The classic reference is: Proc Natl Acad Sci U S A. May 30, 2006; 103(22): 8487–8492.

Published online May 10, 2006. doi: 10.1073/pnas.0602138103

PMCID: PMC1482519

Genetic adaptation by Pseudomonas aeruginosa to the airways of cystic fibrosis patients

Eric E. Smith,*† Danielle G. Buckley,‡ Zaining Wu,‡ Channakhone Saenphimmachak,‡ Lucas R. Hoffman,§ David A. D’Argenio,¶ Samuel I. Miller,¶‖ Bonnie W. Ramsey,§ David P. Speert,** Samuel M. Moskowitz,§ Jane L. Burns,§ Rajinder Kaul,‡†† and Maynard V. Olson‡‖††‡‡

Susanna Remold at the Univ of Louisville (http://louisville.edu/biology/faculty-information/remold/susanna.remold.home) has been interested in this question, and with her former grad student Megan Purdy presented at least one poster at the North American Cystic Fibrosis Conf within the past few years on the topic of environmental acquisition. However, this is a very challenging question given the uncertainty of what came first for any given patient and their immediate environment (i.e., was there primary acquisition from the immediate environment, or only secondary contamination?). To my knowledge, the occurrence of epidemic strains still does not account for the majority of CF pseudomonal strain acquisition in most places with reasonable infection control practices, but you are correct that it has not been well documented.

By the way, the reference that Rick Moss has cited above was an outstanding piece of work by Eric Smith and Maynard Olson, on which I was privileged to collaborate, but does not address the issue of environmental acquisition, rather addresses the question of persistence and in vivo evolution.

There are a few references that describe local, regional and worldwide predominant CF-related P. aeruginosa clones consisting of strains originated from natural habitats, including river, drinking water, etc.

Dear Kirstin:

Your question is simple but frustratingly difficult to answer! You are correct. There are lots descriptions of natural environmental reservoirs for Pseudomonas; in contrast I couldn’t find any directly linking these to acquisition. Even the Cheng et al 1996 Lancet paper doesn’t specifically suggest natural environments as a reservoir. My own “conversion” to this hypothesis comes from experience of investigating acquisition of Pseudomonas by two CF individuals who acquired the same strain whilst sharing a single hydrotherapy session. This was followed three months later by the isolation of mucoid colony morphotypes of the infecting strain. Interestingly, we also found the infecting strain (which was one of several cultured from the pool) to be highly chemotactic towards CF mucin. The relevant citations are:

Govan JRW, Nelson JW. Microbiology of lung infection in cystic fibrosis. British Medical Bulletin 1992; 48: 912-930.

Nelson JW, Tredgett MW, Sheehan JK, Thornton DJ, Notman D, Govan JRW. Mucinophilic and chemotactic properties of Pseudomonas aeruginosa in relation to pulmonary colonization in cystic fibrosis. Infect Immunol 1990; 58: 1489-1495