As a greater number of research teams begin to use molecular technology rather than standard cultivation mechanisms to detect bacteria in their samples, it is becoming increasingly obvious why doctors and researchers are unaware that their patients with chronic inflammatory disease are infected with large quantities of L-form and biofilm bacteria - the techniques they are using to look for bacteria prove rather useless in actually identifying the pathogens.

This month yet another paper was published whose results confirm that the Petri dish is a thing of the past. The study, which was published in BMC Microbiology, used a series of molecular techniques to identify the species of biofilm bacteria present inside several different kinds of wounds.

Bioflims are formed when a complex and varied group of bacteria aggregate together inside a protective and adhesive protein matrix. The bacteria inside a biofilm cooperate to promote their own survival and the chronic nature of an infection. While dentists have long realized that bacteria in the mouth often reside inside biofilms - they form much of the goo that they remove from teeth - researchers are just starting to investigate bioflim communities that form in other areas of the body.

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Could people 800 years ago have benefited from the Marshall Protocol? Did cave men suffer from infection with L-form bacteria? Nobody knows for sure when these stealthy pleiomorphic bacteria first began to infect human beings, but a new study published in the Proceedings of the National Academy of Sciences by researchers at Pennsylvania State University suggests that Th1 disease was already common during the middle ages.

The team analyzed 490 skeletons from a London cemetery for Black Death victims – the name given to those people who succumed to the plague epidemic of 1347 to 1351. Black Death – named after the black spots the bubonic form of the plague caused on the skin - was one of the deadliest recorded in human history, killing about 75 million people, according to some estimates, including more than a third of Europe’s population.

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For decades, scientists working with L-form bacteria have warned that the pathogens are not killed by the purification processes used when pharmaceutical companies creates vaccines. A recent drug trial by Merck and Co., Inc. suggests that the failure of mainstream medicine to take the presence of L-form bacteria seriously has put a large group of people of people for developing a wide range of chronic diseases.

Several months ago, two international trials aimed at testing an experimental AIDS vaccine were stopped after it became clear that the vaccine did not prevent infection with the AIDS virus. The trials were conducted in conducted in the United States, Peru, Brazil, Dominican Republic, Haiti, Jamaica, Australia and South Africa. Today, the researchers conducting the trial are faced with another problem. Earlier this month they reported “worrying” indications that the thousands of people who received the vaccine are now at greater risk for infection. They have already begun counseling volunteers about the fact that they could be at higher risk for acquiring HIV - the fatal and incurable virus that causes AIDS.

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The question has puzzled scientists for decades – how are L-form bacteria able to divide if they lack cell walls? The answer remained elusive until recently, when medical researcher Josep Casadesus at the University of Sevilla, Spain published on the subject in the medical journal Bioessays. The findings he reports provide valuable clues about how L-form bacteria are able to propagate and reproduce.

In the case of the more commonly studied classical bacterial forms, the creation of a septum, or a wall separating two cavities or spaces, is an essential requisite for cell division. The main structure of a septum is composed of chains of amino acids made from the substance peptidoglycan. In fact, classical bacterial divide only after a double layer of peptidoglycan is laid down in the middle of the cell. The septum subsequently splits – forming two daughter cells. The septum itself is formed by several different proteins that unite to form a ring-like complex.

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“I’m sixty going on sixteen.” “I think that at the moment my brain functions even better than it did when I graduated from college 50 years ago.” “I’m convinced that I will live longer because I’m doing the Marshall Protocol.” Comments like these - which were made by actual patients in the MP phase II study trial - are increasingly common as people reach the later stages of the treatment. In fact, many Marshall Protocol patients who have recovered from inflammatory conditions, such as sarcoidosis, rheumatoid arthritis, diabetes, and others report that recovery feels like “being 20 years younger.”

The wear and tear created by the inflammatory response plays a large role in generating the stress and tissue damage that leads to old age.

In a 2006 paper in the Journal of Immunity and Aging, Italian researcher Sergio Giunta argues that inflammation and aging are intricately connected, to the point where the term “Inflammaging” has been coined “to explain the now widely accepted phenomenon that ageing is accompanied by a low-grade chronic, systemic up-regulation of the inflammatory response and that the underlying inflammatory changes are also common to most age-associated diseases.”

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There’s little doubt about it – the Th1 pathogens (L-form, biofilm and other metagenomic bacteria) generate inflammation, and the eye does not appear to be spared from the actions of these persistent pathogens.

In many people who suffer from eye disease, the pigmented middle of the three concentric layers that make up an eye becomes inflamed. This condition is referred to as uveitis. Other parts of the eye can also become inflamed, causing conditions such as scleritis – a disease that affects the white outer coating of the eye. These conditions are both included in the umbrella name ocular inflammatory disease.

Many cases of ocular inflammatory disease are associated with “autoimmune diseases” like Crohn’s disease and rheumatic arthritis, or with illnesses of “unknown cause” such as Chronic Fatigue Syndrome and sarcoidosis – all of which have been linked over the years and most recently by biomedical researcher Trevor Marshall to the Th1 pathogens. Thus, it comes as no surprise that these same cell wall deficient pathogens may also be responsible for causing the many ocular inflammatory diseases. It’s also logical that people who have acquired enough of the Th1 pathogens to develop one form of Th1 disease (and begin to suffer from decreased immune function) find that these same pathogens more easily infect other areas of the body, like the eye.

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Sam is a 32-year-old patient who is using the Marshall Protocol to treat CFS and depression (and doing extremely well). But Sam is certainly not the only person in his family suffering from Th1 disease – the name given to inflammatory illness caused by bacteria that reside undetected inside biofilms and the cells of the immune system. These bacteria, which are often in a cell-wall-deficient form (the L-form), are collectively referred to as the Th1 pathogens.

Sam’s mother suffers from fibromyalgia, accompanied by insomnia, fatigue, and irritable bowel disorder. His father recently had a stroke, and deals with substantial fatigue and depression. His older brother has debilitating back pain and is hard of hearing. His youngest sister suffers from alopecia, brain fog, depression, excessive fatigue, and mild attention deficit disorder. The youngest brother in the family has a severe case of bipolar disorder, as well as irritable bowel syndrome.

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As we progress into the age of molecular medicine, unraveling the intricacies of the human immune system is an increasingly achievable goal. One can only marvel at the carefully regulated feedback pathways that, under a range of conditions, allow the immune system to maintain a natural state of homeostasis. What happens though when pathogens, medications, and supplements upset this delicate balance? Research that reveals how the immune system can be affected during an infant’s first weeks of life is shedding light on many of the factors driving the current epidemic of chronic disease.

The human immune system has two components – the innate immune system and the adaptive immune system. The innate immune system is the body’s first line of defense against invading pathogens. White blood cells of the innate immune system called phagocytes engulf and kill bacteria. The adaptive immune system is primarily made up of white blood cells called lymphocytes. Once lymphocytes encounter a pathogen, they create proteins called antibodies that allow the adaptive immune system to ‘remember’ the infectious agent and prevent it from causing disease at a later time.

A diagram from Rolf Zinkernagel’s paper showing how the group of newborn mice injected with CMV died when exposed to the virus at a later date

While the innate immune system is functioning at birth, it takes several weeks for an infant to develop a working adaptive immune system. Little is known about what happens when a baby encounters pathogens during this early period of life. However, a recent study by 1996 Nobel Laureate Rolf Zinkernagel and team at the Institute of Experimental Immunology in Switzerland illustrates how pathogens may affect infants during the period before their adaptive immune systems are up and running.

Zinkernagel and team injected a virus called Cytomegalovirus (CMV) into the brains of a group of mice that were only a few days old. Their adaptive immune systems had not yet developed and consequently they were not producing lymphocytes. The researchers found that the innate immune systems of the mice were able to eliminate CMV from most of the tissues except for those of the central nervous system. As a result, the virus persisted in the brains of the mice. Later in life, when the same mice were challenged by infection with a similar virus, they developed a condition resembling a type of autoimmune disease and died. The team referred to this concept as viral “deja-vu.”

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Many people who are chronically ill are given antibiotics. But are these medications working in the correct manner to kill the pathogens responsible for their disease? New molecular modeling research strongly suggests that the stealth pathogens responsible for causing a wide array of chronic diseases can only be killed if carefully chosen antibiotics are taken in a very specific manner.

In what is emerging as a new understanding of chronic disease, researchers are increasingly implicating what are often referred to as the Th1 pathogens in a wide array of illnesses previously considered to be of unknown cause or “autoimmune” in nature. “It is our contention that several diseases that are usually regarded as ‘autoimmune’ or ‘idiopathic’, including rheumatoid arthritis, Crohn’s disease, ulcerative colitis, sarcoidosis and psoriasis, are caused by infection with related slow-growing bacteria,” states G.A.W. Rook in the journal Immunology Today.

The Th1 pathogens are hypothesized to be an intraphagocytic, metagenomic microbiota of bacteria, meaning that they are able to persist inside the cells of the immune system as well as group into colonies called biofilms. The bacteria inside a biofilm produce a protective matrix that allows them to more effectively evade the immune system and develop resistance to antibiotics administered in a standard manner. Essentially, high-dose antibiotics fail to eliminate all the cells that form a biofilm, leaving what are referred to as persister cells behind. The persister cells are eventually able to re-create the biofilm, allowing it to thrive again. There is a tremendous number of different species of these chronic pathogens.

Many of the bacteria that compose this microbiota are in what is referred to as the L-form. For over a century, scientists have realized that classical bacteria can transform into small forms that lack cell walls. These pathogens are known as L-form bacteria. Researchers have currently identified over 50 different species of bacteria capable of transforming into the L-form, and it is likely many other bacteria also have this ability. Brown et al have found evidence of L-form bacteria in the blood of more than 60% of healthy controls. In fact, the diseases generated by L-form bacteria are far more common than currently realized, and are often only noticed as subtle signs of aging, such as osteoporosis, obesity, fatigue and arthritis.

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“An apple a day keeps the doctor away.” Regardless of whether apples have proven to ward off disease, this statement reflects a long-held understanding of the fact that the foods and supplements we consume can impact our health. Recent research, which has demonstrated that a vast array of chronic diseases are bacterial in origin, now allows us to better understand the actions of the substances we ingest. By analyzing research that reveals how bacteria use and obtain vital nutrients, we can adapt our diets to ensure that we do not provide the pathogens we harbor with extra amounts of substances that foster their growth, including iron, folic acid, and carbohydrates. Furthermore, molecular modeling research now allows us to understand how various foods, including vitamin D, chlorogenic acid, carnosic acid, and soy, can alter the activity of the immune system. Together, this research reveals that eating large quantities of certain foods that make us feel good is not necessarily beneficial, and that a number of supplements may do more harm than good.

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Do genetic defects cause the vast majority of chronic diseases? Not according to evolutionary biologist Paul Ewald, who teaches biology at University of Louisville. If chronic diseases were genetic in origin, he argues, “A disease-causing gene that reduces survival and reproduction would normally eliminate itself over a number of generations.” He contends that the thinking underlying today’s “Human Genome Mania” often violates the fundamental principle of biology, Darwin’s Theory of Natural Selection.

Paul Ewald

One example of this is schizophrenia; patients with this mental illness rarely reproduce. Ewald posits that if schizophrenia were a genetic illness, the genes that cause the disease would have gradually been eliminated from the population. And what about identical twins who share the exact same DNA? When one identical twin develops breast cancer the other twin has only a 10% - 20% chance of also developing the disease. Ewald argues that “for the common damaging chronic diseases, the evidence considered in light of evolutionary principles implicates infection” and that “adding infectious causation into the mix can best explain the documented epidemiological patterns, and does so in accordance with evolutionary principles.”

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“Bacterial L-forms are among the most unusual creatures in nature. Once one has seen their strange habits and life style, one starts to work on L-forms with great enthusiasm because their existence in vivo and in vitro gives rise to more questions in classical microbiology, immunology and infectious diseases.

And just who is able to describe the process of culturing L-form bacteria so eloquently? She’s an Associate Professor at the Department of Pathogenic Bacteria Institute of Microbiology at the Bulgarian Academy of Sciences, who’s worked with L-form bacteria for the last 15 years. Meet Nadya Markova.

1. What led you to become interested in L-form bacteria?

I graduated as a medical doctor, but my interest in microbiology led me to the Bulgarian Academy of Sciences (where I defended my PhD thesis in the field of medical microbiology). Researchers already working there at the time had great experience in L-form research and had made many interesting observations about the bacteria, all of which sparked my interest. They were my teachers, who inspired me to continue their research in the same field.

2. How long have you been working with L-form bacteria? How many people do you currently work with and how to they contribute to the research environment?

I started thinking about how L-form bacteria change form in the beginning of the 90s, and my interest in them has risen ever since. Unfortunately, our research team is comprised of only 5 people. One of them must be mentioned, my teacher Professor Lilia Michailova. She is an excellent electron microscopist and, without her, our achievements wouldn’t have been possible. I’m really glad that she is still active and that we continue to work together.

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All images of bacteria in this post are taken, with author’s permission from Clinical Microbiological Reviews, published in 1997, 10(2), 320-344.

Gerald Domingue

Gerald Domingue is a medical researcher and academic who served as Professor of Urology, Microbiology and Immunology in the Tulane University School of Medicine and Graduate School for thirty years and also as Director of Research in Urology. He is currently retired and resides in Zurich, Switzerland where he is engaged in painting and creative writing. At retirement he was honored with the title of Professor Emeritus at Tulane. Prior to Tulane, he served on the faculty of St. Louis University, was a lecturer at Washington University and director of clinical microbiology in St. Louis City Hospital, St. Louis, MO.

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A wide body of research has shown that classical forms of bacteria often transform into tiny variants of the same species, losing their cell walls in the process. They are then referred to as L-form or cell wall deficient (CWD) bacteria. Although researchers have known about L-form bacteria for over a century, up until recently they have not fully understood their connection to chronic disease. It is now known that these bacteria are responsible for causing a wide array of chronic diseases including rheumatoid arthritis, Chronic Fatigue Syndrome, Lyme disease, and sarcoidosis.

L-forms of various shapes and sizes inside the cells of a patient with breast cancer, photo taken by Alan Cantwell

Over the past century researchers have identified over 50 different species of bacteria capable of transforming into the L-form and it is likely that even more species will be discovered in the coming years. The vast majority of researchers and doctors are not aware that L-form bacteria are present in their patients because the pathogens will not grow under standard laboratory conditions and must be cultured in a different medium and at a different temperature than classical bacteria.

In 2005, a team of researchers at the Royal Brompton Hospital in London published a paper that reviewed the clinical significance of the L-form as an infectious agent. The review discussed the work of hundreds of researchers who have cultivated the L-form and implicated it in a wide array of diseases.

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In a 2006 the Centers for Disease Control and Prevention (CDC) released a paper stating, “Infectious agents have emerged as notable determinants, not just complications, of chronic diseases. To capitalize on these opportunities, clinicians, public health practitioners, and policymakers must recognize that many chronic diseases may indeed have infectious origins.”

According to the CDC, infectious agents likely determine more cancers, immune-mediated syndromes, neurodevelopmental disorders, and other chronic conditions than currently appreciated. In fact, they argue that the potential to avoid or minimize chronic disease by preventing or treating infections may yet be substantially underestimated. Those of us familiar with the Marshall Protocol know that they are absolutely correct.

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