{'fraction_non_alphanumeric': 0.020610687022900764, 'fraction_numerical': 0.015267175572519083, 'mean_word_length': 5.621212121212121, '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}}
Molecular Mechanisms of Antimicrobial Resistance Technical report #14

In the last 50 years bacteria have demonstrated a remarkable ability to develop and share resistance to every antibiotic that has been developed, often by quite unexpected mechanisms and much more readily than was originally predicted (Spratt, 1994). Antibiotic resistant bacteria can live and multiply in the presence of therapeutic levels of antibiotics. They can be resistant in their natural state or they can acquire resistance genes by mutation or from other bacteria. There is a large reservoir of resistance genes, in bacterial genomes and in extra-chromosomal pieces of DNA, that encode different mechanisms of drug resistance such as efflux pumps, enzymes that inactivate antibiotics and altered antibiotic targets. During times of stress, commensal and pathogenic bacteria demonstrate the ability to become hypermutable (Shapiro, 1999) and they duplicate and share survival information (Roberts, 1999), such as resistance genes that can be encoded on plasmids, transposons and integrons. Bacteria have demonstrated a large capacity to retain genetic material that will provide an evolutionary advantage and they conserve advantageous mutations even in the presence of DNA repair mechanisms that can correct them (Shapiro, 1999).