# Treatment Methods for Antibiotic Mycelial Residues: A Review
## 1 Introduction  
Following [PERSON]'s landmark discovery of penicillin in 1928, the development and deployment of antibiotics have profoundly reshaped strategies for combating bacterial infections in humans [1]. Beyond therapeutic applications in human medicine, these agents are extensively employed as growth enhancers within agriculture, aquaculture, and livestock production [2]. As the world's predominant antibiotic manufacturer, Chinese annual output surpasses 248,000 tons, encompassing more than 70 distinct antibiotic varieties and representing approximately 70% of production [3]. Significantly, Chinese facilities supply roughly 75% of the global penicillin industrial salts, 80% of cephalosporors, and an estimated 90% of streptomycin-class antibiotics globally [4]. Antibiotic manufacturing predominantly utilizes microbial fermentation, a process generating substantial quantities of organic solid waste termed antibiotic mycelial residue (AMR). This residue arises during the fermentation of substrates (e.g., starch, corn syrup, inorganic salts) and consists chiefly of spent mycelial biomass from the antibiotic-producing microorganisms, alongside metabolic byproducts, unconsumed nutrients, and residual antibiotic compounds [5]. Estimates based on a production ratio of roughly 10 metric tonsof AMR per metric ton of antibiotic indicate that China's yearly AMR generation exceeds 2 million metric tons [3; 6]. Due to its high organic matter and moisture content, AMR is prone to fermentation during storage, producing malodorous gases containing compounds, such as pyridine and pyrrole, which severely impact local air quality [7]. The ecological risks posed by residual antibiotics are particularly critical. [PERSON] et al. [8] investigated the ecotoxicological effects and toxicity mechanisms of fluoroquinolone antibiotics on photosynthetic organisms. Their findings demonstrated that fluoroquinolones disrupt energy transfer in chloroplasts of _Spinacia oleraea_, impairing photosynthesis and significantly inhibiting plant growth. In animal toxicological studies, \(\beta\)-diketone antibiotics have been demonstrated to inhibit superoxide dismutase activity in _Danio rerio_, resulting in elevated intracellular oxidative stress levels and oxidative damage to biomacromolecules, such as proteins and nucleic acids. This molecular damage progressively accumulates during embryonic zebrafish development, ultimately manifesting as significant teratogenic effects, including developmental abnormalities and morphological malformations [9]. Beyond the inherent chemical pollution from antibiotics, their usage may induce the emergence of antibiotic-resistant bacteria (ARB) and the evolution of antibiotic resistance genes (ARGs), posing latent threats to ecological equilibrium and public health security. The environmental half-lives of antibiotics vary significantly across different classes, ranging from just a few days for chloramphenicol and sulfaryridine to up to 300 days for compounds, like tetracycline [10; 11; 12]. This substantial variability dictates divergent environmental persistence and behavioral patterns, enabling certain antibiotics to remain biologically active in ecosystems over extended durations. As a byproduct of antibiotic production and usage, antibiotic residues in AMR may trigger a series of complex biological chain reactions once exposed to the natural environment [13]. Specifically, residual antibiotics could induce selective pressure on bacteria, promoting the development of antibiotic resistance in both non-pathogenic and pathogenic organisms, thereby driving the generation of ARBs. The ARGs carried by these ARBs possess a unique transmission mechanism, capable of horizontal gene transfer and dissemination among bacterial populations through mobile genetic elements [14]. This genetic propagation mechanism transcends traditional vertical inheritance limitations, enabling rapid diffusion of ARGs within bacterial communities.