Dr. Dao Nguyen, now at McGill University, trained in the University of Washington lab of Dr. Pradeep Singh, a lung specialist who studies bacterial biofilm infections.

“A chief cause of the resistance of biofilms is that bacteria on the outside of the clusters have the first shot at the nutrients that diffuse in,” said Pradeep Singh, associate professor of medicine and microbiology at the University of Washington.

“This produces starvation of the bacteria inside clusters, and severe resistance to (their) killing,” added the senior study author, the journal Science reports.

“Bacteria become starved when they exhaust nutrient supplies in the (infected) body, or if they live clustered together in groups known as biofilms,” said study co-author Dao Nguyen, assistant professor of medicine at Montreal’s McGill University.

Preventing pathogenic bacteria from sensing nutrient starvation may present a new therapeutic approach to increasing antibiotic efficacy and preventing drug resistance, researchers claim. A team led by McGill University investigators has found that blocking an active mechanism used by bacteria to respond to starvation by slowing their growth significantly reduces the natural tolerance to antibiotics that infectious organisms develop when nutrient supplies become low.

The investigators work is reported in Science in a paper titled “Active Starvation Responses Mediate Antibiotic Tolerance in Biofilms and Nutrient-Limited Bacteria.” Pradeep K. Singh, Ph.D., Dao Nguyen, Ph.D., and colleagues

Abstract:

Bacteria become highly tolerant to antibiotics when nutrients are limited. The inactivity of antibiotic targets caused by starvation-induced growth arrest is thought to be a key mechanism producing tolerance. Here we show that the antibiotic tolerance of nutrient-limited and biofilm Pseudomonas aeruginosa is mediated by active responses to starvation, rather than by the passive effects of growth arrest. The protective mechanism is controlled by the starvation-signaling stringent response (SR), and our experiments link SR-mediated tolerance to reduced levels of oxidant stress in bacterial cells. Furthermore, inactivating this protective mechanism sensitized biofilms by several orders of magnitude to four different classes of antibiotics and markedly enhanced the efficacy of antibiotic treatment in experimental infections.

You can read all of my biofilm posts here

My Testimonial

Growth at the age of 18 usually pertains to mental and physical changes of an affirmative nature-one entering long awaited adulthood. This transition is a defining moment, submerge within human mushrooming, that manifests the liberating self within-the adult. A period as such begs for last youthful, teenage, adolescent kicks before the initial throw into survival for personal prevail.. We always look back years later, reminisce of the high school times, of its euphoric, trivially troubled, apathetic and awkwardly clumsy moments with jubilance and just sigh. This sort of ease I was not granted with, for at this time I developed a gluten and dairy intolerance.

Starting with just simple pain, it escalated to chronic visits to the bathroom, metamorphose into crude IBS, simultaneously arousing a type of acid relax which brought nothing but unprecedented pain, discomfort, or simply-terrible depressing life. After many visits to the doctor, pills, pills, and more pills were prescribed. The assumed acid reflux did nothing but add to the issues. My stomach felt destroyed. I thought if I limited my food intake, such as spice, and just eat simple foods like bread symptoms would ease-they only showered. The details are terrible of the pain I underwent every day for about a year.

Turning to the internet and easing of pills helped. Soon I was on some holistic herbal pills (name I do not recall), which seemed to help. After months and months I finally stumbled onto a forum that matched my symptoms and I dove into its contents. Having never heard of gluten intolerance, and having an imbedded humor towards lactose intolerance there was no consideration of it. And then, somehow, by some cosmic infinitesimally small chance, Dr. Ettinger had a meager response to someone’s statement on this ambiguous forum. After reluctant search I reached his website and made an appointment. BEST DECISION, EVER.

At this point in time, I entered his office hopeless and depressed. The chemical spark within was never this lifeless. Following thorough dietary details Dr. Ettinger’s immediate response and conclusion was that I, in fact, was gluten intolerant and everything my body digested was poison for it. Skipping the initial shock, it was quite difficult to cope with such news and to develop an acute sensory as well as filtration system to accommodate my bodily needs. Trials and errors persisted, stumbles and falls waved in. Still, improvement showed. Slowly, but in actuality promptly, my body underwent a speedy rehabilitation and I felt amazing.

Remembrance of such joy, such avid taste of my anatomies equilibrium was elusive. I finally returned to my body’s normalcy. I still took in diary, only to realize a bit later that that too was an allergen. After its elimination I never felt better. It has now been about a year since I’ve been gluten and dairy free. It has been difficult but worth it. Crudely, perhaps in a bit exaggerated manner, I do not know if I would have survived without this simple analysis. I can now have gluten and dairy occasionally and feel no symptoms (if necessary). This is not some requested testimonial, there is no higher truth. Dr. Ettinger possesses healing knowledge for all, and I still joke around that he should somehow replicate himself in the health profession for others to benefit from. If I was a millionaire I would definitely pay him generously. Unfortunately I’m not, and I owe him greatly for all he’s done. I still visit whenever I can just for a check-up.

Best regards,

-Rokas

Previous treatments: multiple rounds of antibiotics without eradication of the H. pylori bacteria.

A pre-test for H. pylori stool antigen was performed on February 07, 2011 and was found to be positive. After  44 days on my H. pylori protocol, a follow-up stool antigen test was performed. The results came back negative for H. pylori.

Current Status: GI symptoms are improving and I expect that with the addition of  a few nutritional supplements to support her specific needs, combined with certain dietary restrictions and additions, this patient will be symptom free in short-order.

Positive BioHealth Diagnostics H. pylori stool antigen test

Hello Dr. Ettinger,

Just a quick thank you note and a recommendation to others.

I was told by my doctor that I had H. pylori and it needed to be handled. She told me it would require three antibiotics. I’m one who prefers not to put antibiotics in my body because I got addicted to them earlier in my life and ended up “having” to take them for 5 years. I was told that I would be sick if I didn’t take them all the time. It took me an equal number of years for my body to be able to heal itself after that. Do NOT believe anyone who tells you that antibiotics do not lower your body’s own defense. I have been completely drug free and sickness free since 1995. So I was very surprised when I learned I had h pylori.

I began my research on the web to cure h. pylori naturally. I followed two website’s protocol for 3 months. I was very disciplined on their protocol but kept testing positive. I then read Dr. Marcus Ettinger’s site and called him. He was extremely professional and very helpful and sensitive to my concerns. He recommended a natural protocol and I followed it for 34 days. BioHealth Diagnostic’s test (Helicobacter pylori Antigen, #418 link added by ME]) came back negative.

I highly recommend everyone try his program before subjecting your body to antibiotics or other protocols.

Thank you Dr. Ettinger.

TDS
Salt Lake City, UT

Negative BioHealth Diagnostics H. pylori stool antigen test

Monolaurin - Monolauroylglycerin - Glycerol monolaurate

Lauric acid is a 12-carbon medium chain fatty acid (MCFA) found naturally in human breast milk (6.2% of total fat) and coconut oil (47.5% by weight). Lauric acid was originally discovered when microbiologists studied human breast milk to determine the protective (anti-viral and anti-bacterial) substances which protected infants from microbial infections. Other fatty acids were also found to have antimicrobial actions but lauric acid was found to be the most active.

The esterification of lauric acid, that naturally occurs in our body, yields an amazing compound known as monolaurin (glycerol monolaurate). Monolaurin is a non-ionic surfactant¹, which possesses an even greater anti-viral and anti-bacterial activity than its precursor, lauric acid. Monolaurin, when given orally, at therapeutic doses between 2,500 – 4,500 mg/day is generally well tolerated, with loose bowels as the only negative concern. Monolaurin has been studied at medical research centers, including the Center for Disease Control (CDC), because of its high antimicrobial (anti-viral, anti-bacterial, anti-fungal, anti-yeast and anti-protozoal) activity. These studies have provided information about the anti-viral and anti-bacterial mechanisms of monolaurin. Monolaurin was found to be effective against certain Lipid Coated Bacteria (LCBs) and Lipid Coated Viruses (LCVs) – enveloped DNA and RNA viruses.

¹Surfactant: Surfactants are compounds that lower the surface tension of a liquid, allowing easier spreading, and lowering of the interfacial tension between two liquids, or between a liquid and a solid. Surfactants may act as: detergents, wetting agents, emulsifiers, foaming agents, and dispersants.

Lipid Coated Virus

HIV-1, Influenza virus, paramyxoviruses, rubeola virus, bronchitis virus, and the herpes family of viruses (Epstein-Barr, cytomegalo, zoster, vericella-zoster and herpes type I and II). Sadly, monolaurin had no effect on diseases caused by non-enveloped viruses such as polio virus, coxsackie virus, encephalomyocarditis virus, rhinovirus, and rotaviruses.

Lipid Coated Bacteria

Helicobacter pylori (H. pylori),  Staphylococcus aureus and Streptococcus agalactiae.

The anti-viral and anti-bacterial action attributed to monolaurin is that of solubilizing the lipids and phospholipids in the protective envelope of these particular infective agents causing the disintegration of the lipid envelope. Recent publications have shown that monolaurin and lauric acid inhibit the replication of viruses by interrupting the communication and binding of virus to host cells and thus preventing the uncoating of viruses necessary for replication and infection. Other studies have shown that monolaurin is able to remove all measurable infectivity by directly disintegrating the protective bacterial and viral lipid envelop. Binding of monolaurin to the viral envelop also makes the virus more susceptible to degradation by host defenses, heat, or ultraviolet light.

Microorganisms Inactivated by Monolaurin

Ecological Formulas Monolaurin (600 mg’s – 90 caps) $34.00 or Lauricidin® The Original Monolaurin 227gr $40.00 Call to Purchase 714-639-4360

microparticles "microbubbles" used for detection of bacterial biofilm

Certain types of bacteria, such as: Borrelia burgdorferi, Escherichia coli, Candida albicans, Clostridium difficile, Helicobacter pylori, Klebsiella pneumoniae, Legionella pneumophila, Listeria monocytogenes, Pseudomonas aeruginosa, Salmonella typhimurium, Staphylococcus aureus, Staphylococcus epidermidis, and Vibrio cholerae, can join forces to form protective communities called biofilms.  These thin layers of bacteria, which grow on the surfaces of medical implants or directly on tissue in the body, can be difficult to treat because they are more resistant to drugs than the bacteria on their own.  Currently there is no established way to image biofilms in or out of the body.

Pavlos Anastasiadis and colleagues at the University of Hawaii at Manoa have developed a method to watch and measure growing biofilms with ultrasound.  The researchers used contrast agents, microparticles, more accurately, microbubbles, that are normally injected into the body to improve the quality of ultrasound images.  They modified the surface of bubbles in the agents to stick to two kinds of infectious bacteria that form biofilms (Staphylococcus aureus and Pseudomonas aeruginosa).   Acoustic pulses of ultrasound cause the bubbles to “ring” like a bell, revealing their location and the attached biofilm.

The research was done on isolated biofilms.  The next step will be to test it in living tissue.  Anastasiadis hopes to develop the technique to diagnose infective endocarditis, a disease in which bacterial biofilms form on the inner walls of damaged heart valves.

“Targeted ultrasound contrast agents for the imaging of biofilm infections” by Pavlos Anastasiadis  – Abstract: http://asa.aip.org/web2/asa/abstracts/search.may09/asa323.html

The discovery that bacteria are able to communicate with each other changed our general perception of many single, simple organisms inhabiting our world. Instead of language, bacteria use signaling molecules which are released into the environment. As well as releasing the signaling molecules, bacteria are also able to measure the number (concentration) of the molecules within a population. Nowadays we use the term ‘Quorum Sensing’ (QS) to describe the phenomenon whereby the accumulation of signaling molecules enable a single cell to sense the number of bacteria (cell density). In the natural environment, there are many different bacteria living together which use various classes of signaling molecules. As they employ different languages they cannot necessarily talk to all other bacteria. Today, several quorum sensing systems are intensively studied in various organisms such as marine bacteria and several pathogenic bacteria.

Quorum Sensing & Biofilm Formation

Why do bacteria talk to each other?

(QS) enables bacteria to co-ordinate their behavior. As environmental conditions often change rapidly, bacteria need to respond quickly in order to survive. These responses include adaptation to availability of nutrients, defense against other microorganisms (biofilm formation) which may compete for the same nutrients and the avoidance of toxic compounds (biofilm formation) potentially dangerous for the bacteria. It is very important for pathogenic bacteria during infection of a host (e.g. humans, other animals or plants) to co-ordinate their virulence in order to escape the immune response of the host in order to be able to establish a successful infection. The University of Nottingham Quorum Sensing Research Group

From Dr. Ettinger’s Biofilm Protocol for Lyme and Gut Pathogens: Pathogenic bacteria known to reside in biofilms include: Borrelia burgdorferi, Escherichia coli, Candida albicans, Clostridium difficile, Clostridium perfringens, Helicobacter pylori, Klebsiella pneumoniae, Legionella pneumophila, Listeria monocytogenes, Pseudomonas aeruginosa, Salmonella typhimurium, Staphylococcus aureus, Staphylococcus epidermidis, and Vibrio cholerae. The number of human diseases shown to be associated with biofilms is expanding and includes chronic bacterial prostatitis, chronic rhinosinusitis, cystic fibrosis pneumonia, infective endocarditis, periodontitis, recurrent otitis media, and virtually all device and implant related infections. Strong evidence is also beginning to emerge for an etiologic role of pathogenic mucosal biofilms in gastrointestinal diseases, such as Irritable Bowel Disorders: Crohn’s disease and ulcerative colitis.

Biofilm Formation

A Brief history of “biofilm”
Center for Biofilm Engineering
Montana State University

Microbial communities attached to surfaces (biofilms) were observed long before people had the tools to study them in detail. In 1684 Antony van Leeuwenhoek remarked on the vast accumulation of microorganisms in dental plaque in a report to the Royal Society of London: “The number of these animalcules in the scurf of a man’s teeth are so many that I believe they exceed the number of men in a kingdom.”

The study of microbes took an important turn in the mid-1800s, when Robert Koch developed methods to create a solid nutrient medium in order to grow and isolate pure cultures of microorganisms. This development led to huge advances in medicine, agriculture, and industry. However, these advances were based on such a simplistic concept of microbial life that many ‘solutions’ generated by these techniques are now being reversed. Microorganisms have proved to be much more complex and less tractable than we ever imagined.

In a 1940 issue of the Journal of Bacteriology, authors H. Heukelekian and A. Heller wrote, “Surfaces enable bacteria to develop in substrates otherwise too dilute for growth. Development takes place either as bacterial slime or colonial growth attached to surfaces.” Claude ZoBell described many of the fundamental characteristics of attached microbial communities in the 1940s. In the late decades of the 20th century, numerous articles were written about microbial films or slime layers; German researchers sometimes used the term “Schmutzdecke.” As the unique properties of microbial communities vs planktonic microbes grew more apparent, it became helpful to use a special term to describe them. “Biofilm” was used colloquially among researchers for some years before it was considered a term acceptable for use in publication. The earliest use of “biofilm” in publication is in the Swedish journal Vatten: Harremoës, P. 1977. “Half-order reactions in biofilm and filter kinetics,” Vatten, 33 122-143. (If you know of an earlier publication with “biofilm” in it, please let us know; we would be happy to make a correction.)

Early biofilm researchers studied the implications of biofilms in waste-water filtration, biofouling of industrial equipment, and dental plaque (Leewenhoek would have been pleased). Since bacteria preferentially attach to surfaces, biofilms are virtually ubiquitous. Biofilm formation is also implicated in microbiologically influenced corrosion (MIC), product contamination, medical device-related infections, and chronic wounds. Biofilm can also be used for positive effects, especially in water pretreatment systems and contaminated soils.

In 1990, recognizing the significance of microbial activity, as well as the tremendous economic costs associated with microbial communities on surfaces, the US National Science Foundation founded the Center for Biofilm Engineering at Montana State University in Bozeman (though, interestingly, NSF would not initially accept the word “biofilm” in the Center’s name; instead the award funded the “Center for Interfacial Microbial Process Engineering”). Since that time, the field of biofilm research has exploded. New tools and techniques are continually pioneered to help understand the secrets of microbial community interactions. In addition to numerous research laboratories in the US, several groups study biofilms worldwide, including centers in Denmark, England, Germany, Australia, and Singapore.

What is a biofilm?

Most of you have never heard of the term “biofilm”, but you have certainly encountered “biofilm” on a routine basis. If you’ve ever been to the dentist and he’s scraped “plaque”, which causes tooth decay, off your teeth; that’s a type of bacterial biofilm. The “slim” that clogs your drains is also biofilm. The slippery coating on rocks, at the water’s edge of a stream or river, is just a  bacterial biofilm-coating. Pond-scum – a biofilm. If you’ve ever been diagnosed with Candida albicans; H. pylori; chronic sinus or prostate infection; or Lyme disease, chances are they’re living, hiding and replicating in a biofilm colony.

Iodine staining of biofilm plaque (upper right)

This is the best product for removing the bacterial biofilm that causes plaque – Biotene PBF Chewing Gum.

These microorganisms (biofilm colonies) are usually encased in an extracellular polysaccharide that they themselves synthesize, via the release of signaling molecules through quorum sensing (QS). This glue-like substance allows them to anchor to all kinds of surfaces – such as metals, plastics, soil particles, medical implant materials, and tissue. As long as sufficient moisture and nutrients are available, a bacterial biofilm can form just about anywhere. In your body that would be from your mouth, especially the teeth, through the stomach and GI tract, all the way down to the rectum. Biofilm in the environment can be found, most often, in ponds, streams, rivers, etc.  A biofilm can be formed by a single bacterial species, but more often than not, biofilms consist of many species of bacteria, as well as fungi/yeast, algae, protozoa, debris and corrosion products. Once anchored to a surface, biofilm microorganisms carry out a variety of detrimental or beneficial reactions, depending on the surrounding environmental or body conditions.

In the human body, biofilm colonies are the main reason that certain conditions take so long to get handled. In my opinion, if it were not for “biofilm”, conditions caused by the microorganisms – Candida albicans, Candida spp,  H. pylori, Lyme’s bacteria (Borrelia burgdorferi) and many others, would be far easier to diagnose and/or treat. It is crucial in any treatment protocol to first handle the biofilm.  By doing so, it will make a significant difference in the amount of time, money and effort spent on treating many, so called, stubborn condition – like the above.

Related Posts: Biofilm Protocol, Quorum Sensing, Lactonase

Biofilm Research and Links/Resources

THE ROLE OF EXTRACELLULAR DNA IN MAINTENANCE OF BIOFILMS FORMED BY E. COLI, H. INFLUENZAE, K. PNEUMONIAE, P. AERUGINOSA, S. AUREUS, S. PYOGENES AND A. BAUMANNII George V. Tetz & Victor V. Tetz Dept. of Microbiology, Virology and Immunology; Saint-Petersburg State Pavlov Medical University, Russia Email: vtetzv@yahoo.com

It is known that bacteria within biofilms are much less susceptible to antibiotics particularly because of poor antimicrobial penetration through surface film that covers microbial community and inactivating role of extracellular matrix. Combined effects of DNase (Enzyme for digesting single and double-stranded DNA) and antibiotics on established biofilms of different unrelated bacteria were displayed. A Combination of antibiotics with DNase I resulted in significant decrease of established biofilm biomass compared to the reduction of biomass achieved when antibiotics or DNase I were used alone.

DETECTION OF HELICOBACTER PYLORI IN BIOFILMS BY USING REAL-TIME POLYMERASE CHAIN REACTION (PCR) Linke, S., Gebel, J., Büttgen, S., Exner, M. Institute for Hygiene and Public Health, University of Bonn

Our results confirmed a possible existence of H. pylori in drinking-water biofilms.

ANALYSIS AND IDENTIFICATION OF THE BIOFILM WOUND MICROFLORA IN HORSE WOUNDS Samantha J. Westgate1, Steven L Percival2*, Derek C. Knottenbelt1 and Christine A. Cochrane1 1University of Liverpool, Department of Veterinary Clinical Science, Division of Equine Studies, Leahurst, Neston, South Wirral, UK *2ConvaTec Wound Therapeutics, Deeside, Flintshire CH5 2NU, UK

Equine wound healing is notoriously problematic on the lower limb, specifically when biofilms are evident. Equine chronic wounds display similar characteristics to chronic wounds in humans thus these cases provide an effective model for human cases. Whether wounds are caused by trauma or surgery their high prevalence is of concern and treatment can be both challenging and costly. Biofilms are considered detrimental to normal healing in non-healing and infected chronic wounds because of their recalcitrant nature towards antimicrobial agents. Biofilms are also known to be resistant to the effects of the immune system. Because of this fact more research in the area of chronic wounds and biofilms is warranted.

Culturable analysis of the microflora revealed that the majority of bacteria isolated from the chronic wounds of horses were Staphylococcus spp, Pseudomonas spp, Micrococcus spp, Enterococcus spp, Corynebacterium spp, Streptococcus spp, Bacillus spp, Aerococcus spp and Clostridium spp. Further analysis of all isolates highlighted their biofilm forming potential and antibiotic resistance profiles. Biofilms were shown to be evident in a large percentage of the chronic wounds. In conclusion these studies provide evidence that biofilms exist in the chronic wounds of horse which may well provide an underlying reason as to why a large percentage of chronic wounds are recalcitrant to antimicrobial therapies, do not heal a timely manner and often become infected.

BACTERIAL BIOFILMS IN SURGICAL SPECIMENS OF PATIENTS WITH CHRONIC RHINOSINUSITIS (sinusitis).
Sanclement JA, Webster P, Thomas J, Ramadan HH. Department of Otolaryngology, West Virginia University, Morgantown, West Virginia 26506-9200, USA.

CONCLUSIONS: Biofilms were demonstrated to be present in 80% the 30 patients undergoing surgery for chronic rhinosinusitis (CRS); none of the (control) patients without CRS had any evidence of biofilms.

Note: According to Andrew Foreman, B.M.B.S., Ph.D., and colleagues from the University of Adelaide in Australia, the most common bacteria reeking havoc in those experiencing CRS is Staphylococcus aureus (S. aureus).

First a little background on biofilm:

Fig. 1: The biofilm life cycle. 1: individual cells populate the surface. 2: extracellular polymeric substance (EPS) is produced and attachment becomes irreversible. 3 & 4: biofilm architecture develops and matures. 5: single cells are released from the biofilm. Related Post – Biofilm Basics and Quorum Sensing and Biofilm

This is an excerpt from a Klaire Labs product monograph which is a basic primer on the topic (My additions are in RED) The National Institutes of Health estimates that 60% of all human infections and 80% of refractory infections (def. unresponsive to medical treatment) are attributable to biofilm colonies.  I have seen this, most commonly, in cases I’ve worked-up, where the pathogen is: Chlamydia pneumoniae, Pseudomonas aeruginosa, Helicobacter pylori, [Lyme disease - Borrelia burgdorferi] and Candida albicans.

• The protection conferred upon microorganisms by biofilm allows them to achieve a high level of antibiotic resistance, stealth and invisibility.

• Biofilm not only provide a physical barrier to antimicrobial agents (pharmaceutical antibiotics) and host antibodies, but facilitate the exchange of antibiotic-resistant genetic material between organisms and may contain antibiotic-degrading (hydrolysing) enzymes such as b-lactamase, effectively neutralizing incoming antibiotic (b-lactam antibiotics) molecules.

• In fact, biofilm communities can be 1000 times more resistant to antibiotics than free-floating bacteria.

• The decreased growth rate of sessile microorganisms (def. Permanently attached to a substrate; not free to move about; “an attached oyster”) also reduces their antibiotic susceptibility as most antimicrobial agents require rapid cell growth in order to effectively kill or inhibit the microbes.  Biofilm thus render pathogenic microorganisms enormously difficult to eradicate, and can almost single-handedly contribute to localized or systemic inflammatory reactions and delayed wound healing.

• Depending on the type of biofilm, one or more species of pathogens may be found embedded in the extracellular polymeric substance (def. Composed primarily of polysaccharides and can either stay attached to the cell’s outer surface, or be secreted into its growth medium).  Bacterial extracellular polymeric substance (EPS) maybe a carrier of, or may have heavy metals embedded in them, thus the indication for chelation w/EDTA. EDTA, ethylenediaminetetraacetic acid, is a chelating agent used to lower one’s body burden of heavy metals).

Pathogenic bacterial known to reside in biofilms include, but are not limited to: Borrelia burgdorferi (Lyme bacteria), Escherichia coli, Candida albicans (yeast and fungal mutation), Clostridium difficile, Clostridium perfringens, Helicobacter pylori, Klebsiella pneumoniae, Legionella pneumophila, Listeria monocytogenes, Pseudomonas aeruginosa, Salmonella typhimurium, Staphylococcus aureus, Staphylococcus epidermidis, and Vibrio cholerae. The number of human diseases shown to be associated with biofilms is ever expanding and includes: chronic bacterial prostatitis, chronic rhinosinusitis (chronic sinus infections), cystic fibrosis pneumonia, infective endocarditis, periodontitis, recurrent otitis media, and virtually all device and implant related infections.  Strong evidence is also beginning to emerge for an etiologic (causative) role of pathogenic mucosal biofilm in gastrointestinal diseases, such as Irritable Bowel Disorders (IBS): Crohn’s disease and ulcerative colitis.

S. aureus biofilm

Dr. Marcus Ettinger’s Biofilm Protocol – Only the eradication phase is presented here.  There is a pre,  post and toxin reduction step as well.  You can get help with any of these steps – HERE

A. Products (mandatory products in red). These are ONLY the basics. Additional nutraceuticals may be needed, based on each individuals unique situation.

1. Monolaurin [AKA Glyceryl laurate or glycerol monolaurate] (monolaurin information) or Lauricidin
2. Nutiva Extra-Virgin Coconut Oil (42-52% Medium Chain Fatty Acids [MCFA], lauric acid, by volume)
3. Nattokinase (a potent fibrinolytic enzyme) I like this better than Lumbrokinase.
4. InterFase Plus™ (broad-spectrum enzyme formula w/EDTA)
5. Serrapeptase (a potent fibrinolytic enzyme)
6. Vitamin C (ascorbic acid – Not buffered, as most of these contain metals)
7. NAC (N-Acetyl-Cysteine)
8. Lactoferrin (specifically Nutricillin by Ecological Formulas) Dr. Anju Usman of Illinois states, “Our bodies make proteins, transferrin and lactoferrin, which mop up iron and block the ability of biofilm to form,” she said. “But pathogenic bacteria secrete iron chelators to snatch up iron and thus compete with the transferrin and lactoferrin for what they need to survive.”

B. Avoid supplemental forms of: magnesium, iron and calcium during the biofilm protocol, as they may contribute to  biofilm formation or decrease the effectiveness of the biofilm protocol.

C. Take a broad-spectrum probiotic and prebiotic.  I like the combination of Now Foods brand Probiotic-10 and their Probiotic Defense Powder (contains gluten).  These products will help to crowd out the bad bacteria, and also help disrupt and replace biofilm colonies along the mucus membrane.

D. Specific additions based on condition (not a complete list):

1. Candida albicans – SF722* (10-Undecenoic Acid  50 mg) Thorne Research. This is as close as you can get to a medication and still be a natural substance.  There are a few chat rooms blasting this product, based on who knows what – can’t make everyone happy.  I’ve used SF722 for over 15 years and it is amazing – never a problem!  *Do not take SF722 if you are allergic to fish. There are many other amazing products that can be added to complement the SF722. It’s really a matter of how many pills someone wants/doesn’t want to take per day or the severity of one’s condition, that will determine, if or which, additional products will be added. If the Candida albicans overgrowth is severe, has not responded to holistic methods or has mutated into its more virulent hyphal form/fungal infection (nails, underarms, groin or skin); Diflucan (fluconazole), a prescription medication, is my personal preference, but Nizarol (ketoconazol) can also be used. In Azole-resistant Candida albicans, lactoferrin must be added to either medication in order to increase their effectiveness. There is a certain B vitamin, mineral and amino acid that possesses synergistic qualities and I find them indispensable when taking Diflucan (fluconazole), Nizarol (ketoconazole) or for supporting candida die-off symptoms.
2. Chlamydia pneumonia, Klebsiella pneumoniae or Pseudomonas aeruginosa – Pneumotrophin PMG by Standard Process, Inc. How it works.  I use this because it helps direct the body’s attention and healing efforts to the lung, where it’s needed most. Apex Energetics, H-PLR is also a mandatory addition. I also like to use OOrganik-15™ and Pneuma-Zyme™ by Biotics Research with some of my patients who manifest asthma, a chronic cough and/or emphysema like symptoms.     
3. H. pylori – Complete write-up on another post.
4. Chronic bacterial prostatitis – Quercitin (600mg’s) and Bromelain (200mg’s) combination by Now Foods. Decreases inflammation and oxidant stress in the prostate while increasing local concentrations of beta-endorphins. Apex Energetics, H-PLR is also a mandatory addition.

E. Certain dietary restrictions and additions will need to be taken. These are determined on a case by case basis.

Important Note:

All dosages will be provided if you purchase some or all of your “biofilm protocol” products through my office. I truly do want to help all who are interested, but it’s finally gotten to the point where too many people want free advice and an increasing amount of my time, and then buy all of their products elsewhere. I am a firm believer in fair exchange and I feel I have done that by providing the information in this post.

I also offer tailor made protocols for your individual situation, please contact our office for product prices and distance patient information (714) 639-4360. 

 

 

 

Biofilm testing is also available through Fry Laboratories. Fry Laboratories, L.L.C. is an independent clinical diagnostic and research laboratory located in Scottsdale, Arizona. We are committed to understanding chronic diseases and contributing to their cure through advancements in diagnostics and basic science research with emphasis on chronic inflammatory diseases, vector-borne diseases, and their intersection. Our clinical diagnostic laboratory offers general and targeted immunology services in conjunction with standard and cutting edge infectious disease detection and identification technologies. Our signature services include microscopy for visual identification and quantification of a wide range of blood-borne pathogens, co-infection serology, biofilm detection, and genus wide molecular detection technology with sequencing for individualized species and/or strain identification. We participate in both CAP and API quality control programs and provide worldwide testing service.

Diseases of Interest: Chronic Fatigue Syndrome, Fibromyalgia, Gulf War Veterans Illness, Chronic Lyme Disease, ALS (Lou Gehrig’s Disease), Parkinson’s Disease, Multiple Sclerosis, Autism, Lupus, Ulcerative Colitis, Scleroderma, Rheumatoid Arthritis, Osteoarthritis, Crohn’s Disease.

Infections of Interest: Borrelia (Lyme), Babesia, Bartonella, Anaplasma, Ehrlichia, Q-Fever (Coxiella), Toxoplasma, Rickettsia, Plasmodium, XMRV

Important: This post is not a substitute for medical advise or treatment and is for informational purposes only. Please consult with a physician before starting any nutritional or biofilm protocol on your own.

Marcus Ettinger BSc, DC – H. pylori treatment – H. pylori protocol.

Disclaimer: This post is not a substitute for medical advise or treatment and is for informational purposes only. Please consult with a physician before starting any nutritional protocol on your own.

Blog post – H. pylori free, in just 34 days, without antibiotics on Dr. Ettinger’s protocol! Lab tests to prove it.

H. pylori – Resources and Links

“Heartburn, chronic active gastritis, GERD, acid reflux, achlorhydria or H. Pylori - that is the question.” William Shakespeare. Are any of these conditions actually due to too much stomach acid (hyperchlorhydria)? Not necessarily. I have to admit here, I experienced a severe bout of gastritis – once, when I started-up my first practice. And yes, it hurt. It felt exactly like someone poured a quart of battery acid down my throat, at the same time I was having a heart attack, while licking a brand-new nine volt battery. I think you get the picture. (The Digestive System)

Well, to make a long story short, my stress wasn’t going to go away in the next five minutes, so I needed to apply my “medical detectiveness” and back-track the pathophysiology of the condition, to figure out the cause. Knowing the cause and predisposing factors would allow me to apply the precise heartburn treatment, H. pylori treatment, chronic active gastritis treatment, GERD treatment or low stomach HCl treatment. The cause and predisposing factors were:

My Predisposing Factors:

1. Chronic Dehydration – There are different types of mucous cells in the stomach and they are easy sources to supply the body with water when dehydrated. The thinning of the gastric mucosa or destruction of that mucous membrane layer, makes the stomach vulnerable to acids – hydrochloric or those produced from fermentation of ingested sugars and purification of ingested proteins. Decreased stomach acid (HCl) also creates the perfect storm for the introduction and/or colonization of the dreaded H. pylori bacterium.

2. Zinc deficiency - I  picked-up on this during a hair-mineral analysis. Zinc deficiency as a single factor would, most likely, not cause anything overtly noticeable. When combined with a Helicobacter pylori (H. pylori) infection, the compounding effects created a more severe inflammatory reaction within the gastric lining.

3.  Wine and Beer - Ethanol on its own can create painful erosion and inflammation of the gastric lining, but when combined with the zinc deficiency, it can compound the degree of inflammation and drastically delay healing.

4.  H. pylori or Lack of HCl? – After testing it was confirmed the H. pylori was present. Now was my lack of HCl the reason I got the H. pylori or was the H. pylori the cause of the reduced stomach acid?

So, at this point, not only was I up shit-creek without a paddle, I was missing the canoe too.

So What Was the True Cause of My Gastritis?

#1, #2, #3 and #4 all played their individual parts in my condition. A little more on #4 – Achlorhydria (lack of stomach HCl) or H. pylori bacteria: This is the, what came first, chicken or the egg dilemma. Did my lack of stomach acid allow the H. pylori a safe haven to take up residence OR did the H. pylori infection cause the lack of stomach acid? Both are possible and both allow the other to exist, and create a painful condition called atrophic gastritis. This is exactly what I had, and, I am sure, a little erosive gastritis as well.

H. pylori bacteria

Diagnostic Testing:

After some diagnostic testing: allopathic (traditional medicine), which included BioHealth Diagnostics Laboratories 401H ( GI Pathogen Screen w/ H. pylori Antigen $270.00) and energetic testing (Applied Kinesiology & Contact Reflex Analysis), I now knew what was going on, what caused it and what to do to get it completely under control. I confirmed that I did have Helicobacter pylori - H. pylori for short.

The True Cause – H. pylori:

Helicobacter pylori (H. pylori) is a spiral-shaped gram-negative bacterium which was identified in 1979[1]. It produces urease in abundance, the activity of which, through the production of   ammonia, together with the bacterium’s motility and ability to adhere to the gastric mucosa, enables its survival in the acid environment of the stomach. About half of the worlds population house H. pylori, in their stomach, and are unphased by it. But in about 15 percent of those infected, the microbes cause peptic ulcers and chronic active gastritis, and in an unluckier bunch the H. pylori is a causative agent for gastric cancer and mucosa associated lymphoid tissue lymphoma[2]. It has also been shown to be associated with extragastric diseases, such as iron deficiency anemia and idiopathic thrombocytopenic purpura[3-5].

1. Pajares JM, Gisbert JP. Helicobacter pylori: its discovery and relevance for medicine. Rev Esp Enferm Dig 2006; 98: 770-785
2. Sari YS, Sander E, Erkan E, Tunali V. Endoscopic diagnoses and CLO test results in 9239 cases, prevalence of Helicobacter pylori in Istanbul, Turkey. J Gastroenterol Hepatol 2007; 22:1706-1711
3. Bohr UR, Annibale B, Franceschi F, Roccarina D, Gasbarrini A. Extragastric manifestations of Helicobacter pylori infection — other Helicobacters. Helicobacter 2007; 12 Suppl 1: 45-53
4. Franceschi F, Roccarina D, Gasbarrini A. Extragastric manifestations of Helicobacter pylori infection. Minerva Med 2006;97: 39-45
5. Franceschi F, Gasbarrini A. Helicobacter pylori and extragastric diseases. Best Pract Res Clin Gastroenterol 2007; 21: 325-334

My H. pylori Treatment Protocol

Pre-treatment – First, I took antacids (over the counter – Zantac OTC) to increase the susceptibility of the H. pylori to treatment/eradication (lesson the need of  H. pylori to defend itself so vigorously) and allow my gastric mucosa a chance to heal.  Note: The H. pylori form protective bacterial colonies called biofilm, which are made up of a protective, extracellular polysaccharide shield. This protective shield is a defensive barrier against stomach hydrochloric acid and other factors, like antibiotics. Being a complex matrix of proteins and carbohydrates, which are probably interdependent, the H. pylori biofilm could possibly offer a protective haven for the survival of this gastric bacterial pathogen in the extragastric environments (Proteomannans in Biofilm of Helicobacter pylori ATCC 43504).

Treatment – Second, my personal H. pylori bomb consisted of: x,xxx mg’s 2x/day of Monolaurin (xxx mg’s lauric acid per cap – also see coconut oil, which is 50% lauric acid by weight) and x caps x times per day of H-PLR (Supports bacterial elimination) from Apex Energetics. I also juiced 1/4 cabbage every day (cabbage contains S-Methylmethionine also known as Vitamin U, a great healer of ulcers and gastritis). After 4 weeks on my protocol I was feeling like a new man! I rechecked myself, after 8 weeks, and was free of the foreign invaders, breath test confirmed the same.

Note: As of September 2009, I’m also adding Klaire Labs – InterFase Plus, x caps x per day on an empty stomach to my H. pylori treatment protocol. InterFase Plus is now an important and mandatory part of the protocol. InterFase Plus aids in the eradication of biofilm, especially H. pylori biofilm colonies. This is a major advancement in my protocol. Understanding BIOFILM is extremely important for a variety of reasons. Please follow any biofilm link to read more about it and also see my biofilm protocol. Additional products taken during the treatment phase: Probiotic Defense Powder (multi-strain pro-biotic and pre-biotic formula), NAC by Now Foods and Psyllium Husk Fiber.

Certain dietary restrictions and additions will need to be taken. These are determined on a case by case basis.

Prevention – Third, was to keep the H. pylori bacteria from coming back and keep the healing process moving forward. I took digestive enzymes w/HCl* – x w/ea. meal, plant based enzymes – x w/ea. meal, zinc** – xx mg’s x per day, L-carnosine** – xxx mg’s x times per day, mastic gum*** x,xxx mg’s x times per day, TheraAloe**** – x ounce x times per day, chlorophyll – xxx mg’s x per day (chlorella or spirulina can be substituted for chlorophyll), a daily broad-spectrum probiotic (Probiotic Defense Powder or Probiotic-10 from Now Foods), psyllium husk fiber (x heaping Tbsp x-x times per day) and tons of distilled water, for 6 weeks. I was now better than before my first symptom.

All-in-all, it was a learning experience, and one that has made me a better doctor and a more diligent medical detective.

FYI: Gastritis is not a single condition, but several different conditions that all share inflammation of the stomach lining as a common symptom. Gastritis, most often, is caused by prolonged use of non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or aspirin, drinking too much alcohol or infection such as Helicobacter pylori bacteria (H. pylori). It may also occur after a major surgery, severe infections, trauma-injury-burns, or severe infections. Some diseases, such as pernicious (B12 deficiency) anemia, autoimmune diseases, and chronic bile reflux, can cause gastritis as well.

*Microscopy studies of the motility of H. pylori in gastric mucin at acidic and neutral pH in the absence of urea show that the bacteria swim freely at high (alkaline – achlorhydria) pH, and are strongly constrained at low (acidic) pH. Also, H. Pylori, through enzyme reactions promote increased ammonia production, which raises the pH of its environment – allowing it to move more freely.

(**)A combination of zinc and L-carnosine has been shown to prevent gross visible damage to gastric mucosa caused by ethanol ingestion. This combination also acts as a potent antioxidant, specifically benefiting the gastric mucosa.

***There is conflicting data on whether mastic gum kills H. pylori effectively in vivo (live human trials). Killing it in a test tube or mice is one thing, but I am interested in living human beings. There is evidence that it aids in the healing of the gastric mucosa, possessing anti-inflammatory properties. I used it for healing rather than as an agent to kill the H. pylori bacteria. Note: there are studies that have shown that mastic gum kills H. pylori. The problem is that it is in less than 30% of the trial groups. So it works in about 1 out of every 3 that try it as a primary treatment (at dosages of 500mg’s 3x/day).

****TherAloe is a high molecular weight polysaccharides containing aloe vera juice product. Its healing capabilities, as far as I am concerned, are quite profound on the gastric mucosa.

Important Note on Purchasing Products:

All dosages will be provided if you purchase some or all of your products through my office. I truly do want to help all who are interested, but it’s finally gotten to the point where too many people want free advice and an increasing amount of my time, and then buy all of their products elsewhere. I am a firm believer in fair exchange and I feel I have done that by providing the information in this post.

I also offer tailor made protocols for your individual situation, please contact our office for product prices and distance patient information (714) 639-4360

H. Pylori Articles:

Updates:

September 13, 2009 Update – I am now taking, Source Naturals – Broccoli Sprouts Extract, which provides 2,000mcg’s sulforaphane daily. This is equivalent to eating more than a pound of fresh broccoli. Dietary Sulforaphane-Rich Broccoli Sprouts Reduce Colonization and Attenuate Gastritis in Helicobacter pylori–Infected Mice and Humans

October 03, 2009 Update - H. pylori most likely will live in biofilm colonies which make them even harder to kill or be identified by our host defenses. Read more about biofilms here and my protocol to remove them. BIOFILMS

November 03, 2009 Update – In my never ending quest for knowledge, I just came across this interesting piece of data. The H. pylori bacteria is thought to have been with us for around 58,000 years and migrated with modern man out of east Africa. Here is the link to this article. – An African origin for the intimate association between humans and Helicobacter pylori

November 18, 2009 Update – Here are two PubMed articles validating the effectiveness of Monolaurin for the prevention and/or eradication of H. pylori.

Int J Antimicrob Agents. 2002 Oct;20(4):258-62
Bactericidal effects of fatty acids and monoglycerides (Monolaurin) on Helicobacter pylori
Bergsson G, Steingrímsson O, Thormar H. Institute of Biology, University of Iceland, Grensasvegur 12, 108, Reykjavik, Iceland. bergsson@here.is

The susceptibility of Salmonella spp., Escherichia coli and Helicobacter pylori to fatty acids and monoglycerides was studied. None of the lipids showed significant antibacterial activity against Salmonella spp. and E. coli but eight of 12 lipids tested showed high activity against H. pylori; monocaprin and monolaurin being the most active. The high activity of monoglycerides against H. pylori suggests that they may be useful as active ingredients in pharmaceutical formulations.

Mol Cell Biochem. 2005 Apr;272(1-2):29-34
Minimum inhibitory concentrations of herbal essential oils and monolaurin for gram-positive and gram-negative bacteria
Preuss HG, Echard B, Enig M, Brook I, Elliott TB. Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, DC 20057, USA. preusshg@georgetown.edu

New, safe antimicrobial agents are needed to prevent and overcome severe bacterial, viral, and fungal infections. Based on our previous experience and that of others, we postulated that herbal essential oils, such as those of origanum, and monolaurin offer such possibilities. We examined in vitro the cidal (def. killing, as in bactericidal) and/or static effects of oil of origanum, several other essential oils, and monolaurin on Staphylococcus aureus, Bacillus anthracis Sterne, Escherichia coli, Klebsiella pneumoniae, Helicobacter pylori, and Mycobacterium terrae. Origanum proved cidal to all tested organisms with the exception of B. anthracis Sterne in which it was static. Monolaurin was cidal to S. aureus and M. terrae but not to E. coli and K. pneumoniae. Unlike the other two gram-negative organisms, H. pylori were extremely sensitive to monolaurin. Similar to origanum, monolaurin was static to B. anthracis Sterne. Because of their longstanding safety record, origanum and/or monolaurin, alone or combined with antibiotics, might prove useful in the prevention and treatment of severe bacterial infections, especially those that are difficult to treat and/or are antibiotic resistant (also see biofilm, as a source of antibiotic resistance).

Note: Monolaurin has been shown to inactive many forms of bacteria and virus’ that are protected by an outer lipid membrane, known as an envelope (H. pylori cell envelope). The mechanism is due to monolaurin’s ability aid in the disintegration of this lipid membrane.

May 02, 2010 Update - A recent review, just published, of available literature on the use of probiotics in the treatment or prevention of H. pylori infection, validated that, “Both in vitro and in vivo studies provide evidence that probiotics may represent a novel approach to the management of H. pylori infection.”

Helicobacter. 2010 Apr;15(2):79-87.
Role of probiotics in pediatric patients with Helicobacter pylori infection: a comprehensive review of the literature.
Lionetti E, Indrio F, Pavone L, Borrelli G, Cavallo L, Francavilla R. Department of Paediatrics, University of Catania, Catania, Italy. elenalionetti@inwind.it

March 28, 1011 Update – Helicobacter pylori infection has been associated with diverse extra-digestive morbidity, including insulin resistance (IR) syndrome (1), atherosclerosis and cardiovascular diseases (2). Insulin resistance is the pathophysiologic background of the clinical features of atherosclerosis and cardiovascular diseases.

Morbidity – The rate of incidence of a disease. (Medicine / Pathology) Also called morbidity rate the relative incidence of a particular disease in a specific locality.

1. Gunji T. Helicobacter pylori infection significantly increases insulin resistance in the asymptomatic Japanese population. Helicobacter. 2009 Oct;14(5):144-50.
2. Polyzos SA. The Association Between Helicobacter pylori Infection and Insulin Resistance: A Systematic Review. Helicobacter. 2011 Apr;16(2):79-88. doi: 10.1111/j.1523-5378.2011.00822.x.