Infectious Disease Compendium

Pseudomonas

Microbiology

Thin gram negative rods includes P. aeruginosa, P. (now Burkholderia) cepacia, P. fluorescens, P. luteola, P. (now Burkholderia) mallei, P. oryzihabitans P. (now Burkholderia) pseudomallei.

Epidemiologic Risks

Found everywhere: dirt, animals, water, plants and humans.

P. pseudomallei: SE Asia, especially with rice fields. N. Australia. Has been found all over the world including Arizona (PubMed).

Syndromes

P. aeruginosa: it can cause infection in any organ and any host, it is often associated with hospital acquired pneumonia and UTI.

Infections in neutropenic patients.

Pneumonia in cystic fibrosis.

How often is it a cause of CAP? Not very in post populations: "The prevalence of P. aeruginosa and antibiotic-resistant P. aeruginosa-CAP was 4.2% and 2.0%, respectively. The rate of P. aeruginosa CAP in patients with prior infection/colonisation due to P. aeruginosa and at least one of the three independently associated chronic lung diseases [i.e., tracheostomy, bronchiectasis and/or very severe COPD]) was 67%. In contrast, the rate of P. aeruginosa CAP was 2% in patients without prior P. aeruginosa infection/colonisation and none of the selected chronic lung diseases (PubMed)."

Increasingly identified in as a cause of progression of COPD (PubMed).

Everyone worries about bacteremia with this organism, but it is rare as a community acquired pathogen. 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.

Hot tub folliculitis and it's cousin, the hot-foot syndrome (PubMed) and hot-hand syndrome (PubMed). The "hot foot syndrome" is painful nodules on the bottom of the foot in people who wade in rough pools; mostly self limited (PubMed).

Ecthyma gangrenosum in the neutropenic.

P. cepacia, P. fluorescens: wound infections, the occasional traumatic osteomyelitis and pneumonia in poor hosts.

P. fluorescens: fin rot in fish. Nosocomial infections. Pseudomonas fluorescens produces mupirocin and glows under UV light, hence the name. Just what we need, a black light Elvis poster done in P. fluorescens.

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. pseudomallei: Melioidosis; bacteremia, pneumonia (PubMed) and sepsis, occasionally traumatic osteomyelitis, in people who have been in the rice fields of SE Asia.

P. stutzeri: most often catheter infections as well as a hodgepodge of organ infections.

Treatment

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).

Ceftolozane/tazobactam is more potent against P. aeruginosa compared to ceftazidime, cefepime, meropenem, piperacillin/tazobactam, aztreonam, levofloxacin, gentamicin and colistin. Second to colistin, had best activity against 310 multidrug resistant strains of P. aeruginosa. Similarly 175 extensively drug resistant strains showed susceptibility, while they were resistant to most other agents.

Extended infusion (a 4­h infusion of 2 g every 8 h) my increase survival (PubMed). Constant, rather than intermittent, iv infusion is associated with decreased mortality in sepsis (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 maybe 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).

P. fluorescens: In one outbreak (PubMed) "Antibiotic susceptibility testing using the E-test showed that the strain was resistant to aztreonam (MIC, 16.0 mg/liter), intermediate resistant to meropenem (MIC, 4.0 mg/liter), and susceptible to ciprofloxacin (MIC, 0.064 mg/liter), ceftazidime (MIC, 0.25 mg/liter), piperacillin-tazobactam (MIC, 0.5 mg/liter), gentamicin (MIC ≤ 0.016 mg/liter), tobramycin (MIC ≤ 0.016 mg/liter), and colistin (MIC, 0.125 mg/liter)."

P. luteola: In one study (PubMed) "Antimicrobial susceptibility testing revealed that all strains of P. luteola were sensitive to amikacin, gentamicin, trimethoprim-sulfamethoxazole, and meropenem, and that all strains were resistant to piperacillin-tazobactam, aztreonam, and colistin."

P. mallei: doxycycline OR ciprofloxacin, streptomycin, novobiocin, gentamicin OR imipenem OR ceftazidime, and the sulfonamides.

P. oryzihabitans: All the anti-pseudomonals.

P. pseudomallei: IV therapy: ceftazidime every 6-8 hours OR meropenem every 8 hours. Oral therapy: trimethoprim-sulfamethoxazole every 12 hours OR doxycycline every 12 hours

P. stutzeri: tends to be susceptible to the usual anti-gram negative rod antibiotics (PubMed)

Notes

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 it has efficacy (PubMed).

Beta-lactamase 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.

In cystic fibrosis patients, resistance to carbapenems can occur even if the patient has not been treated with these agents (PubMed).

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 boogie 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.

Curious Cases

Relevant links to my Medscape blog

Bloody Bullae

Next time use a toothpick

The Real Monas

Concepts

A Repeat After 29 Years

Grumpy Old Man On Call

I have seen the only two cases. Ever.

Double Coverage Rant

What Medicine Takes Away Medicine Gives Back

More Like Cool Tub

Last Update: 07/15/18.