Biofilm and Cyst Overview

 

Fibrin Biofilms in Bacterial & Viral Chronic Diseases

 

The combination of Monolaurin, Biofilm Enzymes (and Heavy Metal Detox in some cases) provides the best natural defense against:

Allergies                         Herpes

Lyme Disease                 Hepatitis

MRSA Staph                    HIV and Aids

Fibromyalgia                   Shingles

Chronic Fatigue               Chronic Diseases

 

New research is coming out that gives us a clearer understanding of what is needed to fight chronic illnesses like those above.  There are hundreds of clinical studies that show Monolaurin will kill all the above – if it can come into contact with them!  Here, we will show how the biofilm enzymes can help speed the process and give longer results.  (We will focus on the bacterial application here but the process applies to both the bacterial and viral diseases.)

Bacteria adapt to survive.  One way that they’re doing this is by creating biofilms.  Biofilms represents a layer of bacteria and other organisms that live together in a jelly like film.  This film protects them from antibiotics, the immune system, ultraviolet light and other “predators”.  It makes them hard to kill.  New research is showing us how to dissolve these biofilms so our Monolaurin can do its job better.

 

What Are Biofilms?

Since the early 19th century people thought that bacteria existed as single cells floating around. However, in recent years, it was discovered that many disease-causing microbes – especially ‘chronic’ ones – actually live in organized, diverse “communities” called biofilms.

These bacteria (and the viruses above) can attach themselves to surfaces naturally, or as a response to an antibiotic or immune system attack. The biofilm matrix shield they build around themselves helps protect them from attack. Even worse, it also gives them an excellent environment for the exchange of genetic material between cells. This “up-and-down regulation of specific genes can help them develop resistance to antibiotics that might have attacked them.

Biofilms were discovered by van Leeuwenhoek, but it was Heukelekian and Heller that observed that bacterial growth and activity were greatly increased in biofilms. (1) Bacteria within these biofilms can also have “co-bacteria” mutually benefitting relationships. They can even consuming the other’s waste products, thus encouraging growth and production via a symbiotic relationship.

Then, in the early 70’s, Characklis showed that, in this form, the bacteria were highly resistant to disinfectants. (2) This changes the ballgame! You see, standard medical research usually takes a few bacteria and adds antibiotics to see which ones are effective against the bacteria. What they leave out of their ‘pure’ petri dish is that chronic infections can form these community biofilms. Standard research techniques don’t allow for biofilms and treats the bacteria as if they grow in sterile conditions.

These biofilms build a mucus-like film called “Extracellular Polymeric Substances” (EPS), or it can form a tighter form like a cocoon cyst you’d see around a caterpillar. The biofilms leave the infections highly resistant to antibiotics! Often, many different co-bacteria or fungi live in the same biofilm. The biofilm prevents the colony from being penetrated by anti-bacterial agents or the immune system.

However, new tests such as PCR or antigen testing offer new hope for being able to diagnose and treat these biofilm infections. This is critical, as the Center for Disease Control estimates that 65-80% of chronic illnesses are caused by biofilms!

The biofilm can even slow down the penetration of our Monolaurin. In order to dissolve these biofilms and speed up the effectiveness of our Monolaurin, we have introduced a special enzyme blend. This is a blend of enzymes, called Bio-Fibrin specifically focuses on dissolving these biofilms.

How Do These Biofilms Work?

A biofilm is a matrix of polysaccharide material held together by fibrin that it grabs from our body’s own fibrinogen.  The biofilm then adds heavy metals, minerals, blood components and anything else it can get to the biofilm matrix.  Sometimes this mess is in a harder, tighter cyst form.  Sometimes it is a gooey mess, usually just called a biofilm.

The solid-liquid action between a body part and the water/blood mix in our body provides an ideal environment for the attachment and growth of microorganisms. The rougher the cell surface is, the easier the microorganisms can attach. (3)  For example, a rough artery lining is easier to attach to than smooth ones.

Researchers have found that some microorganisms (such as Lyme disease) can form biofilms within minutes of attack and continued to grow them for several hours.  The nature of a particular biofilm may differ for different surfaces in the human host.  There are a number of different materials a biofilms can paste in – such as blood, tears, urine, saliva, intravascular fluid, and (mucus) respiratory secretions. (4-5).

Other things can help ‘trigger’ the growth rate of biofilms.  Blood pH, nutrient levels, sodium, calcium, lanthanum, ferric iron ionic strength, and stress (physical or an illness) can play a role in biofilm development. (6-7)  This is one of the reasons we recommend a heavy metal detox and multi-nutrient to help prevent these triggers.

Fimbriae and flagella influence the rate and extent of attachment of the microorganisms.  Fimbriae are simple filaments attached to the microorganism.  They are like tiny appendages in many gram-negative bacteria (the most common type) that are used to attach to each other or to surfaces for colonization.  Flagella are longer and thicker than fimbria and used in locomotion by many single-celled organisms.  Their role is more to overcome repulsive forces rather than to act as adhesives themselves.  However, it is the fimbriae which have been shown to cause attachment to body cells. (8).

As we will see more later, several studies have shown that treatment of adsorbed cells with proteolytic enzymes causes a dissolving and release of attached bacteria (9), providing evidence for the role of proteins in attachment.

Some viruses use lectins to attach themselves to the cells of the host organism during infection. So, some have suggested binding the lectins would help.  However, Beech and Gaylarde (10) found that this did not prevent attachment unless polysaccharides were involved in attachment.  Once again, the best answer is biofilm enzymes.

Mutation in the Biofilms!

A scarier situation explains why some people have had short term relief with antibiotics –only to have Lyme return again!  When Lyme spirochetes encounter antibiotics (or the immune defenses), they will quickly build their fibrin biofilms for protection.  They are less active behind the biofilms so people experience relief.  However, behind the biofilms, they can easily trade genes and develop resistance to that antibiotic!  Then, when symptoms return, doctors are forced to switch to another antibiotic.  Many patients have spent decades in that vicious cycle, using several different antibiotics.

Now, evidence is mounting that up-and-down regulation of genes in individual bacterial cells can occur within minutes of attachment to surfaces.  A scary 22% of these genes were up-regulated in the biofilm state, and 16% were down-regulated. (11)  In fact, biofilms of MRSA staphylococcus aureus were up-regulated for genes encoding enzymes involved in glycolysis. (16)

Biofilms are primarily made of polysaccharides in extracellular polymeric substance (EPS).  It is the gooey mess we mentioned and be 50% to 90% of the total organic carbon of biofilms. (12)  Then you can add in the heavy metals, minerals blood cells and co-infections and we have biofilm.  The EPS may also contribute to the antimicrobial resistance properties of biofilms by resisting of antibiotics through the biofilm.  Monolaurin appears to slowly absorb through ESP biofilms (the cyst form might be an exception).  We want to speed that process up and get even better results.

It is this atmosphere of easy flow of cell motility in biofilms.  Each organism initially formed small micro colonies.  Then they intermixed.  It is in this looser structure where the micro colonies were observed to be motile. (13)

Fibrin accumulates, as the biofilm forms, in a matrix of platelets, fibrin, and EPS. (14)  The fibrin cyst or biofilm that develops will protect the organisms in these biofilms from the immune system leukocytes.  The minerals become entrapped in the biofilm and can cause encrustation.

Now, we have biofilms that provide an ideal niche for the exchange of extra chromosomal DNA.  Conjugation (the mechanism of plasmid transfer) occurs at a greater rate between cells in biofilms. (15)  Unfortunately, the more chronic diseases, the medically relevant strains of bacteria that contain conjugative plasmids, readily develop biofilms!  (Perhaps that is why they are “chronic”.)

Plasmid-carrying strains have also been shown to transfer plasmids to recipient organisms, resulting in biofilm formation.  However, since plasmids may encode for resistance to multiple antimicrobial agents, biofilms provide a mechanism for selecting and promoting the spread of bacterial resistance to antibiotics!

The Result: Resistance to Antibiotics

The net result of biofilms are that:

1. They are highly resistant to most antimicrobial agents. (17)
2. Organisms within biofilms acquire resistance through the transfer of

resistance plasmids. (18)

3. Transfer of plasmids within biofilms has been well established.
4. Resistant organisms such as methicillin-resistant Staphylococcus aureus

have also been shown to form biofilms. (19)

5.  Biofilms could overcome the host immune system and cause an infection. (20)

Viruses

Though we have focused on bacteria here, the viruses above are included also. For example, Dr. Jose Montoya, at Stanford University, has spent 20 years identifying the protein (biofilm) responsible for chronic Herpes Epstein-Barr HHV-6 and EBV virus.  It is also found in the brains of those with CFS Chronic Fatigue Syndrome (but not in those that are healthy). (21)  This is helping us give answers that work for these viruses as well.

The more we become aware of fibrin biofilms, the more it becomes obvious that we need biofilm enzymes to dissolve them!

(Link to Biofilm Enzymes.)

References

  (Special thanks for excerpts from: Rodney M. Donlan, Centers for Disease Control and Prevention, Atlanta, Georgia, USA, Volume 8, Number 9—September 2002.)

1.  Heukelekian H, Heller A. Relation between food concentration and surface for bacterial growth. J Bacteriol. 1940;40:547–58.PubMed

2. Characklis WG. Attached microbial growths-II. Frictional resistance due to microbial slimes. Water Res. 1973;7:1249–58. DOI

3. Pringle JH, Fletcher M. Influence of substratum wettability on attachment of freshwater bacteria to solid surfaces. Appl Environ Microbiol. 1983;45:811–7.PubMed

4. Mittelman MW. Adhesion to biomaterials. In: Fletcher M, editor. Bacterial adhesion: molecular and ecological diversity. New York: Wiley-Liss, Inc.; 1996. p. 89–127.

5. Ofek I, Doyle RJ. Bacterial adhesion to cells and tissues. In: Ofek I, Doyle RJ, editors. New York: Chapman & Hall; 1994.

6. Fletcher M. The applications of interference reflection microscopy to the study of bacterial adhesion to solid surfaces. In: Houghton DR, Smith RN, Eggins HOW, editors. Bio-deterioration 7. London: Elsevier Applied Science; 1988. p. 31–5.

7. Cowan MM, Warren TM, Fletcher M. Mixed species colonization of solid surfaces in laboratory biofilms. Bio-fouling. 1991;3:23–34. DOI

8. Corpe WA. Microbial surface components involved in adsorption of microorganisms onto surfaces. In: Bitton G, Marshall KC, editors. Adsorption of microorganisms to surfaces. New York: John Wiley & Sons; 1980. p. 105–44.

9. Danielsson A, Norkrans B, Bjornsson A. On bacterial adhesion – the effect of certain enzymes on adhered cells in a marine Pseudomonas sp. Bot Mar. 1977;20:13–7. DOI

10. Beech IB, Gaylarde CC. Adhesion of Desulfovibrio desulfuricans and Pseudomonas fluorescens to mild steel surfaces. J Appl Bacteriol. 1989;67:2017.

11. Becker P, Hufnagle W, Peters G, Herrmann M. Detection of different gene expression in biofilm-forming versus planktonic populations of Staphylococcus aureus using micro-representational-difference analysis. Appl Environ Microbiol. 2001;67:2958–65. DOIPubMed

12. Flemming H-C, Wingender J. Griegbe, Mayer C. Physico-chemical properties of biofilms. In: Evans LV, editor. Biofilms: recent advances in their study and control. Amsterdam: Harwood Academic Publishers; 2000. p. 19–34.

13. Tolker-Nielsen T, Brinch UC, Ragas PC, Andersen JB, Jacobsen CS, Molin S. Development and dynamics of Pseudomonas sp. biofilms. J Bacteriol. 2000;182:6482–9. DOIPubMed

14. Tunney MM, Jones DS, Gorman SP. Biofilm and biofilm-related encrustations of urinary tract devices. In: Doyle RJ, editor. Methods in enzymology, vol. 310. Biofilms. San Diego: Academic Press; 1999. p. 558–66.

15. Hausner M, Wuertz S. High rates of conjugation in bacterial biofilms as determined by quantitative in situ analysis. Appl Environ Microbiol. 1999;65:3710–3.PubMed

16. Raad II, Sabbagh MF, Rand KH, Sherertz RJ. Quantitative tip culture methods and the diagnosis of central venous catheter-related infections. Diagn Microbiol Infect Dis. 1992;15:13–20. DOIPubMed

17. Donlan RM. Role of biofilms in antimicrobial resistance. ASAIO J. 2000;46:S47–52. DOIPubMed

18. Sedor J, Mulholland SG. Hospital acquired urinary tract infections associated with the indwelling catheter. Urol Clin North Am. 1999;26:821–8. DOIPubMed

19. Murga R, McAllister S, Miller JM, Tenover F, Bell M, Donlan RM. Effect of vancomycin treatment of methicillin-resistant S. aureus (MRSA) biofilms on central venous catheters in a model system. Poster No. C276 presented at the 2001 American Society for Microbiology Annual Meeting, Orlando, FL, May 23, 2001.

20. Yasuda H, Ajiki Y, Aoyama J, Yokota T. Interaction between human polymorphonuclear leucocytes and bacteria released from in vitro bacterial biofilm models. J Med Microbiol. 1994;41:359–67. DOIPubMed

21. Biofilms and Chronic Infections. JAMA June 11, 2008. P 2682-3.