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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/advagg_css\/css__ce2QY63WIanKyr8eSq7eavr1XQRRmFD6ZSmwpyJi8lM__zXwFqpqmxrZOXXcd_TpBQpjuELbmIP9wBR5UuTDWAO4__YJWWMMdfCJuAFm5cUEp88OsodhO3ZA-2lzRfoBsSlk4.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EToday, increasing numbers of patients are experiencing multispecies infections, often bacterial-fungus infections, due to greater use of medical devices, transplantation, and other interventions that allow patients to live longer with chronic diseases. Understanding the interplay between co-infecting organisms and how they affect their hosts may lead to refinements in patient management.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EBacterial Infections\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ELower Respiratory Infections\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EFungal Infections\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EDeborah Hogan, PhD, Department of Microbiology and Immunology, Dartmouth Medical School, Hanover, New Hampshire, USA, has been hard at work exploring the love-hate relationship between two important pulmonary pathogens that are common among patients with cystic fibrosis (CF). She shared the institution\u0027s discoveries and discussed the clinical relevance of microbe-microbe interactions in the State-of-the-Art lecture, \u201c\u003Cem\u003EPseudomonas\u003C\/em\u003E and \u003Cem\u003ECandida\u003C\/em\u003E: Friends or Foes?\u201d\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EToday, increasing numbers of patients are experiencing multispecies infections, often bacterial-fungus infections, due to greater use of medical devices, transplantation, and other interventions that allow patients to live longer with chronic diseases. Understanding the interplay between co-infecting organisms and how they affect their hosts may lead to refinements in patient management.\u003C\/p\u003E\u003Cp id=\u0022p-4\u0022\u003EIn the environment, \u003Cem\u003EPseudomonads\u003C\/em\u003E have a rather fickle relationship to fungi\u2014sometimes synergistic, as with the colonization and protection of the chanterelle mushroom, and sometimes antagonistic. Dr. Hogan\u0027s laboratory is attempting to untangle a similarly convoluted relationship between \u003Cem\u003EPseudomonas aeruginosa\u003C\/em\u003E, a gram-negative bacterium that is common in soil and hospitals, and \u003Cem\u003ECandida albicans\u003C\/em\u003E, a ubiquitous fungus that is capable of causing invasive disease. \u003Cem\u003EP. aeruginosa\u003C\/em\u003E readily attaches to filamentous \u003Cem\u003EC. albicans\u003C\/em\u003E, creating a biofilm, and together they infect catheters, ventilator tubing, and other devices, as well as eyes, wounds, burns, and the lungs of CF patients. Coinfection can negatively affect patients. A 2010 prospective study in \u003Cem\u003EP. aeruginosa\u003C\/em\u003E-infected CF patients demonstrated a correlation between the advent of \u003Cem\u003EC. albicans\u003C\/em\u003E colonization and an increase in exacerbations [Chotirmall et al. \u003Cem\u003EChest\u003C\/em\u003E 2010].\u003C\/p\u003E\u003Cp id=\u0022p-5\u0022\u003EOn a cellular level, this seeming kinship between \u003Cem\u003EP. aeruginosa\u003C\/em\u003E and \u003Cem\u003EC. albicans\u003C\/em\u003E is actually highly contentious, as it is subject to a kind of interspecies molecular warfare and continual adaptation in the effort to survive. Dr. Hogan highlighted various facets of the relationship, both friendly and antagonistic. \u003Cem\u003EP. aeruginosa\u003C\/em\u003E is able to kill filamentous \u003Cem\u003EC. albicans\u003C\/em\u003E hyphae by secreting a group of toxic small molecules, called phenazines [Peleg et al. \u003Cem\u003ENat Rev Microbiol\u003C\/em\u003E 2010]. Candida fights back by secreting farnesol, which, in some instances, dismantles \u003Cem\u003EP. aeruginosa\u003C\/em\u003E\u0027s phenazine production [Hornby et al. \u003Cem\u003EAppl Environ Microbiol\u003C\/em\u003E 2001] but, in other instances increases it by bumping up downstream production [Cugini et al. \u003Cem\u003EMicrobiol\u003C\/em\u003E 2010]. Farnesol also promotes the conversion of filamentous fungal elements to the more stable yeast morphology, resistant to \u003Cem\u003EP. aeruginosa\u003C\/em\u003E attachment and killing [Westwater et al. \u003Cem\u003EEukaryot Cell\u003C\/em\u003E 2005; Deveau et al. \u003Cem\u003EEukaryot Cell\u003C\/em\u003E 2010]. Over time, a chronic coinfection milieu may select for a more synergistically inclined \u003Cem\u003EP. aeruginosa\u003C\/em\u003E variant that demonstrates reduced antifungal capacity (due to defective quorum sensing and phenazine production) but improved growth. However, \u003Cem\u003EP. aeruginosa\u003C\/em\u003E is also armed with a novel, highly toxic 5-methylphenazine, possibly specifically intended for its \u003Cem\u003EC. albicans\u003C\/em\u003E foe, as it is not generally produced by solitary \u003Cem\u003EPseudomonas\u003C\/em\u003E species.\u003C\/p\u003E\u003Cp id=\u0022p-6\u0022\u003EImportantly, microbe-microbe interactions may also impact a host\u0027s ability to clear the infection. Recent data show that the presence of \u003Cem\u003EP. aeruginosa\u003C\/em\u003E may suppress host immune response to \u003Cem\u003EC. albicans.\u003C\/em\u003E In a recent study, single-pathogen infection models with \u003Cem\u003EP. aeruginosa\u003C\/em\u003E and \u003Cem\u003EC. albicans\u003C\/em\u003E produced the expected immune responses in total cell count and cell differential, with \u003Cem\u003EP. aeruginosa\u003C\/em\u003E causing a strong neutrophilic response and \u003Cem\u003EC. albicans\u003C\/em\u003E inducing more of a macrophage and eosinophilic response. However, when the two organisms were combined, the immune response more closely resembled that of \u003Cem\u003EP. aeruginosa\u003C\/em\u003E, as if \u003Cem\u003EC. albicans\u003C\/em\u003E was not present [Allard and Whittaker. \u003Cem\u003EMed Mycol\u003C\/em\u003E 2010]. This suggests that coinfection may allow organisms, such as \u003Cem\u003EC. albicans\u003C\/em\u003E, to evade immune recognition and set up persistent infections in patients.\u003C\/p\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2011 MD Conference Express\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/11\/12\/27.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzmxm1\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}