For a number of years I have referred in my lectures to the word I have termed “Pseudomonaphobia”.  Basically, this is an irrational fear of the organism Pseudomonas aeruginosa (PA) when isolated from a culture of a wound in the foot.  I really believe that this arises in most Podiatrists during the residency interview process when, without fail they are asked by the interviewer “How would you treat a Pseudomonas infection in the foot?”  I remember being prepped for that question way back in 1981 when we were instructed that the correct response was “You use a combination of gentamicin and carbenicillin”.  Unfortunately, that was incorrect even back then since the more “current” schools were teaching their students to respond with a combination of tobramycin & ticarcillin, the so-called T&T therapy. (This may explain why I did not get my first choice of residency program!)  Fortunately, today the well prepared student should be able to recite about a dozen different, non-aminoglycoside options.  But, that is beside the point.  It really is a moot issue.  You see, despite the ability to readily culture the organism from lower extremity wounds, PA is RARELY a pathogen in lower extremity infections.   In fact, I would go as far as saying that about the only time PA should be empirically considered pathogenic is in a case of osteomyelitis following a puncture wound. 

Pseudomonas colonizing a heel wound

A number of randomized, controlled clinical trials have actually substantiated this viewpoint.  Most have looked at the clinical outcome of patients who grew PA from a wound/infection when treated empirically with an antibiotic that was ineffective against PA vs. one which had anti-pseudomonal activity. In this entry I will present 3 such trials.  

In 2002 Graham, published the results of the pivotal phase III trials comparing ertapenem to piperacillin/tazobactam for complicated skin and skin structure infections (PubMed link:  Of these two antibiotics ertapenem has no inherent anti-PA activity while pip/tazo does.  Despite this difference in spectrum, the positive clinical response in patients growing PA was 70% for ertapenem and 60% for pip/tazo.  In a very similar trial comparing the same two antibiotics specifically for diabetic foot infection, Lipsky et. al. had similar outcomes with a positive clinical response in 76.9% of patients on ertapenem vs. 70% for pip/tazo. (The SIDESTEP trial  More recently, in September 2010, Corey, et. al.  published the results of the clinical trials on the new anti-MRSA cephalosporin ceftaroline .  This drug has no inherent anti-PA activity yet there was a positive clinical response in 80% of the patients from which the organism was isolated.   

None of these trials are meant to show that the study drug had some previously undiscovered anti-PA activity.  They just point to the role of PA as a notorious colonizer of lower extremity wounds/infections. Nannini stated it quite succinctly in his review paper of ceftaroline (

“The demonstration of efficacy in patients with P. aeruginosa receiving ceftaroline, a pathogen against which ceftaroline has little activity, most probably reflects the presumptive role of P. aeruginosa as a colonizer rather than a true pathogen in many of these infections.”

Please do not misinterpret me.  I am not saying that PA is always a colonizer and is never pathogenic.  If this bug is found from a reliable, deep surgical culture, consideration should be given to covering it. However, this is a ubiquitous organism that has been found in tap water and on plants and vegetables.  Just culturing it from a superficial wound swab will lead the clinician to treat an organism that can most likely be handled with thorough debridement and topical therapy, with an anti-PA antibiotic that may be unnecessary.  This may increase resistance of the organism against these antibiotics so that they are not available for the next time…when we may really need them.