The purpose of this study was to introduce a new method of bedside assessment of both the motor and sensory components of swallowing called fiberoptic endoscopic evaluation of swallowing with sensory testing (FEESST). This approach combines the established bedside endoscopic swallowing evaluation with a more recently described technique that allows objective determination of laryngopharyngeal (LP) sensory discrimination thresholds by delivering air pulse stimuli to the mucosa innervated by the superior laryngeal nerve via a flexible endoscope. A prospective study was conducted of FEESST in 20 healthy control subjects, mean age of 34 +/- 11 years. LP sensory thresholds were defined as either normal (< 4.0 mmHg air pulse pressure [APP]), moderate deficit (4.0-6.0 mmHg APP), or severe deficits (> 6.0 mmHg APP). Subsequent to LP sensory testing, food of varying consistencies, mixed with green food coloring, was given and attention was paid to spillage, laryngeal penetration, pharyngeal residue, aspiration, and reflux. Therapeutic maneuvers such as postural changes and airway protection techniques were performed on each subject to determine if the assessed swallowing parameters were affected by maneuvers. All patients completed the study; all had normal LP sensory discrimination thresholds (2.9 +/- 0.7 mmHg APP). There were no instances of spillage, laryngeal penetration, or aspiration. Two of 20 subjects had pharyngeal residue and 2 of 20 had reflux. Institution of therapeutic maneuvers resulted in a predictable change in the endoscopic view of the laryngopharyngeal anatomy. FEESST provides comprehensive, objective sensory and motor information about deglutition in the bedside setting and might have implications for the bedside diagnosis and management of patients with dysphagia.
Treatment failure did not differ between patients receiving trimethoprim/sulfamethoxazole or minocycline monotherapy for treatment of S. maltophilia infections.
Pseudomonas aeruginosa is a widespread opportunistic pathogen and a major cause of morbidity and mortality in cystic fibrosis patients. Microbe-virus interactions play a critical role in shaping microbial populations, as viral infections can kill microbial populations or contribute to gene flow among microbes. Investigating how P. aeruginosa uses its CRISPR immune system to evade viral infection aids our understanding of how this organism spreads and evolves alongside its viruses in humans and the environment. Here, we identify patterns of CRISPR targeting and immunity that indicate P. aeruginosa and its viruses evolve in both a broad global population and in isolated human “islands.” These data set the stage for exploring metapopulation dynamics occurring within and between isolated “island” populations associated with CF patients, an essential step to inform future work predicting the specificity and efficacy of virus therapy and the spread of invasive viral elements and pathogenic epidemic bacterial strains.
As a heritable sequence-specific adaptive immune system, CRISPR-Cas is a powerful force shaping strain diversity in host-virus systems. While the diversity of CRISPR alleles has been explored, the associated structure and dynamics of host-virus interactions have not. We explore the role of CRISPR in mediating the interplay between host-virus interaction structure and eco-evolutionary dynamics in a computational model and compare results with three empirical datasets from natural systems. We show that the structure of the networks describing who infects whom and the degree to which strains are immune, are respectively modular (containing groups of hosts and viruses that interact strongly) and weighted-nested (specialist hosts are more susceptible to subsets of viruses that in turn also infect the more generalist hosts with many spacers matching many viruses). The dynamic interplay between these networks influences transitions between dynamical regimes of virus diversification and host control. The three empirical systems exhibit weighted-nested protection networks, a pattern our theory shows is indicative of hosts able to suppress virus diversification.Previously missing from studies of microbial host-pathogen systems, the protection network plays a key role in the coevolutionary dynamics. 2.
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