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Bacteria living in a biofilm usually have significantly different properties from free-floating bacteria of the same species, as the dense and protected environment of the film allows them to cooperate and interact in various ways.
Bacteria living in a biofilm usually have significantly different properties from free-floating bacteria of the same species, as the dense and protected environment of the film allows them to cooperate and interact in various ways.
One benefit of this environment is increased resistance to [[detergent]]s and [[antibiotic]]s, as the dense extracellular matrix and the outer layer of cells protect the interior of the community. In some cases antibiotic resistance can be increased a thousandfold.<ref>{{Cite journal|author=Stewart PS, Costerton JW |title=Antibiotic resistance of bacteria in biofilms |journal=Lancet |volume=358 |issue=9276 |pages=135–8 |date=July 2001 |pmid=11463434 |doi=10.1016/S0140-6736(01)05321-1}}</ref> [[Lateral gene transfer]] is greatly facilitated in biofilms and leads to a more stable biofilm structure.<ref>{{cite journal|pmid=12849777 | doi=10.1016/S0958-1669(03)00036-3 | volume=14 | issue=3 | title=Gene transfer occurs with enhanced efficiency in biofilms and induces enhanced stabilisation of the biofilm structure |date=June 2003 | author=Molin S, Tolker-Nielsen T | journal=Current Opinion in Biotechnology | pages=255–61}}</ref>
One benefit of this environment is increased resistance to [[detergent]]s and [[antibiotic]]s, as the dense extracellular matrix and the outer layer of cells protect the interior of the community. In some cases antibiotic resistance can be increased a thousandfold.<ref>{{Cite journal|author=Stewart PS, Costerton JW |title=Antibiotic resistance of bacteria in biofilms |journal=Lancet |volume=358 |issue=9276 |pages=135–8 |date=July 2001 |pmid=11463434 |doi=10.1016/S0140-6736(01)05321-1}}</ref> [[Lateral gene transfer]] is greatly facilitated in biofilms and leads to a more stable biofilm structure.<ref>{{cite journal|pmid=12849777 | doi=10.1016/S0958-1669(03)00036-3 | volume=14 | issue=3 | title=Gene transfer occurs with enhanced efficiency in biofilms and induces enhanced stabilisation of the biofilm structure |date=June 2003 | author=Molin S, Tolker-Nielsen T | journal=Current Opinion in Biotechnology | pages=255–61}}</ref> Extracellular DNA is a major structural component of many different microbial biofilms.<ref name="pmid23848166">{{cite journal |author=Jakubovics NS, Shields RC, Rajarajan N, Burgess JG |title=Life after death: the critical role of extracellular DNA in microbial biofilms |journal=Lett. Appl. Microbiol. |volume=57 |issue=6 |pages=467–75 |year=2013 |month=December |pmid=23848166 |doi=10.1111/lam.12134 |url=http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0266-8254&date=2013&volume=57&issue=6&spage=467}}</ref> Enzymatic degradation of extracellular DNA can weaken the biofilm structure and release microbial cells from the surface.


However, biofilms are not always less susceptible to antibiotics. For instance, the biofilm form of ''[[Pseudomonas aeruginosa]]'' has no greater resistance to antimicrobials than do stationary-phase planktonic cells, although when the biofilm is compared to logarithmic phase planktonic cells, the biofilm does have greater resistance to antimicrobials. This resistance to antibiotics in both stationary phase cells and biofilms may be due to the presence of [[persister cell]]s.<ref>{{Cite journal|author=Spoering AL, Lewis K |title=Biofilms and planktonic cells of Pseudomonas aeruginosa have similar resistance to killing by antimicrobials |journal=Journal of Bacteriology |volume=183 |issue=23 |pages=6746–51 |date=December 2001 |pmid=11698361 |pmc=95513 |doi=10.1128/JB.183.23.6746-6751.2001}}</ref>
However, biofilms are not always less susceptible to antibiotics. For instance, the biofilm form of ''[[Pseudomonas aeruginosa]]'' has no greater resistance to antimicrobials than do stationary-phase planktonic cells, although when the biofilm is compared to logarithmic phase planktonic cells, the biofilm does have greater resistance to antimicrobials. This resistance to antibiotics in both stationary phase cells and biofilms may be due to the presence of [[persister cell]]s.<ref>{{Cite journal|author=Spoering AL, Lewis K |title=Biofilms and planktonic cells of Pseudomonas aeruginosa have similar resistance to killing by antimicrobials |journal=Journal of Bacteriology |volume=183 |issue=23 |pages=6746–51 |date=December 2001 |pmid=11698361 |pmc=95513 |doi=10.1128/JB.183.23.6746-6751.2001}}</ref>
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===Dental plaque===
===Dental plaque===
[[Dental plaque]] is an oral biofilm that adheres to the [[teeth]] and consists of many species of both fungal and bacterial cells (such as ''Streptococcus mutans'' and ''Candida albicans''), salivary [[polymers]] and microbial extracellular products. The accumulation of microorganisms subjects the teeth and gingival tissues to high concentrations of bacterial [[metabolite]]s which results in dental disease.<ref name=AnthonyHRogers>{{Cite book|author=Rogers A H |title=Molecular Oral Microbiology |publisher=Caister Academic Press |year=2008 |url=http://www.horizonpress.com/oral2 |isbn=978-1-904455-24-0|pages=65–108}}</ref><ref name="RevistaOMF">{{cite journal |author= Augustin Mihai, Carmen Balotescu-Chifiriuc, Veronica Lazăr, Ruxandra Stănescu, Mihai Burlibașa, Dana Catrinel Ispas |title= Microbial biofilms in dental medicine in reference to implanto-prostethic rehabilitation |language= {{ro icon}} |journal= Revista de chirurgie oro-maxilo-facială și implantologie |issn= 2069-3850 |volume= 1 |issue= 1 |pages= 9–13 |year= 2010 |month= Dec |url= http://www.revistaomf.ro/(8) |id= 8 |accessdate= 2012-06-03 }}(webpage has a translation button)</ref>
[[Dental plaque]] is an oral biofilm that adheres to the [[teeth]] and consists of many species of both fungal and bacterial cells (such as ''Streptococcus mutans'' and ''Candida albicans''), salivary [[polymers]] and microbial extracellular products. The accumulation of microorganisms subjects the teeth and gingival tissues to high concentrations of bacterial [[metabolite]]s which results in dental disease.<ref name=AnthonyHRogers>{{Cite book|author=Rogers A H |title=Molecular Oral Microbiology |publisher=Caister Academic Press |year=2008 |url=http://www.horizonpress.com/oral2 |isbn=978-1-904455-24-0|pages=65–108}}</ref><ref name="RevistaOMF">{{cite journal |author= Augustin Mihai, Carmen Balotescu-Chifiriuc, Veronica Lazăr, Ruxandra Stănescu, Mihai Burlibașa, Dana Catrinel Ispas |title= Microbial biofilms in dental medicine in reference to implanto-prostethic rehabilitation |language= {{ro icon}} |journal= Revista de chirurgie oro-maxilo-facială și implantologie |issn= 2069-3850 |volume= 1 |issue= 1 |pages= 9–13 |year= 2010 |month= Dec |url= http://www.revistaomf.ro/(8) |id= 8 |accessdate= 2012-06-03 }}(webpage has a translation button)</ref>

The biofilm on the surface of teeth is frequently subject to oxidative stress<ref name="pmid8519478">{{cite journal |author=Marquis RE |title=Oxygen metabolism, oxidative stress and acid-base physiology of dental plaque biofilms |journal=J. Ind. Microbiol. |volume=15 |issue=3 |pages=198–207 |year=1995 |month=September |pmid=8519478 |doi= |url=}}</ref> and acid stress.<ref name=Lemos>{{cite journal |author=Lemos JA, Abranches J, Burne RA |title=Responses of cariogenic streptococci to environmental stresses |journal=Curr Issues Mol Biol |volume=7 |issue=1 |pages=95–107 |year=2005 |month=January |pmid=15580782 |doi= |url=http://www.horizonpress.com/cimb/v/v7/07.pdf}}</ref> Dietary carbohydrates can cause a dramatic decrease in pH in oral biofilms to values of 4 and below (acid stress).<ref name=Lemos /> A pH of 4 at body temperature of 37oC causes depurination of DNA, leaving apurinic (AP) sites in DNA<ref name="pmid14938354">{{cite journal |author=TAMM C, HODES ME, CHARGAFF E |title=The formation apurinic acid from the desoxyribonucleic acid of calf thymus |journal=J. Biol. Chem. |volume=195 |issue=1 |pages=49–63 |year=1952 |month=March |pmid=14938354 |doi= |url=http://www.jbc.org/cgi/pmidlookup?view=long&pmid=14938354}}</ref>, especially loss of guanine. <ref name="pmid13701660">{{cite journal |author=FREESE EB |title=Transitions and transversions induced by depurinating agents |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=47 |issue= |pages=540–5 |year=1961 |month=April |pmid=13701660 |pmc=221484 |doi= |url=}}</ref>

A peptide pheromone quorum sensing signaling system in ''S. mutans'' includes the Competence Stimulating Peptide (CSP) that controls genetic competence.<ref name=Li>{{cite journal |author=Li YH, Lau PC, Lee JH, Ellen RP, Cvitkovitch DG |title=Natural genetic transformation of Streptococcus mutans growing in biofilms |journal=J. Bacteriol. |volume=183 |issue=3 |pages=897–908 |year=2001 |month=February |pmid=11208787 |pmc=94956 |doi=10.1128/JB.183.3.897-908.2001 |url=http://jb.asm.org/cgi/pmidlookup?view=long&pmid=11208787}}</ref><ref name="pmid18792689">{{cite journal |author=Senadheera D, Cvitkovitch DG |title=Quorum sensing and biofilm formation by Streptococcus mutans |journal=Adv. Exp. Med. Biol. |volume=631 |issue= |pages=178–88 |year=2008 |pmid=18792689 |doi=10.1007/978-0-387-78885-2_12 |url=http://dx.doi.org/10.1007/978-0-387-78885-2_12}}</ref> This system is optimally expressed when ''S. mutans'' cells reside in an actively growing biofilm. Biofilm grown ''S. mutans'' cells are genetically transformed at a rate 10- to 600-fold higher than ''S. mutans'' growing as free-floating planktonic cells suspended in liquid.<ref name=Li />

When the biofilm, containing ''S. mutans'' and related oral streptococci, is subjected to acid stress, the competence regulon is induced, leading to resistance to being killed by acid.<ref name=Lemos /> Genetic competence is the ability of a cell to take up DNA released by another cell. Competence can lead to genetic transformation, a form of sexual interaction, favored under conditions of high cell density and/or stress where there is maximal opportunity for interaction between the competent cell and the DNA released from nearby donor cells. As pointed out by Michod et al., sex, due to transformation in bacterial pathogens, provides for effective and efficient recombinational repair of DNA damages.<ref name=Michod>{{cite journal |author=Michod RE, Bernstein H, Nedelcu AM |title=Adaptive value of sex in microbial pathogens |journal=Infect. Genet. Evol. |volume=8 |issue=3 |pages=267–85 |year=2008 |month=May |pmid=18295550 |doi=10.1016/j.meegid.2008.01.002 |url=}}http://www.hummingbirds.arizona.edu/Faculty/Michod/Downloads/IGE%20review%20sex.pdf </ref> It appears that ''S. mutans'' can survive the frequent acid stress in oral biofilms through the recombinational repair provided by competence and transformation.

===''Streptococcus pneumoniae''===
''S. pneumoniae'' is the main cause of community-acquired pneumonia and meningitis in children and the elderly, and of septicemia in HIV-infected persons. When ''S. pneumonia'' grows in biofilms, genes are specifically expressed that respond to oxidative stress and induce competence.<ref name="pmid16925554">{{cite journal |author=Oggioni MR, Trappetti C, Kadioglu A, Cassone M, Iannelli F, Ricci S, Andrew PW, Pozzi G |title=Switch from planktonic to sessile life: a major event in pneumococcal pathogenesis |journal=Mol. Microbiol. |volume=61 |issue=5 |pages=1196–210 |year=2006 |month=September |pmid=16925554 |pmc=1618759 |doi=10.1111/j.1365-2958.2006.05310.x |url=http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0950-382X&date=2006&volume=61&issue=5&spage=1196}}</ref> Formation of a biofilm depends on competence stimulating peptide (CSP). CSP also functions as a quorum-sensing peptide. It not only induces biofilm formation, but also increases virulence in pneumonia and meningitis.

It has been proposed that competence development and biofilm formation is an adaptation of ''S. pneumoniae'' to survive the defenses of the host.<ref name=Michod /> In particular, the host’s polymorphonuclear leukocytes produce an oxidative burst to defend against the invading bacteria, and this response can kill bacteria by damaging their DNA. Competent ''S. pneumoniae'' in a biofilm have the survival advantage that they can more easily take up transforming DNA from nearby cells in the biofilm to use for recombinational repair of oxidative damages in their DNA. Competent ''S. pneumoniae'' can also secrete an enzyme (murein hydrolase) that destroys non-competent cells (fratricide) causing DNA to be released into the surrounding medium for potential use by the competent cells.<ref name="pmid22706053">{{cite journal |author=Wei H, Håvarstein LS |title=Fratricide is essential for efficient gene transfer between pneumococci in biofilms |journal=Appl. Environ. Microbiol. |volume=78 |issue=16 |pages=5897–905 |year=2012 |month=August |pmid=22706053 |pmc=3406168 |doi=10.1128/AEM.01343-12 |url=http://aem.asm.org/cgi/pmidlookup?view=long&pmid=22706053}}</ref>


===Legionellosis===
===Legionellosis===

Revision as of 19:18, 3 April 2014

For biographic motion picture, see Biographical film.
Staphylococcus aureus biofilm on an indwelling catheter
IUPAC definition

Aggregate of microorganisms in which cells that are frequently
embedded within a self-produced matrix of extracellular polymeric
substance (EPS) adhere to each other and/or to a surface.

Note 1: A biofilm is a fixed system that can be adapted internally to
environmental conditions by its inhabitants.

Note 2: The self-produced matrix of extracellular polymeric substance, which is also referred to as
slime, is a polymeric conglomeration generally composed of extracellular
biopolymers in various structural forms.[1]

A biofilm is any group of microorganisms in which cells stick to each other on a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS). Biofilm extracellular polymeric substance, which is also referred to as slime (although not everything described as slime is a biofilm), is a polymeric conglomeration generally composed of extracellular DNA, proteins, and polysaccharides. Biofilms may form on living or non-living surfaces and can be prevalent in natural, industrial and hospital settings.[2][3] The microbial cells growing in a biofilm are physiologically distinct from planktonic cells of the same organism, which, by contrast, are single-cells that may float or swim in a liquid medium.

Microbes form a biofilm in response to many factors, which may include cellular recognition of specific or non-specific attachment sites on a surface, nutritional cues, or in some cases, by exposure of planktonic cells to sub-inhibitory concentrations of antibiotics.[4][5] When a cell switches to the biofilm mode of growth, it undergoes a phenotypic shift in behavior in which large suites of genes are differentially regulated.[6]

Formation

An iridescent biofilm on the surface of a fishtank.

Formation of a biofilm begins with the attachment of free-floating microorganisms to a surface. These first colonists adhere to the surface initially through weak, reversible adhesion via van der Waals forces. If the colonists are not immediately separated from the surface, they can anchor themselves more permanently using cell adhesion structures such as pili.[7] Hydrophobicity also plays an important role in determining the ability of bacteria to form biofilms, as those with increased hydrophobicity have reduced repulsion between the extracellular matrix and the bacterium.[8] Some species are not able to attach to a surface on their own but are sometimes able to anchor themselves to the matrix or directly to earlier colonists. It is during this colonization that the cells are able to communicate via quorum sensing using products such as AHL. Some bacteria are unable to form biofilms as successfully due to their limited motility. Nonmotile bacteria cannot recognize the surface or aggregate together as easily as motile bacteria.[9] Once colonization has begun, the biofilm grows through a combination of cell division and recruitment. Polysaccharide matrices typically enclose bacterial biofilms. In addition to the polysaccharides, these matrices may also contain material from the surrounding environment, including but not limited to minerals, soil particles, and blood components, such as erythrocytes and fibrin.[10] The final stage of biofilm formation is known as dispersion, and is the stage in which the biofilm is established and may only change in shape and size. The development of a biofilm may allow for an aggregate cell colony (or colonies) to be increasingly antibiotic resistant. Bacteria form biofilms, matrix-enclosed multicellular assemblages that appear to provide increased survival ability under various stress conditions Cell-cell communication or quorum sensing (QS) has been shown to be involved in the formation of biofilm in several bacterial species.[11]

Development

Five stages of biofilm development: (1) Initial attachment, (2) Irreversible attachment, (3) Maturation I, (4) Maturation II, and (5) Dispersion. Each stage of development in the diagram is paired with a photomicrograph of a developing P. aeruginosa biofilm. All photomicrographs are shown to same scale.

There are five stages of biofilm development (see illustration at right):

  1. Initial attachment:
  2. Irreversible attachment:
  3. Maturation I:
  4. Maturation II:
  5. Dispersion:

Dispersal

Dispersal of cells from the biofilm colony is an essential stage of the biofilm life cycle. Dispersal enables biofilms to spread and colonize new surfaces. Enzymes that degrade the biofilm extracellular matrix, such as dispersin B and deoxyribonuclease, may play a role in biofilm dispersal.[12][13] Biofilm matrix degrading enzymes may be useful as anti-biofilm agents.[14][15] Recent evidence has shown that a fatty acid messenger, cis-2-decenoic acid, is capable of inducing dispersion and inhibiting growth of biofilm colonies. Secreted by Pseudomonas aeruginosa, this compound induces cyclo heteromorphic cells in several species of bacteria and the yeast Candida albicans.[16] Nitric oxide has also been shown to trigger the dispersal of biofilms of several bacteria species [17][18] at sub-toxic concentrations. Nitric oxide has the potential for the treatment of patients that suffer from chronic infections caused by biofilms.[19]

Properties

Biofilms are usually found on solid substrates submerged in or exposed to an aqueous solution, although they can form as floating mats on liquid surfaces and also on the surface of leaves, particularly in high humidity climates. Given sufficient resources for growth, a biofilm will quickly grow to be macroscopic (visible to the naked eye). Biofilms can contain many different types of microorganism, e.g. bacteria, archaea, protozoa, fungi and algae; each group performs specialized metabolic functions. However, some organisms will form single-species films under certain conditions. The social structure (cooperation, competition) within a biofilm highly depends on the different species present.[20]

Extracellular matrix

The biofilm is held together and protected by a matrix of secreted polymeric compounds called EPS. EPS is an abbreviation for either extracellular polymeric substance or exopolysaccharide. This matrix protects the cells within it and facilitates communication among them through biochemical signals. Some biofilms have been found to contain water channels that help distribute nutrients and signalling molecules.[21] This matrix is strong enough that under certain conditions, biofilms can become fossilized (Stromatolites).

Bacteria living in a biofilm usually have significantly different properties from free-floating bacteria of the same species, as the dense and protected environment of the film allows them to cooperate and interact in various ways. One benefit of this environment is increased resistance to detergents and antibiotics, as the dense extracellular matrix and the outer layer of cells protect the interior of the community. In some cases antibiotic resistance can be increased a thousandfold.[22] Lateral gene transfer is greatly facilitated in biofilms and leads to a more stable biofilm structure.[23] Extracellular DNA is a major structural component of many different microbial biofilms.[24] Enzymatic degradation of extracellular DNA can weaken the biofilm structure and release microbial cells from the surface.

However, biofilms are not always less susceptible to antibiotics. For instance, the biofilm form of Pseudomonas aeruginosa has no greater resistance to antimicrobials than do stationary-phase planktonic cells, although when the biofilm is compared to logarithmic phase planktonic cells, the biofilm does have greater resistance to antimicrobials. This resistance to antibiotics in both stationary phase cells and biofilms may be due to the presence of persister cells.[25]

Examples

Biofilm in Yellowstone National Park. Longest raised mat area is about half a meter long.
Thermophilic bacteria in the outflow of Mickey Hot Springs, Oregon, approximately 20 mm thick.

Biofilms are ubiquitous. Nearly every species of microorganism, not only bacteria and archaea, have mechanisms by which they can adhere to surfaces and to each other. Biofilms will form on virtually every non-shedding surface in a non-sterile aqueous (or very humid) environment.

  • Biofilms can be found on rocks and pebbles at the bottom of most streams or rivers and often form on the surface of stagnant pools of water. In fact, biofilms are important components of food chains in rivers and streams and are grazed by the aquatic invertebrates upon which many fish feed.
  • Biofilms can grow in the most extreme environments: from, for example, the extremely hot, briny waters of hot springs ranging from very acidic to very alkaline, to frozen glaciers.
  • In the human environment, biofilms can grow in showers very easily since they provide a moist and warm environment for the biofilm to thrive. Biofilms can form inside water and sewage pipes and cause clogging and corrosion. Biofilms on floors and counters can make sanitation difficult in food preparation areas.
  • Biofilms in cooling- or heating-water systems are known to reduce heat transfer.[26]
  • Biofilms in marine engineering systems, such as pipelines of the offshore oil and gas industry,[27] can lead to substantial corrosion problems. Corrosion is mainly due to abiotic factors; however, at least 20% of corrosion is caused by microorganisms that are attached to the metal subsurface (i.e., microbially influenced corrosion).
  • Bacterial adhesion to boat hulls serves as the foundation for biofouling of seagoing vessels. Once a film of bacteria forms, it is easier for other marine organisms such as barnacles to attach. Such fouling can reduce maximum vessel speed by up to 20%, prolonging voyages and consuming fuel. Time in dry dock for refitting and repainting reduces the productivity of shipping assets, and the useful life of ships is also reduced due to corrosion and mechanical removal (scraping) of marine organisms from ships' hulls.
  • Biofilms can also be harnessed for constructive purposes. For example, many sewage treatment plants include a treatment stage in which waste water passes over biofilms grown on filters, which extract and digest organic compounds. In such biofilms, bacteria are mainly responsible for removal of organic matter (BOD), while protozoa and rotifers are mainly responsible for removal of suspended solids (SS), including pathogens and other microorganisms. Slow sand filters rely on biofilm development in the same way to filter surface water from lake, spring or river sources for drinking purposes. What we regard as clean water is effectively a waste material to these microcellular organisms.
  • Biofilms can help eliminate petroleum oil from contaminated oceans or marine systems. The oil is eliminated by the hydrocarbon-degrading activities of microbial communities, in particular by a remarkable recently discovered group of specialists, the so-called hydrocarbonoclastic bacteria (HCB).[28]
  • Stromatolites are layered accretionary structures formed in shallow water by the trapping, binding and cementation of sedimentary grains by microbial biofilms, especially of cyanobacteria. Stromatolites include some of the most ancient records of life on Earth, and are still forming today.
  • Biofilms are present on the teeth of most animals as dental plaque, where they may cause tooth decay and gum disease.
  • Biofilms are found on the surface of and inside plants. They can either contribute to crop disease or, as in the case of nitrogen-fixing Rhizobium on roots, exist symbiotically with the plant.[29] Examples of crop diseases related to biofilms include Citrus Canker, Pierce's Disease of grapes, and Bacterial Spot of plants such as peppers and tomatoes.[30]
  • Biofilms are used in microbial fuel cells (MFCs) to generate electricity from a variety of starting materials, including complex organic waste and renewable biomass.[3]


Biofilms and infectious diseases

Biofilms have been found to be involved in a wide variety of microbial infections in the body, by one estimate 80% of all infections.[31] Infectious processes in which biofilms have been implicated include common problems such as urinary tract infections, catheter infections, middle-ear infections, formation of dental plaque,[32] gingivitis,[32] coating contact lenses,[33] and less common but more lethal processes such as endocarditis, infections in cystic fibrosis, and infections of permanent indwelling devices such as joint prostheses and heart valves.[34][35] More recently it has been noted that bacterial biofilms may impair cutaneous wound healing and reduce topical antibacterial efficiency in healing or treating infected skin wounds.[36]

It has recently been shown that biofilms are present on the removed tissue of 80% of patients undergoing surgery for chronic sinusitis. The patients with biofilms were shown to have been denuded of cilia and goblet cells, unlike the controls without biofilms who had normal cilia and goblet cell morphology.[37] Biofilms were also found on samples from two of 10 healthy controls mentioned. The species of bacteria from interoperative cultures did not correspond to the bacteria species in the biofilm on the respective patient's tissue. In other words, the cultures were negative though the bacteria were present.[38]

Biofilms can also be formed on the inert surfaces of implanted devices such as catheters, prosthetic cardiac valves and intrauterine devices. [39]

New staining techniques are being developed to differentiate bacterial cells growing in living animals, e.g. from tissues with allergy-inflammations .[40]

Research has shown that sub-therapeutic levels of β-lactam antibiotics induce biofilm formation in Staphylococcus aureus. This sub-therapeutic level of antibiotic may result from the use of antibiotics as growth promoters in agriculture, or during the normal course of antibiotic therapy. The biofilm formation induced by low-level methicillin was inhibited by DNase, suggesting that the sub-therapeutic levels of antibiotic also induce extracellular DNA release.[41]

Dental plaque

Dental plaque is an oral biofilm that adheres to the teeth and consists of many species of both fungal and bacterial cells (such as Streptococcus mutans and Candida albicans), salivary polymers and microbial extracellular products. The accumulation of microorganisms subjects the teeth and gingival tissues to high concentrations of bacterial metabolites which results in dental disease.[32][42]

The biofilm on the surface of teeth is frequently subject to oxidative stress[43] and acid stress.[44] Dietary carbohydrates can cause a dramatic decrease in pH in oral biofilms to values of 4 and below (acid stress).[44] A pH of 4 at body temperature of 37oC causes depurination of DNA, leaving apurinic (AP) sites in DNA[45], especially loss of guanine. [46]

A peptide pheromone quorum sensing signaling system in S. mutans includes the Competence Stimulating Peptide (CSP) that controls genetic competence.[47][48] This system is optimally expressed when S. mutans cells reside in an actively growing biofilm. Biofilm grown S. mutans cells are genetically transformed at a rate 10- to 600-fold higher than S. mutans growing as free-floating planktonic cells suspended in liquid.[47]

When the biofilm, containing S. mutans and related oral streptococci, is subjected to acid stress, the competence regulon is induced, leading to resistance to being killed by acid.[44] Genetic competence is the ability of a cell to take up DNA released by another cell. Competence can lead to genetic transformation, a form of sexual interaction, favored under conditions of high cell density and/or stress where there is maximal opportunity for interaction between the competent cell and the DNA released from nearby donor cells. As pointed out by Michod et al., sex, due to transformation in bacterial pathogens, provides for effective and efficient recombinational repair of DNA damages.[49] It appears that S. mutans can survive the frequent acid stress in oral biofilms through the recombinational repair provided by competence and transformation.

Streptococcus pneumoniae

S. pneumoniae is the main cause of community-acquired pneumonia and meningitis in children and the elderly, and of septicemia in HIV-infected persons. When S. pneumonia grows in biofilms, genes are specifically expressed that respond to oxidative stress and induce competence.[50] Formation of a biofilm depends on competence stimulating peptide (CSP). CSP also functions as a quorum-sensing peptide. It not only induces biofilm formation, but also increases virulence in pneumonia and meningitis.

It has been proposed that competence development and biofilm formation is an adaptation of S. pneumoniae to survive the defenses of the host.[49] In particular, the host’s polymorphonuclear leukocytes produce an oxidative burst to defend against the invading bacteria, and this response can kill bacteria by damaging their DNA. Competent S. pneumoniae in a biofilm have the survival advantage that they can more easily take up transforming DNA from nearby cells in the biofilm to use for recombinational repair of oxidative damages in their DNA. Competent S. pneumoniae can also secrete an enzyme (murein hydrolase) that destroys non-competent cells (fratricide) causing DNA to be released into the surrounding medium for potential use by the competent cells.[51]

Legionellosis

Legionella bacteria are known to grow under certain conditions in biofilms, in which they are protected against disinfectants. Workers in cooling towers, persons working in air conditioned rooms and people taking a shower are exposed to Legionella by inhalation when the systems are not well designed, constructed, or maintained.[52]

See also

References

  1. ^ "Terminology for biorelated polymers and applications (IUPAC Recommendations 2012)" (PDF). Pure and Applied Chemistry. 84 (2): 377–410. 2012. doi:10.1351/PAC-REC-10-12-04.
  2. ^ Hall-Stoodley L, Costerton JW, Stoodley P (February 2004). "Bacterial biofilms: from the natural environment to infectious diseases". Nature Reviews Microbiology. 2 (2): 95–108. doi:10.1038/nrmicro821. PMID 15040259.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ a b Lear, G; Lewis, GD (editor) (2012). Microbial Biofilms: Current Research and Applications. Caister Academic Press. ISBN 978-1-904455-96-7. {{cite book}}: |author= has generic name (help)CS1 maint: multiple names: authors list (link)
  4. ^ Karatan E, Watnick P (June 2009). "Signals, regulatory networks, and materials that build and break bacterial biofilms". Microbiology and Molecular Biology Reviews. 73 (2): 310–47. doi:10.1128/MMBR.00041-08. PMC 2698413. PMID 19487730.
  5. ^ Hoffman LR, D'Argenio DA, MacCoss MJ, Zhang Z, Jones RA, Miller SI (August 2005). "Aminoglycoside antibiotics induce bacterial biofilm formation". Nature. 436 (7054): 1171–5. doi:10.1038/nature03912. PMID 16121184.{{cite journal}}: CS1 maint: multiple names: authors list (link) (primary source)
  6. ^ An D, Parsek MR (June 2007). "The promise and peril of transcriptional profiling in biofilm communities". Current Opinion in Microbiology. 10 (3): 292–6. doi:10.1016/j.mib.2007.05.011. PMID 17573234.
  7. ^ JPG Images: niaid.nih.gov erc.montana.edu
  8. ^ Donlan, Rodney M. 2002. Biofilms: Microbial Life on Surfaces. Emerging Infectious Diseases. Vol. 8, No. 9: pg. 881-890.
  9. ^ Ibid.
  10. ^ Ibid.
  11. ^ Quorum-Sensing Regulation of the Biofilm Matrix Genes (pel) of Pseudomonas aeruginosa
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