Found everywhere: dirt, animals, plants and humans.
P. pseudomallei: SE Asia, especially with rice fields.
P. aeruginosa: it can cause infection in any organ and any host, it associated often with hospital acquired pneumonia and UTI.
Infections in neutropenic patients.
Pneumonia in cystic fibrosis.
Everyone worries about bacteremia with this organism, but it is rare as a community acquired. Except, and I quote, " P. aeruginosa caused 6.8% of 4114 unique patient episodes of GNR bacteremia upon hospital admission (incidence ratio, 5 cases per 10,000 hospital admissions). Independent predictors of P. aeruginosa bacteremia were severe immunodeficiency, age 190 years, receipt of antimicrobial therapy within past 30 days, and presence of a central venous catheter or a urinary device. Among 250 patients without severe immunodeficiency, if no predictor variables existed, the likelihood of having P. aeruginosa bacteremia was 1 : 42. If > 2 predictors existed, the risk increased to nearly 1:3 (PubMed)."
Malignant otitis externa in the diabetic.
Ecthyma gangrenosum in the neutropenic.
Also causes "hot foot syndrome" with painful nodules on the bottom of the foot in people who wade in rough pools; mostly self limited (PubMed).
P. cepacia, P. fluorescens: wound infections, the occasional traumatic osteo and pneumonia in poor hosts.
P. luteola: most often catheter infections as well as a hodgepodge of organ infections.
P. mallei: glanders in horses.
P. oryzihabitans: most often catheter infections as well as a hodgepodge of organ infections.
P. stutzeri: most often catheter infections as well as a hodgepodge of organ infections.
P. aeruginosa: ceftazidime OR ciprofloxacin OR imipenem OR meropenem OR piperacillin OR cefepime OR tobramycin OR amikacin are the all antipseudomonal antibiotics. Which to pick empirically depends, as always, on local susceptibility patterns. Avoid Piperacillin-tazobactam as initial therapy; variability in sensitivity is too high and as the MIC creeps up, so does mortality (PubMed).
Extended infusion (a 4h infusion of 2 g every 8 h) my increase survival (PubMed).
I am not so certain that "double coverage" is needed outside of sepsis, it is mostly a myth. It does not improve outcomes (except sepsis) and does not prevent the emergence of resistance and it does add to cost and toxicity (PubMed). So what people do is extrapolate from a therapy that isn't beneficial (beta lactam and aminoglycoside) to beta lactam and quinolone because of worries of toxicity and for which there is no proven benefit. Stupide, n'est pas? As long as one drug is effective, even for bacteremia, there is no benefit of two antibiotics over one (PubMed) (PubMed) (PubMed) (PubMed).
Macrolides have been used in cystic fibrosis and sepsis where, despite in vitro resistance, the antibiotics improved outcomes. It may be resistant in a test tube but when tested in cell culture have efficacy (PubMed).
Beta-lactamse inhibitor combinations are problematic with some gram negative rods, depending on the strain and the type of beta-lactamase. Clavulanate can be antagonistic for ticarcillin (PubMed) and other beta lactam antibiotics (PubMed). This is less of a problem with tazobactam, maybe occurring 1% of the time (PubMed).
If the MIC is 32 to 64, use of pip/tazo in associated with increased death rates.
And if for some weird reason you have a patient on both a cephalosporin and a beta-lactamase inhibitor combination (a sign, I am sure, of early dementia) then the beta-lactamase inhibitor not only inhibits the penicillin, but the cephalosporin as well, making everything less effective.
This organism is the boogy monster of modern medicine. Where they worried about demons and evil spirits in the 1600's, we worry about pseudomonas with the same intensity and almost the same degree of rationality. Gotta cover that pseudomonas.