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Intravenous beta-lactam antibiotics in the gastrointestinal tract refer to the fraction of systemically administered antibiotics, such as penicillins and cephalosporins, that reach the gut via biliary excretion (Kokai-Kun et al., 2017, The Lancet Infectious Diseases). While these agents are essential for treating systemic infections, their presence in the intestinal lumen leads to the destruction of beneficial commensal bacteria (De Gunzburg et al., 2018, Journal of Infectious Diseases). This disruption, or dysbiosis, creates an environment conducive to the overgrowth of opportunistic pathogens, most notably Clostridioides difficile (Burdet et al., 2017, Antimicrobial Agents and Chemotherapy). Furthermore, the exposure of gut flora to sub-therapeutic or residual concentrations of these drugs promotes the emergence and spread of antimicrobial resistance (AMR) genes (De Gunzburg et al., 2018). To address this, therapeutic strategies like ribaxamase (an oral beta-lactamase) have been developed to specifically degrade these antibiotics in the upper GI tract (Kokai-Kun et al., 2017). These microbiome-protecting therapies aim to neutralize the antibiotic's active structure before it reaches the colonic microbiota, thereby preventing infection and the spread of resistance without compromising systemic therapeutic efficacy.
Targeted degradation of the beta-lactam ring by orally administered, non-absorbable beta-lactamase enzymes or physical adsorption by activated charcoal to prevent antibiotic-induced dysbiosis in the colon.
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