(Continued from the previous blog) However, this mechanism ultimately leads to the emergence of antibiotic-resistant bacteria  due to the rapid generation turnover of bacteria (short generation time) and evolutionary changes, such as mutations in the drug target sites.  Additionally, genetic transfer through conjugation (the transmission of genetic information similar to sexual reproduction in higher organisms) or  transduction by bacteriophages (viruses that infect bacteria, facilitating the transfer of genetic material between bacteria) enables the rapid  horizontal gene transfer and recombination of genetic traits across bacterial species. This results in the inevitable emergence of bacteria that are  resistant to the toxic effects of antibiotics.

This is referred to as drug-resistant bacteria. For example, in the case of penicillin-based or cephalosporin-based antibiotics (which are modified  to target penicillin-resistant bacteria), some bacteria exposed to these antibiotics produce an enzyme called beta-lactamase. This enzyme  alters the antibiotic’s drug component, preventing it from binding to its target site, the PBP (penicillin-binding protein), by transforming  (evolving) to counteract the drug. Even with other antibiotics that operate through different mechanisms, similar processes occur, such as  bacteria producing enzymes or changing their target sites (for example, altering cell membrane permeability so that the drug cannot reach its intended target).

Ultimately, the issue lies not only in the perspective that these artificial bactericidal or bacteriostatic agents (which suppress bacterial growth)  lead to the emergence of multidrug-resistant bacteria but also in the fact that administering such drugs selects for bacteria capable of surviving even under these stressful conditions. Incidentally, one theory suggests that the pathogenic Escherichia coli O157 acquired its virulence factor, the Shiga toxin, through  transduction by a bacteriophage from Shigella, which naturally carries this toxin.