Bacterial Resistance: What Is the Epidemiological Scenario?

Bacterial antibiotic resistance arises randomly, by mutation and gene transfer. Antibiotic use then favors resistant strains, which accumulate over time. In the case of UTIs—regardless of complexity—the predominant pathogen is Escherichia coli, though other Enterobacterales, Pseudomonas aeruginosa, enterococci, and staphylococci are also important. E. coli has become progressively more resistant to fluoroquinolones, trimethoprim and sulfonamides, β-lactams, and aminoglycosides. Multiresistance is substantially associated with biologically fit strains, adept at colonizing the urinary tract, notably E. coli ST131. In community cystitis, resistance has driven a shift to resistance-escaping drugs, notably nitrofurantoin, fosfomycin, and mecillinam, though these risk failure if infection has begun to ascend. In the hospital, resistance to empirical agents increases the urosepsis risk. Global resistance rates vary greatly. They are highest in South Asia, high also in East Asia and Latin America, but lower in northwest Europe, Canada, and Australasia. Exact prevalence data are often lacking, with estimates confounded owing (1) to laboratory testing being biased to severe infections and patients failing to respond to primary empirical therapy; (2) to antibiograms being presented for UTIs collectively, rather than by type of UTI; and (3) to a failure to stratify data by patient risk factors, although resistant infection more often occurs in those with a history of prior infection. Radically improved surveillance is needed to better guide the empirical therapy of UTIs.