Exploring chronic disease
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.
Since few studies have performed extensive surveys of the bacterial populations within different types of chronic wound biofilms, the BMC team, comprised of individuals from the United States Department of Agriculture, the Medical Biofilm Research Institute in Texas, and the Center for Biofilm Engineering at Montana State University, used several advanced molecular techniques to survey the major populations of bacteria in the pathogenic biofilms of three types of chronic wounds:
The researchers used several different molecular methods – ribosomal amplification and cloning, Sanger sequencing (FRACS), partial ribosomal amplification, density gradient gel electrophoresis (DGGE), and Sanger sequencing (PRADS) – to provide a comprehensive survey of microbial populations.
Together, these molecular techniques revealed that some specific populations of bacteria were evident in the biofilms of all chronic wound types. These bacteria included Staphylococcus, Pseudomonas, Peptoniphilus, Enterobacter, Stenotrophomonas, Finegoldia, and Serratia.
But there were also marked difference between the bacterial populations in each of the wounds. For example, in pressure ulcers, 62% of the populations identified were from a class of bacteria called obligate anaerobes – bacteria that do not require oxygen for growth and may even die in its presence.
In fact, every wound that the research team tested with new molecular technology was also tested for the presence of bacteria using traditional based culture methods. When the results of molecular analysis were compared to the bacteria obtained using these traditional methods, the team found that culture methods were only able to correctly identify the primary bacterial population in one wound type.
“Here we show that culturing failed to identify major contributing populations, especially strict anaerobes, within the given wound types,” state the team, “Standard culturing techniques are inherently biased as they only examine only the 1% of all microorganisms which are able to grow fairly rapidly in pure culture.”
The team also commented on the fact that it takes several days for bacteria grown by culturing methods to be identified, whereas molecular methods such as PCR can typically be completed within several hours. They also stress the fact that some forms of bacteria can simply not grow under the conditions required for standard cultivation, stating that “In addition, certain of the isolates that we have shown to be primary populations within a wound type may never be cultured in the laboratory due to reduced metabolic activity, obligate cooperation with other bacteria, requirements for specialized nutrients, or growth in specific environmental conditions.”
They also argue that molecular methods, unlike culture methods, have more potential to provide quantitative data, stating “arguably, we have shown that molecular methods will allow populations residing within biofilms to be more fully characterized.”
Furthermore, they make it clear that doctors will greatly benefit by knowing the exact composition of bacteria that each of their individual patients harbors. “The continued development of molecular methods may lead to vastly improved tools or diagnostics that will identify and provide quantification of the diverse species potentially present in chronic wounds thereby allowing physicians to better tailor their treatment to each patient’s unique pathogenic biofilm populations,” states the team.
Thus, much like other teams who are using molecular methods to detect bacteria, the researchers make an urgent call for the standardized use of improved diagnostic methods. Not only that, but they also hope the results of their study might actually “foster the pioneering, and development of new diagnostic tools.”
One of the study’s findings that also bears pertinence to the Marshall Protocol is the fact that the bacterial species Staphylococcus was found inside all chronic wound types. Two of the other largest studies to date to seek bacteria using molecular technology (one which looking at bacteria removed prosthetic joints, and another that looked at bacterial populations in patients with Cystic Fibrosis) also found Staphylococcus to be a common pathogen in their samples. Since minocycline is one of the antibiotics that best targets Staphpylococcus, these findings suggest that the decision to use minocycline as the base antibiotic for the Marshall Protocol was well warranted.
Also interesting is that researchers at the University of Turku in Finland just released the results of a study which found that infants who harbor theStaphylococcus aureus are more likely to become overweight and obese later in life.  Again, this suggests that Staphylococcus is a common cause of Th1 symptoms, and that obesity should respond to the MP antibiotic regimen that allows the bacterial species to be killed.
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 theProceedings 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.
Experts have long believed that the Black Death killed indiscriminately regardless of age, sex or level of health because it was so virulent. But anthroplogists Sharon deWitte and James Wood, who led the Penn State team, have demonstrated that the infection did not affect everyone equally.
The anthropologists found that while many perfectly healthy people certainly were cut down, those already in poor health prior to the arrival of the plague were more likely to have perished.
“A lot of people have assumed that the Black Death killed indiscriminately, just because it had such massive mortality,” states DeWitte. “People already in poor health often are more vulnerable in epidemics. “But there’s been a tradition of thinking that the Black Death was this unique case where no one was safe and if you were exposed to the disease that was it. You had three to five days, and then you were dead.”
DeWitte analyzed skeletons unearthed from the East Smithfield cemetery in London, dug especially for plague victims and excavated in the 1980s, for bone and teeth abnormalities that would show that people had health problems before they died of plague.
She found such abnormalities in many skeletons, suggesting these people had experienced malnutrition, iron deficiencies and infections well before succumbing to the Black Death.
Today we understand that, due to the chronic nature of bone deterioration and dental problems, these infections were almost certainly caused by L-form bacteria.
Bone loss results after L-form bacteria create substances that block the Vitamin D Receptor – preventing it from transcribing an enzyme that keeps the level of the hormone/cytokine 1,25-D in check. As 1,25-D rises above a certain range (around 43 pg/ml), it stimulates bone osteoclasts, or cells that remove minerals from the bone. Stimulated osteoclasts dissolve bone material, causing it to be reabsorbed into the bloodstream – leading to osteoporosis and osteopenia.
We are also familiar with the “anemia of chronic disease”, or the fact that people with Th1 disease are frequently deficient in iron. This deficiency is the direct result of the fact that L-form and biofilm bacteria secrete iron-binding complexes called siderophores that remove iron from host proteins, making it available for use by the pathogens.
Futhermore, tooth decay is almost certainly impacted by L-form bacteria, as a wide range of treatment resistant bacteria, including those that persist in bioflims, have been detected in the mouth, not to mention the fact that dental immunopathology and subsequent improvement of dental issues is common among patients on the Marshall Protocol.
Thus it comes as no surprise that DeWitte and team found that the proportion of people with such signs of Th1 disease in the cemetery, compared to those who appeared to have been of robust health before the epidemic, indicate that Black Death was somewhat selective in who it killed.
“The Black Death was highly virulent and undoubtedly killed many otherwise healthy people who would have been unlikely to die under normal-mortality conditions,” they wrote. But people already in poor health were more likely to die.”
Those people in poor health were certainly immunosuppressed, thanks to the fact that as L-form and other stealth bacteria accumulate, the pathogens produce substances that block the VDR, causing the innate immune system to become increasingly compromised. It’s no wonder their lives were claimed by the Black Death, just as today people with Th1 disease are easy victims for the HIV virus.
All images of bacteria in this post are taken, with author’s permission fromClinical Microbiological Reviews, published in 1997, 10(2), 320-344.
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.
Over the course of his thirty-nine year career, Domingue received funding from the National Institutes of Health, Veterans Administration, and a variety of national and international research foundations. He enjoys international recognition as an authority on the basic biology and medical significance of atypical bacterial organisms and is considered an expert on the role of these bacteria in the persistence and expression of kidney and urological infectious diseases.
He first became interested in the role of atypical bacterial forms after noting that a large number of patients with urinary tract infections suffer from continual relapsing illness. Using a direct phase microscope, he examined the urine specimens of several patients with urinary tract infections and found L-form bacteria in his sample.
He began to investigate L-form bacteria, striving to better understand their biology and the role they play in causing disease. Over the course of the next 30 years, he was able to explain much of the mystery behind how the bacteria are able to persist in the body, and published a wide array of clinical and experimental studies on the subject.
Domingue worked with a team that included pre and post doctoral students and fellows along with faculty colleagues and laboratory assistants. Together they discovered that L-form bacteria are able to form tiny dense bodies within parent cells that already lack cell walls. They noted that the forms, which they called electron dense bodies were so small that they could pass through bacterial filters that normally withheld ordinary bacteria with cell walls.
The electron dense bodies could persist inside tissue culture cells in the laboratory. After applying this data to the human condition, Domingue reasoned that in some patients who suffer from chronic bacterial infections, the disease process could be related to the fact that bacteria are able to differentiate into the resistant electron dense bodies that he observed in tissue cultures.
In 1974, he and his graduate student, Mary Green, along with Paul Heidger, a faculty collaborator, published two landmark companion papers in the prestigious journal Infection and Immunity. The papers detail how L-form bacteria inside an experimental human embryonic kidney tissue culture system are able to persist in cells and explains how they are able to revert into the cell wall-containing parent bacterial form. They also proposed a detailed reproductive cycle for L-form bacteria, followed by electron microscopy of the microorganisms.
These papers set the stage for Domingue and his team to delve even further into the role that cryptic atypical bacteria play in causing persistent and recurrent infections.
In 1997, he and a colleague, the late Hannah Woody published an invited extensive review article on chronic bacterial infection in Clinical Microbiological Reviews. Among their conclusions was the claim that “difficult to culture and dormant bacteria are involved in the latency of infection and that these persistent bacteria may be pathogenic.”
He implicated L-form bacteria in several kidney-related diseases including pyelonephritis, glomerulonephritis, idiopathic hematuria, and interstitial cystitis. He also speculated about their role in other diseases such as rheumatic fever, tuberculosis, syphilis, and rheumatoid arthritis.
In the review Domingue stated, “Clearly, any patient with a history of recurrent infection and persistent disability is sending the signal that the phenomenon (infection with L-form bacteria) could be occurring. The so-called autoimmune diseases in which no organism can be identified by routine testing techniques are particularly suspect.”
He went on to conclude, “Bacteriologic advances, which include special culture media and stains, electron microscopy and molecular techniques such as PCR (polymerase chain reaction), have revealed an increasing number of previously unidentifiable organisms in a variety of pathologic conditions. It is unwise to dismiss the pathogenic capacities of any microbe in a patient with a mysterious disease.”
Over the course of his thirty-nine year career Domingue published 160 papers, monographs, and book chapters; 65 devoted to L-form research. He was invited to deliver over fifty international and national lectures about L-form bacteria and wrote a book on the subject, Cell Wall-Deficient Bacteria: Basic Principles and Clinical Significance. His papers are filled with photos of cultures of L-form bacteria taken with an electron microscope. They show the microbes inside human and animal cells.
Although Domingue’s primary research focused on bacterial L-forms, he also published extensively on the relationship between a molecule that stimulates the immune response called the Entobacterial Common Antigen (CA) and certain types of bacteria. He detailed the structure of the antigen and explained how it is able to elicit antibodies in humans and in animal models. He also detailed how the antigen could serve as a possible vaccine against urinary tract infections. He also studied the effects that a vasectomy might have on the immune system and performed studies on the relationship between the host and various species of bacteria in the disease pyelonephritis.
He delved into the effects of antibiotic therapy and chemotherapy on patients with urinary tract infections, and performed several studies on bacteria that produce a substance called chorionic gonadotropin-like hormone, detailing the way the bacteria might be involved in an experimental tumor model. He was even the co-author of a publication that characterized the oral microbial flora of alligators in order to develop better therapy for alligator bites.
When asked recently about his work Domingue replied, “I worked in a controversial research area for decades, and I found that sticking to the facts and hard data are the best ways to make progress in a field. Meaningful experimental designs and careful interpretation and discussion of the results are of prime importance in science. The ultimate aim was always to seek the truth about the problem at hand. Unfortunately, in the area of L-form or cell wall-defective bacteriology, too often there have been conclusions (anecdotal) drawn without supporting scientific data. In my opinion, many of these studies have hampered progress in the field and especially the role of these cryptic organisms in bacterial persistence and expression of disease. Sometimes the controversial issues have become political, which is unfortunate.
As far as I am concerned, modern technological tools are presently at hand to support all of the above microbiological and immunological findings at the molecular level… which is really what present day medical scientists, clinicians, pathologists are willing to accept as proof (maybe) of the role of such aberrant bacteria in disease.”
Indeed, molecular modeling has revealed how L-form bacteria are able to persist in the body and disable the immune system. Over the past few years, L-form bacteria have been linked to a wide array of chronic diseases, many of them previously considered to be autoimmune in nature. In 2002, biomedical researcher Trevor Marshall created a medical treatment that effectively kills L-form bacteria.
Now that L-form bacteria are known to cause a wide array of chronic inflammatory diseases, Domingue’s work is of utmost importance in allowing researchers to correctly demonstrate and understand their behavior.
Domingue, G., Lloyd, K., & Schlegel, J. U. (1974). In vitro phagocytosis of transitional phase bacterial variants utilizing autoradiography. Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), 146(2), 635-42.
Domingue, G. J. (1980). Filterable cell-associated cryptic bacterial forms in immunologic renal diseases. Urological survey, 30(1), 1-4.
Domingue, G. J., Ghoniem, G. M., Bost, K. L., Fermin, C., & Human, L. G. (1995). Dormant microbes in interstitial cystitis. The Journal of urology, 153(4), 1321-6.
Domingue, G. J., & Schlegel, J. U. (1970). The possible role of microbial L-forms in pyelonephritis. The Journal of urology, 104(6), 790-8.
Domingue, G. J., & Schlegel, J. U. (1977). Novel bacterial structures in human blood: cultural isolation. Infection and immunity, 15(2), 621-7.
Domingue, G. J., & Schlegel, J. U. (1978). Novel bacterial structures in human blood. II. Bacterial variants as etiologic agents in idiopathic hematuria. The Journal of urology, 120(6), 708-11.
Domingue, G. J., Thomas, R., Walters, F., Serrano, A., & Heidger, P. M. (1993).Cell wall deficient bacteria as a cause of idiopathic hematuria. The Journal of urology, 150(2 Pt 1), 483-5.
Domingue, G. J., Woody, H. B., Farris, K. B., & Schlegel, J. U. (1979). Bacterial variants in urinary casts and renal epithelial cells. Archives of internal medicine, 139(12), 1355-60.
Domingue, G., & Woody, H. (1997). Bacterial persistence and expression of disease. Clin Microbiol Rev, 10(2), 320-344.
Domingue, G. J. (1982). Cell-wall Deficient Bacteria: Basic Principles and Clinical Significance. Reading, MA: Addison-Wesley Publishing Co.
Green, M. T., Heidger, P. M., & Domingue, G. (1974a). Demonstration of the phenomena of microbial persistence and reversion with bacterial L-forms in human embryonic kidney cells. Infection and immunity, 10(4), 889-914.
Green, M. T., Heidger, P. M., & Domingue, G. (1974b). Proposed reproductive cycle for a relatively stable L-phase variant of Streptococcus faecalis. Infection and immunity, 10(4), 915-27.
Ponig, B., Domingue, G., & Schlegel, J. (1972). The role of in vitro induced microbial L-forms in experimental hematogenous pyelonephritis. Investigative urology, 9(4), 282-5.
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.
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.
This piece describes several of the doctors and researchers discussed in the review who have perfected the lab methods needed to correctly culture L-form bacteria and have consequently been able to observe and document their behavior. L-forms have also been studied extensively in veterinary literature but those findings are not presented here.
In 1895 a scientist named Richard Pfeiffer described an altered form of the bacteria Vibrio cholerae that was difficult to see with a light microscope. Other workers in his lab confirmed that the bacteria lacked cell walls and were difficult to grow using standard laboratory techniques.
Around the same time, Ernest Alnquist, a friend of Louis Pasteur, began to culture the L-form. Alnquist was the first to suggest how extensive and diverse L-forms are. He once commented that “nobody can pretend to know the complete life cycle and all the varieties of even a single bacterial species. It would be an assumption to think so.”
In 1941, German scientist Emmy Klieneberger-Nobel began to study the L form at the Lister Institute in England. A meticulous lab worker, Klieneberger-Nobel, perfected the method of growing the pathogens on serum (blood) agar.
After growing colonies of the bacterium Streptobacillus monliforme she confirmed that several of the pathogens in her Petri dish did indeed lack cell walls. She named the wall-less variants L-forms after the Lister Institute where she worked. In the years that followed she studied other species of L-forms and published several papers describing their characteristics and behavior. She once said that “the L-form is an entity of its own as different from bacteria as the tadpole from the frog.”
A few years later, Harvard Medical School researcher Louis Dienes began to work with the L-form. He applied penicillin to various species of classical bacteria such as Salmonella typhosacoule and discovered that some of the pathogens transformed into cell wall-less variants of the same species. They also found that exposing the original strains to other antibiotics in the same class as penicillin, chemical injury, high levels of amino acids, lithium, calcium, chromatin and mercuric salts could cause L-form variants to form as well.
In many of his experiments Dienes noted that the individual L-forms in his samples often swelled into large round bodies. He also found that small colonies of L-form bacteria such as S.moniliformis are able to revert back to the classical form. He published numerous papers detailing his discoveries and was one of the first scientists to warn the medical community that some antibiotics such as penicillin can actually precipitate the formation of L-form bacteria.
Dienes kept his lab open at all times so that anyone interested could see his L-form cultures and ask questions about how to grow them correctly. Nevertheless, few of the other researchers at Harvard took note of his work. He once remarked that he only became known to the medical staff after a hospital art show displayed some of his watercolors.
Around the same time, a team of doctors under Virginia Wuerthele-Caspe Livingston cultured L-form bacteria from patients with the skin disease scleroderma. Livingston noted that some of the L-forms she observed were as small as viruses. But others were the size of classical bacteria and some were larger forms resembling spores of fungi and yeasts
Livingston and her colleagues injected the L-form bacteria they collected from patients with scleroderma into chicks and guinea pigs. The chicks died. Some of the guinea pigs developed hardening of the skin like scleroderma, and some developed cancer. In the years that followed Livingston was also able to grow L-forms from various human cancer tumors.
Her work was published in the American Journal of Medical Sciences and in the years that followed she wrote several books on the subject.
In 1975, H.M Butler and team wrote a review of L-forms, describing their resistance to penicillin and ability to change form. They concluded that “such organisms may be clinically significant in cases of chronic and recurrent infection.”
At the same time, Bisset and Barlett identified L-form variants of Bacillus licheniformia during different stages of its life cycle. They hypothesized that the wall-less variants of the bacteria they observed had previously been wrongly classified as other species of pathogens.
A decade later, a doctor working at Columbia University by the name of Emil Wirostko began to culture and photograph L-form. In a series of related experiments, he took white blood cells from the liquid inside the eyes of patients with sarcoidosis, juvenile rheumatoid arthritis and Crohn’s disease and observed them under an electron microscope.
He detected L-forms in many of the specimens and noticed that the bacteria were grouped into colonies and encased inside tubuoles. He also noted that they were separated from the environment inside the cell by a membrane or exoskeleton that kept them from being digested by the cell.
Wirostko published three papers that detailed his findings and took many pictures of the L-forms he observed, 20 of which are dispersed throughout his papers.
Around the same time, researcher Alan Cantwell took great interest in Livingston’s work and proceeded to study the L-form. He applied a technique called acid fast staining to the tissue sections of the skin and lymph nodes of patients with the lung disease sarcoidosis and found L-forms in his samples. Cantwell later isolated the L-form of Streptococcus B from the lymph nodes and blood of patients with HIV. He noted that the L-forms he observed could grow into extremely large forms and determined that they were what are known as “Russell bodies.”
In the years that followed, Cantwell took samples from the lymph nodes, skin tumors and other organs from the corpses of patients who had died from Hodgkin’s disease and cancer. He found copious amounts of L-form bacteria in his samples, including round forms resembling the bacterial species staphylococci and rod-shaped bacteria known as corynebacteria.
Over the course of his career Cantwell published over 30 papers and wrote several books that implicate the L-forms in chronic disease, including a book about Livingston and three other women who had worked on her research team.
Around the same time, researcher Lida Mattman began to study the L-form. After working as senior bacteriologist at the University of Massachusetts, she became the director of a laboratory that evaluated specimens sent by mail from doctors around the world. Mattman, who would study and photograph the L-from over the course of decades, confirmed that the pathogens could vary widely in size and shape.
Mattman’s success in growing L-forms was due in part to a relentless drive to perfect the laboratory techniques which allowed her to culture the pathogens. She used fluorescent antibodies and a variety of staining techniques to view the various cell wall deficient forms. She even figured out how to grow them directly on slides.
Mattman studied patients with Tuberculosis and found that in every patient tested, the blood was saturated with a variety of L-forms.
She identified two different species of L-form bacteria in patients with Parkinson’s Disease. The L- form species of Borrellia burgdoferi was detected in patients with Lyme disease. She cultured serum from forty patients with multiple sclerosis and found a different species of the borrelia L-form present in her samples. Soon after, she detected Chlamydia pneumonia in the blood of patients who had suffered a pulmonary thrombosis. She also found bacteria that resembled M. tuberculosis in the blood of patients with the lung disease sarcoidosis.
In the end, Mattman detected dozens of species of L-form bacteria and was able to culture these wall-less forms of bacteria from the blood samples of patients with over 20 incurable illnesses. She published numerous papers throughout her career and in authored an entire medical textbook in which she details her findings.
In 1997 a team of researchers at Tulane University under Gerald Domingue published an extensive review article on chronic bacterial infection in Clinical Microbiological Reviews. Among their conclusions was the claim that ”the difficult to culture and dormant bacteria are involved in latency of infection and that these persistent bacteria may be pathogenic.”
The review also detailed how L-form bacteria are able to form electron dense bodies within previously infected cells. Domingue implicated L-form bacteria in several kidney-related diseases including pyelonephritis, glomerulonephritis, idiopathic hematuria, and Interstitial cystitis. He also speculated about their role in other diseases such as rheumatic fever, tuberculosis, syphilis, and rheumatoid arthritis.
In the review Domingue states “Certainly, any patient with a history of recurrent infection and persistant disability is sending the signal that the phenomenon (infection with L-form bacteria) is occurring. The so called autoimmune diseases in which no organism can be identified by routine testing techniques are particularly suspect.”
Over the course of his thirty-nine year career Domingue published 65 papers, monographs, and book chapters about L-form bacteria. He was invited to deliver over fifty international and national lectures about atypical forms of bacteria and wrote a book on the subject called Cell Wall-Deficient Bacteria: Basic Principles and Clinical Significance.
Several years later, Kenneth Nilsson, a researcher at Uppsala University Hospital in Sweden, published photos of the bacteriaRickettsia helvetica living inside the white blood cells of patients with sarcoidosis. The fact that the bacteria was able to persist inside the cells suggested that something was very wrong with the patient’s immune systems. Dozens of other researchers have also implicated other species of L-forms in sarcoidosis.
A decade later, researchers at the Academy of Science in Bulgaria infected rats with the L-form of Staphylococcus aureus and found that the pathogen were able to “internalize, replicate and persist “ in the lungs of the infected rats. They concluded that “cell wall deficient bacterial forms may be involved in the pathogenesis of chronic and latent lung infections.”
A team of researchers and doctors in the United Kingdom are currently studying the L-form in patients with Chronic Fatigue Syndrome (CFS). The microbiology team, lead by CFS clinician Dr. Andy Wright has detected L-forms in every single one of the CFS patients they have tested (about 600 to date).
Wright has developed a method of taking pinprick blood (usually from the ear) and allowing it to degrade for 6-36 hours. The process causes the L-form bacteria to break out of the cells and they can subsequently be observed with a dark field microscope. The bacteria can be stained with fluorescent dye. If the L-forms are alive they will stain green, while dying/dead L-forms stain orange. Wright has created several videos of L-forms under the microscope in which the pathogens can be seen quite clearly.
In the videos, the bacteria often lengthen into long filamental forms that look thin and snakelike. They can be seen weaving in between infected cells. Sometimes “giant” L-forms, which are more rectangular in shape, begin to grow inside the cells.
Danish researcher Marie Kroun has also taken several videos of L-form bacteria under a high-resolution microscope.
However it’s quite possible that L-form bacteria might have remained in relative obscurity if a scientist from Adelaide Australia by the name of Trevor Marshall hadn’t taken an interest in their ability to persist in the body. Marshall wasn’t a medical doctor – he was an biomedical engineer with an impressive grasp of molecular modeling software. Whereas a doctor can look at a patient and infer a mechanism for disease based only on symptom presentation, a biomedical researcher can take the actual compounds created by L-form bacteria and mathematically determine how they affect the body’s receptors and enzymes.
Thus, after decades of research, Marshall was able to succeed in two areas where the L-form researchers before him had failed. By combining precise molecular modeling data with previous research on stealth bacteria, he was able to create a model that explained exactly how L-form bacteria are able to dysregulate the immune system and persist in the body. Secondly, he was able to use his model in order to create a treatment that effectively kills L-form bacteria. The Marshall Protocol was born. Patients on the treatment use pulsed, low-dose antibiotics, along with a medication that activates the immune system to eliminate L-form bacteria over a period of several years.
Patients with a wide array of chronic diseases are using the treatment. Most are reporting symptomatic improvement and a number of patients have claimed complete resolution of symptoms.
Marshall has since written several papers and given numerous presentations that detail the pathogenesis of chronic disease.
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Amy Proal graduated from Georgetown University in 2005 with a degree in biology. While at Georgetown, she wrote her senior thesis on Chronic Fatigue Syndrome and the Marshall Protocol.