{'fraction_non_alphanumeric': 0.016538037486218304, 'fraction_numerical': 0.004410143329658214, 'mean_word_length': 5.878787878787879, '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}}
Update on vancomycin resistance.

Enterococci can be responsible for severe infections such as endocarditis, meningitis and septicaemia and are one of the most important causes of nosocomial infections. Resistance in enterococci concerns many classes of antibiotics including, since 1986, glycopeptides. These antibiotics act by blocking cell wall formation, and resistance is due to synthesis of modified peptidoglycan precursors. Resistance can be acquired or intrinsic and strains may be resistant to vancomycin and teicoplanin, or to vancomycin only. Five types of glycopeptide resistance and their biochemical mechanisms have been described. Furthermore, strains that are dependent on vancomycin for growth have been isolated from clinical samples. Data suggest that resistance could originate in glycopeptide-producing organisms or in enterococcal species intrinsically resistant to these antibiotics.