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Staphylococcus aureus Biofilms: Characteristics and Impacts on the Treatment of Infectious Diseases

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Nara Juliana Santos Araújo, Vanessa Lima Bezerra, Maria do Socorro Costa, Camila Aparecida Pereira da Silva, Ana Raquel Pereira da Silva, Damiana Gonçalves de Sousa Freitas, Josefa Sayonara dos Santos, Juliete Bezerra Soares and Jacqueline Cosmo Andrade-Pinheiro

Submitted: 24 August 2024 Reviewed: 28 August 2024 Published: 14 December 2024

DOI: 10.5772/intechopen.1007304

Advances and Perspectives of Infections Caused by <em>Staphylococcus aureus</em> IntechOpen
Advances and Perspectives of Infections Caused by Staphylococ... Edited by Jaime Bustos-Martínez

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Advances and Perspectives of Infections Caused by Staphylococcus aureus [Working Title]

Jaime Bustos-Martínez, Juan José Valdez-Alarcón and Aída Hamdan-Partida

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Abstract

Bacterial biofilms have been the subject of studies, mainly because they are responsible for a significant fraction of persistent infections that are resistant to both the action of antimicrobials and the action of the host’s immune system. Staphylococcus aureus is a pathogen with remarkable virulence, present in a significant portion of infectious diseases that affect humans, and its ability to form biofilms contributes to the risks associated with outbreaks involving this agent. This chapter aims to highlight and understand the molecular components involved in the formation and maturation of S. aureus biofilms, as well as the host’s immune responses. These factors are crucial for developing effective strategies to overcome the resistance barrier imposed by biofilms, with the goal of implementing more effective treatments and improving patients’ quality of life. Additionally, the chapter will address the current therapies available for treating infections caused by S. aureus biofilms.

Keywords

  • Staphylococcus aureus
  • biofilms
  • infection
  • resistance
  • treatment

1. Introduction

Staphylococcus aureus is widely recognized as one of the main etiological agents causing several hospital infections and diseases, such as endocarditis, osteomyelitis, bacteremia, pneumonia, skin infections, and complications associated with implanted devices [1].

Biofilm formation is a crucial virulence factor that influences the pathogenicity of the genus Staphylococcus in infections related mainly to devices. Biofilms are defined as microbial communities adhered to surfaces, encapsulated by an extracellular polymeric matrix that offers protection against the host immune system and conventional antimicrobial treatments [2].

Staphylococcus aureus biofilms represent one of the greatest challenges in the treatment of infectious diseases, resulting in an incidence of the infectious process in approximately 80% of cases, especially when it comes to infections occurring within intensive care units [3]. Its ability to form biofilms is associated with chronic infections, which contributes to resistance to conventional therapies. Studies focused on the molecular components involved in the process of biofilm formation and maturation are important for the development of strategies that contribute to reversing resistance and ensuring effective treatments, improving patients’ quality of life [4, 5].

It is well known that the formation of biofilms in Staphylococcus aureus contributes significantly to the development of resistance to conventional antibiotics, biocides, and even the host’s natural defenses, in addition to promoting the production of several virulence factors [1, 2]. In view of this clinical emergency, the need to explore new alternatives in the development of effective drugs against biofilm-associated diseases has become an urgent priority in modern medicine. Continued research and advancement of innovative therapeutic strategies are crucial to combating this growing public health threat.

This study aims to analyze the molecular mechanisms involved in the formation and maturation of Staphylococcus aureus biofilms and how these mechanisms contribute to resistance to antimicrobial treatments. Additionally, it aims to explore host immune responses and evaluate both current and emerging therapies for the control and treatment of biofilm-associated infections. Understanding these aspects is essential for developing more effective and innovative therapeutic strategies that can improve infection management and patient’s quality of life.

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2. Characteristics of Staphylococcus aureus biofilms

2.1 Composition and structure of biofilms

Staphylococcus aureus presents two main structures in biofilm formation: the extracellular matrix and microcolonies. Several characteristics of biofilms, such as increased resistance to antibiotics, adaptability, and strong adhesion to surfaces, are closely related to the extracellular matrix secreted by this microorganism. This matrix, of viscous consistency, represents about 90% of the dry mass of the biofilm and is composed of polymeric substances, extracellular DNA (eDNA), proteins, and polysaccharides [2, 6].

Unlike other microorganisms that possess several exopolysaccharides (EPS), Staphylococci produce only one dominant EPS molecule, the polysaccharide intercellular adhesin (PIA) or poly-β (1–6)-N-acetylglucosamine (PNAG) which is the agent of intercellular adhesion and adhesion to external surfaces [5, 7, 8].

The cell surface of S. aureus is composed of more than 20 proteins covalently anchored to peptidoglycan by the enzyme sortase A. These proteins, known as cell wall proteins (CWA), can be classified into different groups based on their structural and functional characteristics [7, 9]. Some examples include Clumping factor A (ClfA) and Clumping factor B (ClfB), which bind to fibrinogen and facilitate the formation of biofilms. Additionally, fibronectin-binding proteins (FnBPs), such as FnbA and FnbB, interact with fibronectin, while Collagen-binding protein (Can) binds to collagen. Serine-aspartate repeat proteins C, D, and E (SdrC, SdrD, and SdrE) also play a role in adhesion and colonization, along with other families of proteins related to bacterial survival [9].

Another important component of the biofilm structure is the extracellular DNA (eDNA) molecules, which are present in the matrix and are released after cell death. S. aureus biofilms show variations in eDNA content between different strains, and these variations are significantly affected by environmental conditions, including antibiotic exposure. It facilitates the process of irreversible attachment, phenazine retention, and contributes to the process of bacterial resistance [5, 10, 11, 12, 13].

The structural process of biofilm formation by S. aureus involves several steps. This structure is established by the attachment of bacterial cells to the surface, followed by the formation of microcolonies. As the microcolonies consolidate, synthesis of the extracellular matrix that provides structural support begins. Biofilms are organized in layers that allow the diffusion of nutrients. In this environment, cells can undergo aerobic growth, fermentation, death, or dormancy [2, 14, 15].

2.2 Mechanisms of biofilm formation

Biofilm formation by S. aureus occurs through the stages of attachment (adhesion to the surface), aggregation (accumulation and multiplication), maturation (mature biofilm), and dispersion (final phase of the biofilm life cycle). One of the crucial stages is the attachment of planktonic cells to the surface which occurs due to hydrophilic and hydrophobic interactions between the bacterial cell and the target surface mediated by adhesion proteins present on the bacterial cell surface. However, this initial stage of formation is potentially reversible [2, 16, 17].

During the initial stage, planktonic cells of S. aureus use different factors and mechanisms, such as adhesins, alteration of the bacterial cell surface, and the production of eDNA to interact with the host, through proteins anchored in the cell wall. In addition to these factors, the autolytic enzymes AtlA are the main facilitators for primary attachment to surfaces [4, 5].

After the adhesion process, cell multiplication begins and the cell is incorporated into the matrix, which is composed of a complex set of extracellular polymeric substances, such as polysaccharides, proteins, lipids, extracellular DNA, and other biomolecules. It has a rigid and thick structure [16, 17, 18, 19].

The last stage is cell dispersal, in which the quorum sensing system, which regulates the behavior of bacteria within the biofilm, releases chemical signals that promote separation and dispersal, allowing the bacterial cells to return to the planktonic state [20].

2.3 Environmental and biological conditions for Staphylococcus aureus biofilm formation

Three main factors contribute to the formation of Staphylococcus biofilm: the ability to adhere to surfaces, the host immune response, and environmental factors [21].

The ability to adhere to these devices occurs through two main pathways. The first occurs through direct interaction with the surface, while the second involves the formation of connections with proteins in the extracellular matrix. In general, biofilms tend to form where nutrients such as carbon, nitrogen, and phosphate are abundant and can begin to dissolve when nutrients are depleted [15, 22, 23].

Biofilms increase the ability of bacteria to survive environmental stresses, in addition to being potential reservoirs of pathogens such as S. aureus [24]. However, factors such as pH, temperature, nutrient availability, salinity, and dissolved oxygen play crucial roles in the development and persistence of Staphylococcus biofilms. According to recent studies, the biofilm formation capacity of S. aureus is optimal at temperatures between 25°C and 37°C, while lower temperatures, such as 10°C and 4°C, significantly reduce this capacity. Furthermore, the addition of NaCl has been shown to further favor biofilm formation [25].

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3. Impacts of Staphylococcus aureus biofilms on the treatment of infectious diseases

3.1 Resistance to antibiotics

The biofilm acts as a shield against environmental conditions that are unfavorable to the survival of the bacteria, protecting it from the action of the host’s immune system and restricting the penetration and damage caused by drugs. This shield plays a fundamental role in the development of antimicrobial resistance and therapeutic failure, especially in the case of strains of Staphylococcus aureus [16, 26].

The main characteristics responsible for the resistance presented by biofilms include the limited diffusion of antimicrobial agents through the biofilm matrix, the communication of antimicrobial agents with the biofilm matrix, enzyme-mediated resistance, the levels of metabolic activity within the biofilm, genetic adaptation, efflux pumps, and the structure of the outer membrane. The matrix has an efflux system and enzymes that are capable of inactivating antimicrobials and protecting the peripheral region of the biofilm [27, 28].

Staphylococcus aureusinfections associated with biofilms do not respond positively to treatment, even when administering antibiotics that show effective results when tested in standard susceptibility tests since the tests used in clinical laboratories to analyze the susceptibility of microorganisms in relation to antibiotics do not cover the behavior of S. aureus associated with biofilms, as they are performed on planktonic bacteria [29, 30].

The Quorum sensing system, in addition to its functions in the formation and intercellular communication in the biofilm, also plays important roles in virulence and antimicrobial resistance in S. aureus. In this species, this system is also called the accessory gene regulator (agr), encoded by the agr locus [31]. The Agr system also regulates the detachment of biofilm cells from the matrix, and these can cause systemic infections or even adhere to another location and form a new biofilm [32].

The S. aureus bacteria present in the biofilm can alter their gene expression in response to antibiotics such as ampicillin, leading to the translation of genes encoding antimicrobial resistance mechanisms. These include genes for the AbcA efflux pump, modified penicillin-binding proteins (PBP1a/2), and antimicrobial resistance protein genes such as VraF, VraG, Dlt, and Aur. Furthermore, the expression of genes encoding surface proteins such as clumping factor B (ClfB), iron-regulated surface determinant (IsdA), and S. aureus surface protein (SasG), as well as genes that promote adhesion (cap5B and cap5C) induced by ampicillin, increases biofilm viability and biomass [33, 34].

Polysaccharide intercellular adhesin (PIA) is the only exopolysaccharide in Staphylococcus aureus and, in addition to its function in biofilm formation and evasion of the host immune system, it also plays a role in the virulence and antibacterial resistance of the species. This molecule, which is part of the extracellular matrix, mainly affects the penetration of antibiotics into the biofilm, but it can also, in some way, limit the activity of antibiotics that have no difficulty in overcoming the matrix barrier [8].

Another important factor in bacterial resistance is the two-component system encoded by the yycFG gene, which consists of the regulatory protein (YycF) and the sensory protein (YycG). This system is responsible for the generation of Staphylococcus aureus strains with intermediate resistance to vancomycin (VISA) and Staphylococcus aureus with heteroresistance to vancomycin (hVISA). This gene also confers resistance to depolarization and/or permeabilization, contributing to resistance to daptomycin and many other resistance mechanisms, such as the metabolism of cell wall peptidoglycans, the metabolism of cell membrane lipids, and evasion of the innate immune system, are directly or indirectly regulated by it [35, 36].

Antibiotic resistance is reinforced by a transition of the colony from an exponentially multiplying state to a slowly multiplying or non-multiplying state. When antibiotics are administered, they kill most of the cells and the immune system kills both the regular cells and the persister cells in the bloodstream, but some persister cells remain in the biofilm [37].

The biofilm community has a high cell density, which can cause an uneven distribution of nutrients and oxygen, which deprives some cells of this supply. Because of this, the cells reduce their metabolic activity and energy status, a state called persistence, and can survive exposure to most bactericidal antibiotics. In addition, an antibiotic concentration gradient is generated, resulting in selective pressure for these cells to change their state to a persistence state, due to the presence of sub-inhibitory concentrations of this drug [38].

These persistent cells, or persisters, are a specific subpopulation of cells capable of developing temporary antibiotic resistance phenotypes, since these cells are in a metabolic state of dormancy, not undergoing cell division. Since antibiotics require active targets to exert their effect and kill the bacterial cell, when an antibiotic is administered to a population, the metabolically active cells die, while the persisters survive and, in the absence of the antibiotic, repopulate the biofilm, and the infection returns. From this, it is possible to suggest that these cells may be the primary contributors to the recurrence of chronic infections resistant to antimicrobial therapy [7, 39].

In S. aureus, there is an eventual shift to a stationary phase in metabolism, generating a decrease in intracellular ATP. The low concentration of ATP is one of the causes of the tolerance of this microorganism to antimicrobials and represents a lower probability of therapeutic efficacy. These cells may be present throughout the growth phase, but increase proportionally to the increase in cell density in the biofilm [5, 40].

Since persister cells are dormant and are not susceptible to antibiotics available in the clinic, biotechnological approaches have been developed to combat these dormant cells, using compounds that are capable of entering the cell without active transport and can kill the cells without the need for any cellular metabolism mechanism [37].

3.2 Immune response to biofilm infection

The immune system responds to biofilm infection, but unlike the action against planktonic cells, the immune response is quite ineffective most of the time and can lead to recalcitrant infections and even chronic infection [41]. This is mainly due to the physical and mechanical properties of these biofilms, which allow them to evade immune cells, including allowing them to resist elimination by phagocytosis. The entire metabolome of the biofilm is modified when it encounters the host’s defense cells, even leading to an increase in damage to the host generated by the inflammatory response itself [42, 43].

Neutrophils, the first line of defense against bacteria, can invade the biofilm structure, but the community can reverse the attack by producing quorum sensing-regulated toxins that inhibit immune recognition and activity. In addition, the biofilm can produce detergent-like molecules that have direct cytotoxic activity against these cells [41].

This inflammatory response occurs early and is ineffective, mainly due to the fact that complement fixation occurs, to which S. aureus and other Gram-positive species are essentially resistant. And, it is this early response that triggers the activation of neutrophils and the release of inflammatory mediators that cause tissue damage, are harmful to the host, and some mediators, such as IL-1β, can even reinforce biofilm formation [44].

The persistence, dissemination, or elimination of infection is determined by the interaction between S. aureus and macrophages, because as the infection persists, macrophages switch to an anti-inflammatory phenotype. S. aureus biofilm increases the challenges in eliminating the bacteria by avoiding recognition by macrophages, tolerating phagocytosis, reprogramming the metabolic patterns of host cells, promoting anti-inflammatory polarization, and inducing cell death [45].

In a chronic response, the host produces IgG-class antibodies to combat the infection. However, due to heterogeneity within the biofilm community, an antigen may be produced in some areas and not in others, leading to ineffective antigen recognition by antibodies and a failure to eliminate these microorganisms [44]. In this way, the biofilm allows bacteria, especially strains of S. aureus, a multicellular strategy that reverses the relationship between the host’s immune cells and the pathogen [46].

3.3 Complications in clinical treatment resulting from the presence of biofilm

Staphylococcus aureus species are among the first biofilm-forming strains recorded on hospital devices, being commonly related to cases of septicemia, especially in patients with burns and implanted medical devices, whether temporary or permanent [47]. Device or wound infections are associated with opportunistic organisms such as Staphylococcus aureus and are difficult to treat, requiring debridement and even removal of the device, depending on the severity, in addition to presenting a high morbidity and mortality rate [48]. Such infections are observed in a considerable number of patients, being more frequent in immunocompromised individuals [49].

The presence of biofilm makes it difficult to treat pathologies because it can inhibit the penetration of antibiotics so that they can act, in addition to being capable of inactivating them through enzymatic decomposition or adsorption, resulting in relapses or complications [50]. In Staphylococcus aureus strains, the presence of biofilm can generate an increase in antibiotic resistance in the range of 10–1000 times, in addition to contributing to the dissemination of the genes responsible for such resistance, making the healing process difficult [51], requiring high doses of antimicrobials which, often, can lead to an increase in the systemic toxicity of the drugs [52], with high rates of mortality, relapse, and treatment failures having been observed [23].

Antimicrobial resistance may be related to phenomena such as the anaerobic metabolism of bacteria, enzyme production, and the presence of the matrix that acts as an efficient physical barrier that can prevent the entry or dispersion of antimicrobials, hindering their action and causing complications in treatment, requiring the need for more extreme interventions such as surgical procedures [53, 54].

3.4 Staphylococcus aureus biofilm in the nosocomial environment

Bacterial biofilm can be observed in clinical conditions such as infective endocarditis, where it disrupts valve function [55], sepsis [56], and osteomyelitis [57]. The presence of this bacterial organization directly contributes to the increased morbidity and mortality of patients with such pathologies [56]. The presence of biofilm can lead to the inefficiency of antimicrobials, leading to inadequate treatment that can result in recurrence in approximately 80% of cases [3].

When it comes to infections occurring within intensive care units, cases of Staphylococcus aureus detection are the second most recorded type, with 10 cases recorded for every 1000 patients using mechanical ventilators and approximately 3.9 cases for every 1000 patients using central catheters and indwelling catheters [58, 59].

The scientific literature classifies the presence of biofilms as a relevant factor of clinical complication, however, it reports the scarcity of studies on this topic and the importance of carrying out more in-depth studies, considering that many deals with detection and eradication and not exclusively with their nosocomial impact [60], which demonstrates the importance of determining factors such as epidemiological, molecular, phenotypic, and pathophysiological aspects of such infections [61].

In addition to developing profiles related to microorganisms and the structure of the biofilm, it is necessary to implement hygiene, disinfection, and antimicrobial exposure processes in order to prevent the transmission of infectious agents in the nosocomial environment [58].

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4. New therapeutic approaches to combat Staphylococcus aureus biofilms

Biofilm production leads to a significant increase in drug resistance of Staphylococcus aureus, demanding the need for new therapies to combat it. Among these, enzyme therapy has been a treatment option due to its potential to disrupt the bacterial matrix [18, 62, 63]. The action of these enzymes, such as glycoside hydrolases and proteases, is directly related to the molecular complexity of the biofilm and the characteristics of the substrate [64, 65]. Its enhancement can be obtained through the mixture of different enzymes, which has shown more effective action, compared to the use of isolated enzymes [66].

Biofilm control by phages emerges as a new paradigm for possible therapies against S. aureus. In addition to phages, proteins synthesized by phages have been widely studied and have shown potential antibacterial agents. Enzymes, such as virion-associated peptidoglycan hydrolases (VAPGHs), endolysins, and depolymerases, are used by phages to interact with and kill hosts [67, 68].

Nanostructures increase the therapeutic efficacy of many drugs by enhancing their efficiency and bioavailability. They also support significant advances in the selectivity of drug-receptor interactions, systemic bioavailability, and controlled drug release. This is exemplified by polymeric nanoparticles, which are more effective in combating bacteria than the free antimicrobial agents themselves [69].

Nanoparticles have diverse applications in multiple areas of modern science [70]. Some studies have presented polypyrrole nanoparticles and phytofabricated metal nanoparticles as a substantial option against S. aureus, as well as silver nanoparticles associated with simvastatin and copper complexes derived from Schiff base combined with oxacillin and vancomycin as potential promising antimicrobial and antibiofilm agents in the fight against infections originating from S. aureus [71, 72, 73, 74].

Essential oils combined with different antibiotics have shown good results in destroying biofilms, probably due to the presence of monoterpenes, phenols, and alcohols in their composition [75, 76]. The combination of traditional antibiotics, such as norfloxacin, oxacillin, and gentamicin, with certain essential oils, such as Cinnamomum zeylanicum, Mentha piperita, Origanum vulgare, and Thymus vulgaris, has shown potent activity against Staphylococcus aureus biofilms. This association may be a beginning for the creation of safer drug formulations [76].

4.1 Emerging technologies and development of antibiofilm materials

Among the most promising approaches, antibiofilm coatings stand out, which mainly aim to prevent the initial adhesion of bacteria to surfaces. In this context, coating nanoengineering falls into this category, as it aims to alter the physicochemical characteristics of substrate surfaces in such a way that interactions with surfaces and bacteria become unfavorable [77].

The creation of low-adhesion surfaces has proven to be a promising technique for the non-toxic control of microbial bioadhesion. Several approaches have been used, such as topographic modifications, which are designed to destabilize biofilms and reduce irreversible attachment, developing selective anti-fouling effects on certain species [78, 79]. Furthermore, the use of antimicrobial substances, such as antibiotics [79, 80], antimicrobial peptides [81, 82], and quaternary ammonium compounds, have been shown to be effective when applied as special coatings to prevent biofilm formation [81, 83, 84].

The use of polymers, in turn, stands out as a widely used approach for non-stick surfaces, using several mechanisms to prevent bacterial adhesion. Among the polymeric strategies, steric hydration is the most investigated, as it forms a layer of strongly associated water, which reduces the contact angle with water and gives these surfaces a superhydrophilic characteristic [85].

In addition to the use of polymers, recent research has explored nature-inspired surfaces to prevent bacterial adhesion [86], such as plant leaves [87], dragonfly wings, cicada wings [88], lizard skin [89], and shark skin [90]. These bio-inspired architectures are replicated by surface engineering due to their anti-fouling and antibacterial properties, being used in the development of synthetic antimicrobial surfaces through nanoscience tools [91, 92].

Photodynamic therapy, which combines visible light, a photosensitizer, and oxygen to induce a phototoxic reaction capable of killing bacteria, has shown promise. Photosensitizers, when exposed to a specific wavelength of light, generate free radicals and reactive oxygen species that cause oxidative damage to bacteria, affecting essential molecules such as DNA, RNA, proteins, and lipids. Due to the distributed nature of this damage, photodynamic therapy has been considered the least likely to promote the development of antimicrobial resistance [93, 94].

Finally, quorum sensing inhibition has emerged as a promising strategy to prevent the synthesis of factors that contribute to biofilm formation. One example is apicidin, a fungal metabolite that acts as an inhibitor in quorum sensing communication [95]. In recent decades, interference in bacterial communication has become an intensely explored field of research. This approach seeks to identify molecules that act specifically on the quorum sensing system, reducing the production of exoenzymes and toxins without interfering with bacterial growth, qualifying as an ideal adjuvant therapy that can be combined with antibiotics to increase the efficacy of antimicrobial therapy and decrease the risk of resistance [4].

4.2 Prevention and control of Staphylococcus aureus biofilms in clinical settings

The application of effective hygiene and sterilization protocols is crucial to prevent infections in clinical settings, especially those caused by Staphylococcus aureus biofilms, which are highly resistant to conventional treatments. Given this resistance, it is essential to implement rigorous and updated control strategies to minimize the risks associated with these infections [96].

Adopting hygienic and sanitary practices and sanitation procedures is essential to prevent the development of infections. These measures include rigorous hand washing, disinfection of materials used, and training staff to recognize the risks of transmission caused by multidrug-resistant bacteria. In environments with a high probability of transmission and development of resistant microorganisms, defining well-structured hygiene and sterilization protocols is essential [97].

In the context of sterilization protocols, the use of autoclaves is widely adopted, as they employ heat and pressure to kill microorganisms and their spores. However, some devices used in clinical settings are heat-sensitive, which necessitates the adoption of alternative sterilization methods [98].

Hydrogen peroxide sterilization, in turn, is widely used due to its compatibility with most medical devices, as well as its proven efficacy and safety [99]. Although ethylene oxide gas sterilization has been considered the gold standard due to its effectiveness, it has significant disadvantages, such as long processing times and the generation of toxic and carcinogenic residues [98].

In addition to these methods, the use of ultrasound for biofilm removal has gained prominence, especially in clinical settings, due to its effectiveness and potential to complement traditional disinfection and cleaning methods. Ultrasound utilizes high-frequency sound waves to generate cavitations, which are the formation of cavities that can destabilize biofilms and even inactivate microorganisms [100]. Other physical methods, such as plasma application, have also been employed in biofilm eradication. Plasma offers advantages over traditional methods, as it contains free radicals, charged particles, electrons, photons, and other particles that can effectively interact to destroy biofilms [100, 101].

Despite the adoption of several disinfection procedures in healthcare settings, the presence of biofilms in these settings suggests that cleaning and disinfection protocols may be insufficient. Although biofilms contribute to failures in prevention and disinfection, they are not the only culprits. To address these challenges, it is essential to train healthcare professionals to recognize the risks associated with biofilms and implement effective measures to prevent contamination and infections [102].

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5. Conclusion

The biofilm acts as a shield that protects Staphylococcus aureus against mechanical actions, immune response, and antimicrobial action. This structure is frequently associated with nosocomial infections and is considered a relevant cause of complications and morbidity and mortality in patients, especially those who are immunocompromised, increasing hospitalization periods and therefore requiring the need for more in-depth studies that can provide elimination and prevention profiles to ensure a better prognosis for patients. Several lines of research have gained prominence in the fight against biofilms, some examples being innovative therapeutic approaches, such as the use of enzymes, combination therapies, and others, which offer new perspectives in the fight against Staphylococcus aureus biofilms. Although promising, these strategies still face challenges for their effective clinical application. The integration of these techniques with rigorous hygiene and sterilization protocols is essential to overcome current limitations and achieve effective control of these resistant infections.

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Acknowledgments

To the Laboratory of Microbiology and Molecular Biology—LMBM, Regional University of Cariri (URCA) Brazil; the Laboratory of Applied Microbiology—LAMAP, Federal University of Cariri©UFCA, to the National Council for Scientific and Technological Development—CNPq, to ​​the Coordination Foundation for the Improvement of Higher Education Personnel—CAPES, and to the Ceará Foundation for the Support of Scientific and Technological Development—FUNCAP, for financing the project Susceptibility of Bacterial Biofilms to Steroidal Sapogenins (#BP5-0197 00189.01.00/22).

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Conflict of interest

The authors declare no conflict of interest.

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Nara Juliana Santos Araújo, Vanessa Lima Bezerra, Maria do Socorro Costa, Camila Aparecida Pereira da Silva, Ana Raquel Pereira da Silva, Damiana Gonçalves de Sousa Freitas, Josefa Sayonara dos Santos, Juliete Bezerra Soares and Jacqueline Cosmo Andrade-Pinheiro

Submitted: 24 August 2024 Reviewed: 28 August 2024 Published: 14 December 2024

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