Exploring chronic disease
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.
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.