Thiamphenicol

Antibiotic residues in waste activated sludge (WAS) may disrupt anaerobic carbon conversion, yet how phenicol antibiotics redistribute carbon between acidogenesis and methanogenesis remains unclear. At 10 mg/g TSS, methane production decreased by 63.2% while VFAs reached 131-fold the control. This functional decoupling was underpinned by microbial fates: hydrolytic-acidogenic bacteria were largely retained or enriched, whereas methanogenic archaea and syntrophic bacteria were severely depleted. Concurrently, bacteria-archaea ecological networks underwent reorganization, with positive correlations partially rebounding at moderate TAP exposure. The network collapsed at high TAP, with substantial loss of connector taxa mediating inter-module metabolite exchange. Metagenomic evidence further revealed a functional asymmetry: genes involved in substrate transport and amino acid metabolism were maintained or showed increased relative abundance, while methanogenic genes and AI-2-associated communication genes exhibited decreased relative abundance. PLS-PM revealed that TAP was positively associated with the acidogenic bacterial community (β = 0.960) but negatively with methanogenic potential (β = -0.998). Accordingly, the methane share dropped from 98.7% to 18.1%, while VFAs increased to 81.9% of the COD-equivalent product pool. This work advances the understanding of antibiotic-driven functional imbalance and carbon flux redirection in sludge anaerobic digestion, providing a mechanistic basis for managing antibiotic-laden sludge prior to energy recovery.