Endocrinology of Pseudomonas aeruginosa.- Mechanisms of Stress-Mediated Modulation of Upper and Lower Respiratory Tract Infections.- Psychological Stress, Immunity, and the Effects on Indigenous Microflora.- The Epinephrine/Norepinephrine/Autoinducer-3 Interkingdom Signaling System in Escherichia coli O157:H7.- Molecular Profiling: Catecholamine Modulation of Gene Expression in Enteropathogenic Bacteria.- Microbial Signaling Compounds as Endocrine Effectors.- Mycologic Endocrinology.- Experimental Design Considerations for In Vitro Microbial Endocrinology Investigations.
"Chapter 9 The Microbial Endocrinology of Pseudomonas aeruginosa (p. 167-168)
John C. Alverdy, Kathleen Romanowski, Olga Zaborina, and Alexander Zaborin
9.1 Epidemiology of Pseudomonas aeruginosa
Pseudomonas aeruginosa is a model pathogen with which to advance the notion that microbial endocrinology plays a central role in the pathogenesis of bacteria and other microbes. P. aeruginosa is a gram-negative opportunistic pathogen that can infect a variety of host species, including Arabidopsis, Drosophila, Caenorhabditis elegans, rodents, and man.
Like many opportunistic pathogens, virulence expression in P. aeruginosa is not an invariant phenotype. Some investigators consider P. aeruginosa to be an accidental pathogen to man given that it does not appear to have co-evolved with the human immune system; as such it has been assumed to be rarely part of the normal commensal flora. Yet more comprehensive genome-based analyses of the human intestinal microflora suggest that P. aeruginosa is present in up to 20% of normal healthy individuals (Marshall 1991).
Although primarily considered to be a nosocomial pathogen that infects the injured and immunocompromised host, P. aeruginosa appears to be the most common cause of infection-related deaths among patients with cystic fibrosis, a genetic disorder of the respiratory epithelium. In this latter host, P. aeruginosa is a chronic colonizer that can persist for many years where it often exerts only moderate virulence.
In hospitalized patients, however, P. aeruginosa is most commonly isolated from the aero-digestive tract where it can colonize up to 50% of patients after as little as 3 days in hospital (Marshall 1991). Widespread and promiscuous use of antibiotics in the critically ill and injured appears to be among the various causes of the persistent prevalence of this pathogen in hospitalized patients. Attempts at predicting which colonizing pathogens are associated with the highest rates of virulence, and hence associated with the worst outcome has traditionally been assessed by genotyping and the use of antibiotic resistance profiles.
Even attempts at predicting outcome from patients who are infected versus colonized have yielded highly paradoxical results. In a recent study, patients with lung infection, i.e., pneumonia versus those with lung colonization (culture positive without pneumonia) demonstrated that the mortality rates were higher in colonized patients versus those that were clinically infected (Zhuo et al. 2008). Despite strict control measures, the prevalence and mortality rate of P. aeruginosa in hospitalized patients remain high and have not appreciably decreased in the last 10 years.
The highly opportunistic nature of P. aeruginosa, its ability to colonize and remain clinically elusive in antibiotic resistant biofilms, and its highly lethal virulence repertoire make this pathogen particularly difficult to detect and treat. The emergence of strains that are multi-drug resistant poses a real and present danger to patients who suffer burn injury, solid organ and bone marrow transplantation, traumatic injury, major surgical intervention, or severe immunocompromise such as HIV/AIDS.
Many of these infections arise from endogenous sources, the most common of which is the digestive tract reservoir. P. aeruginosa continues to carry the highest case fatality rate (60%) among nosocomial pathogens and is responsible for a variety of clinical infections, including keratitis, otitis, pneumonia, bacteremia, catheter-related sepsis, echthema gangrenosa, and severe diarrhea (Neuhauser et al. 2003)."
