Pseudomonas aeruginosa is a Gram-negative organism that confers a high mortality risk, especially in cases of bloodstream infection or bacteraemia.1-3 The most common sources of bacteraemia include pneumonia, intra-abdominal infections, urinary tract infections, and skin and soft tissue infections.1-3 Antimicrobial resistance among P. aeruginosa isolates, including to novel fifth-generation cephalosporins have been reported.4 With the increased incidence of beta-lactam treatment failure, researchers from Taiwan investigated the role of fluoroquinolones as monotherapy against P. aeruginosa bacteraemia.5
Ping-Feng Wu and colleagues performed a retrospective analysis of adult patients admitted at Taipei Veterans General Hospital who had P. aeruginosa bacteraemia and received definitive monotherapy with either a beta-lactam or a fluoroquinolone. The study period was between November 2013 and November 2014. The investigators compared 28-day mortality rates between the two groups. Predictors of 28-day mortality were identified using logistic regression and propensity score-adjusted analysis.
A total of 105 patients met the inclusion criteria. Majority (n=78) received beta-lactams, while 27 received a fluoroquinolone (ciprofloxacin, n=20; levofloxacin, n=7). Beta-lactam use was as follows: 22 piperacillin-tazobactam, 15 ceftazidime, 15 cefepime, 11 imipenem/cilastatin, 8 meropenem and 7 doripenem. There was no difference in the clinical characteristics of the patients who received definitive therapy with beta-lactam compared with those who received fluoroquinolones. Specifically, no statistically significant difference was found between age, gender, Charlson comorbidity index, underlying diseases, proportion of surgery, presence of indwelling device, use of immunosuppressive agents, source of infection (community versus healthcare-associated) and source of bacteraemia. The most common sources of bacteraemia were urinary tract infections (37.1%) and primary bacteraemia (39.0%).
Twenty-eight-day mortality was 32.1% for patients who received beta-lactams and 11.1% for patients who received fluoroquinolones. This difference in 28-day mortality did not reach statistical significance (P=0.062). There was also no significant difference in 28-day mortality when patients were further stratified by Acute Physiology and Chronic Health Evaluation II (APACHE II) and Pitt bacteraemia scores. These scoring systems are used to predict mortality among inpatients with bacteraemia or sepsis, taking into account several factors such as cardiovascular and neurologic status, presence of fever, hypotension, and use of mechanical ventilation.6,7 The patients who received fluoroquinolones tended to have lower APACHE II score and Pitt bacteraemia scores than the group treated with beta-lactams. Although this difference was not statistically significant, the authors surmised that physicians may have prescribed fluoroquinolones to patients who appeared less clinically ill.
Propensity-score adjusted multivariate analysis revealed that Pitt bacteraemia score was the only independent factor associated with 28-day mortality (adjusted odds ratio 2.04, P<0.001). Importantly, the use of fluoroquinolone was not associated with mortality. The authors concluded that definitive monotherapy with fluoroquinolones was non-inferior to the use of a beta-lactam in P. aeruginosa bacteraemia when the isolate is proven to be fluoroquinolone-susceptible in vitro. Fluoroquinolones may be a useful alternative to beta-lactams, especially among less severely ill patients. The authors recommended larger studies to verify these results.
Is fluoroquinolone monotherapy a useful alternative treatment for Pseudomonas aeruginosa bacteraemia?