Pathogenicity 3 Flashcards
explain dental plaque
Dental plaque is a complex, multispecies biofilm that forms on the surfaces of teeth and plays a significant role in oral health. Here are some key points about dental plaque:
Biofilm Formation: Dental plaque is a biofilm, which is a community of microorganisms that adhere to a surface and are enclosed within a protective extracellular matrix. Plaque formation is an organized process that occurs in several stages.
Diverse Microbial Community: Dental plaque consists of a diverse community of microorganisms, including bacteria, fungi, and sometimes even viruses. The predominant members are bacteria, and various species of bacteria work together in a symbiotic manner within the biofilm.
Digestion of Mucins: Plaque bacteria collaborate to digest mucins, which are complex glycoproteins found in saliva. This process requires a wide range of enzymes to break down the mucins into simpler components that can serve as a nutrient source for the bacteria.
Protein Pellicle: When a person brushes their teeth, proteins from saliva, such as lysozyme, IgA antibodies, and mucins, quickly deposit over the tooth surfaces. This forms a protein pellicle that provides several functions, including protecting teeth from acidic substances, providing lubrication, and preventing mineral deposition or erosion.
Bacterial Colonization: Bacteria, particularly aerobic Gram-positive Streptococcus species, are among the early colonizers of the protein pellicle. These initial colonizers prepare the surface for subsequent bacterial species, including Gram-negative bacteria.
Slime Matrix: Plaque bacteria are embedded in a slimy matrix that consists of a combination of bacterial and host-derived substances. This matrix helps anchor the biofilm to the tooth’s surface and provides protection to the microorganisms.
suggest why biofilms are about 1000 x as resistant to antibiotics than planktonic cells
Biofilms are significantly more resistant to antibiotics compared to planktonic (free-floating) bacterial cells due to a combination of factors that enhance their resilience. Some key reasons include:
Physical Barrier: Biofilms create a protective physical barrier. The extracellular polymeric substance (EPS) matrix produced by biofilm-forming bacteria acts as a shield, limiting the penetration of antibiotics. This matrix consists of polysaccharides, proteins, and DNA, which can trap antibiotics and hinder their diffusion into the biofilm.
Reduced Antibiotic Penetration: The EPS matrix, along with the close proximity of bacterial cells within the biofilm, restricts the diffusion and penetration of antibiotics. This makes it difficult for antibiotics to reach all the bacterial cells, especially those deeper within the biofilm.
Nutrient and Oxygen Gradients: Biofilms have nutrient and oxygen gradients, with greater availability at the surface and decreasing levels toward the core. This gradient can create variations in bacterial metabolic states, with some cells entering a dormant or slow-growing state, which is less susceptible to antibiotics.
Phenotypic Changes: Bacteria within biofilms can undergo phenotypic changes. This includes altered gene expression and the development of antibiotic resistance mechanisms, such as efflux pumps or biofilm-specific resistance genes.
Quorum Sensing: Biofilm bacteria can communicate through quorum sensing, a process in which they release signaling molecules to coordinate their behavior. This communication can trigger the expression of genes that protect against antibiotics.
Diversity of Species: Biofilms often contain diverse bacterial species, and some species may produce enzymes or molecules that break down or inactivate antibiotics. The interactions among different species can contribute to antibiotic resistance.
Tolerance to Antibiotics: Bacterial cells within biofilms can exhibit increased antibiotic tolerance. While they may not be truly resistant, their tolerance allows them to survive exposure to antibiotics for extended periods.
Antibiotic Sequestration: Biofilm components can adsorb and sequester antibiotics, reducing the effective concentration of the drugs within the biofilm and limiting their ability to exert a sufficient antimicrobial effect
explain the formation of dental plaque
Pellicle Formation: As soon as the tooth surface is exposed to saliva, a thin layer called the pellicle forms. This pellicle consists of proteins and lipids, including the salivary agglutinin glycoprotein.
Primary Colonization: The initial step involves primary colonizing bacteria, including Streptococcus oralis, Streptococcus mitis, Streptococcus gordonii, and Streptococcus sanguis. These bacteria express receptors that specifically interact with components of the pellicle, such as the salivary agglutinin glycoprotein. This interaction allows them to adhere to the pellicle-coated tooth surface.
Secondary Colonization: Once the primary colonizers have attached, they create a foundation for the subsequent colonization by other bacteria. Secondary colonizers, often more diverse species, utilize various receptors and adhesins to adhere to the primary colonizers or the tooth surface directly. This step contributes to the maturation of the dental plaque.
Biofilm Formation: Over time, as more bacterial species join the biofilm, they begin to produce extracellular polymeric substances (EPS) that form a matrix around the bacterial cells. This matrix is known as the biofilm, and it provides structural support and protection for the bacterial community.
Biofilm Maturation: The biofilm continues to mature as different species of bacteria adapt and interact within the complex community. It can develop into a three-dimensional structure with water channels and gradients of nutrients and metabolic byproducts.
Biofilm Stability: The mature dental plaque biofilm can be quite stable and difficult to remove. It can resist mechanical forces like brushing and flossing due to its structural integrity and the protective nature of the biofilm matrix.
Pathogenic Implications: While some of these oral bacteria are part of the normal oral microbiota, if not properly managed, dental plaque can lead to oral health problems. Bacteria within the biofilm can metabolize sugars and produce acids, which can erode tooth enamel and lead to dental cavities
explain the gut microflora
Species Richness: The gut microbiota is the most species-rich group of microflora in the human body. It comprises a vast and diverse community of microorganisms, including bacteria, viruses, fungi, and other microorganisms.
Development: The gut microbiota begins to develop shortly after birth. It is not fully established at birth but gradually populates the gastrointestinal tract during infancy. By the age of 1 to 2 years, the gut microbiota is typically well-developed and relatively stable.
Commensals: Many of the microorganisms in the gut are commensals, meaning they have a mutually beneficial relationship with the host. Commensal bacteria live in the gastrointestinal tract without causing harm and, in turn, benefit from the environment and nutrients available.
Mutualists: Some of the gut microorganisms are mutualists, which means they provide clear benefits to the host. For example, these microorganisms help break down complex carbohydrates and dietary fiber that are otherwise indigestible by the host, converting them into short-chain fatty acids (SCFAs) that can be absorbed and used as an energy source.
Metabolic Functions: The gut microbiota contributes to various metabolic functions within the host. It aids in the digestion of certain dietary components, produces essential nutrients like vitamins (e.g., vitamin K and certain B vitamins), and plays a role in the metabolism of xenobiotics (foreign substances) and drugs.
Microbial Composition: The composition of the gut microbiota is predominantly composed of obligate anaerobes. Bacteroides is one of the prominent genera in the gut and is known for its role in fermenting dietary fibers and producing SCFAs.
Protection Against Pathogens: A diverse and balanced gut microbiota is important for protecting the host against enteric (intestinal) pathogens. The presence of commensal and mutualistic microorganisms can help prevent the colonization and overgrowth of harmful pathogens by competing for resources and niches within the gut.
Balance and Health: Maintaining a balanced and diverse gut microbiota is associated with overall health and well-being.
explain the roles of Bacteroides fragilis
The description you’ve provided is consistent with Bacteroides fragilis, a common obligate anaerobic bacterium found in the human gut microbiota. Here are some key characteristics and roles of Bacteroides fragilis:
Gram-Negative Rod: Bacteroides fragilis is classified as a Gram-negative bacterium due to the structure of its cell wall.
Obligate Anaerobe: This bacterium thrives in environments devoid of oxygen, such as the anaerobic conditions found in the human colon.
Gut Microflora: Bacteroides fragilis is a significant component of the gut microbiota, making up approximately 1% to 2% of the microorganisms present in the human intestine.
Commensal and Mutualist: Like many members of the gut microbiota, Bacteroides fragilis can be considered both a commensal and a mutualist. It typically exists in the gut without causing harm and may provide benefits to the host, particularly in the digestion of complex carbohydrates and dietary fiber.
Biofilm Formation: In conditions like inflammatory bowel diseases (IBD), Bacteroides fragilis has been associated with the formation of intestinal biofilms. These biofilms can have complex interactions with the host and other microorganisms.
Opportunistic Pathogen: While Bacteroides fragilis is typically benign in the gut, it can become an opportunistic pathogen if it escapes from the intestine. In such cases, it may cause infections like intra-abdominal abscesses.
Inner Mucus Layer: The human intestinal mucus layer consists of an inner and outer layer. The inner mucus layer is typically devoid of bacteria, serving as a protective barrier against direct contact between bacteria and the epithelial cells lining the gut.
explain a mechanism by which a bacterium, likely a commensal or mutualistic species, utilizes outer membrane vesicles (OMVs) and a specific molecule called PSA (Polysaccharide A) to modulate the host’s immune response
The description you’ve provided relates to a mechanism by which a bacterium, likely a commensal or mutualistic species, utilizes outer membrane vesicles (OMVs) and a specific molecule called PSA (Polysaccharide A) to modulate the host’s immune response. This modulation results in the suppression of inflammation and the facilitation of long-term colonization of the host without causing harm. Here’s a summary of the process:
PSA Secretion: The bacterium secretes a molecule known as PSA.
Packaging into OMVs: PSA is specifically packaged into outer membrane vesicles (OMVs). OMVs are small, spherical structures that can be released by certain Gram-negative bacteria. They contain various biomolecules, including proteins, lipids, and polysaccharides.
Long-Distance Communication: OMVs serve as a means of long-distance communication between the bacterium and the host’s immune system.
Interaction with Dendritic Cells (DCs): OMVs interact with dendritic cells (DCs), which are a type of antigen-presenting immune cell found in various tissues, including the intestinal wall.
PSA Binding to TLR2: Within DCs, PSA from the OMVs binds to Toll-like receptor 2 (TLR2), a receptor involved in recognizing pathogen-associated molecular patterns (PAMPs). PSA- TLR2 binding triggers a signaling cascade in the DC.
DC Activation: Activation of the dendritic cells occurs in response to PSA binding to TLR2. Activated DCs play a crucial role in initiating and regulating immune responses.
T Regulatory Cell Activation: The activated dendritic cells stimulate the activation of regulatory T cells (Tregs). T regulatory cells, or Tregs, are a subset of T cells that are known to suppress excessive immune responses.
IL-10 Secretion: Tregs secrete the anti-inflammatory cytokine Interleukin-10 (IL-10). IL-10 is a key player in suppressing inflammation, and it helps maintain immune homeostasis by preventing the immune system from overreacting.
Suppression of Inflammation: IL-10, secreted by T regulatory cells, exerts its anti-inflammatory effects, which can lead to the suppression of inflammation and immune responses.
Facilitated Long-Term Colonization: By modulating the host’s immune response and suppressing inflammation, the bacterium can achieve long-term colonization without eliciting a harmful immune reaction.
suggest the consequences of failure of DC cells to respond to PSA
Reduced Tolerance Induction: One of the key roles of DCs is to initiate immune responses and regulate tolerance. When DCs do not respond to PSA, the induction of immune tolerance may be compromised. This could lead to an increased likelihood of inappropriate or exaggerated immune responses.
Hyperactive Immune Responses: In the absence of DC-mediated tolerance, the host’s immune system may exhibit hyperactivity, leading to exaggerated inflammatory responses. This could manifest as chronic inflammation and autoimmune reactions.
Loss of Immune Homeostasis: The inability of DCs to activate regulatory T cells (Tregs) in response to PSA may result in the loss of immune homeostasis. Tregs play a critical role in dampening excessive immune reactions, and their absence could disrupt the balance between pro-inflammatory and anti-inflammatory responses.
Increased Susceptibility to Autoimmune Diseases: Dysregulation of the immune system due to the failure of DCs to respond to PSA might increase the host’s susceptibility to autoimmune diseases. Autoimmune diseases are characterized by the immune system mistakenly targeting and damaging the host’s own tissues.
Compromised Gut Health: Since the described mechanism involves interactions in the gut, the loss of immune tolerance and increased inflammation in this region could negatively impact gut health. It may contribute to gut disorders, such as inflammatory bowel diseases (IBD) like Crohn’s disease or ulcerative colitis.
Impaired Long-Term Microbiota Interactions: Failure to respond to PSA might disrupt the balance between commensal microorganisms and the host’s immune system. This could affect the establishment of long-term, mutually beneficial interactions between the gut microbiota and the host.
Increased Risk of Infection: Some bacteria exploit immune regulation mechanisms to establish persistent and harmless colonization within the host. The inability of DCs to respond to PSA might impair this process and increase the risk of pathogenic infections.
explain bacteriocins
Bacteriocins are proteins secreted by certain strains of bacteria that exhibit antibacterial activity, primarily against closely related bacterial strains or species. These antimicrobial peptides play a role in microbial competition, allowing the producing bacteria to outcompete and inhibit the growth of potential competitors in their ecological niche. Here are some key characteristics and functions of bacteriocins:
Narrow Spectrum: Bacteriocins typically have a narrow spectrum of activity, meaning they are effective against specific bacterial strains or species, often those closely related to the producer.
Competition Mechanism: Bacteriocins are part of the competitive arsenal used by bacteria to compete for resources and niche occupancy. They help the producer bacteria gain a competitive advantage by inhibiting the growth of competing bacterial strains.
Species or Genus-Specific: Some bacteriocins target bacterial strains within the same species or genus, while others may affect a broader range of bacteria, depending on their specificity.
Various Producing Bacteria: Bacteriocins are produced by different bacterial species. For example, colicins are bacteriocins produced by Escherichia coli (E. coli), a bacterium commonly found in the human colon. Additionally, some strains of Bacteroides, which are part of the human colon’s microbiota, produce bacteriocins.
Mechanisms of Action: Bacteriocins can have diverse mechanisms of action. Some are pore-forming, meaning they create channels or pores in the target bacteria’s membranes, leading to cell lysis. Others may interfere with essential cellular processes, such as DNA replication or protein synthesis.
Immunity: In many cases, bacteriocin-producing bacteria also produce immunity proteins that protect them from the harmful effects of their own bacteriocins. This allows the producing bacteria to coexist with their toxic proteins.
Applications: Bacteriocins and bacteriocin-producing strains have been explored for various applications, including in the food industry as natural preservatives, in probiotics to support gut health, and for their potential in developing new antibiotics.
explain bacteriocin production by human faecal isolates of Bacteroides
The production and action of bacteriocins in the human colon involve complex interactions between different strains of bacteria, particularly within the Bacteroides group. Here are some key points regarding bacteriocin production by human faecal isolates of Bacteroides:
Bacteriocin T1-1: Bacteriocin T1-1 is produced by some human faecal isolates of Bacteroides. It exhibits remarkable stability over a wide range of pH (from 1 to 12) and temperature (up to 121°C for 15 minutes) conditions. However, exposure to trypsin can inactivate it.
Target Specificity: Bacteriocin T1-1 primarily targets other Bacteroides strains within the same ecological niche. This specificity allows producing strains to gain a competitive advantage against closely related competitors.
Resistance and Susceptibility: Bacteriocin-producing strains are generally resistant to the bacteriocin they produce. In contrast, non-bacteriocin producing strains of Bacteroides are susceptible to the action of bacteriocin T1-1.
Cost of Production: Producing bacteriocins can be metabolically expensive for the bacteria, as it diverts resources and energy away from growth and reproduction. This cost may slow the growth of bacteriocin-producing strains.
Minority Population (Hawks vs. Doves): Within the colon’s microbial community, bacteriocin-producing strains (often referred to as “hawks”) are usually a minority, while the majority consists of non-bacteriocin producing strains (referred to as “doves”). This balance is a result of complex ecological dynamics.
Competitive Outcomes: In a well-mixed microbial culture, the competitive interactions between bacteriocin-producing strains (“hawks”) and non-bacteriocin producing strains (“doves”) determine which strain will dominate. The producing strain’s advantage is the ability to inhibit the growth of susceptible strains, but this advantage may be counteracted by the metabolic costs of bacteriocin production.
suggest why most bacteriocins target closely-related strains
Bacteriocins, which are antimicrobial peptides produced by bacteria to inhibit the growth of other bacteria, often exhibit specificity for closely related strains or species. Several factors can explain why most bacteriocins target closely-related strains:
Ecological Niche: Bacteria that belong to the same species or closely related species often occupy similar ecological niches. This means they share similar habitats, compete for the same resources, and interact with each other more frequently. Bacteriocins have evolved to serve as competitive weapons in these niches.
Receptor Specificity: Bacteriocins typically recognize and bind to specific receptor molecules on the surface of target bacteria. These receptor molecules are often components of the cell envelope or membrane. Closely related strains are more likely to have similar or identical receptor molecules, making them susceptible to the action of a particular bacteriocin.
Genetic Relatedness: Bacteriocin production is genetically encoded, and the genes responsible for bacteriocin synthesis and immunity are often carried on plasmids or within the bacterial genome. Closely related strains are more likely to share similar genetic elements, including bacteriocin-producing genes. This genetic relatedness allows the genes for bacteriocin production and immunity to be more conserved among related strains.
Competitive Advantage: Bacteriocins provide a competitive advantage to the producing strain by inhibiting the growth of competing strains within their ecological niche. In this context, closely related strains are more direct competitors, making them the primary targets for bacteriocin action.
Evolutionary Pressure: The constant competition for limited resources within a niche exerts evolutionary pressure on bacteria. Over time, bacteriocin-producing strains that can effectively target closely related competitors have a selective advantage. As a result, the genes for bacteriocin production and immunity may become fixed or prevalent in the bacterial population.
Efficiency: Bacteriocins are more efficient when they target closely related strains because they are more likely to have evolved receptor molecules that allow for specific recognition.
explain Nisin
Nisin is a polycyclic peptide antibiotic produced by certain strains of the bacterium Lactococcus lactis. It is primarily known for its use as a food preservative to inhibit the growth of spoilage bacteria and foodborne pathogens, especially in dairy products like cheese. Nisin has a unique mode of action that involves disrupting the cell membranes of target bacteria, leading to cell death. Its ability to form pores in the bacterial cell membrane is a key aspect of its antimicrobial activity.
Here’s how nisin works as an antimicrobial agent:
Pore Formation: Nisin acts by binding to a specific molecule called lipid II, which is involved in cell wall synthesis. When nisin binds to lipid II, it forms pores or holes in the bacterial cell membrane.
Permeabilization: The pores created by nisin allow ions, including potassium, to leak out of the bacterial cell. This disrupts the electrochemical balance across the cell membrane, which is essential for many cellular processes.
ATP Efflux: The loss of ions, particularly potassium, affects the energy balance of the cell. This disruption leads to the efflux of adenosine triphosphate (ATP), a molecule critical for energy storage and cellular function.
Cell Exhaustion and Death: As ATP is lost and essential ions leak from the cell, the bacterium experiences cellular exhaustion, which ultimately leads to cell death. Without a functioning membrane and energy production, the bacterium cannot maintain its essential processes.
Nisin is effective against a range of Gram-positive bacteria, including some foodborne pathogens and food spoilage organisms. In addition to its use in food preservation, nisin has also shown promise in medical and clinical settings. Research has indicated that nisin can be effective against both planktonic (free-floating) bacterial cells and bacterial biofilms. This makes it a potential candidate for combating biofilm-associated infections, as biofilms often protect bacteria from antibiotics.
Nisin’s ability to disrupt the integrity of bacterial cell membranes, leading to cell death, has made it a valuable tool in various applications, from food preservation to potential treatments for bacterial infections, including those associated with biofilms.
explain Bdellovibrio bacteriovorus
Bdellovibrio bacteriovorus is a unique bacterium known for its predatory nature. It preys upon other Gram-negative bacteria, serving as a natural predator of various pathogenic or non-pathogenic Gram-negative bacterial species. Here are some notable features of Bdellovibrio bacteriovorus:
Predatory Behavior: Bdellovibrio is a predatory bacterium that actively seeks out and preys upon other Gram-negative bacteria. It attaches to its target host, invades the host’s periplasmic space (the space between the inner and outer membranes of Gram-negative bacteria), and ultimately lyses the host cell to consume its contents.
High Speed: Bdellovibrio is known for its remarkable swimming speed, which can range from 40 to 400 micrometers per second. This speed allows it to quickly locate and attach to its prey.
Diverse Habitats: Bdellovibrio bacteriovorus can be found in various natural environments, including soil, water, and even the human intestine, particularly in the duodenum.
Obligate Predator: It is an obligate predator, which means that it relies on predation for its nutrition and cannot grow or reproduce without a host bacterium to prey upon.
Potential Applications: Research on Bdellovibrio has shown potential applications in biotechnology and biomedicine. It has been investigated for its ability to control and reduce populations of pathogenic bacteria. In some studies, Bdellovibrio has demonstrated the ability to combat antibiotic-resistant strains of bacteria, which makes it an interesting candidate for the development of new antibacterial therapies.
Microbiome Interactions: Understanding the role of Bdellovibrio in the human gut microbiome is an active area of research. It may play a role in influencing the composition and dynamics of the microbial communities in the intestine.
Bdellovibrio bacteriovorus serves as an intriguing example of the diversity and complexity of the microbial world, highlighting the relationships between different microorganisms within ecosystems.
explain a general process of a bacteriophage transitioning from a dormant state to actively infecting a host bacterial cell
Dormant Phase: Bacteriophages can exist in a dormant or inactive state until they encounter a suitable host bacterium. During this phase, they may have protective structures or proteins that shield their genetic material and help them survive in various environmental conditions.
Whiskers Sensing the Environment: Bacteriophages may possess sensory structures or proteins often referred to as “whiskers” (which are not actual whiskers but rather receptor proteins) on their surfaces. These sensory proteins can detect environmental cues such as pH levels, ion concentrations, and temperature.
Depolymerization of Long Tail Fibers: When the bacteriophage senses that it has encountered a suitable host bacterium, it can initiate the process of depolymerizing long tail fibers. These long tail fibers are appendages that help the bacteriophage attach to the host cell’s surface.
Adhesion: After depolymerization of long tail fibers, the bacteriophage can then attach to the host bacterial cell. This attachment is crucial for the subsequent steps of infection.
Injecting DNA into Host Cell: Once attached to the host cell, the bacteriophage uses a structure called a tail sheath to inject its genetic material (usually DNA) into the host cell. This genetic material carries the instructions necessary to hijack the host cell’s machinery for the replication of new phages.
The entire process is a part of the bacteriophage life cycle, which involves recognizing a host, adhering to it, injecting genetic material, replication within the host, and eventually, the lysis (rupture) of the host cell to release new phage particles.
It’s important to note that specific details of bacteriophage infection can vary between different types of phages, and not all bacteriophages have “whiskers” or long tail fibers.
explain the bacteriophage T4 life cycle and the process by which it infects Escherichia coli (E. coli) bacteria
Bacteriophage T4: Bacteriophage T4 is a type of bacteriophage, which is a virus that infects and replicates within bacterial cells.
Viral Structure: Like all viruses, bacteriophages such as T4 have a protein shell, or capsid, that encloses their genetic material. T4 specifically contains double-stranded DNA (dsDNA) as its genetic material.
Injection of Genetic Material: T4 infects E. coli bacteria by attaching to the bacterial surface and injecting its dsDNA into the host cell. Once inside, the viral DNA takes control of the host cell’s machinery.
Replication: Within the host cell, the viral DNA is replicated, and the host cell’s ribosomes and other cellular components are hijacked to produce new viral particles.
DNA Packaging: T4 uses a molecular motor to package its replicated DNA into the phage head at high pressure. This process results in the formation of new viral particles.
Lysis of Host Cell: After about 60 minutes post-infection, T4 enzymatically lyses the host cell, causing it to burst open. This allows the newly formed T4 virions to be released and infect other bacterial cells.
The T4 bacteriophage is an example of a well-studied and highly efficient virus that targets E. coli, making it a valuable model system for studying viral infection and the molecular mechanisms involved in the viral life cycle.
explain biofilms
Biofilms can significantly impact the rates and mechanisms of horizontal gene transfer (HGT) in bacterial communities. HGT refers to the transfer of genetic material (e.g., plasmids, genes) between bacteria through mechanisms like conjugation, transformation, and transduction. Here’s how biofilms influence these processes:
Conjugation in Biofilms: Biofilms provide a structured environment where cells are in close proximity. This proximity can enhance the occurrence of conjugation, a process where genetic material is transferred through direct cell-to-cell contact. In biofilms, cells are physically close, making it easier for conjugative plasmids to be transferred among neighboring cells. Conjugation can stabilize biofilms by allowing bacteria to share beneficial traits like antibiotic resistance.
Transformation in Biofilms: Transformation is the uptake of free DNA by bacteria, which can lead to the acquisition of new genetic material. In biofilms, the extracellular polymeric substance (EPS) matrix can trap DNA, particularly from dead bacteria within the biofilm. The EPS matrix serves as a natural genetic exchange platform, facilitating transformation and allowing biofilm bacteria to incorporate DNA from their surroundings.
Transduction in Biofilms: Transduction is a process where bacteriophages (viruses that infect bacteria) carry bacterial DNA from one cell to another. The structure of biofilms can impact the interactions between bacteriophages and bacteria. Bacteriophages can penetrate biofilm matrices and infect biofilm-resident bacteria, potentially transferring genetic material as they move through the biofilm.
In summary, biofilms create unique environments that promote horizontal gene transfer among bacteria. The physical proximity of cells within biofilms, the presence of trapped DNA in the EPS matrix, and the interaction with bacteriophages all contribute to the enhanced rates of HGT within these complex communities.
