{'fraction_non_alphanumeric': 0.03723404255319149, 'fraction_numerical': 0.004835589941972921, 'mean_word_length': 5.568253968253968, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Virulence Factors in Escherichia coli

Drews et al. convincingly demonstrate a lower prevalence of beta-hemolysis and papEF among nalidixic acid- or ciprofloxacin-resistant Escherichia coli urine isolates from their locale, compared with susceptible isolates (1). However, several of the authors' assumptions and conclusions deserve comment. First, in studies not cited by Drews et al., similar (and more extensive) associations have been demonstrated among extraintestinal E. coli isolates for ciprofloxacin resistance, nalidixic acid resistance, and multidrug resistance (3-8). Thus, the present study is confirmatory, rather than adding “a new dimension to previous work.” Second, the concept that “fluoroquinolone resistance is linked to loss of beta-hemolysis and papEF” must be strongly challenged. There actually is no evidence that the hemolysin- and pap-negative strains ever had these traits and, consequently, that they have lost them. On the contrary, abundant evidence now indicates that quinolone-resistant and -susceptible E. coli clinical isolates represent two quite distinct populations. Resistant isolates derive predominantly from non-B2 E. coli phylogenetic groups, within which hemolysin and pap are quite uncommon, whereas susceptible isolates tend to be from (virulence factor-rich) phylogenetic group B2 (3-6). Thus, differences in phylogenetic distribution can largely account for observed differences in virulence factor prevalence between resistant and susceptible isolates (3-5). Likewise, experimental data now show that conversion to fluoroquinolone resistance in E. coli is not accompanied by significant loss of virulence genes (2). Finally, it is unclear what proportion of the isolates studied by Drews et al. truly represented “uropathogenic” E. coli, since urine organisms were collected without epidemiological data regarding clinical manifestations (or lack thereof) and underlying host status. Thus, an undefined proportion of the isolates likely represented low-virulence colonizers or opportunists, rather than true pathogens.