Beyond immediate effects: Microbial mechanisms and ecological feedback in year-long in situ cyanobacterial control using artemisinin sustained-release algaecides

In situ cyanobacterial control has become an important complement to watershed management, but long-term efficacy and ecological impacts remain underexplored. We conducted a one-year enclosure experiment using artemisinin sustained-release algaecides (ASAs) at a dosage of 1:200 (v/v, ASAs to water column) to assess ecosystem effects and persistence, specifically on Microcystis blooms. ASAs temporarily altered carbonate chemistry and carbon pools. Combined with artemisinin's allelopathic oxidation (increases to 100 μg/L in 2–5 days), this triggered cyanobacteria death, reducing chl-a (reduced by 63.9–80.4 %) and algal density (reduced by 23.7–96.4 %) while causing brief Microcystin-LR (MC-LR) spikes (4.7–5.4 μg/L). ASAs also suppressed certain rare prokaryotes, enhanced deterministic community assembly, reduced eukaryotic α-diversity (notably Arthropoda ), marginalized cyanobacteria in microbial networks, and raised Bacillariophyta centrality. Over subsequent months, sustained bloom suppression was driven by microbial dynamics: ASAs altered carbon isotope signatures, weakening cyanobacterial fractionation; increased prokaryote and eukaryote abundances; promoted diversity recovery; and reduced cyanobacterial network centrality to prevent rebound. Network analyses revealed a keystone-taxa shift from Microcystis to zooplankton genera Eucyclops and Neodiaptomus , reflecting the long-term resistance of the microbial community to cyanobacteria. Ecological modeling showed that ASAs rewired water chemistry-microbe-cyanobacteria interactions, and random forests showed that under ASAs treatment, the temperature sensitivity of cyanobacteria decreased and microbial competition increased. These findings elucidate distinct short- and long-term mechanisms of ASAs-mediated bloom control and provide a theoretical foundation for sustainable field applications.