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Bactericide
Bactericide
Bactericide
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A bactericide or bacteriocide, sometimes abbreviated Bcidal, is a substance which kills bacteria. Bactericides are disinfectants, antiseptics, or antibiotics.[1] However, material surfaces can also have bactericidal properties based solely on their physical surface structure, as for example biomaterials like insect wings.

Disinfectants

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The most used disinfectants are those applying

Antiseptics

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As antiseptics (i.e., germicide agents that can be used on human or animal body, skin, mucosae, wounds and the like), few of the above-mentioned disinfectants can be used, under proper conditions (mainly concentration, pH, temperature and toxicity toward humans and animals). Among them, some important are

Others are generally not applicable as safe antiseptics, either because of their corrosive or toxic nature.

Antibiotics

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Bactericidal antibiotics kill bacteria; bacteriostatic antibiotics slow their growth or reproduction.

Bactericidal antibiotics that inhibit cell wall synthesis: the beta-lactam antibiotics (penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems) and vancomycin.

Also bactericidal are daptomycin, fluoroquinolones, metronidazole, nitrofurantoin, co-trimoxazole, telithromycin.

Aminoglycosidic antibiotics are usually considered bactericidal, although they may be bacteriostatic with some organisms.

As of 2004, the distinction between bactericidal and bacteriostatic agents appeared to be clear according to the basic/clinical definition, but this only applies under strict laboratory conditions and it is important to distinguish microbiological and clinical definitions.[2] The distinction is more arbitrary when agents are categorized in clinical situations. The supposed superiority of bactericidal agents over bacteriostatic agents is of little relevance when treating the vast majority of infections with gram-positive bacteria, particularly in patients with uncomplicated infections and noncompromised immune systems. Bacteriostatic agents have been effectively used for treatment that are considered to require bactericidal activity. Furthermore, some broad classes of antibacterial agents considered bacteriostatic can exhibit bactericidal activity against some bacteria on the basis of in vitro determination of MBC/MIC values. At high concentrations, bacteriostatic agents are often bactericidal against some susceptible organisms. The ultimate guide to treatment of any infection must be clinical outcome.

Surfaces

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Material surfaces can exhibit bactericidal properties because of their crystallographic surface structure.

Somewhere in the mid-2000s it was shown that metallic nanoparticles can kill bacteria. The effect of a silver nanoparticle for example depends on its size with a preferential diameter of about 1–10 nm to interact with bacteria.[3]

In 2013, cicada wings were found to have a selective anti-gram-negative bactericidal effect based on their physical surface structure.[4] Mechanical deformation of the more or less rigid nanopillars found on the wing releases energy, striking and killing bacteria within minutes, hence called a mechano-bactericidal effect.[5]

In 2020 researchers combined cationic polymer adsorption and femtosecond laser surface structuring to generate a bactericidal effect against both gram-positive Staphylococcus aureus and gram-negative Escherichia coli bacteria on borosilicate glass surfaces, providing a practical platform for the study of the bacteria-surface interaction.[6]

See also

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References

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Bactericide

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from Grokipedia
A bactericide, also spelled bacteriocide, is a substance or agent capable of killing , distinguishing it from bacteriostatic agents that only inhibit and reproduction. Bactericides encompass a broad category of chemical and biological compounds, including disinfectants applied to inanimate surfaces, antiseptics used on living tissues, and antibiotics administered systemically to combat infections. Bactericides are essential for across healthcare, environmental, and industrial settings, where they target bacterial cells through mechanisms such as protein denaturation, membrane disruption, oxidation of cellular components, or interference with nucleic acids and enzymes. Common types include alcohols (e.g., and isopropanol), which denature proteins and dissolve for rapid surface disinfection; halogens like and iodine, which oxidize microbial structures; phenolics that inactivate enzymes and disrupt membranes; and peroxygen compounds such as , which generate free radicals to damage cells. These agents vary in spectrum, with many exhibiting broad bactericidal activity against both Gram-positive and , though efficacy can be influenced by factors like concentration, contact time, , and the presence of . In clinical and applications, bactericides like and quaternary ammonium compounds are widely used for skin preparation, wound care, and equipment sterilization to reduce healthcare-associated infections, while antibiotics such as penicillins function as bactericides by inhibiting synthesis. Despite their effectiveness, challenges include potential toxicity, development of bacterial resistance, and environmental impacts, necessitating careful selection and regulated use.

Overview

Definition and Scope

A bactericide is defined as any substance or agent that kills , exerting a bactericidal effect by directly causing bacterial death, in distinction from bacteriostatic agents that only inhibit bacterial growth and reproduction without necessarily eliminating the population. The term "bactericide" originates from the combination of "," referring to the microbial , and the Latin "-cide," meaning "to kill," with the adjective form "bactericidal" first appearing in in 1877 and the noun in the early 1880s during the burgeoning field of . Bactericides encompass a range of chemical and biological agents specifically effective in destroying , including broad-spectrum variants that target diverse bacterial across Gram-positive and Gram-negative categories, as well as narrow-spectrum ones selective for particular types to minimize disruption to non-target microbes. A representative example of a bactericide is , an oxidizing chemical agent widely recognized for its ability to disrupt bacterial cell components and achieve rapid killing. This scope excludes agents like virucides or fungicides that primarily target viruses or fungi, unless they demonstrate concurrent bactericidal activity against . Antibiotics constitute a key biological subset of bactericides.

Classification

Bactericides, agents that kill , are primarily classified by their , which determines their , , and profile. Common chemical classes include alcohols such as ethyl and , which are volatile and evaporate quickly after application; like chlorine (e.g., ) and iodine compounds, known for their oxidative properties; and phenolic derivatives (e.g., orthophenylphenol), which disrupt microbial cell membranes; and quaternary compounds (QACs), such as , that act as cationic . These classes vary in stability and compatibility with different environments, with alcohols being non-corrosive but flammable, while can be corrosive at higher concentrations. Classification by application context distinguishes bactericides based on their intended use: disinfectants target inanimate surfaces and objects to eliminate pathogens; antiseptics are formulated for safe application on living tissues, such as or mucous membranes, to reduce microbial load without causing ; and antibiotics, a subset of bactericidal agents, are administered systemically or topically for therapeutic treatment inside the body to combat bacterial infections. This distinction ensures appropriate selection, as disinfectants like may irritate tissues if misused as antiseptics. Bactericides are further categorized by spectrum of activity, referring to the range of bacteria they target: broad-spectrum agents effectively kill both Gram-positive and Gram-negative bacteria, as well as some fungi and viruses, exemplified by halogens and alcohols; narrow-spectrum agents primarily affect specific groups, such as QACs, which are more potent against Gram-positive bacteria due to their thicker peptidoglycan layer but less effective against Gram-negative ones with outer membranes that impede penetration. Classification factors include environmental sensitivities, such as pH dependence—QACs perform optimally at pH 9-10, while efficacy drops in acidic conditions—and temperature requirements, where phenols require at least 60°F (15.6°C) for stability. While chemical agents dominate bactericide use, physical methods such as and provide non-chemical alternatives for controlling .
ClassExamplesPrimary UsesSpectrum Notes
AlcoholsEthyl alcohol, Surface disinfection, antisepsisBroad (Gram+ and Gram-, enveloped viruses)
Halogens, iodine, surface disinfectionBroad (Gram+ and Gram-, spores at high concentrations)
PhenolsOrthophenylphenolEnvironmental disinfectionBroad (Gram+ and Gram-, limited sporicidal)
Quaternary Ammonium CompoundsSurface cleaning, equipment Narrow (favors Gram+, weaker on Gram-)

Mechanisms of Action

Primary Cellular Targets

Bactericides primarily target essential structures and processes within bacterial cells to disrupt viability and proliferation. These targets include the , cytoplasmic membrane, intracellular components such as nucleic acids and ribosomes, and specialized structures like endospores in certain species. By focusing on these sites, bactericides exploit differences between bacterial and host cell architecture to achieve selective . The bacterial cell wall serves as a critical barrier and shape-maintaining structure, making it a prime target for many bactericides. In , the features a thick layer, often 20-80 nm in thickness, composed of cross-linked chains that provide rigidity and protection. In contrast, possess a thinner layer, approximately 1.5-10 nm thick, sandwiched between an inner cytoplasmic membrane and an outer membrane containing lipopolysaccharides, which acts as an additional permeability barrier. This structural variation influences the susceptibility of and to cell wall-targeting agents, with species generally more accessible due to the absence of the outer membrane. The cytoplasmic membrane, a bilayer that regulates nutrient transport, energy generation, and cellular , is another key target. Disruption of its can lead to leakage, loss of , and eventual cell lysis. This semi-permeable structure is conserved across bacterial species, allowing membrane-targeting bactericides to exhibit broad-spectrum activity by compromising essential transport functions. Intracellular targets encompass vital macromolecules and pathways within the cytoplasm. Bactericides can interfere with DNA and RNA, which are central to replication and transcription machinery, halting genetic processes necessary for bacterial survival. Ribosomes, responsible for protein synthesis, represent a major intracellular site, where some antibiotics bind to inhibit translation, as explored in the antibiotics subsection. Additionally, metabolic enzymes, such as those in the folic acid synthesis pathway (e.g., dihydropteroate synthase), are targeted to block essential biosynthesis, depriving bacteria of critical cofactors for growth. For endospore-forming bacteria like those in the genera Bacillus and Clostridium, bactericides must address the resilient spore structures, including the exosporium, spore coat, peptidoglycan cortex, and inner core. These multilayered defenses confer resistance to harsh conditions, necessitating agents capable of penetrating the tough, proteinaceous coats to reach and damage the dormant DNA or vital enzymes within the core. Effective sporicidal bactericides thus target these protective layers to induce germination or direct inactivation.

Common Mechanisms

Bactericides exert their lethal effects on through several distinct biochemical and physical processes that target essential cellular structures and functions. These mechanisms include disruption of the , damage to the cytoplasmic membrane, interference with proteins and nucleic acids, and disruption of metabolic pathways. Each process ultimately leads to by compromising bacterial integrity or viability, often in a concentration- and time-dependent manner. Cell wall disruption occurs primarily through the inhibition of cross-linking, which is essential for maintaining structural rigidity. By blocking transpeptidase enzymes responsible for cross-linking, bactericides weaken the , rendering susceptible to osmotic in hypotonic environments, where internal causes the to burst. This mechanism exploits the unique composition of bacterial s, particularly in Gram-positive species with thicker layers. Membrane damage represents another prevalent mode, involving the formation of pores or detergent-like solubilization of the . Pore formation allows uncontrolled leakage of intracellular and metabolites, while solubilization disrupts the membrane's fluidity and integrity, leading to ion imbalance, collapse of the proton motive force, and eventual . These actions cause rapid and loss of cellular , often within minutes of exposure. Interference with proteins and DNA prevents essential cellular processes such as replication and transcription. This can involve alkylation of nucleic acids, which covalently modifies bases and inhibits strand separation, or inhibition of topoisomerases, enzymes critical for relieving during replication. Consequently, halts, leading to stalled and death. Additionally, oxidative damage arises from the generation of (ROS), which oxidize proteins, lipids, and DNA, amplifying cellular injury; for instance, contribute to oxidation in disinfectants. A key ROS production pathway is the Fenton reaction, simplified as: H2O2→OH∙+OH−\text{H}_2\text{O}_2 \rightarrow \text{OH}^\bullet + \text{OH}^- This reaction, facilitated by transition metals like iron, produces highly reactive hydroxyl radicals that exacerbate oxidative stress. Metabolic disruption targets energy production by blocking critical pathways, such as the electron transport chain in the inner membrane. Inhibition uncouples oxidative phosphorylation, preventing ATP synthesis and causing energy starvation, which impairs active transport, biosynthesis, and motility. This leads to a cascade of metabolic failure, rendering the bacterium non-viable even if structural integrity is initially preserved. The of these mechanisms is modulated by several factors, including concentration, exposure time, and environmental conditions. Higher concentrations generally enhance activity by increasing the probability of target interaction, while sufficient exposure time allows complete penetration and reaction. Environmental factors, such as organic load, , and temperature, can reduce ; for example, adsorbs bactericides, diminishing their availability, and low temperatures slow diffusion and reaction rates.

Types of Bactericides

Chemical Disinfectants

Chemical disinfectants are chemical agents designed to eliminate or reduce bacterial populations on inanimate surfaces and objects, targeting non-living materials where higher concentrations and toxicity levels are tolerable compared to applications on living tissues. These agents function primarily through oxidation, protein denaturation, or disruption, achieving bactericidal effects by inactivating essential cellular components. Common classes include alcohols, , phenolics, ammonium compounds, and aldehydes, each with distinct compositions, mechanisms, and limitations that influence their suitability for specific uses. Alcohols, such as at 70% concentration or isopropanol, act rapidly by denaturing proteins and dissolving in bacterial cell membranes, providing bactericidal action within seconds against vegetative . However, they evaporate quickly, limiting contact time, and are ineffective against bacterial spores, necessitating their use in combination with other agents for comprehensive disinfection. In settings, 60-90% alcohol solutions are applied to non-critical items like thermometers and small surfaces for quick . Halogens, including compounds like (household ) and iodine-based iodophors, serve as oxidizing agents that disrupt proteins and nucleic acids in . solutions, diluted to 0.5-5% available , are widely used for surface disinfection and , achieving rapid bactericidal effects, such as ≥99.9% reduction in under 10 minutes against pathogens like . Limitations include inactivation by and lack of sporicidal activity for , while iodine can stain and irritate. In , chlorination maintains a free residual of 0.2-1 mg/L in distribution systems to ensure ongoing bactericidal efficacy and prevent regrowth. Phenolics, derivatives of phenol such as ortho-phenylphenol, penetrate bacterial cell walls and inactivate enzymes, offering bactericidal and tuberculocidal properties at use-dilutions. They are effective against a broad range of vegetative but not spores, and their residual activity on surfaces aids in prolonged protection, though they may cause discoloration or if residues remain. These compounds are commonly employed for cleaning non-critical environmental surfaces in healthcare facilities. Quaternary ammonium compounds (quats), such as alkyl dimethyl benzyl ammonium chloride, are cationic that disrupt bacterial membranes and inactivate enzymes, providing bactericidal and fungicidal effects with low to users. They exhibit surface-active properties that allow adhesion to materials, but efficacy diminishes in or against biofilms, and they lack sporicidal or tuberculocidal action. Quats are favored for routine disinfection of medical equipment and non-critical surfaces in hospitals due to their ease of use and minimal . Aldehydes, notably in 2-3.4% aqueous solutions, alkylate proteins and nucleic acids, penetrating deeply to achieve high-level disinfection and sterilization against , including mycobacteria, with log reductions of 2.4-6.4 against in 10-20 minutes. Their toxicity to handlers and potential for vapor irritation limit use to well-ventilated areas, and they are not suitable for routine low-level disinfection. is primarily applied to heat-sensitive instruments like endoscopes in healthcare settings for thorough . Efficacy of chemical disinfectants is evaluated using standards like , where a 5-log kill (99.999% reduction) is often required for high-level disinfection claims against target . Testing follows methods, such as the Use-Dilution Method (AOAC 955.14), which assesses bactericidal performance under simulated use conditions by inoculating carriers with organisms like Staphylococcus aureus and measuring survivors after exposure. These protocols ensure disinfectants meet regulatory criteria for and environmental applications, accounting for factors like contact time and organic load. In cleaning, chemical disinfectants like diluted bleach (1:10-1:100 ) and quats are standard for surfaces and equipment, reducing bacterial contamination to prevent healthcare-associated infections. For , chlorination at residual levels of 0.2-1 mg/L provides continuous bactericidal protection in distribution systems, effectively controlling pathogens without excessive byproduct formation. Limitations across classes, such as spore resistance and environmental inactivation, underscore the need for proper selection, concentration, and application protocols to maximize efficacy while minimizing risks.

Antiseptics

Antiseptics are bactericidal agents designed for safe application on living tissues, particularly for wound care and skin disinfection, distinguishing them from disinfectants by their emphasis on to minimize tissue damage while effectively reducing microbial load. The concept of antisepsis originated in the , with introducing carbolic acid (phenol) in 1867 as the first for surgical wounds, applying it as a to prevent by targeting airborne and contact-transmitted . This pioneering approach marked a shift from empirical to evidence-based infection control, laying the foundation for modern antiseptic use in clinical settings. Key antiseptics include , a 10% solution that provides broad-spectrum activity against Gram-positive and , fungi, and viruses by releasing free iodine to disrupt microbial proteins and membranes, though it temporarily stains skin and fabrics yellow-brown. , typically used at concentrations of 0.5% to 4%, offers persistent action lasting up to 48 hours due to its binding to skin proteins, effectively killing through membrane disruption and protein precipitation. at 3% concentration produces an effervescent reaction via oxygen release that mechanically dislodges debris and kills anaerobes, but it can damage healthy tissues by generating that impair cell viability. Biguanides, such as polyhexamethylene (PHMB), function similarly to by penetrating bacterial cell walls and inhibiting metabolic processes, often incorporated into wound dressings for sustained release. Silver compounds, exemplified by applied topically for burn wounds, release silver ions that disrupt bacterial cell membranes, interfere with electron transport, and bind to DNA, providing broad-spectrum coverage particularly against and species. Safety profiles of these agents are critical for human use, with carrying risks of in iodine-sensitive individuals, manifesting as rash or , though true allergies are rare and often misattributed to the carrier povidone rather than iodine itself. like carbolic acid are limited to concentrations no greater than 1% for application to avoid severe burns or systemic , as higher levels (above 1.5%) cause rapid tissue and absorption leading to organ damage. and generally exhibit low at recommended dilutions but can provoke or in rare cases, necessitating patch testing for prolonged use. poses minimal systemic risk but may delay in burns if overused due to potential from ion accumulation. Overall, these agents are formulated to balance efficacy with tolerability, avoiding concentrations that exceed safe thresholds for mucosal or open-wound exposure. Efficacy against , such as , is well-documented for these antiseptics, with and achieving rapid log reductions in viable on intact , often exceeding 4 logs within minutes of application. However, their bactericidal performance is notably reduced in the presence of like or serum, which can inactivate up to 50-90% of the active agents through protein binding or dilution, necessitating thorough prior to use in contaminated wounds. Silver compounds maintain activity against staphylococcal biofilms even in protein-rich environments, making them suitable for chronic wounds, while biguanides like PHMB show consistent inhibition of Gram-positive flora regardless of mild organic loads.

Antibiotics

Antibiotics represent a cornerstone of bactericidal agents, comprising synthetic or semi-synthetic compounds that target essential bacterial processes to achieve direct killing of pathogens. The era of antibiotics began with the by in 1928, when he observed the inhibition of growth by notatum mold in a contaminated . Although initial purification efforts were limited, large-scale production and clinical trials in the early 1940s, led by and , enabled its widespread use during for treating bacterial infections such as and wound . This breakthrough spurred the development of diverse classes, many of which exhibit bactericidal activity by disrupting vital cellular functions, distinguishing them from bacteriostatic agents that merely inhibit growth. Major classes of bactericidal antibiotics include beta-lactams, aminoglycosides, glycopeptides, and fluoroquinolones, each targeting distinct bacterial components. Beta-lactams, such as penicillins (e.g., penicillin G) and cephalosporins, act as inhibitors by binding to (PBPs), preventing cross-linking and leading to osmotic . For severe infections like streptococcal , penicillin G is typically dosed at 1-4 million units intravenously every 4-6 hours to maintain therapeutic levels. Aminoglycosides, exemplified by gentamicin, disrupt protein synthesis by irreversibly binding to the ribosomal subunit, causing mRNA misreading and membrane damage that culminates in . Glycopeptides like inhibit synthesis by forming hydrogen bonds with the D-ala-D-ala terminus of precursors, blocking transpeptidation and polymer elongation. Fluoroquinolones, such as , exert their bactericidal effect through inhibition of and topoisomerase IV, enzymes critical for DNA supercoiling and replication, resulting in double-strand breaks and bacterial demise. Bactericidal antibiotics differ from bacteriostatic ones in their capacity to reduce viable bacterial counts by at least 99.9% (3-log kill), often measured via the (MBC), which is typically close to the (MIC). Their killing efficacy follows either time-dependent (e.g., beta-lactams, where prolonged exposure above MIC is key) or concentration-dependent (e.g., aminoglycosides and fluoroquinolones, where peak levels relative to MIC drive maximal effect) . Pharmacokinetic considerations are crucial for optimization; for instance, has a half-life of 6-7 hours in patients with normal renal function, with dosing adjusted to achieve trough levels of 15-20 mcg/mL for serious infections like MRSA bacteremia to ensure adequate area under the curve (AUC) exposure. Post-2004 updates, including the 2009 consensus guidelines, emphasized higher trough targets over traditional 10-15 mcg/mL to combat rising resistance while minimizing risks through .

Emerging Agents

Bacteriophage therapy represents a targeted approach using viruses to selectively infect and lyse specific bacterial cells, offering a precision alternative to broad-spectrum bactericides. Post-2020, numerous clinical trials have advanced this modality, with approximately 35 ongoing worldwide as of 2025, including around 15 in the United States focused on multidrug-resistant (MDR) infections. Phage cocktails, combining multiple phages for enhanced efficacy, have shown promise against pathogens like Pseudomonas aeruginosa, demonstrating sustained bacterial load reduction in compassionate-use cases and Phase I/II trials approved under FDA investigational new drug applications since 2020. For instance, a 2023 trial reported effective clearance of P. aeruginosa biofilms in cystic fibrosis patients without significant adverse effects. As of November 2025, key ongoing trials include Phase 2 studies for phage therapy in cystic fibrosis and prosthetic joint infections. Nanomaterials have emerged as potent bactericides due to their high surface area and ability to disrupt bacterial structures at the nanoscale. Silver nanoparticles (AgNPs), typically in the 1-100 nm range, exert effects primarily through the release of silver s that generate (ROS), damaging bacterial membranes and DNA. A study highlighted magnetically doped AgNPs (10-50 nm) that enhanced penetration, achieving up to 90% reduction in Staphylococcus aureus biomass by perforating extracellular matrices. Similarly, nanoparticles (CuO NPs), synthesized via green methods, exhibit broad-spectrum activity against Gram-positive and Gram-negative bacteria, with minimum inhibitory concentrations (MICs) as low as 6.25 μg/mL against S. aureus, attributed to release and ROS production. Recent 2023-2025 reviews confirm CuO NPs' in combating MDR strains, including enhanced photocatalytic degradation of bacterial cells under exposure. Phytocompounds, derived from plants, provide natural bactericidal agents that often synergize with existing antimicrobials by targeting resistance mechanisms. , extracted from , inhibits the NorA efflux pump in , restoring susceptibility to antibiotics like with up to 8-fold potency increases in 2024 studies. , a phenolic monoterpenoid from , disrupts bacterial membranes and inhibits efflux pumps in , reducing MICs by 4-16 times when combined with conventional drugs. A 2024 review emphasized these compounds' role in efflux pump inhibition across MDR , highlighting their low toxicity and biofilm-disrupting potential in preclinical models. Antimicrobial peptides (AMPs) mimic host-defense molecules, offering rapid bactericidal action via membrane permeabilization and intracellular targeting, particularly against MDR infections. , a lantibiotic AMP produced by , shows promise for topical applications based on preclinical studies, with efficacy against MDR and Clostridium difficile with MICs below 2 μg/mL in combination therapies. Broader AMP classes, including cathelicidins and , disrupt biofilms and inhibit , with 2025 preclinical data indicating over 80% bacterial kill rates in models when delivered via nanoparticles to overcome stability issues. These peptides address resistance by multi-targeting, reducing the likelihood of evasion compared to single-site inhibitors. Recent innovations include novel enzyme inhibitors and gene-editing tools to counter resistance enzymes. inhibitors like enmetazobactam, approved in 2024 as part of cefepime combinations, restore beta-lactam efficacy against carbapenem-resistant , achieving 90% susceptibility in Phase III trials with MIC reductions up to 64-fold. CRISPR-based antimicrobials, utilizing Cas13 or to cleave bacterial genes or plasmids, remain in preclinical stages as of 2025, with engineered phages delivering CRISPR payloads demonstrating 99% elimination of MDR E. coli in models by targeting antibiotic-resistance genes. These approaches, while promising, face delivery challenges that may contribute to emerging resistance patterns.

Applications

Medical and Healthcare

In clinical settings, bactericides play a crucial role in prevention, particularly through preoperative skin preparation using gluconate (CHG) in alcohol solutions for surgical scrubs, which has been shown to reduce surgical site s (SSIs) compared to alternatives. Similarly, silver alloy-coated urinary catheters are employed to minimize catheter-associated urinary tract s (CAUTIs), with meta-analyses indicating a reduction in asymptomatic bacteriuria and limited evidence for symptomatic s in short-term use. For therapeutic applications, bactericides are integral to managing severe infections like , where intravenous combination therapies such as plus piperacillin-tazobactam are commonly used as empiric treatment to cover (MRSA) and gram-negative pathogens, though studies highlight potential risks prompting alternatives like cefepime. In wound care, dressings impregnated with medical-grade or silver ions promote healing by providing broad-spectrum antibacterial activity; 's osmotic and acidic properties inhibit bacterial growth, while silver disrupts microbial cell walls, both reducing infection rates in chronic s like diabetic ulcers. Guidelines from authoritative bodies emphasize standardized bactericide protocols to enhance safety. The (WHO) recommends alcohol-based hand rubs (at least 60% alcohol) as the preferred method for hand hygiene in healthcare, with improvement programs preventing up to 50% of avoidable healthcare-associated infections (HAIs). The Centers for Disease Control and Prevention (CDC) outline sterilization protocols requiring steam or for critical medical devices, ensuring a of 10^-6 to prevent HAIs from contaminated instruments. A notable case study involves MRSA control through nasal , where targeted application in colonized patients reduced postdischarge MRSA infections by approximately 30% in cohorts, as demonstrated in randomized trials supporting its role in universal or targeted strategies. Following the 2020 , bactericide use in healthcare surged for surface disinfection, with (HOCl) mists gaining prominence due to their efficacy against ; low-concentration HOCl (0.01%) inactivates the virus on high-touch surfaces and mucosal barriers, contributing to enhanced environmental cleaning protocols in hospitals.

Environmental and Industrial

Bactericides play a crucial role in processes to ensure the safety of by inactivating pathogens. remains one of the most widely used methods, where free at concentrations around 1 mg/L can achieve 4-log inactivation of viruses within approximately 6 minutes, effectively reducing viral loads by 99.99%. Ozonation offers an alternative, employing doses typically ranging from 1 to 2 mg/L to disinfect , with the advantage of leaving no persistent residuals due to ozone's rapid decomposition into oxygen. In , bactericides help extend and prevent spoilage, particularly in products. Nisin, a natural produced by , is approved for use in items such as cheese at levels up to 250 mg/kg, providing targeted inhibition against like . For spices and dehydrated herbs, gamma at doses of 1 to 10 kGy effectively reduces microbial contamination, including bacteria and molds, without significantly altering sensory qualities. Industrial applications of bactericides focus on controlling microbial growth in manufacturing systems to prevent and contamination. In cooling towers, biocides such as isothiazolinones are employed to suppress proliferation, often in combination with oxidizing agents to manage biofilms in recirculating water systems. For textiles, quaternary ammonium compounds (QACs) are applied as finishes to impart properties, effectively reducing odor-causing by disrupting their cell membranes and preventing static-related microbial adhesion. Regulatory frameworks govern bactericide use to balance efficacy with environmental and health risks. The U.S. Environmental Protection Agency (EPA) sets a Maximum Residual Level (MRDL) of 4.0 mg/L for in , based on running annual averages to minimize exposure while maintaining disinfection. However, chlorination can generate disinfection byproducts like trihalomethanes (THMs), with the EPA establishing a Maximum Contaminant Level (MCL) of 0.080 mg/L for total THMs to address potential carcinogenic risks from reactions. concerns include byproduct formation and persistence, prompting shifts toward alternatives that reduce ecological impacts. Recent advancements emphasize bio-based bactericides for . In 2024, research highlighted the integration of bacteriophages into treatment systems as sustainable disinfectants, targeting specific pathogens in with minimal environmental disruption and reduced resistance development compared to chemical biocides.

Antimicrobial Surfaces

surfaces represent engineered materials and natural structures designed to inhibit or kill upon contact, primarily through physical or chemical disruption without relying on leachable agents. These surfaces leverage , embedded particles, or photocatalytic properties to prevent bacterial adhesion and proliferation, offering passive protection in high-contact environments. Natural inspirations, such as the nanopillar arrays on wings, have guided the development of biomimetic designs that mechanically rupture bacterial cell membranes, particularly for Gram-negative . A seminal example from is the wing surface of the Cryptotympana atrata, which features hexagonally arranged nanopillars approximately 200 nm in height and 70 nm in diameter. These structures induce shear forces that stretch and rupture the outer membranes of like Pseudomonas aeruginosa, leading to cell death without harming mammalian cells. A 2013 biophysical study modeled this interaction, demonstrating that the pillars cause irreversible deformation and upon bacterial contact, achieving near-complete killing efficiency . This mechanism highlights how nanoscale topography can provide inherent bactericidal activity, inspiring synthetic mimics. Engineered antimicrobial surfaces often draw from such natural models, including shark skin-inspired micropatterns known as riblets or . These diamond-shaped protrusions, typically 2–5 μm in size, disrupt and adhesion by creating unfavorable attachment sites, reducing formation. Studies on Sharklet-patterned surfaces have shown reduced colonization by uropathogenic compared to smooth controls, with up to 77% less colony size and over 80% inhibition of migration. Similarly, femtosecond laser-etched , combined with layer-by-layer deposition of silver and silica , creates hierarchical micro- and nanostructures that kill both Gram-positive () and Gram-negative () bacteria through mechanical piercing and ion release. A 2020 study reported over 99% reduction in viable bacteria after 24 hours of contact, attributed to the synergistic and effects. Nanoparticle-embedded coatings further enhance surface bactericidal properties, particularly with copper or silver particles integrated into polymer matrices. For instance, copper-carbon hybrid nanoparticles embedded in polymethyl methacrylate (PMMA) coatings provide contact-killing activity against E. coli through ion release and oxidative stress on bacterial membranes. These coatings maintain activity over multiple cycles without significant leaching. Complementing this, titanium dioxide (TiO₂) photocatalytic coatings enable self-cleaning under UV light, generating reactive oxygen species that degrade bacterial cell walls. A 2023 review of TiO₂-modified surfaces highlighted their antibacterial activity against S. aureus and E. coli under UV exposure, with applications in persistent disinfection. Such overlaps with emerging nanomaterials underscore their versatility, though surface-specific implementations prioritize durable adhesion over solubility. In practical applications, antimicrobial surfaces are deployed on touch surfaces like handles and bed rails to curb healthcare-associated infections, including catheter-associated urinary tract infections (CAUTIs). Sharklet-patterned catheters have demonstrated reduced bacterial colonization by 77% in studies, potentially lowering CAUTI incidence by minimizing on indwelling devices. In food packaging, nanoparticle-embedded polymer films prevent microbial spoilage; for example, silver-infused coatings achieve >99% inhibition of on meat surfaces, extending without altering . is typically assessed via contact-killing assays, such as ISO 22196 standards, where surfaces show >5-log reduction in bacterial counts after 24 hours, establishing their role in reducing transmission risks.

Challenges and Resistance

Bacterial Resistance Mechanisms

Bacterial resistance to bactericides encompasses both intrinsic and acquired mechanisms that enable survival and proliferation in the presence of agents. Intrinsic resistance refers to pre-existing cellular features that inherently limit bactericide , while acquired resistance develops through genetic changes that confer adaptive advantages. These mechanisms collectively contribute to the global burden of (AMR), with bacterial AMR directly causing 1.14 million deaths in 2021 and associated with 4.71 million more, a trend projected to escalate to 1.91 million direct deaths and 8.22 million associated deaths by 2050 without intervention. Intrinsic resistance in bacteria, particularly Gram-negative species, often stems from structural barriers that reduce bactericide penetration. The outer membrane of Gram-negative bacteria acts as a selective permeability barrier, with porins—such as OmpF and OmpC in Escherichia coli—forming narrow channels that restrict the entry of hydrophilic molecules like beta-lactams and quinolones. Additionally, natural efflux pumps actively expel bactericides from the cell interior, preventing accumulation at lethal concentrations; for instance, the AcrAB-TolC tripartite efflux system in E. coli and other Enterobacterales efficiently pumps out quinolones, tetracyclines, and chloramphenicol, contributing to baseline multidrug tolerance. These mechanisms are chromosomally encoded and ubiquitous, providing a foundational level of protection without requiring evolutionary adaptation. Acquired resistance arises through genetic alterations that enhance these intrinsic defenses or introduce novel countermeasures. Chromosomal mutations can modify bactericide targets, reducing binding affinity; a prominent example is the Ser83Leu mutation in the gyrA gene, which alters in , conferring resistance to fluoroquinolones like by inhibiting drug-induced DNA cleavage. (HGT) further accelerates resistance dissemination via plasmids, transposons, or integrons; beta-lactamase genes, such as those encoding extended-spectrum beta-lactamases (ESBLs), are frequently mobilized on conjugative plasmids, enabling enzymatic hydrolysis of beta-lactam antibiotics in recipients like Klebsiella pneumoniae. HGT facilitates rapid spread across bacterial populations and species, amplifying resistance in clinical and environmental settings. Specific enzymatic and modification strategies exemplify acquired resistance pathways. Enzyme degradation inactivates bactericides post-entry; the AmpC , often derepressed in Gram-negative pathogens like , hydrolyzes cephalosporins such as ceftazidime, rendering third-generation cephalosporins ineffective. Target site modification alters essential bacterial components; the gene in methicillin-resistant Staphylococcus aureus (MRSA) encodes penicillin-binding protein 2a (PBP2a), a low-affinity transpeptidase that maintains synthesis despite beta-lactam exposure. Biofilms represent a multifaceted resistance strategy, where bacterial communities embed in an (EPS) matrix that shields cells from bactericides. In chronic infections, such as P. aeruginosa biofilms in patients' lungs, the EPS matrix—composed of , proteins, and extracellular DNA—impedes diffusion of antibiotics like tobramycin, creating concentration gradients that protect inner layers. Within biofilms, persister cells, a subpopulation of metabolically dormant , exhibit phenotypic tolerance by entering a non-growing state, evading bactericides that target active processes like replication or protein synthesis. Recent developments highlight the ongoing evolution of resistance, including the emergence of novel proteins like MCR-10, a plasmid-mediated resistance enzyme detected in isolates from humans, animals, and environments since 2022, with sporadic global distribution raising concerns for last-resort polymyxin efficacy. Such innovations, often driven by HGT, underscore the dynamic threat of AMR.

Mitigation Strategies

Antimicrobial stewardship programs play a crucial role in mitigating bacterial resistance by promoting judicious use of bactericides, particularly . The World Health Organization's AWaRe classification system categorizes into Access, Watch, and Reserve groups to guide prescribing practices and monitor consumption, with updates in 2023 incorporating new evidence on resistance patterns and lists. Surveillance networks like the WHO's Global Antimicrobial Resistance and Use Surveillance System () provide standardized data on resistance trends and use, with the 2025 report analyzing over 23 million bacterial isolates to inform global policy responses. These efforts aim to reduce unnecessary prescriptions and track progress toward targets like the 60% usage by 2024, as outlined in WHO guidelines. Combination therapies enhance bactericide efficacy by pairing antibiotics with inhibitors to overcome resistance mechanisms, such as beta-lactamase production. For instance, ceftazidime-avibactam combines a beta-lactam antibiotic with a non-beta-lactam beta-lactamase inhibitor, approved by the FDA in 2015 for complicated infections and expanded in indications through the 2020s. More recently, aztreonam-avibactam received FDA approval in 2025 for treating multidrug-resistant gram-negative infections in adults with limited options, demonstrating synergistic activity against metallo-beta-lactamase-producing pathogens. These combinations restore susceptibility in resistant strains and are recommended in stewardship protocols to preserve monotherapy efficacy. Alternative bactericides offer resistance-sparing options beyond traditional antibiotics. , using bacteriophages to target specific bacteria, has advanced through regulatory protocols in the EU, with the adopting Chapter 5.31 in 2024 to establish quality standards for phage medicinal products, facilitating approvals for compassionate use and trials by 2025. The European Medicines Agency's 2025 draft guideline further clarifies quality documentation for phage active substances, enabling broader clinical implementation. development targets key pathogens like , with ongoing phase I/II trials in 2025 evaluating candidates such as LTB-SA7 to induce immunity against toxins and reduce infection risk in high-burden populations. These approaches minimize selective pressure on antibiotics by preventing infections at the source. Environmental strategies address resistance dissemination outside clinical settings. In agriculture, the EU's Regulation (EU) 2019/6, fully effective from 2022, prohibits s like for growth promotion in and restricts therapeutic use to cases without alternatives, significantly reducing environmental loading from animal sources. Enhanced processes, such as advanced oxidation and membrane filtration, have demonstrated up to 90% removal of resistance genes in municipal plants, with 2025 studies confirming their role in mitigating ARG abundance before effluent discharge. These interventions curb the spread of resistant bacteria into water bodies and chains. Research innovations drive long-term mitigation through novel bactericide development. AI-driven has accelerated pipelines, with 2024 applications identifying novel scaffolds against resistant gram-negatives, contributing to over 10 new classes in preclinical and clinical stages by screening vast chemical spaces efficiently. Global initiatives like the AMR Action Fund have invested in 10 later-stage projects as of July 2025, committing over $1 billion to advance therapeutics for priority pathogens toward market by 2030. These efforts prioritize high-impact mechanisms to replenish the bactericide arsenal.

References

  1. https://www.biology-online.org/dictionary/Bactericide
  2. https://bio.libretexts.org/Courses/Northwest_University/MKBN211%253A_Introductory_Microbiology_%28Bezuidenhout%29/07%253A_Antimicrobial_Drugs/7.01%253A_Overview_of_Antimicrobial_Therapy/7.1.05%253A_Antibiotic_Classifications
  3. https://www.cdc.gov/infection-control/hcp/disinfection-sterilization/glossary.html
  4. https://bio.libretexts.org/Bookshelves/Microbiology/Microbiology_(OpenStax)/13:_Control_of_Microbial_Growth/13.03:_Using_Chemicals_to_Control_Microorganisms
  5. https://www.ncbi.nlm.nih.gov/books/NBK574540/
  6. https://www.cfsph.iastate.edu/Disinfection/Assets/Disinfection101.pdf
  7. https://www.cdc.gov/infection-control/hcp/disinfection-sterilization/chemical-disinfectants.html
  8. https://pmc.ncbi.nlm.nih.gov/articles/PMC11695898/
  9. https://www.merriam-webster.com/dictionary/bactericidal
  10. https://www.collinsdictionary.com/us/dictionary/english/bactericide
  11. https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/bactericide
  12. https://bio.libretexts.org/Courses/Northwest_University/MKBN211%253A_Introductory_Microbiology_%28Bezuidenhout%29/07%253A_Antimicrobial_Drugs/7.01%253A_Overview_of_Antimicrobial_Therapy/7.1.04%253A_Spectrum_of_Antimicrobial_Activity
  13. https://pubmed.ncbi.nlm.nih.gov/31195444/
  14. https://www.sciencedirect.com/science/article/pii/S0362028X24000905
  15. https://www.open.edu/openlearn/mod/oucontent/view.php?id=75460&section=4.2
  16. https://www.cdc.gov/infection-control/media/pdfs/guideline-disinfection-h.pdf
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC4613276/
  18. https://pmc.ncbi.nlm.nih.gov/articles/PMC9544107/
  19. https://www.nature.com/articles/srep38610
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC2857177/
  21. https://pmc.ncbi.nlm.nih.gov/articles/PMC3496266/
  22. https://www.sciencedirect.com/science/article/pii/S0005273615003582
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC2896384/
  24. https://pmc.ncbi.nlm.nih.gov/articles/PMC3531234/
  25. https://biomedres.us/fulltexts/BJSTR.MS.ID.003500.php
  26. https://pubs.acs.org/doi/10.1021/acs.analchem.0c04519
  27. https://pmc.ncbi.nlm.nih.gov/articles/PMC88911/
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC11426018/
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC3171981/
  30. https://www.who.int/publications/i/item/9789240045064
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC9854334/
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC7449185/
  33. https://pmc.ncbi.nlm.nih.gov/articles/PMC7951395/
  34. https://www.ncbi.nlm.nih.gov/books/NBK507853/
  35. https://pmc.ncbi.nlm.nih.gov/articles/PMC5423571/
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC5423573/
  37. https://pubmed.ncbi.nlm.nih.gov/36630111/
  38. https://www.ncbi.nlm.nih.gov/books/NBK556054/
  39. https://pmc.ncbi.nlm.nih.gov/articles/PMC9976080/
  40. https://ehs.cornell.edu/research-safety/chemical-safety/laboratory-safety-manual/appendix-p-phenol-first-aid-guide-and-ppe
  41. https://www.merckvetmanual.com/pharmacology/antiseptics-and-disinfectants/phenols-and-related-compounds-as-antiseptics-and-disinfectants-for-use-with-animals
  42. https://pmc.ncbi.nlm.nih.gov/articles/PMC10390165/
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC8209993/
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC4520913/
  45. https://www.ars.usda.gov/midwest-area/peoria-il/national-center-for-agricultural-utilization-research/docs/penicillin-opening-the-era-of-antibiotics/
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC5403050/
  47. https://www.ncbi.nlm.nih.gov/books/NBK545311/
  48. https://globalrph.com/renal/penicillin-g/
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC5754804/
  50. https://doseme-rx.com/vancomycin/articles/vancomycin-mechanisms-of-action
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC5008060/
  52. https://www.merckmanuals.com/professional/infectious-diseases/bacteria-and-antibacterial-medications/overview-of-antibacterial-medications
  53. https://www.ncbi.nlm.nih.gov/books/NBK535443/
  54. https://www.unmc.edu/intmed/_documents/id/asp/pharm-pk.pdf
  55. https://www.idsociety.org/practice-guideline/vancomycin/
  56. https://www.iqvia.com/locations/emea/blogs/2025/06/the-good-virus-phage-therapeutics
  57. https://www.sciencedirect.com/science/article/pii/S147149142500084X
  58. https://jintensivecare.biomedcentral.com/articles/10.1186/s40560-024-00759-7
  59. https://www.oaepublish.com/articles/mrr.2025.31
  60. https://www.jci.org/articles/view/187996
  61. https://clinicaltrials.gov/study/NCT05453578
  62. https://pubs.rsc.org/en/content/articlehtml/2022/nr/d2nr03902h
  63. https://pmc.ncbi.nlm.nih.gov/articles/PMC12390974/
  64. https://www.mdpi.com/1422-0067/25/21/11563
  65. https://www.nature.com/articles/s41598-025-10700-z
  66. https://publishing.emanresearch.org/CurrentIssuePDF/EmanPublisher_1_5419angiotherapy-859664.pdf
  67. https://www.sciencedirect.com/science/article/pii/S2590098625000259
  68. https://onlinelibrary.wiley.com/doi/10.1111/jfs.70013?af=R
  69. https://www.researchgate.net/publication/381662759_Mechanism_of_antibacterial_phytoconstituents_an_updated_review
  70. https://pmc.ncbi.nlm.nih.gov/articles/PMC11981355/
  71. https://www.dovepress.com/antimicrobial-peptides-mechanisms-applications-and-therapeutic-potenti-peer-reviewed-fulltext-article-IDR
  72. https://pmc.ncbi.nlm.nih.gov/articles/PMC12029989/
  73. https://www.dovepress.com/promising-future-of-novel-beta-lactam-antibiotics-against-bacterial-re-peer-reviewed-fulltext-article-DDDT
  74. https://pubs.acs.org/doi/10.1021/acsinfecdis.2c00649
  75. https://www.genesispub.org/crispr-cas-systems-transformative-precision-tools-to-combat-antimicrobial-resistance-in-multidrug-resistant-gram-negative-pathogens
  76. https://www.nejm.org/doi/full/10.1056/NEJMoa0810988
  77. https://www.cdc.gov/infection-control/media/pdfs/Guideline-CAUTI-H.pdf
  78. https://betsylehmancenterma.gov/assets/uploads/general/Partners-Healthcare-Sepsis-Guidelines-2018.pdf
  79. https://pmc.ncbi.nlm.nih.gov/articles/PMC8496555/
  80. https://pmc.ncbi.nlm.nih.gov/articles/PMC4531195/
  81. https://www.who.int/campaigns/world-hand-hygiene-day/2021/key-facts-and-figures
  82. https://www.nejm.org/doi/full/10.1056/NEJMoa1716771
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC8598944/
  84. https://www.epa.gov/sites/default/files/2021-05/documents/effectiveness_of_disinfectant_residuals_final_-_3-7-07.pdf
  85. https://nepis.epa.gov/Exe/ZyPURL.cgi?Dockey=20014CNC.TXT
  86. https://www.journalofdairyscience.org/article/S0022-0302%2820%2930009-6/pdf
  87. https://units.cals.ncsu.edu/foodsafety/wp-content/uploads/sites/2/2019/06/foodsafety_irradiation.pdf
  88. https://stacks.cdc.gov/view/cdc/193924
  89. https://pubs.acs.org/doi/10.1021/acs.est.2c08244
  90. https://www.waterboards.ca.gov/drinking_water/certlic/drinkingwater/documents/disinfectionregulations/63FedReg69390Dec161998.pdf
  91. https://www.epa.gov/dwreginfo/stage-1-and-stage-2-disinfectants-and-disinfection-byproducts-rules
  92. https://link.springer.com/article/10.1007/s42398-024-00322-y
  93. https://pmc.ncbi.nlm.nih.gov/articles/PMC3576530/
  94. https://pmc.ncbi.nlm.nih.gov/articles/PMC3168968/
  95. https://www.sciencedirect.com/science/article/pii/S0021979720305713
  96. https://link.springer.com/article/10.1557/s43579-022-00294-2
  97. https://pmc.ncbi.nlm.nih.gov/articles/PMC10333809/
  98. https://pmc.ncbi.nlm.nih.gov/articles/PMC11281112/
  99. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(24)01867-1/fulltext
  100. https://www.who.int/news-room/fact-sheets/detail/antimicrobial-resistance
  101. https://pmc.ncbi.nlm.nih.gov/articles/PMC6604941/
  102. https://journals.asm.org/doi/10.1128/cmr.00117-14
  103. https://portlandpress.com/essaysbiochem/article/61/1/49/78496/Intrinsic-adaptive-and-acquired-antimicrobial
  104. https://www.nature.com/articles/s41598-021-99230-y
  105. https://onlinelibrary.wiley.com/doi/10.1111/1348-0421.13222
  106. https://pmc.ncbi.nlm.nih.gov/articles/PMC11939227/
  107. https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2018.02928/full
  108. https://www.sciencedirect.com/science/article/pii/S2590207523000266
  109. https://journals.asm.org/doi/10.1128/spectrum.00418-22
  110. https://www.nature.com/articles/s43856-025-01109-w
  111. https://www.who.int/publications/i/item/WHO-MHP-HPS-EML-2023.04
  112. https://www.who.int/publications/i/item/9789240116337
  113. https://www.who.int/teams/surveillance-prevention-control-AMR/control-and-response-strategies/AWaRe
  114. https://www.accessdata.fda.gov/drugsatfda_docs/nda/2015/206494Orig1s000ODMemo.pdf
  115. https://www.cidrap.umn.edu/antimicrobial-stewardship/fda-approves-combination-antibiotic-difficult-treat-infections
  116. https://www.edqm.eu/en/w/new-general-chapter-on-phage-therapy-medicinal-products-5.31-adopted-and-pre-published-on-the-edqm-website
  117. https://www.ema.europa.eu/en/documents/scientific-guideline/draft-guideline-quality-aspects-phage-therapy-medicinal-products_en.pdf
  118. https://www.med.navy.mil/Media/News/Article/4318968/nmrc-researchers-conduct-first-in-human-clinical-trials-for-staph-a-treatment/
  119. https://clinicaltrials.gov/study/NCT06719219
  120. https://www.sciencedirect.com/science/article/pii/S0928098723001033
  121. https://www.nature.com/articles/s41545-025-00456-4
  122. https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2017.02603/full
  123. https://www.wisdomgale.com/jmrr/index.php?fulltxt=199792&fulltxtj=267&fulltxtp=267-1714456952.pdf
  124. https://www.amr-insights.eu/wp-content/uploads/2025/09/20250917_IFPMA_AMR-incentives-position-paper.pdf
  125. https://www.amractionfund.com/investments
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