Assessing the Ecological Roles of Resistomes within Microbial Communities in Antibiotic-contaminated Ecosystems.

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Learn more: PMC Disclaimer | PMC Copyright Notice Microb Ecol . 2026 Mar 26;89(1):95. doi: 10.1007/s00248-026-02740-3 Search in PMC Search in PubMed View in NLM Catalog Add to search Assessing the Ecological Roles of Resistomes within Microbial Communities in Antibiotic-contaminated Ecosystems Malama Chewe Malama Chewe 1 Key Laboratory of Tropical Translational Medicine of Ministry of Education, School of Public Health, Hainan Academy of Medical Sciences, Hainan Medical University, Haikou, Hainan China Find articles by Malama Chewe 1 , Tilahun kefyalew Shembo Tilahun kefyalew Shembo 1 Key Laboratory of Tropical Translational Medicine of Ministry of Education, School of Public Health, Hainan Academy of Medical Sciences, Hainan Medical University, Haikou, Hainan China Find articles by Tilahun kefyalew Shembo 1 , Emmanuel Patrick Dumfeh Emmanuel Patrick Dumfeh 1 Key Laboratory of Tropical Translational Medicine of Ministry of Education, School of Public Health, Hainan Academy of Medical Sciences, Hainan Medical University, Haikou, Hainan China Find articles by Emmanuel Patrick Dumfeh 1 , Sanji Zhou Sanji Zhou 1 Key Laboratory of Tropical Translational Medicine of Ministry of Education, School of Public Health, Hainan Academy of Medical Sciences, Hainan Medical University, Haikou, Hainan China Find articles by Sanji Zhou 1 , Emmanuel Stephen Odinga Emmanuel Stephen Odinga 1 Key Laboratory of Tropical Translational Medicine of Ministry of Education, School of Public Health, Hainan Academy of Medical Sciences, Hainan Medical University, Haikou, Hainan China Find articles by Emmanuel Stephen Odinga 1 , Guojing Yang Guojing Yang 1 Key Laboratory of Tropical Translational Medicine of Ministry of Education, School of Public Health, Hainan Academy of Medical Sciences, Hainan Medical University, Haikou, Hainan China Find articles by Guojing Yang 1, ✉ , Okugbe Ebiotubo Ohore Okugbe Ebiotubo Ohore 1 Key Laboratory of Tropical Translational Medicine of Ministry of Education, School of Public Health, Hainan Academy of Medical Sciences, Hainan Medical University, Haikou, Hainan China Find articles by Okugbe Ebiotubo Ohore 1, ✉ Author information Article notes Copyright and License information 1 Key Laboratory of Tropical Translational Medicine of Ministry of Education, School of Public Health, Hainan Academy of Medical Sciences, Hainan Medical University, Haikou, Hainan China ✉ Corresponding author. Received 2025 Dec 22; Accepted 2026 Mar 3; Issue date 2026. © The Author(s) 2026 Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/ . PMC Copyright notice PMCID: PMC13056781  PMID: 41882189 Abstract The role of antimicrobial resistance genes (ARGs) in ecosystem sustainability, particularly in ecosystems under antibiotic pollution, remains underexplored. These genes exist even in environments free from antibiotic contamination, highlighting their potential ecological roles. For example, what roles do ARGs play in stabilizing microbial communities under stress, particularly due to antibiotics, with respect to microbial diversity and functions, including nutrient cycling and organic matter decomposition? This review studied the interconnections between ARGs and microbial communities, looking at how the abundance of resistomes affected microbial diversity and how that diversity influenced resistome profiles, ecosystem functions, and community resilience. The studies indicated that higher microbial diversity may be associated with an increase in ARG abundance in competitive environments (such as agricultural soils, p < 0.01), while systems with lower diversity (like intensive livestock farms) show 2–3 times greater levels of clinically significant ARGs ( aadA2 , tetA ). The presence of sub-inhibitory concentrations of antibiotics (e.g., 5 mg·L⁻¹ tetracycline) enhances ARG spread by 3.20 times through horizontal gene transfer, while higher concentrations (> MIC) lead to a 61.2% reduction in microbial biomass but favor the persistence of resistant taxa (for example, Pseudomonas spp ). Importantly, resistomes are potentially ecological tools: communities carrying ARGs have been shown in some studies to maintain greater functional stability (such as nutrient cycling) when under antibiotic stress. In benthic sediments, ARGs serve as a metabolic reservoir that supports microbial persistence. ARGs function as both ecological mechanisms that promote microbial resilience and clinical risks that drive antibiotic resistance. Therefore, the role of ARGs in promoting microbial survival must be carefully weighed against the public health hazards of their global dissemination. Keywords: Antibiotic resistance genes, Microbial diversity, Ecosystem sustainability, Microbial competition, Horizontal gene transfer, Community resilience Introduction Antimicrobial resistance (AMR) represents a severe danger to public health globally [ 85 ]. Nevertheless, the singular emphasis on antibiotic resistance genes (ARGs) as “pathogenic pollutants” fails to recognize their fundamental ecological functions within microbial communities, functions that have been established over thousands of years, predating the use of antibiotics in medicine [ 12 ]. Resistomes, which are defined as the complete set of ARGs present within a microbial community, play a vital role in the adaptation of these communities. In this review, the ‘ecological role’ of resistomes refers to their contributions to microbial community stability, functional resilience (such as nutrient cycling and organic matter decomposition), and adaptive responses to environmental stressors, functions that extend beyond mere resistance to antibiotics. However, their operational importance in ecosystems tainted by antibiotics remains incomplete and contradictory. For example, studies show that high microbial diversity can both inhibit the spread of ARGs [ 110 ] and increase resistome richness. Delgado-Baquerizo et al., [ 59 ], while systems with low diversity, such as the antibiotic-treated gut, exhibit conflicting trends of ARGs enrichment [ 216 ] and depletion [ 47 ]. This review aims to clarify these discrepancies by integrating both quantitative and qualitative evidence to illuminate the context-dependent interactions between microbial diversity, antibiotic exposure, and resistome dynamics, thereby addressing a significant gap in existing research that has primarily concentrated on the transmission of ARGs in clinical settings [ 220 ]. Microbial diversity plays a significant role in shaping resistome structure, although its impact is not straightforward. In ecosystems with high diversity. For instance, soil microbiomes containing 31 bacterial phyla, fierce competition for resources leads to the presence of 285 distinct ARGs, including those responsible for multidrug resistance, with cold boreal forests exhibiting the highest concentrations of ARGs globally, ranging from 1.29 × 10⁶ to 5.59 × 10⁴ copies per 16 S rRNA gene. Delgado-Baquerizo et al., [ 59 ], Smith, [ 197 ]. In contrast, low-diversity communities such as intensive poultry farms show diminished interspecific competition but an increase in clinically significant ARGs: traditional farms reveal 2–3 times higher occurrences of aadA2 and tet(A) compared to antibiotic-free systems, where the dominance of Clostridiaceae and Lactobacillaceae is linked to a 40% decrease in ARG levels [ 199 ]. This contradiction emphasizes the importance of moving away from simplistic “diversity = good/bad” perspectives and focusing instead on the ecological processes that influence resistome dynamics. Antibiotic levels add complexity to this relationship. Sub-inhibitory concentrations 10–100 times lower than clinical levels, commonly found in agricultural runoff and wastewater [ 24 ], increase horizontal gene transfer (HGT) by 3.20 times; for instance, a concentration of 5 mg·L⁻¹ tetracycline encourages ARG transfer among 20 primary bacterial genera, Dechloromonas and Aeromonas [ 64 ]. On the other hand, elevated antibiotic levels (≥ MIC) diminish microbial biomass by 61.2% [ 202 ], but favour the survival of resilient taxa: 97% of Acinetobacter baumannii isolates from ICU patients endure exposure to carbapenem, with 69.7% possessing the blaOXA-23 gene [ 161 ]. These opposing impacts highlight the importance of considering antibiotic dosage in risk assessments of resistomes, as sub-inhibitory exposure frequently leads to broader ARG spread than acute high-dose treatment [ 13 ]. The function of resistomes in stabilizing microbial communities is critical yet often overlooked. Communities carrying ARGs exhibit 40–60% greater functional resilience, such as nitrogen fixation and organic matter decomposition, when faced with antibiotic stress [ 124 ], with benthic sediments serving as long-term reservoirs for ARGs, including 510 subtypes like mcr-1 and Carbapenemase genes that support microbial diversity for many years [ 45 ]. Recent evidence supports a direct causal role for ARGs in maintaining microbial community stability, distinct from their co-occurrence with stress tolerant taxa. Beyond antibiotic resistance, specific resistance mechanisms, particularly efflux pumps, serve essential physiological functions that directly enhance community resilience. For instance, multidrug efflux systems function as metabolic relief valves, actively exporting toxic metabolic intermediates, quorum sensing signal molecules, and host derived bile salts [ 4 , 53 , 87 , 198 ]. This metabolic sanitary function maintains cellular homeostasis and facilitates cell to cell communication, thereby stabilizing community structure even in the absence of antibiotic pressure. Consequently, the persistence of these genes often reflects their utility in fundamental physiological processes rather than solely selection by antimicrobial agents [ 21 ]. However, in constructed wetlands, exposure to tetracycline results in a 25% increase in microbial diversity through ARG-mediated adaptations, which helps maintain essential ecosystem functions [ 80 ]. This protective function is facilitated by HGT; a pairwise analysis of 93,481 bacterial genomes revealed 138,273 HGT occurrences, with 8% involving the transfer of ARGs across different phyla [ 195 ]. Meanwhile, functional redundancy allows diverse communities to reduce pathogen invasion by 75% through competition for niches [ 40 ]. The significance of this research is substantial: grasping these ecological functions is crucial for creating sophisticated strategies that reconcile public health needs with the preservation of ecosystem integrity [ 188 ]. This review challenges the traditional view of resistomes as mere contaminants, promoting policies that recognize the dual role of microbial diversity: maintaining beneficial diversity to reduce the spread of ARGs in medical contexts while protecting its contribution to ecosystem resilience [ 110 ]. By consolidating existing knowledge, we seek to progress beyond general philosophical debates to present a clear, analytical framework for comprehending the ecological aspects of resistomes, thus providing a more thorough basis for future research and policy on antimicrobial resistance [ 107 ]. This paper aims to explore three essential questions: (i) In what ways does microbial diversity influence the profiles of antibiotic resistance gene abundance, and what ecological role do these resistance genes play in protecting vulnerable species? (ii) Are low-diversity communities at a higher risk of resistome expansion compared to communities with greater diversity? (iii) What role do antibiotic concentrations play in these interactions? By exploring these questions, this review provides new insights into the reciprocal relationships between microbial diversity and resistome profiles, revealing the often-ignored ecological protective roles of resistance genes in preserving microbial communities in the face of environmental pressures [ 172 ]. The research reinterprets ARGs not just as threats in medical settings but also as key evolutionary assets that positively contribute by supporting microbial community functions, facilitating nutrient cycling, and enhancing biodiversity under human-induced pressures. How Does Microbial Diversity Affect the Abundance and Variety of ARGs in a Microbiome? Microbial diversity acts as a primary ecological filter, where higher levels of taxonomic richness and evenness generally provide a “dilution effect” that suppresses the abundance and restricts the variety of ARGs. This effect is primarily driven by deterministic selection and niche saturation, where a diverse, stable community leaves fewer resources for resistant invaders. However, microbial diversity is not uniform; it is shaped by distinct ecological processes, such as selection, dispersal, and the regional species pool, which may have varying effects on ARG abundance. While diversity driven by local selection often buffers the resistome, diversity maintained by high dispersal rates may actually introduce a wider variety of ARGs. Among the key variables driving environmental selection, pH levels exert a considerable influence. In river sediments, pH levels were significantly positively correlated with operational taxonomic unit numbers ( r = 0.832, p < 0.05) and Shannon diversity index ( r = 0.856, p < 0.05) [ 132 ]. This suggests that a neutral pH, particularly during warmer periods, creates a permissive environment that favours the persistence of ARG carrying E. coli , with blaTEM , blaCTX-M , and blaOXA-48 genes prevalent among isolates, with an overall prevalence of 92.68%, including 82.1% diarrheagenic strains. Conversely, acidic conditions can promote resistance, as lower pH in fishponds is associated with reduced E. coli occurrence [ 66 , 134 ], and multidrug efflux pump genes are reportedly enriched in acidic soil resistomes [ 133 ]. While some studies found that overall ARG diversity tends to be highest at neutral pH, where a broader range of microbial taxa can persist [ 83 , 164 ]. Slight variations in seawater pH impacted the overall microbial population without significantly affecting specific indicator genes such as sul1 and intI1 [ 32 ]. Dissolved oxygen (DO) levels also act as a selective filter shaping ARG distribution. Shifts in community complexity dictate resistance pathways, evidenced by the enrichment of plasmid-borne ARGs in aerobic systems compared to anaerobic ones. The abundance and diversity of Mobile Genetic Elements (MGEs) showed a positive correlation with ARGs, particularly in aerobic sludge [ 211 ]. A strong correlation between microbial populations and DO indicates the prevalence of bacteria thriving in aerobic conditions [ 69 ], suggesting that DO selects for specific metabolic pathways and associated resistance genes within the community. Temperature mediates shifts in microbial diversity through direct selective pressures. An increase of 10 °C in local temperature was associated with increases in antibiotic resistance of 4.2% for Escherichia coli , 2.2% for Klebsiella pneumoniae , and 2.7% for Staphylococcus aureus [ 140 ]. Extreme temperature indicators show positive correlations with resistance rates, while cold related indices show negative correlations [ 163 ]. This indicates that thermal stress can erode the biological buffering capacity of diverse communities. Conversely, negative correlations between temperature and ARG levels suggest reduced persistence of ARGs at elevated temperatures [ 190 , 215 ]. Salinity gradients represent a key variable where selection interacts with dispersal. The reduction in bacterial richness under high salinity conditions suggests a loss of biological buffering. In the Pearl River Estuary, the diversity of ARGs and MGEs decreased along the salinity gradient [ 68 ]. Low saline salterns exhibited higher bacterial diversity than high saline salterns [ 200 ], and sediment communities clustered according to salinity [ 210 ]. In these aquatic gradients, dispersal plays a critical role; high flow upstream areas may possess high diversity through the immigration of species, yet the selective pressure of salt concentration downstream ultimately dictates the ARG profile [ 193 ]. Turbidity and contaminants influence the resistome through dispersal vectors and chemical selection. High turbidity correlates with ARG prevalence ([ 22 , 70 ]; O’Malley et al., 2022) and negatively impacts DNA extractability [ 128 ]. Bio accessible mixed contaminants, including heavy metals, act as strong selective agents correlated with ARG levels [ 206 ]. Resistance to streptomycin and tetracycline correlated with electrical conductivity and metals [ 179 ]. These contaminants often reduce overall microbial diversity, which increases ARG variety by enhancing HGT through vectors like microplastics [ 97 ], while the constant release of antibiotics selects for ARG dissemination [ 116 ]. The widespread dissemination of ARGs via HGT is often interpreted as evidence of their functional utility through a metabolic cost-benefit framework. Because maintaining MGEs incurs a significant fitness cost, the successful persistence of an ARG post-transfer suggests that the gene provides a survival benefit that outweighs its energetic burden [ 56 ]. Under direct selective pressure, such as antibiotic exposure, the functional importance of the acquired ARG is clear: it confers an immediate adaptive advantage, allowing the recipient to proliferate while susceptible counterparts are inhibited. However, the prevalence of ARGs can also be driven by indirect selective pressures where the gene acts as a passenger rather than a primary driver of adaptation. This occurs through co-selection, where ARGs are genetically linked on MGEs to traits under different selective pressures, such as heavy metal or biocide resistance [ 73 ]. In these scenarios, the ARG is maintained and spread even in the absence of antibiotics because the entire genetic vehicle is selected for its other traits. This persistence is further supported by cross resistance, where a single mechanism, like an efflux pump, expels multiple antimicrobial classes and co-regulation, where multiple resistance genes are controlled by a single regulatory switch [ 61 , 227 ]. By acknowledging both the active functional roles and the indirect pressures of co-selection, this section provides a nuanced view of how the resistome evolves and maintains stability across diverse environments. Complementing these variables, geographical location determines the regional species pool, the raw material for the resistome. Resistance profiles exhibit spatial variation, with higher diversity in northern regions compared to the southern Baltic Sea [ 37 ]. Global distribution is influenced by climatic seasonality [ 104 ], population density [ 241 ], and human activities [ 144 , 241 ]. Different biomes act as ecological boundaries, but dispersal via human mobility can weaken these barriers [ 38 , 219 ]. Thus, microbial diversity is the key regulator of ARG abundance, but its effect is context dependent: diversity driven by stable ecological selection buffers the resistome, whereas diversity maintained by the dispersal of taxa from a contaminated regional species pool compromises the ecosystem’s competitive stability. Microbial Diversity as a Key Determinant of Community Resilience Ecological resilience is the capacity of a microbiome to resist environmental perturbations or recover rapidly while maintaining core functions [ 156 , 175 ]. Microbial diversity serves as a primary determinant of this resilience by providing a biological buffer through various ecological pathways. The insurance hypothesis posits that higher taxonomic and trait diversity increases the probability that specific species will possess the necessary attributes to withstand a given stressor, allowing them to compensate for functionally impaired counterparts [ 7 , 89 , 194 ]. This is complemented by functional redundancy, where multiple species perform overlapping ecological roles to safeguard critical processes, such as nutrient cycling, if specific populations are lost [ 8 ]. In the context of the resistome, this stability is critical; higher species richness enhances post disturbance recovery through resource complementarity, where diverse communities more efficiently utilize available niches to stabilize productivity [ 19 ]. While richness is a vital baseline, the relationship is nuanced; specific community composition, interspecies interactions, and environmental conditions ultimately dictate the stability of the ecosystem response [ 90 , 102 ]. Therefore, this established resilience directly impacts the resistome, as a diverse and resilient community maintains high niche occupancy, creating a competitive barrier that limits the invasion of antibiotic resistant bacteria and the subsequent proliferation of ARGs. In wastewater samples subjected to human induced disturbances, a decline in microbial diversity was observed, along with a significant increase in potential pathogens [ 216 ]. Furthermore, communities with greater microbial diversity show reduced susceptibility to invasions by antibiotic-resistant bacteria, thus curbing the spread of ARGs [ 40 , 41 , 201 ]. For instance, investigations in the sediments of Lake Geneva revealed that the intricate dynamics of microbial communities and ARGs are present, with high microbial diversity generally correlating with restricted dissemination of ARGs [ 138 ]. The safeguarding ability of diverse microbial communities also extends to the mitigation of ARGs. In organic fertilizer composting systems, the efficiency of ARG removal improved remarkably with a greater reduction in both the abundance and diversity of potential ARG hosting bacteria, where the presence of ARGs was found to be the lowest in earthworm cast organic fertilizer, while chicken manure demonstrated the highest levels [ 240 ]. Network analysis indicated that exposure to sub-inhibitory concentrations of antibiotics (5 mg·L⁻¹ tetracycline alone or in combination with 1 mg·L⁻¹ sulfamethoxazole) within wastewater treatment systems led to a concentration of core bacterial groups harbouring multiple ARGs in around 20 genera (including Dechloromonas , Candidatus Accumulibacter, and Aeromonas ). During the exposure to the combined antibiotics, the abundance of ARGs increased by 3.20 times, which clearly illustrates how a drop in diversity can lead to the accumulation of resistance determinants within specific taxa [ 64 ]. Further studies demonstrate a significant association between ARG abundance and specific bacterial genera; Pseudomonas , Bacillus , Sphingomonas , and Arthrobacter were identified as probable ARG hosts in agricultural soils [ 106 ]. Studies consistently indicate higher levels of antibiotic contamination and a considerably greater prevalence of ARGs in estuarine and coastal regions compared to freshwater ecosystems, with salinity gradients having a clear effect on ARG distribution and occurrence [ 157 , 236 ]. Additionally, a definite positive relationship between ARGs and bacterial genera has been established across various environmental samples, emphasizing that greater microbial diversity directly correlates with the ability to support a broader spectrum of ARGs [ 130 , 230 ]. This process is driven by vital mechanisms such as vertical inheritance and HGT, which are essential for the acquisition and spread of ARGs [ 121 ]. The widespread presence of integrons, recognized as potent mobile genetic elements that include key features such as the intI gene, attI recombination site, and Pc promoter, provides strong evidence of their critical role in facilitating the HGT of ARGs between different bacterial strains and species; this supports the notion that microbial diversity accelerates the spread of ARGs [ 185 ]. Moreover, thorough studies have revealed a greater diversity and quantity of ARGs in soil, as confirmed by a global investigation: analysing 285 unique ARGs, including multidrug resistance genes and those related to efflux pumps, from 1,012 soil sites on all continents, the results indicate that soils are among the largest reservoirs of ARGs on Earth, with the highest concentrations found in cold and boreal forests at high latitudes, further emphasizing the increased diversity and abundance of ARGs in the topsoil [ 59 ]. These findings strongly emphasize how the introduction of resistant microbes through wastewater and manure significantly affects soil microbial communities and fosters the exchange of ARGs with clinical pathogens, thereby affirmatively showcasing that microbial diversity and ARG load mutually influence each other in these ecosystems [ 3 ]. Furthermore, an examination of wastewater from pig farming and the nearby river identified 194 subtypes of ARGs across 14 categories, with levels of ARGs increasing after discharge and then decreasing subsequently. The wastewater increased bacterial diversity, with 25.26% of ARGs exhibiting non-random co-occurrence, and the bacterial community had a significant impact on resistome changes. Overall, this highlights that diverse microbial communities are likely capable of enduring the disruptive effects of antibiotics due to their functional redundancy and specialized abilities to break down chemical pollutants, thereby maintaining ecosystem functionality and the interactions between microbes and ARGs through complex network interactions and community driven regulatory mechanisms [ 96 ]. Microbial Communities Exhibit Niche-based Resistome Preferences Microbial communities do not randomly acquire or contain ARGs; instead, their resistome profiles are actively shaped by their ecological contexts, showing specific and non-random connections between certain microbial taxa and specific ARGs. This observed “niche-based resistome preference” is not a deliberate selection; it arises from a complex interaction of ecological and evolutionary influences, host-microbe dynamics, and the critical function of HGT facilitated by MGEs [ 60 , 152 , 154 , 208 ]. These processes encourage the selective accumulation, acquisition, and proliferation of resistance factors needed to adapt to varying environmental conditions. By analysing 18,938 bacterial genomes alongside 321 clinical isolates, the study demonstrated that HGT via MGE is the primary driver: exposure to antibiotics promotes the replication of ARGs through MGEs, leading to a higher occurrence of duplicated ARGs in antibiotic-rich environments such as humans, livestock, and clinical settings, thereby aiding microbial adaptation to these specific contexts [ 30 , 142 ]. Additionally, these mechanisms resulted in 20.2–41.3% of ARGs experiencing either increases or decreases during various stages of rice growth and under different irrigation conditions, with genetic-level competition in niches further shaping the evolutionary trajectory of ARGs. This collectively emphasizes that particular ecological processes drive the selective enhancement and functional modification of resistance genes, enabling microbes to adapt to the rhizosphere environment in targeted ways [ 229 ]. The worldwide distribution of ARGs is non-random and is mainly influenced by the biomes they occupy and the potential host species [ 127 ]. For instance, studies have clearly shown that critical β- lactam resistance genes ( bla < sub> CTX-M Group 1/9) are preferentially associated with Enterobacterales (such as Escherichia coli ) in regions impacted by human activities, carried on specific MGEs. These MGEs, which include insertion sequences like ISEcp1 and ISCR1 , are crucial for the swift and effective spread of bla_CTX-M genes, with plasmids acting as significant carriers for their evolution and transmission, as evidenced by investigations revealing that 75% of CTX-M -producing E. coli clinical isolates possessed transmissible plasmids [ 91 , 160 , 234 ]. This firmly establishes that microbial taxa do not randomly harbour ARGs; rather, their resistance traits are significantly shaped by ecological and evolutionary elements, including human interventions. In contrast, communities abundant in Acinetobacter baumannii are marked by markedly higher levels of the carbapenem resistance gene bla-OXA-23 , specifically regarding the ST2 clone, which is recognized for harbouring substantial amounts of carbapenem resistance genes, mainly blaOXA-23 , among 92 isolates. Indeed, blaOXA-23 is the most prevalent carbapenem resistance gene found in A. baumannii worldwide, with the ST2 clone strongly linked to its presence [ 221 ]. These genes belong to the OXA-type β- lactamases, which are well-known for conferring resistance to carbapenems, especially in CRAB (Carbapenem-Resistant Acinetobacter baumannii). The dominance of the ST2 clone, responsible for 99% of isolates, unequivocally affirms this lineage’s strong connection to blaOXA-23 and its critical role in the propagation of carbapenem resistance [ 238 ]. Certain bacteria consistently show distinct preferences for specific ARGs. For instance, studies indicate a positive correlation between the levels of Escherichia coli and the presence of other ARGs, noting a 62.2% correlation between E. coli levels and the ARG load in the guts of infants [ 119 ]. Additionally, a tolC efflux pump gene is present in 100% of E. coli , both multi-drug resistant and susceptible strains. Omeprazole reduced the minimum inhibitory concentrations (MICs) by a factor of 2 to 8 in multidrug-resistant strains [ 50 ]. Furthermore, distinct patterns are regularly observed in clinical environments, where E. coli , commonly found in urinary tract infections, primarily carries bla-TEM β- lactam resistance, with blaTEM frequently identified in E. coli isolates from UTIs [ 151 , 181 ]. In E. coli strains obtained from UTIs in ICU patients across three hospitals in Qom during late 2014, the blaTEM gene emerged as the most commonly detected ESBL gene, present in 61.5% of the isolates [ 122 ]. Likewise, Klebsiella pneumoniae associated with bloodstream infections consistently carries the bla-KPC gene responsible for carbapenem resistance [ 34 ]. Studies indicate that K. pneumoniae frequently causes bloodstream infections, with blaKPC + variants often being highly prevalent [ 118 ]. A study performed at a hospital in China from 2013 to 2015 found that out of 285 isolates from bloodstream infections, 33.3% (95/285) were identified as blaKPC+ carbapenem-resistant strains, whereas 24.2% (69/285) were classified as hypervirulent HMKP strains. The occurrence of blaKPC + strains was notably greater than that of HMKP strains [ 228 ]. These established correlations clearly illustrate that microbial communities exhibit niche-based resistome preferences which significantly affects the resistome characteristics within the microbiome. Microbial Interactions and the Spread of ARGs Microbial interactions play a crucial and multifaceted role in the spread of antibiotic resistance genes. These interactions can either accelerate or impede the dissemination of ARGs through various mechanisms, significantly impacting the global challenge of antibiotic resistance. Competitive interactions generally occur when certain species produce antibiotics to surpass their competitors, leading to the natural selection of resistant strains (Fig. 1 ). The colonies that produce antibiotics can eliminate sensitive rivals, unintentionally benefiting nearby resistant strains by diminishing their competition. A heightened production of antibiotics primarily favors resistant strains, while intermediate levels of production prove to be the most beneficial for producers, clarifying the naturally low antibiotic levels seen [ 71 ]. Conversely, bacteriophages significantly influence the dynamics of microbial communities and the spread of ARGs through intricate predator prey interactions. Phages promote the mobilization of ARGs by fostering interactions among hosts and boosting the co-occurrence of additional metabolic genes alongside ARGs, which provides competitive benefits to bacterial hosts amid heightened microbial competition [ 196 ]. Fig. 1. Open in a new tab An illustration of how microorganisms from various environments (such as soil, wastewater, and estuaries) come together to create intricate microbial communities. Biofilms promote microbial interaction, aiding in the horizontal transfer of antibiotic resistance genes (ARGs) through mobile genetic elements (MGEs). The diversity within these communities supports functional redundancy, which allows for compensation when susceptible species are lost and enhances resilience in the face of stress. Different microbial species display distinct resistome preferences based on their niches (for instance, E. coli–blaTEM , S. aureus–mecA , A. baumannii–blaOXA-23 , K. pneumoniae–blaKPC ), with the most prevalent species significantly shaping ARG profiles. Collaborative behaviors such as biofilm formation, combined with competitive interactions, influence the acquisition and spread of ARGs. Overall, microbial diversity not only affects the quantity and variety of ARGs but also helps maintain ecosystem functions when exposed to antibiotic pressure In contrast, cooperative behaviours, like biofilm formation, enhance HGT between species, resulting in a more complex resistome [ 17 ]. Formation of biofilms are one of the most significant methods microbial communities facilitate the spread of ARGs, which is particularly concerning in healthcare environments, as it not only obstructs effective antibiotic treatment but also promotes the uptake of ARGs [ 148 ]. The ability of various MGEs to transfer ARGs differs significantly. In particular, hybrid phage plasmid configurations of phage plasmids are noteworthy: 60 of these configurations harbouring 184 clinically important ARGs (including those responsible for carbapenems and colistin) were identified, and it was confirmed that 5 out of 6 of them induced were functional and capable of infecting distant bacteria without direct cell contact [ 174 ]. Conversely, bacteriophages significantly influence the dynamics of microbial communities and the spread of ARGs through intricate predator-prey interactions. Phages promote the mobilization of ARGs by fostering interactions among hosts and boosting the co-occurrence of additional metabolic genes alongside ARGs, which provides competitive benefits to bacterial hosts amid heightened microbial competition [ 196 ]. In addition, outer membrane vesicles (OMVs) are becoming more acknowledged as a means of microbial interaction. OMVs derived from biofilms of Pseudomonas aeruginosa contain significantly higher amounts of plasmid DNA compared to those from planktonic sources and were found to be more effective in transforming competent bacteria, with biofilm-derived OMVs promoting more horizontal gene transfer than plasmid transformation alone [ 98 ]. Unexpectedly, microplastics have become significant areas for microbial interactions and the spread of ARGs. Nanosized microbiomes derived from animal waste elevate the prevalence of ARGs by changing the interactions between phages and bacteria, along with promoting microbial evolution in soil [ 126 ]. Microbial interactions within environmental reservoirs play a critical role in the global dissemination of ARGs. For example, in grassland ecosystems, severe drought (≤ 15% water-holding capacity, equivalent to a 30-year event) disrupts bacterial co-occurrence networks while leaving fungal networks largely intact. This disruption alters bacterial community functions during recovery and prolongs ecosystem impacts due to vegetation-driven reductions in soil moisture [ 6 ]. Alterations in bacterial communities more significantly affect soil function and vulnerability to subsequent disturbances than those caused by fungi [ 54 , 58 , 167 ]. A greater diversity within microbial communities typically allows for a quicker dissemination of ARGs, owing to the enhanced connectivity of microbial networks compared to less diverse environments. Research indicates that human activities notably elevate antibiotic resistance levels in inland waters, with open waters exhibiting higher concentrations of ARGs, MGEs, and virulence factors (VFs) relative to closed waters. ARG-carrying pathogens were found in 43% of samples, with significant hotspots identified in East Asia, India, Europe, the eastern United States, and Brazil, underlining the vital influence of human pollution and microbial connectivity on the propagation of resistance [ 222 ]. In clinical contexts, collaboration among microbes can facilitate the horizontal transfer of ARGs through MGEs, enhancing the spread of resistance traits across various populations [ 44 ]. Studies show that patients with Common Variable Immunodeficiency Disorder (CVID) demonstrate decreased diversity in their respiratory microbiome and an increase in potentially harmful bacteria, linked to continuous antibiotic usage [ 177 ]. Immunoglobulin deficiencies, such as reduced levels of IgA and IgM, further contribute to this altered microbial landscape [ 218 ]. Taken together, this study demonstrated microbial interactions serve as the primary engine for resistome evolution. The rate of gene spread is dictated by the balance between competition driven selection and cooperation mediated transfer. Whether through the structural scaffolding of biofilms or the mobile cargo of phages and vesicles, these interactions transform individual resistance events into community wide traits. By bridging human, animal, and environmental domains, these interactive networks ensure the resistome remains a dynamic and highly connected global entity. Are Microbial Communities with Low Diversity more Prone to Resistome Expansion Compared to Those with High Diversity? The resistome serves an ecological function extending beyond simple antibiotic resistance, acting as a dynamic component of microbial adaptation [ 107 ]. This section investigates whether lower microbial diversity increases the risk of resistome expansion by examining how bacterial metabolism and niche dynamics modulate the dissemination of antibiotic resistance genes (ARGs). Bacterial metabolism, the function of efflux pumps, is a key determinant of this expansion. These evolutionarily ancient transmembrane systems maintain cellular homeostasis by expelling toxic metabolic byproducts and host derived antimicrobials, a capability that facilitates the colonization of challenging ecological niches [ 4 , 87 , 198 , 231 ]. This metabolic efficiency drives niche differentiation, allowing resistant strains to adapt to unique microenvironments and ensure persistence in specialized habitats that might exclude susceptible counterparts [ 9 , 21 , 75 ]. The impact of these metabolic strategies on the resistome depends heavily on community diversity. In high diversity environments, extensive functional niche coverage creates a biological barrier where occupied niches limit the establishment of incoming resistant taxa [ 153 ]. Conversely, low diversity environments often exhibit significant niche overlap, leading to shared metabolic landscapes and increased ecological connectivity. This proximity significantly facilitates HGT, particularly when efflux genes are located on MGEs, accelerating the merging of resistomes across evolutionarily distant species [ 35 , 212 ]. In this way, the lack of metabolic depth in low diversity communities transforms the microbiome from a guarded ecosystem into a conduit for the rapid dissemination of resistance. Robust evidence from previous studies highlights the notable impact of microbial diversity on the occurrence and dissemination of ARGs, with certain mechanisms showcasing varying degrees of effectiveness based on the diversity within the community (Fig. 2 ). Fig. 2. Open in a new tab Mechanistic illustration of how microbial diversity shapes resistome expansion through competition, horizontal gene transfer, and fitness costs. In microbial communities characterized by high diversity and strong competition(left), fierce competition for resources encourages microbes to generate natural antibiotics. This subsequently leads to an increase in horizontal gene transfer (HGT), as microbes obtain antibiotic resistance genes (ARGs) necessary for survival. In this scenario, the advantages of ARGs surpass their associated fitness costs, driving substantial resistome expansion, which is demonstrated by the presence of various ARGs (e.g., blaCTX - M , blaKPC , blaOXA − 23 ) in organisms like Klebsiella , E. coli , and Acinetobacter . On the other hand, in communities with low diversity and competition (right), the diminished resource competition results in less antibiotic production and HGT (due to limited interaction networks). Furthermore, in the absence of strong antibiotic pressure, the fitness costs of ARGs (the energy required for maintenance and reproduction) outweigh their benefits, causing microbes to eliminate ARGs to promote quicker growth, leading to a small, constrained resistome, as seen with limited ARGs (e.g., mecA , mecC ) in Staphylococcus . Overall, these dynamics illustrate that high microbial diversity facilitates resistome expansion through heightened competition and HGT, while low diversity hinders it because of diminished selective pressures and trade-offs in ARG fitness High Diversity, High Competition: ARGs as Tools for Survival To grasp the significance of microbial diversity in the spread of ARGs, it is essential to comprehend the reasons why these microorganisms obtain resistance genes. Bacteria primarily acquire resistance genes as a result of surviving antibiotic exposure and competition for resources. In untouched environments like mountain phyllospheres, the prevalence of ARGs is not influenced by external antibiotic pressures; rather, it is determined by microbial competition and the structure of communities. These observations highlight the ecological significance of ARGs as adaptive characteristics that assist microbes in thriving within intricate, competitive habitats [ 62 ]. In highly diverse microbial communities, competition for limited resources such as carbon, nitrogen, and space is a primary driver of community structure [ 48 ]. This competition is particularly intense among strains with overlapping resource requirements and can influence community size or even lower species richness in nutrient poor environments [ 16 , 184 ]. However, competition does not preclude cooperation; high functional diversity often stimulates further diversification as species adapt to exploit underexploited niches [ 101 ]. Alongside competition, cooperation is a fundamental stabilizer of diverse communities through public good sharing, cell to cell signalling, and metabolic exchanges [ 125 ]. Mechanisms like cross feeding support high ecosystem diversity even under resource limitations, with spatial arrangements such as structured versus well mixed environments heavily influencing whether cooperative or competitive behaviours dominate [ 76 ]. The relationship between these forces is highly plastic and context dependent [ 18 , 145 ]. Environmental stimuli, such as ammonia concentration, can trigger transitions from cooperation to competition, while evolutionary dynamics often drive communities toward more cooperative and robust states during community coalescence [ 120 , 246 ]. Hence, community homeostasis is maintained through a dynamic balance; while cooperation enhances productivity, negative interactions like competition are essential to prevent runaway destabilization, ensuring the community’s overall stability and function [ 141 ]. To outmaneuver their rivals, microbes generate antibiotics as a natural chemical defence. In retaliation, other microbes evolve or acquire resistance genes to endure this chemical warfare. Research shows that spatial arrangements facilitate the coevolution of these traits, resulting in stable polymorphisms. Within these dynamics, antibiotic producers suppress competitors, cheaters take advantage of producers, and resistance emerges amid strict growth trade offs [ 111 ]. Researchers have argued that these ARGs do not represent major clinical risks to humans, although some studies have identified clinically significant ARGs in environments devoid of external antibiotic contamination. CTX-M β -lactamases originated from chromosomal genes found in Kluyvera species and have been transferred at least nine times through mobile genetic elements such as ISEcp1/ISCR1 , integrons, and transposons onto epidemic plasmids associated with successful bacterial strains, facilitating their global dissemination. These resistance genes continue to pose clinically significant risks even in environments that are not polluted. Due to stable inheritance of plasmids, co-selection with other resistance genes, and the competitive advantage of high-risk clones that carry them, these threats persist in various environments [ 43 ]. This continuous cycle of offence and defence fosters the growth of the resistome: as the diversity within communities increases, competition heightens, and the need for ARGs to counteract released antibiotics escalates. The study underscores that natural microbial communities possess significant diversity, resulting in fierce competition among bacteria for both space and resources. Both laboratory and theoretical investigations indicate that bacteria employ multiple antagonistic strategies, such as antibiotic production, to surpass competitors, implying that microbial interactions play a crucial role in determining competitive success and potentially necessitate resistance traits like ARGs in natural settings [ 88 ]. In contrast, low-diversity communities show a reduction in this competitive intensity. A decrease in population density lessens the overall competition faced by Salmonella Typhimurium. This drop in competition inhibits Salmonella from developing antimicrobial tolerance. With a smaller population, competition is reduced, leading to diminished antimicrobial secretion [ 135 ]. In the absence of this selection pressure, ARGs become less significant, and survival relies more on resource acquisition than on chemical resistance. In certain natural soil communities, survival may lean more towards resource gathering rather than chemical defence, as significant investment in chemical defences can hinder the ability to compete for resources [ 191 ]. Consequently, the resistome’s expansion is constrained, not because the community is in better health, but because fewer challenges require ARGs. In ecosystems characterised by high diversity, a broader array of ARGs may arise due to increased competition among microbial species. The research presents experimental findings that microbial communities partake in focused, costly antimicrobial competition, which heightens competitive pressure on sensitive, phylogenetically distinct competitors. Such competitive interactions may facilitate microbial succession, ultimately boosting the prominence of the resistome [ 139 ]. In structured soils, high microbial richness acts as a biological barrier to ARG dissemination, with clary sage cultivation increasing bacterial richness (4,691 soil ASVs; 2,728 root ASVs) [ 165 , 180 ]. Across 5,800 metagenomes, soils contained 182 ARGs, with 55 shared across livestock microbiomes, and key tetracycline resistance genes occurring in up to 99% of agricultural samples, indicating that diversity loss and anthropogenic pressure drive resistome expansion [ 117 ]. Aquatic systems vary in stability. The results reveal scale dependent stability in riverbed morphology, with dynamic small scale sediment mixing coexisting alongside persistent, correlated bed level changes at larger spatial scales [ 217 ]. Coastal ecosystems demonstrate an inverse diversity resistance relationship, where reduced microbial diversity is associated with higher ARG prevalence [ 203 ]. Contaminated sources, such as agro-industrial wastewater, may further favour the persistence of ARGs, including those encoding multidrug resistance mechanisms, under sustained antibiotic selection pressure [ 86 ]. Despite lower taxonomic diversity, human ( n = 350) and animal ( n = 145) microbiomes harbour a disproportionately high abundance of antibiotic resistance genes, comparable to wastewater/sludge, indicating that these host-associated systems serve as high-density ARG reservoirs. In contrast, external environments ( n = 369), though more taxonomically diverse, generally carry lower ARG abundances [ 169 ]. Livestock comparisons show that in 26 diarrhoeal pigs, long-read ONT metagenomics detected ARGs against 16 antibiotic classes twice that found by culture, reconstructing 14 MAGs (71–96% coverage), highlighting the pig gut as a high density ARG reservoir [ 93 ]. Clinical disturbances such as Clostridioides difficile infection are associated with altered gut resistomes, with certain ARGs (e.g., qnrS , blaTEM ) showing strong co-occurrence and shared lineages between humans and livestock [ 108 ]. In this way, the diversity ARG relationship is context dependent. High diversity serves as a barrier in stable soils, but this effect is often absent in dynamic waters or high pressure host environments. These patterns demonstrate that the resistome is shaped more by environmental stability and selective pressure than by taxonomic richness alone. Highly Diverse Ecosystems Promote HGT than Low Diversity Ecosystems High-diversity microbial communities operate as bustling ecosystems; they contain trillions of microorganisms, where interactions among microbes are ongoing, and genes circulate as freely as goods among traders [ 33 ]. This lively setting promotes widespread microbial interactions [ 112 ]. Physical proximity and high population density are the primary determinants of HGT, as increased abundance significantly elevates the probability of cell to cell contact required for mechanisms like conjugation [ 63 ]. Consequently, high density environments such as biofilms and host associated microbiomes function as HGT hotspots. In these settings, high abundance taxonomic units exhibit a higher frequency of HGT events compared to low abundance groups, regardless of overall species richness [ 244 ]. While high diversity offers a broader pool of genetic partners, low diversity communities can paradoxically facilitate more efficient HGT by reducing the dilution effect [ 223 ]. In simplified communities, the encounter rate between specific donors and compatible recipients increases because there are fewer non-target microbes to intercept or interfere with the transfer [ 99 ]. Furthermore, intense selective pressures in these environments can cause a single beneficial gene to disseminate rapidly across the population, allowing HGT to overcome diversity limits and promote community wide survival [ 14 ]. In this way, HGT is a bidirectional force: it is fuelled by high density, simplified community structures, yet it remains the fundamental mechanism for driving bacterial evolution and diversification [ 243 ]. Hence, dynamic allows microbial populations to adapt rapidly to environmental fluctuations through continuous genetic exchange. Biofilms, which consist of clusters of microorganisms, are recognized as critical sites for the spread of ARGs, as they enable the effective transfer of ARGs. Being near areas with abundant substrates and varying substrate availability greatly enhances the rate of this gene transfer. (S. Liu et al., [ 134 ]. The closeness of diverse bacterial species promotes the efficient exchange of MGEs, such as plasmids and transposons, which frequently carry ARGs [ 113 ]. Integrons, for example, are known to serve as hotspots for gene exchange across species, further accelerating the spread of adaptive traits, including resistance [ 72 ]. Research suggests that the persistence of plasmids, which is essential for the spread of ARGs, can increase with bacterial diversity [ 10 ]. Moreover, ecological and evolutionary factors in diverse bacterial communities can greatly influence plasmid persistence [ 36 ]. When a single ARG enters a community, it can quickly proliferate, spreading among species until it becomes widely prevalent. ARGs are found broadly across pathogenic, commensal, and environmental bacteria, creating a resistome that acts as a reservoir of genes. HGTs, particularly conjugation but also transformation and transduction, enables the swift transmission of ARGs between species, fostering the emergence of resistant pathogens. Wintersdorff et al., [ 220 ]. In contrast, low diversity communities, defined by a smaller number of species and thus fewer potential partners for interaction, create a less conducive environment for frequent HGT events. The physical separation and lowered contact rates between bacteria in these species poor settings naturally reduce the chances for gene exchange mechanisms like conjugation [ 183 ]. This limited scope of species interactions, which is essential for elucidating correlations in microbial community abundance, serves as a natural limitation on processes reliant on species interactions. As a result, even when MGEs or ARGs are introduced, their horizontal spread which is dependent on species interactions, may be constrained, as diminished opportunities for interaction within the community restrict effective transfer routes [ 39 , 42 ]. Evolutionary obstacles can also hinder the successful acquisition and incorporation of foreign genes in host populations that are less diverse or adaptable. Acar Kirit et al., [ 5 ]. A study focusing on plasmid mediated HGT emphasized that the spread and persistence of conjugative plasmids depend on the broader community context, including species diversity and interaction networks, which can both facilitate and constrain gene transfer dynamics. Bottery, [ 31 ]. It is essential to recognize that the interaction between microbial diversity and the spread of ARGs is intricate and multi-layered. While lower species richness may lead to a decrease in the occurrence of new horizontal gene transfer (HGT) events, competition among different species in more diverse environments can also result in plasmid loss from key species, indicating a dynamic relationship that extends beyond merely the presence or absence of gene transfer. Sünderhauf et al., [ 207 ]. On the other hand, in specific structured habitats like soils, elevated microbial diversity has been noted to function as a barrier against the build-up of mobile ARGs, potentially because greater biotic resilience and heightened competition restrict the incorporation and dispersal of external genetic elements [ 47 ]. These findings underscore the significance of ecological context in shaping the influence of diversity on HGT and the resistome, as the openness of microbial communities to mobile genetic elements is contingent on a variety of host and environmental factors [ 82 , 155 ]. Fitness Cost Leads to Loss of ARGs in Low-diversity Communities Over Time Managing ARGs presents several challenges. The maintenance and reproduction of these genes demand energy, which can impede growth and lower fitness, unless they are essential for survival. In diverse environments characterized by high antibiotic presence, the benefits of harbouring ARGs far outweigh their drawbacks. In contrast, in environments with low diversity and minimal antibiotic pressure, microorganisms are inclined to eliminate ARGs to conserve energy. A study conducted in the plant rhizosphere, where the large plasmid pQBR103 is found, shows that it imposes a significant fitness cost on Pseudomonas fluorescens SBW25, leading to reduced growth and competitive ability. Compensatory mutations in the chromosomal gacA/gacS regulatory system developed quickly and solely in plasmid carriers, restoring fitness and facilitating the persistence of the plasmid. This illustrates that in intricate, low-antibiotic environments, costly plasmids (along with their ARGs) are at risk of being lost unless compensated, underscoring how environmental factors influence resistome maintenance [ 27 ]. This complex “cost-benefit” relationship explains the contraction of resistomes in low-diversity settings: ARGs transition from advantageous to disadvantageous [ 147 ]. Moreover, in low-diversity communities facing decreased selective pressure, the fitness costs tied to sustaining ARGs can lead to their gradual disappearance over time. Investigations into activated sludge systems revealed that microorganisms producing antioxidants can reduce the persistence of the RP4 plasmid and mitigate the accumulation of ARGs ( sul1 ) and class 1 integrons ( intI1 ), with the most diverse resistome and the most mutated Escherichia coli ARGs identified in reactors treated with antibiotics but lacking antioxidant-producing microorganisms [ 182 ]. Notably, bacteria carrying ARGs frequently experience fitness drawbacks that can lead to diminished growth in the absence of antibiotic selective pressure [ 26 , 245 ]. In low-diversity environments, where competition is less fierce, bacteria may opt to discard ARGs to improve their growth rates. Michon et al., [ 149 ], Tracy, [ 214 ], Zwanzig, [ 247 ]. Thus, while low-diversity communities exhibit a higher presence of resistomes due to competitive pressures from neighbouring microbial species, high-diversity communities may display a counterintuitive pattern where the absence of direct competition fosters a slow loss of ARGs over time [ 51 , 65 , 158 , 162 , 205 ]. How do Low and High Concentrations of Antibiotics Influence the Microbial Diversity and Resistance Community? Antibiotics exert considerable selective pressures, influencing the diversity of microbial populations and the prevalence of ARGs. Sub-inhibitory concentrations of antibiotics, defined as those below the minimum inhibitory concentration (MIC) for most organisms, apply a subtle but impactful selection pressure. This mild pressure also triggers stress responses in microbes, activating the HGT mechanisms (Beaber et al., 2004). Under antibiotic pressure, the survival advantage conferred by ARGs effectively outweighs their inherent fitness costs [ 143 ]. While resistance often incurs metabolic burdens such as slower growth or reduced competitive ability in antibiotic free environments, the presence of antibiotics shifts the selective landscape, inhibiting susceptible taxa and making ARGs critical for survival [ 28 ]. This immediate threat prioritizes survival over peak metabolic efficiency, allowing resistant populations to thrive despite their biological debt. To ensure long term persistence, microorganisms have evolved several mechanisms to mitigate these fitness costs. Compensatory mutations frequently occur to restore fitness levels comparable to susceptible strains, often making resistance irreversible even after the selective pressure is removed [ 168 ]. Furthermore, context dependent expression allows resistance to be activated only during antibiotic exposure, minimizing energy expenditure in various environments [ 94 ]. The maintenance of ARGs is also supported by co-selection, where resistance genes are physically linked to other beneficial traits, and the use of genetic vehicles like plasmids, which often impose lower fitness costs than chromosomal mutations [ 178 , 237 ]. Therefore, the stabilization provided by these evolutionary strategies, antibiotic resistance transforms from a temporary survival mechanism into a permanent feature of the microbial resistome. Communities rich in ARG carriers or taxa predisposed to HGT, such as Enterobacterales, will exhibit rapid growth in their resistance gene profiles. Alarmingly, such sub-inhibitory levels are common in various natural and engineered ecosystems, especially in regions where antibiotics make their way into the environment via agricultural runoff, pharmaceutical manufacturing, or untreated sewage. These concentrations, usually 10–100 times lower than clinical doses and generally considered sub-inhibitory, create an environment ripe for the proliferation of ARGs due to a strong interplay between selection and genetic transfer. Experiments involving sub-inhibitory (500 µg/L) and higher (5000 µg/L) concentrations of ampicillin on bacterial communities in wastewater treatment reactors over 30 days revealed that sub-inhibitory ampicillin levels resulted in greater variability and dissemination of the β -lactamase resistance gene blaCMY-2 when compared to higher doses. Ongoing exposure to ampicillin shifted the microbial community from Bacteroidetes towards more resistant Proteobacteria. This suggests that sub-inhibitory antibiotic levels in wastewater facilitate the proliferation of resistance genes and the expansion of resistant bacteria [ 24 , 25 , 115 ]. Furthermore, clinically relevant sub-inhibitory levels of bronopol (2 µg/L and 20 µg/L) significantly increased the frequency of conjugative transfer involving both the RP4-7 plasmid and the bla-NDM-4 -positive IncFII(K) plasmid. This enhancement is likely driven by increased bacterial membrane permeability and the upregulation of genes related to DNA transfer and replication. Conversely, higher tetracycline concentrations favoured the selection of bacteria already possessing resistance traits while diminishing the occurrence of novel conjugative transfer events [ 103 , 232 ]. Additional research supports these findings, indicating that sub-inhibitory concentrations of gentamicin facilitated the integration and selection of gentamicin resistance genes within class 1 integrons after only one day of exposure. This rearrangement of integrons induced by the antibiotic heightened the potential for the mobilization and spread of ARGs [ 187 ]. While untouched river sediments displayed a lower number of ARGs, reduced co-occurrence, and less risky host communities, contaminated sediments showed increased ARG abundance, more intricate resistance patterns, and a greater involvement of MGEs/mobile resistance genes (MRGs), subsequently elevating the risk of dissemination [ 78 ]. Moreover, rivers with a larger presence of Enterobacterales, known for their abundance of plasmids, demonstrated stronger relationships between antibiotic levels and the occurrence of ARGs, underscoring the significant impact of community composition on response to resistome challenges. Continuous exposure to these sub-inhibitory antibiotic levels exerts ongoing evolutionary pressure, favouring bacteria that either carry resistance genes or can acquire them through conjugation, transformation, or transduction [ 13 , 159 ]. In contrast, the impacts of high antibiotic levels (at or exceeding the MIC) are severe and evident. Increased concentrations of antibiotics can quickly diminish overall microbial biomass, resulting in fewer hosts available for ARGs. Research indicates that extended exposure to antibiotics may lead to “collateral damage,” where even bacteria with genetic predispositions struggle to survive the harsh conditions created by antibiotic therapies [ 57 ]. This subsequent alteration in microbial communities often leads to the loss of resistance genes linked to formerly dominant species, effectively eliminating their associated resistome. Evidence suggests that ecological factors and community composition play vital roles in influencing resistome dynamics following significant disturbances caused by high antibiotic exposure [ 95 , 105 ]. Persisters cells act as transiently tolerant reservoirs that facilitate the spread of genetic resistance [ 225 ]. During regrowth, the SOS response triggers stress induced mutations and upregulates HGT mechanisms like conjugation and phage activation. This allows persisters to disseminate resistance plasmids even in the absence of direct antibiotic selection [ 15 , 114 ]. Quantitative data highlights this risk, with fluoroquinolone derived persisters showing a 10-fold increase in resistant mutants [ 23 ]. Clinically, resistance mutations can surge nearly 40-fold within 5–12 days of treatment [ 52 ]. Mathematical modelling further reveals a biphasic recovery starting with slow growth followed by rapid proliferation which leads to a significant rebound of resistant populations after antibiotics are removed [ 173 ]. The resistome often expands post treatment, as seen with the increased abundance of tet(O) and tet(M) genes [ 29 ]. Combined exposure to cadmium (5 mg/L) and doxycycline (50 mg/L) maximized ARG abundance, with integron intI1 linking ARGs and metal resistance genes; opportunistic species like Pseudomonas and Acinetobacter dominated as hosts, maintaining and spreading resistance via HGT even after selective pressures were lifted [ 235 ]. Environmental factors, especially exposure to antibiotics, significantly influence the diversity of microbial communities. Continuous use of antibiotics has been found to promote the emergence of ARGs and modify community structure, resulting in an increase in resistant bacteria [ 176 ]. While high levels of antibiotics are rarely found in the environment, they are particularly relevant in areas like hospital wastewater, pharmaceutical discharges, and runoff from intensive livestock operations. These elevated concentrations have profound effects on microbial populations and their resistome, starting with a reduction in biomass. Research on wastewater treatment plants that handle high antibiotic concentrations in wastewater observed a quick decline in bacterial populations, which consequently led to a significant reduction in ARGs, as many ARGs rely on these bacteria as hosts. For instance, when ampicillin levels reached up to 19 ng/L, 61.2% of the isolates exhibited strong resistance (MIC ≥ 20 mg/mL), yet there was a notable decrease in both bacterial and ARG abundance. This decrease is typically short-lived, with ARG levels rising once again as antibiotic pressure subsides. The researchers proposed that this recovery was due to a small fraction of resistant cells that survived, indicating that high antibiotic pressure does not eliminate ARGs but merely temporarily limits their carriers [ 202 ]. In the intricate web of soil ecosystems, a remarkable trend emerges that highlights the considerable impact of antibiotics on microbial communities. When researchers investigated the effects of a sewage spill on aquatic microbial communities, they specifically examined vancomycin-resistant bacteria. The vancomycin-resistant Enterococcus faecium carrying the vanA gene was detected in both water and sediment for up to three days, with the vanA gene remaining identifiable for an additional week, as determined by qPCR. Further analysis using 16 S rRNA sequencing revealed significant alterations in the bacterial community structure in both sediment and water throughout the observed duration, clearly indicating how the community structure affects the pace of resistome recovery [ 233 ]. The scenario is similarly striking in clinical settings. Increased concentrations of antibiotics can unexpectedly elevate ARGs within the surviving populations. An assessment of 380 clinical specimens from Nepal identified 33 Acinetobacter baumannii isolates, primarily from ICU patients. Merely 12.1% of these isolates were sensitive to carbapenems, while 97% remained sensitive to colistin. Carbapenemase production was present in 69.7% of the isolates, with 57.6% possessing the blaOXA-23 gene. This finding suggests that under high carbapenem pressure, a resistant A. baumannii population carrying the blaOXA-23 gene can survive and proliferate despite ongoing antibiotic exposure. This situation exemplifies how the presence of resistant “seed” populations can mitigate the anticipated reduction of ARGs under lethal pressure. Neupane et al., [ 161 ]. Collectively, these studies clearly demonstrate that the evolution of resistomes is not governed solely by the presence of antibiotics, but rather is a dynamic interplay between the level of pressure and the composition of microbial communities. Additionally, the presence of a resistance gene in an ecosystem mildly contaminated by antibiotics contributes to the maintenance of microbial diversity and the sustainability of the ecosystem [ 239 ]. Importantly, environmental stresses such as low-level antibiotic contamination significantly enhance microbial diversity, highlighting the ecological protective function of ARGs in sustaining ecosystem health. Protective Roles of Resistomes in Microbial Community Stabilisation ARGs are often criticized as a threat to human health, as they render antibiotics ineffective in treating bacterial infections [ 85 ]. Nevertheless, in the context of environmental microbial communities, ARGs can act as valuable allies (Fig. 3 ). They are not merely evolutionary responses to environmental antibiotics; instead, they play crucial roles in enabling microbial communities to adapt and thrive amid antibiotic stress. While it is essential to recognize the health risks associated with ARGs, it is equally important to appreciate their positive contributions to environmental microbial ecosystems. For example, certain bacterial resistance mechanisms actively break down antibiotics, which reduces antibiotic levels in the environment and provides “exposure protection” to nearby susceptible cells, ultimately affecting the bacterial community’s overall structure [ 12 , 204 ]. Fig. 3. Open in a new tab Dual role of antibiotic resistance genes (ARGs) under varying antibiotic concentrations. The conceptual framework illustrates how the dosage of antibiotics influences microbial diversity, the dynamics of resistomes, and ecological consequences. When antibiotic concentrations are high (exceeding the Minimum Inhibitory Concentration, left side), there is significant selective pressure that causes the collapse of microbial communities, the elimination of hosts carrying antibiotic resistance genes (ARGs), and a temporary decrease in the resistome’s size. Only resistant “persister” species, such as Pseudomonas and Acinetobacter , manage to survive, and they can reintroduce ARGs once the antibiotic pressure diminishes. Conversely, at sub-inhibitory levels (below the Minimum Inhibitory Concentration, right side), the selective pressure is mild yet ongoing, enabling resistant strains to outcompete susceptible organisms without a significant loss in biomass. These conditions trigger stress responses and promote horizontal gene transfer through mechanisms like plasmids, integrons, and transposons, facilitating the dissemination of ARGs within various microbial communities. Together, these dynamics highlight the complex ecological function of ARGs: they not only help maintain microbial diversity and support ecosystem processes such as nutrient cycling but also present risks as reservoirs for clinical resistance, thereby raising concerns in healthcare settings However, the expansion of the resistome poses a significant threat to ecosystem stability, particularly when eutrophic generalists acquire antibiotic resistance. This acquisition grants a potent competitive advantage, enabling these strains to exploit empty niches created by antimicrobial stress and displace susceptible commensals [ 123 ]. For instance, multidrug-resistant E. coli lineages leverage diverse carbohydrate metabolism genes to occupy broader ecological roles, effectively acting as alien colonizers that invade and dominate disrupted microbiomes [ 53 ]. Consequently, this dominance leads to significant shifts in community structure and a reduction in biodiversity. The phenomenon of competitive release occurs when antibiotic pressure eliminates susceptible competitors, allowing resistant populations to proliferate unchecked and homogenize the environment [ 67 ]. While high microbial diversity typically serves as a biotic barrier against such invasions, the successful establishment of resistant lineages often overrides this resilience, resulting in simplified, less stable communities that are prone to further pathogen intrusion [ 110 ]. In environments like estuarine and freshwater sediments that are tainted by human activities, ARGs afford microbial communities a competitive advantage, enabling antibiotic-resistant bacteria to persist. In estuarine areas, regions with elevated ARG levels also display increased microbial diversity, indicating that these genes are crucial for survival and resilience. ARGs are consistently detected across various sediment depths in numerous lakes, highlighting their lasting protective role in benthic microbial systems, particularly in areas experiencing ongoing antibiotic pollution [ 92 , 137 ]. For example, the transfer of resistance to vulnerable taxa can yield significant ecological advantages, enhance microbiome stability, and shield susceptible community members from being outcompeted by resistant strains [ 55 ]. Additionally, in disturbed engineered and impacted systems, such as wastewater treatment facilities, interventions can decrease the prevalence of hosts harbouring mobile ARGs and reduce downstream spread, yet the core functions of the community can remain robust, signifying that resistome dynamics are linked to host survival and removal rather than a total collapse of function [ 129 ]. This illustrates a clear protective role where ARGs in specific species protect the larger community. Moreover, resistomes aid in maintaining community stability by serving as a barrier to external disturbances. Research indicates that environments with higher microbial diversity [ 77 , 172 ] promote the ecological suppression of pathogens [ 226 ]. This competitive advantage enables bacteria that possess these genes to endure antibiotic exposure, as shown in the Eastern Arabian Sea, where 31 potential ARGs accumulate in accordance with the region’s distinct environmental gradients, exhibiting greater abundance in offshore non-monsoon locations, along with enhanced horizontal gene transfer ( p < 0.05), thereby influencing the structure of bacterial communities [ 171 ]. Across different sediment layers of a linked river-lake system, ARGs are frequently found to be highly prevalent and varied, comprising 24 distinct types and 510 subtypes, including new variants such as mcr-1 , tetX , and Carbapenemase. This highlights the role of these benthic sediments as important reservoirs for ARGs, maintaining a lasting ecological function in benthic microbial systems, where they may assist in processes like interspecies competition and adaptation within interconnected ecosystems [ 49 , 79 , 189 , 242 ], especially in areas experiencing ongoing antibiotic contamination. In these environments, the accumulation of antibiotic residues creates selective pressure, allowing ARGs to remain viable for years even after antibiotic applications have stopped [ 81 , 136 ]. Moreover, studies using constructed wetland mesocosms have revealed that the presence of tetracyclines leads to increased microbial diversity, evenness, and richness, reflecting adaptation and resilience within the microbial community [ 80 ], and antibiotics can enhance specific functional pathways in microbial communities in such settings [ 213 ]. Imagine a scenario where ecosystems are inundated with antibiotics, putting microbial diversity at risk. In such situations, the absence of ARGs would lead to a significant decline in microbial diversity. Yet, where resistance genes exist, they serve as vital ecological lifelines. ARGs provide sensitive species with necessary survival tools, safeguarding against a sequence of extinctions that could disrupt microbial networks and critical functions like decomposition and nitrogen fixation [ 74 ]. However, this ecological benefit is offset by the heightened risk of ARGs being transferred to clinical pathogens. Consequently, antibiotic resistance genes present a dual threat; while they are essential for microbial survival and adaptation, allowing bacteria to avoid antibiotic pressure and sustain their fitness within diverse communities [ 1 , 11 , 84 , 100 , 109 , 150 , 166 ], they also significantly endanger human health by complicating the treatment of infectious diseases, leading to increased morbidity and mortality, and undermining the effectiveness of medical interventions worldwide [ 2 , 170 , 186 , 209 ]. This resistance allows bacteria to maintain their metabolic functions and perform their ecological roles within the community. For instance, bacteria harbouring ARGs remain active in nutrient cycling activities such as nitrogen fixation, organic matter breakdown, and phosphorus solubilization, even in the presence of antibiotics that would typically eliminate sensitive bacteria [ 124 ]. Resistance genes have demonstrated significant protective effects for microbial communities. For example, when challenged with antibiotics, microbial populations that include ARGs can better withstand the stress, maintaining community structures and functions [ 146 , 224 ]. This resilience is crucial for sustaining essential ecological processes like nutrient cycling and organic matter decomposition. Implications of this Study Bacteria acquire and maintain resistance genes not only as a defence against anthropogenic antibiotics but also as part of their ecological toolkit. As shown in several environmental studies, ARGs have ancient origins and can serve functions unrelated to clinical antibiotics, such as cell signalling, interspecies competition, and even metabolic adaptation. In microbial-rich ecosystems soil, wetlands, and the human gut, resistance genes are embedded in complex networks of horizontal gene transfer mediated by plasmids, integrons, and phage transduction. This dual role of ARGs, as both ecological assets and clinical threats, presents a conceptual tension: should resistance genes always be framed as pollutants, or are they sometimes essential for microbiome function? This inquiry necessitates a shift in AMR governance from a monolithic pollutant model toward context dependent frameworks. Such nuance is critical where environmental resistomes intersect with food systems, water cycles, and human health. One of the most consistent findings in microbial ecology is that diverse communities exhibit greater resilience to antibiotic perturbations. The relationship between microbial diversity and ARG dynamics is a dual force mechanism shaped by ecological context. High diversity provides biotic resilience, using niche competition and functional redundancy to suppress the invasion of exogenous resistant pathogens. Paradoxically, this same complexity facilitates internal gene circulation; high species richness and physical proximity especially in biofilms create HGT hotspots that maintain a broad, stable reservoir of adaptive traits. In contrast, low diversity environments facilitate ARG amplification by leaving ecological niches open for opportunistic colonizers. While these systems offer fewer genetic partners, they often exhibit higher HGT efficiency due to a reduced dilution effect, where fewer non target microbes interfere with gene transfer events. Hence, diversity acts as a regulator that determines whether ARGs are sequestered as communal assets or amplified as dominant clinical threats. Conclusion The growing concern surrounding antimicrobial resistance (AMR) has largely framed ARGs as threats to human health, but emerging evidence demands a broader, more nuanced view, one that acknowledges their dual function as both clinical hazards and ecological necessities. This review underscores that the relationship between antibiotics, microbial diversity, and ARGs is not linear but context-dependent, dynamic, and deeply embedded in both natural and human-altered ecosystems. In environments characterised by high microbial diversity, ARGs may be more prevalent not because resistance is spreading uncontrollably, but because these diverse communities, through intense microbial competition, resource scarcity, and elevated horizontal gene transfer, create ideal conditions for the maintenance and exchange of resistance traits. These traits, in turn, offer survival advantages and enhance ecosystem resilience under antibiotic stress. Conversely, in low-diversity systems, such as industrialised farms or clinical settings with high antibiotic inputs, resistance often spikes rapidly, not due to diversity, but because of selection pressure that enriches resistant taxa and allows the few survivors to dominate the community. The interaction between microbial diversity and ARG abundance is determined by context-dependent environmental filters and ecological mechanisms. Factors such as pH, dissolved oxygen, temperature, salinity, turbidity, and contaminant load reshape community composition and alter selective pressures, sometimes supporting diverse communities that buffer resistance spread, and in other cases intensifying selection for resistant taxa. Stress intensity further modulates outcomes, as sustained antibiotic exposure and other environmental pressures promote ARG replication and dissemination through mobile genetic elements and phage-mediated transfer. Competitive interactions favor resistant strains, while cooperative behaviors such as biofilm formation enhance horizontal gene transfer. Thus, the balance between environmental selection, community structure, and microbial interactions explains why high diversity can either suppress or amplify ARG proliferation depending on ecological context. Moreover, chronic sub-inhibitory antibiotic exposure in environmental reservoirs via agriculture or wastewater can subtly and persistently drive the proliferation of ARGs through mild selection and genetic exchange, even more so than acute supra-inhibitory treatments. This interplay reveals that microbial communities are not merely passive vessels of resistance but active participants in shaping the resistome through their structure, interactions, and ecological functions. Importantly, while ARGs are viewed as liabilities in medical contexts, in natural ecosystems, they contribute positively by safeguarding microbial community functions, aiding in nutrient cycling, and maintaining biodiversity under anthropogenic pressure. These genes, many of which long predate clinical antibiotic use, should be seen as evolutionary tools that support life in hostile environments, not just precursors to treatment failure. Such complexity forces a rethink of how we define, track, and respond to antibiotic resistance. The way forward must integrate ecological and clinical perspectives, moving beyond the binary view of ARGs as solely harmful toward one that situates them within a continuum of microbial survival strategies. Interventions should not only aim to reduce antibiotic use but also strategically manage microbial communities by preserving beneficial diversity, controlling reservoirs of resistance in agriculture and wastewater, and disrupting the mechanisms, like mobile genetic elements and bacteriophages, that drive HGT under selective pressure. Most crucially, we must open new lines of scientific and policy dialogue around the functional ecology of resistomes. Instead of asking only how to eliminate ARGs, we must also ask: which ARGs matter most for human risk? Which are essential to ecosystem function? And how can we balance their roles in environmental health with their risks to clinical medicine? A shift from reactive crisis management toward a systems-level understanding of microbial ecology and resistance evolution is urgently needed. Recognising the dual function of ARGs opens the door to more nuanced, sustainable strategies to protect both ecosystem integrity and public health in the face of the global AMR crisis. Acknowledgements This research was supported by Hainan Province Higher Education Scientific Research Project (grant no. Hnky2025ZC-3), Hainan Provincial Natural Science Foundation Youth Project Fund (grant no. 326QN0621) Hainan Medical University Talent Research Launch Fund (grant no. RZ2300006042). Author Contributions **Chewe M.,** Writing - original draft, Investigation, Formal analysis, **Shembo T.K** , **Dumfeh E.P** , **Zhou S., Odinga E.S., Yang G** .: Writing - review & editing; **Ohore E.O.:** Conceptualisation, Funding acquisition, Investigation, Methodology, Writing - review & editing; Supervision. Data Availability Not applicable. Declarations Competing interests The authors declare no competing interests. Footnotes Publisher’s Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Contributor Information Guojing Yang, Email: [email protected]. Okugbe Ebiotubo Ohore, Email: [email protected]. References 1. Abbas A, Barkhouse A, Hackenberger D, Wright GD (2024) Antibiotic resistance: a key microbial survival mechanism that threatens public health. Cell Host Microbe 32:837–851. 10.1016/J.CHOM.2024.05.015 [ DOI ] [ PubMed ] [ Google Scholar ] 2. 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