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English research about biofilm





As humans, our environment consistently exposes us to a variety of dangers. Tornadoes, lightning, flooding and hurricanes can all hamper our survival. Not to mention the fact that most of us can encounter swerving cars or ill-intentioned people at any given moment.

Biofilms form when bacteria adhere to surfaces in aqueous environments and begin to excrete a slimy, glue-like substance that can anchor them to all kinds of material

Thousands of years ago, humans realized that they could better survive a dangerous world if they formed into communities, particularly communities consisting of people with different talents. They realized that a community is far more likely to survive through division of labor– one person makes food, another gathers resources, still another protects the community against invaders. Working together in this manner requires communication and cooperation.

Inhabitants of a community live in close proximity and create various forms of shelter in order to protect themselves from external threats. We build houses that protect our families and larger buildings that protect the entire community. Grouping together inside places of shelter is a logical way to enhance survival.

With the above in mind, it should come as no surprise that the pathogens we harbour are seldom found as single entities. Although the pathogens that cause acute infection are generally free-floating bacteria – also referred to as planktonic bacteria – those chronic bacterial forms that stick around for decades long ago evolved ways to join together into communities. Why? Because by doing so, they are better able to combat the cells of our immune system bent upon destroying them.





According to the Center for Biofilm Engineering at Montana State University, biofilms form when bacteria adhere to surfaces in aqueous environments and begin to excrete a slimy, glue-like substance that can anchor them to all kinds of material – such as metals, plastics, soil particles, medical implant materials and, most significantly, human or animal tissue. The first bacterial colonists to adhere to a surface initially do so by inducing weak, reversible bonds called van der Waals forces. If the colonists are not immediately separated from the surface, they can anchor themselves more permanently using cell adhesion molecules, proteins on their surfaces that bind other cells in a process called cell adhesion.

These bacterial pioneers facilitate the arrival of other pathogens by providing more diverse adhesion sites. They also begin to build the matrix that holds the biofilm together. If there are species that are unable to attach to a surface on their own, they are often able to anchor themselves to the matrix or directly to earlier colonists.





During colonization, things start to get interesting. Multiple studies have shown that during the time a biofilm is being created, the pathogens inside it can communicate with each other thanks to a phenomenon called quorum sensing. The phenomenon allows a single-celled bacterium to perceive how many other bacteria are in close proximity. If a bacterium can sense that it is surrounded by a dense population of other pathogens, it is more inclined to join them and contribute to the formation of a biofilm.

Bacteria that engage in quorum sensing communicate their presence by emitting chemical messages that their fellow infectious agents are able to recognize. When the messages grow strong enough, the bacteria respond en masse, behaving as a group. Quorum sensing can occur within a single bacterial species as well as between diverse species, and can regulate a host of different processes, essentially serving as a simple communication network. “Disease-causing bacteria talk to each other with a chemical vocabulary,” says Doug Hibbins of Princeton University.


The final stage of biofilm formation is known as development and is the stage in which the biofilm is established and may only change in shape and size. This development of a biofilm allows for the cells inside to become more resistant to antibiotics administered in a standard fashion. In fact biofilm bacteria can be up to a thousand times more resistant to antimicrobial stress than free-swimming bacteria of the same species.

Biofilms grow slowly, in diverse locations, and biofilm infections are often slow to produce overt symptoms. However, biofilm bacteria can move in numerous ways that allow them to easily infect new tissues. Biofilms may move collectively, by rippling or rolling across the surface, or by detaching in clumps. Sometimes, in a dispersal strategy referred to as “swarming/seeding”, a biofilm colony differentiates to form an outer “wall” of stationary bacteria, while the inner region of the biofilm “liquefies”, allowing planktonic cells to “swim” out of the biofilm and leave behind a hollow mound.[4]

Biofilm bacteria can move in numerous ways: Collectively, by rippling or rolling across the surface, or by detaching in clumps. Individually, through a “swarming and seeding” dispersal.

When cells switch from planktonic to community mode, they also undergo a shift in behaviour that involves alterations in the activity of numerous genes. There is evidence that specific genes must be transcribed during the attachment phase of biofilm development. In many cases, the activation of these genes is required for synthesis of the extracellular matrix that protects the pathogens inside.

Once a biofilm has officially formed, it often contains channels in which nutrients can circulate. Cells in different regions of a biofilm also exhibit different patterns of gene expression. Because biofilms often develop their own metabolism, they are sometimes compared to the tissues of higher organisms, in which closely packed cells work together and create a network in which minerals can flow. When bacteria are under stress—which is the story of their lives—they team up and form this collective called a biofilm. If you look at naturally occurring biofilms, they have very complicated architecture. They are like cities with channels for nutrients to go in and waste to go out.





Researchers often note that, once biofilms are established, planktonic bacteria may periodically leave the biofilm on their own. When they do, they can rapidly multiply and disperse.

According to Costerton, there is a natural pattern of programmed detachment of planktonic cells from biofilms. This means that biofilms can act as what Costerton refers to as “niduses” of acute infection. Because the bacteria in a biofilm are protected by a matrix, the host immune system is less likely to mount a response to their presence.[1]

But if planktonic bacteria are periodically released from the biofilms, each time single bacterial forms enter the tissues, the immune system suddenly becomes aware of their presence. It may proceed to mount an inflammatory response that leads to heightened symptoms. Thus, the periodic release of planktonic bacteria from some biofilms may be what causes many chronic relapsing infections.





Any pathogen that survives in a chronic form benefits by keeping the host alive. After all, if a chronic bacterial form simply kills its host, it will no longer have a place to live. So A chronic infection often results in a “disease stalemate” where bacteria of moderate virulence are somewhat contained by the defence system of the host. The infectious agents never actually kill the host, but the host is never able to fully kill the invading pathogens either.

The optimal way for bacteria to survive under such circumstances is in a biofilm, stating that “Increasing evidence suggests that the biofilm mode of growth may play a key role in both of these adaptations. Biofilm growth increases the resistance of bacteria to killing and may make organisms less conspicuous to the immune system… ultimately this moderation of virulence may serve the bacteria’s interest by increasing the longevity of the host.”





Research on internal biofilms has been largely neglected, despite the fact that bacterial biofilms seem to have great potential for causing human disease.

The lag in studying heterogeneous biofilms is due to the fact it is easy to work in a lab with homogeneous planktonic populations. Biofilms are complex “organisms” existing of hundreds cooperating bacteria organised in a matrix and as such extremely difficult to culture in a laboratory environment.

In just a short period of time, researchers studying internal biofilms have already pegged them as the cause of numerous chronic infections and diseases, and the list of illnesses attributed to these bacterial colonies continues to grow rapidly.

According to a recent public statement from the National Institutes of Health, more than 65% of all microbial infections are caused by biofilms. Common infections as described below are just a few examples of diseases caused by biofilms. These diseases are hard to treat or frequently relapsing!

-urinary tract infections (caused by E. coli and other pathogens)

-Catheter infections (caused by Staphylococcus aureus and other gram-positive pathogens)

-Child middle-ear infections (caused by Haemophilus influenzae, for example)

-Common dental plaque formation

-Gingivitis (inflammation of the gums)

-Chronic sinusitis

-The formation of kidney stones

-Osteomyelitis, a disease in which the bones and bone marrow become infected

-Chronic prostatitis

-Microbes that colonize vaginal tissue and tampon fibers can also form into biofilms, causing inflammation and disease such as Toxic Shock Syndrome.

-Endocarditis, a disease that involves inflammation of the inner layers of the heart.

-Biofims are also commonly found on medical devices such as joint prostheses and heart valves. Patients will often experience pain, but not other symptoms usually associated with infection. Often what happens is that the bacteria that cause infection on prosthetic joints are the same as bacteria that live harmlessly on our skin. However, on a prosthetic joint they can stick, grow and cause problems over the long term.

-Biofilms also cause Leptospirosis, a serious but neglected emerging disease that infects humans through contaminated water.

-cystic fibrosis (infection by the bacterium Pseudomonas aeruginosa in the lungs)

-Fungal biofilm can form in contact lens solution leading to potentially virulent eye infections

-the sludge covering diabetic wounds is largely made up of biofilms.

-Dr. Randall Wolcott recently discovered and confirmed that the sludge covering diabetic wounds is largely made up of biofilms. Whereas before Wolcott’s work such limbs generally had to be amputated, now measures can be taken to stop the spread of infection and save the limb.

Biofilms have the potential to cause a tremendous array of infections and diseases.





At this point in time in allopathic medicine probably the best protocol developed is called “The Marshall Protocol”. Key to the ability of the Marshall Protocol to effectively target biofilm bacteria is the fact that the specific pulsed, low-dose bacteriostatic antibiotics used by the treatment are taken in conjunction with a medication called Benicar. Benicar binds and activates the Vitamin D Receptor, displacing bacterial substances and 25-D from the receptor, so that it can once again activate the innate immune system. Benicar is so effective at strengthening the innate immune response that the patient’s own immune system ultimately helps destroy the biofilm weakened by pulsed, low-dose antibiotics.





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