Turning the Phage on Treatment of Antimicrobial-Resistant Pneumonia
Abstract
Lower respiratory tract infections cause 79% of all infectious disease deaths in the United States each year (1). Many of these pneumonia deaths are from community-acquired pneumonia or severe viral pneumonia, but hospital-acquired pneumonia (HAP), including ventilator-associated pneumonia (VAP), continues to play a major role. Sixty-four percent of the infections being treated in the ICU on any single day are pneumonia (2). The development of multidrug-resistant, extremely drugresistant, and pandrug-resistant bacterial pathogens is forcing changes in the manual of nosocomial pneumonia treatment. For decades, the backbone of antibiotic treatment for serious gram-negative pneumonia has been a b-lactam (penicillins, cephalosporins, or carbapenems). Of particular concern with regard to antimicrobialresistant (AMR) pneumonia are new and emerging carbapenemresistant pathogens, including Pseudomonas aeruginosa, Acinetobacter spp., and carbapenem-resistant Enterobacteriaceae. Previous “new” chapters in AMR pneumonia treatment have really been edits of prior chapters—adding various b-lactamase inhibitors to address specific resistance mechanisms (3, 4), optimizing pharmacokinetic/pharmacodynamics to treat borderline resistance (5), and even aerosolizing antibiotics to address adverse tissue penetration issues (6). A rereading of truly early chapters has been needed to correctly dose colistin and be reminded of its associated nephrotoxicity (4). Not since linezolid came on the market…
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Evidence Hub reads this as a randomized trial, done in people. Its evidence level is 2 of 5 (High · randomized trial). Randomized trials of a reasonable size are the strongest single-study design.
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