Related article: Symptoms

According to the Marshall PathogenesisA description for how chronic inflammatory diseases originate and develop., chronic inflammatory disease is caused by a microbiotaThe bacterial community which causes chronic diseases - one which almost certainly includes multiple species and bacterial forms. of bacteria, including L-form bacteriaDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria., biofilm A structured community of microorganisms encapsulated within a self-developed protective matrix and living together. bacteria, and intracellular bacterial forms. These bacterial forms are collectively known as the Th1 pathogens, and they collectively cause the Th1 diseasesThe chronic inflammatory diseases caused by bacterial pathogens.. Although the exact species and forms of bacteria, as well as the location and extent of the infection, vary between one patient suffering from chronic disease and the next, the disease process is common: bacterial pathogens persist and reproduce by disabling the innate immune response.

As counterintuitive as the theory of a Th1 Spectrum DisorderThe overlap of different disease symptoms in different patients with similar diagnoses - caused by the fact that any one bacterial species can contribute to numerous disease states. may seem to some medical specialists, it has been the experience of Autoimmunity Research FoundationNon-profit foundation dedicated to exploring a pathogenesis and therapy for chronic disease. that nearly all MP patients with inflammatory disease eventually respond with immunopathology–the predictable rise and fall of symptoms, which is taken to be a sign of progress.

Some diseases are represented by more patients trying the therapy than others. As more patients join the MP cohort, the Autoimmunity Research Foundation will gather more data about the efficacy of the treatment with respect to individual diseases. In the meantime, the MP may be an appropriate treatment option for some of the diseases listed below.

Many patients have shared their stories of recovery on Marshall protocol study site.

What is a chronic inflammatory disease?

Difficulty in diagnosing specific diseases

Main article: Th1 Spectrum Disorder

Th1 Spectrum Disorder refers to the group of chronic inflammatory diseases, which are caused by the Th1 pathogens, a microbiota of bacteria which include L-formDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria., biofilm, and intracellular bacterial forms. Although the exact species and forms of bacteria, as well as the location and extent of the infection, vary between one patient suffering from chronic disease and the next, the disease process is common: bacterial pathogens persist and reproduce by disabling the innate immune response.

Although patients who become infected with the Th1 pathogens are given a variety of diagnoses, there are often no clear cut distinctions between one disease and the next. Rather, symptoms frequently overlap creating a spectrum of illness in which diseases are more connected to one another than mutually exclusive disease states.

Microbial communication

Here we show that an EHEC luxS mutant, unable to produce the bacterial autoinducer, still responds to a eukaryotic cell signal to activate expression of its virulence genes. We have identified this signal as the hormone epinephrine and show that β- and α-adrenergic antagonists can block the bacterial response to this hormone. 1)

The contribution of cell-cell signaling and motility to bacterial biofilm formation. 2)

Bacterial Biofilm Control by Perturbation of Bacterial Signaling Processes.3)

List of diseases

The following is a list of diseases physicians have reported they have used the Marshall Protocol to treat. Number of patients varies by disease.

As far as we know, there is no one on the MP with the following types of conditions. But, since these diseases are inflammatory, it's possible the Marshall Protocol could be helpful as well. However, once again, there's no available patient or physician reports supporting this.

===== Notes and comments =====

Under site map diagnosis could you add prostatitis and interstitial cystitis .

50 % norwegian men around 50 years of age start to suffer !

How about including preeclampsia in the list of diseases that the MP possibly could treat?

Hypertens Pregnancy. 2010;29(4):468-77. Chlamydia pneumoniae infection in preeclampsia. Xie F, Hu Y, Magee LA, Money DM, Patrick DM, Brunham RM, Thomas E, von Dadelszen P; Toxaemia group. Collaborators (5)

Source Department of Obstetrics and Gynaecology, University of British Columbia, Vancouver, Canada. Abstract OBJECTIVE: The maternal syndrome of preeclampsia results from systemic endothelial activation by a number of factors that primarily derive from the intervillous space, so-called intervillous soup. Co-precipitants, such as innate immune activators, may lower the threshold to develop the maternal syndrome in preeclampsia. We examined whether, like atherosclerosis, preeclampsia is associated with infection with Chlamydia pneumoniae (C. pneumoniae).

STUDY DESIGN: A case-control study was performed on 50 women with preeclampsia, 57 women with normal pregnancies at term, and 25 non-pregnant controls. Anti-C. pneumoniae antibodies were examined by enzyme-linked immunosorbent assay and C. pneumoniae genomic DNA (gDNA) loads were measured by real-time PCR. We also performed a data synthesis of the relationship between anti-C. pneumoniae seroprevalence and preeclampsia risk.

RESULTS: Neither the number of women with measurable copy numbers of C. pneumoniae gDNA, the anti-C. pneumoniae seroprevalence, nor antibody indices of IgG, IgM, or IgA to C. pneumonia varied between groups. However, when measurable, gDNA copy numbers of C. pneumoniae were increased in women with preeclampsia compared with the normal pregnant (p < 0.05) and non-pregnant controls (p < 0.05). For women with measurable C. pneumoniae gDNA, their copy numbers were correlated with anti-C. pneumoniae IgG concentrations (r2 = 0.49; p < 0.0001). Data synthesis reveals that anti-C. pneumoniae IgG seroprevalence is associated with preeclampsia risk.

CONCLUSION: Our data suggest an association between C. pneumoniae infection and preeclampsia. While not a uniform and singular precipitant of the maternal syndrome of preeclampsia, C. pneumoniae infection may be a co-precipitant with other components of the intervillous soup. Further investigations appear warranted.

PMID: 20818953

Am J Ther. 2008 Jul-Aug;15(4):373-6. Subclinical infection as a cause of inflammation in preeclampsia. López-Jaramillo P, Herrera JA, Arenas-Mantilla M, Jáuregui IE, Mendoza MA. Source Vilano Group, Research Institute, Cardiovascular Foundation of Colombia, Floridablanca, Santander, Colombia. joselopez@fcv.org Abstract Preeclampsia, a pregnancy-exclusive hypertensive disorder, is the major cause of maternal and perinatal mortality, with a greater importance in developing countries. The role of inflammation in the pathogenesis of preeclampsia has been the object of recent studies by our group. We have described elevated levels of inflammatory markers (tumor necrosis factor alpha, interleukin-6, and C-reactive protein) in preeclamptic patients and demonstrated that Latin-American women present a higher degree of inflammation than women from developed countries. We have results that suggest that chronic subclinical infections and insulin resistance are the most probable causes of the increased inflammation in preeclampsia. Moreover, we showed that early treatment of urinary and vaginal infections decreased the incidence of preeclampsia. We also have evidence that suggests that inflammation leads to endothelial dysfunction, predisposing women to develop preeclampsia. Increased levels of inflammation markers and endothelial dysfunction are found in the early stages of pregnancy in women who later on develop preeclampsia. Appropriate prenatal care programs, including screening and treatment of urinary, vaginal, and periodontal infections in early pregnancy and prevention of factors that predispose to insulin resistance, such as excessive weight gain during pregnancy, may reduce the incidence of preeclampsia in Latin-American women.

PMID: 18645342

A persistent and diverse airway microbiota present during chronic obstructive pulmonary disease exacerbations.Huang YJ, Kim E, Cox MJ, Brodie EL, Brown R, Wiener-Kronish JP, Lynch SV. Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California San Francisco, San Francisco, California 94143-0538, USA. Abstract Acute exacerbations of chronic obstructive pulmonary disease (COPD) are a major source of morbidity and contribute significantly to healthcare costs. Although bacterial infections are implicated in nearly 50% of exacerbations, only a handful of pathogens have been consistently identified in COPD airways, primarily by culture-based methods, and the bacterial microbiota in acute exacerbations remains largely uncharacterized. The aim of this study was to comprehensively profile airway bacterial communities using a culture-independent microarray, the 16S rRNA PhyloChip, of a cohort of COPD patients requiring ventilatory support and antibiotic therapy for exacerbation-related respiratory failure. PhyloChip analysis revealed the presence of over 1,200 bacterial taxa representing 140 distinct families, many previously undetected in airway diseases; bacterial community composition was strongly influenced by the duration of intubation. A core community of 75 taxa was detected in all patients, many of which are known pathogens. Bacterial community diversity in COPD airways is substantially greater than previously recognized and includes a number of potential pathogens detected in the setting of antibiotic exposure. Comprehensive assessment of the COPD airway microbiota using high-throughput, culture-independent methods may prove key to understanding the relationships between airway bacterial colonization, acute exacerbation, and clinical outcomes in this and other chronic inflammatory airway diseases. PMID: 20141328

Does Helicobater pylori infection play a role in extragastric diseases?de Korwin J. [Does Helicobacter pylori infection play a role in extragastric diseases?]. Presse Med. 2008 Mar;37(3 Pt 2):525-34. doi: 10.1016/j.lpm.2007.07.029. Epub 2008 Feb 4.
[PMID: 18249521] [DOI: 10.1016/j.lpm.2007.07.029]

       more options

Author(s): de Korwin JD (de Korwin, Jean-Dominique) Source: PRESSE MEDICALE Volume: 37 Issue: 3 Pages: 525-534 Part: Part 2 Published: MAR 2008 Times Cited: 1 References: 89 Citation Map Abstract: Since the discovery of Helicobacter pylori (H. pylori), numerous studies hove considered the possibility that it ploys a role in different extragastric diseases. Most of these studies may be classified as epidemiological studies or investigations of H. pylori eradication, but there are also case reports and in vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory. studies. This review reveals the limitations common to most of them. Idiopathic thrombocytopenic purpura is the disease for which the strongest association with H. pylori infection has been shown. Data are also accumulating about the role of H. pylori infection in idiopathic iron deficiency anemia and chronic idiopathic urticaria. Interesting results show that H. pylori infection affects atherosclerosis and is weakly associated with ischemic heart disease and stroke. Moreover, CagA-positive H. pylori strains may play a role in the natural history of atherosclerotic stroke. Recent studies suggest a link between H. pylori and Parkinson's disease. Preliminary data indicate that H. pylori infection impairs gastric ghrelin production and may influence nutritional status. The association between H. pylori infection and other extragastric diseases remains controversial. H. pylori infection may cause extragastric manifestations directly or indirectly, by various mechanisms including atrophic gastritis, the release of inflammatory mediators, molecular mimicry, and systemic immune response. Evidence suggests that anti-H. pylori therapy improves idiopathic thrombocytopenic purpura (significant increase of platelet count in half of the cases), iron-deficiency anemia, and chronic urticaria (30% remission rate), but the data from randomized controlled trials are insufficient to confirm these positive effects.

J Infect Dis. 2008 Jul 15;198(2):226-33. Anti-ganglioside antibody induction by swine (A/NJ/1976/H1N1) and other influenza vaccines: insights into vaccine-associated Guillain-Barré syndrome. Nachamkin I, Shadomy SV, Moran AP, Cox N, Fitzgerald C, Ung H, Corcoran AT, Iskander JK, Schonberger LB, Chen RT. Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-4283, USA. nachamki@mail.med.upenn.edu Abstract BACKGROUND: Receipt of an A/NJ/1976/H1N1 “swine flu” vaccine in 1976, unlike receipt of influenza vaccines used in subsequent years, was strongly associated with the development of the neurologic disorder Guillain-Barré syndrome (GBS). Anti-ganglioside antibodies (e.g., anti-GM(1)) are associated with the development of GBS, and we hypothesized that the swine flu vaccine contained contaminating moieties (such as Campylobacter jejuni antigens that mimic human gangliosides or other vaccine components) that elicited an anti-GM(1) antibody response in susceptible recipients. METHODS: Surviving samples of monovalent and bivalent 1976 vaccine, comprising those from 3 manufacturers and 11 lot numbers, along with several contemporary vaccines were tested for hemagglutinin (HA) activity, the presence of Campylobacter DNA, and the ability to induce anti-Campylobacter and anti-GM(1) antibodies after inoculation into C3H/HeN mice. RESULTS: We found that, although C. jejuni was not detected in 1976 swine flu vaccines, these vaccines induced anti-GM(1) antibodies in mice, as did vaccines from 1991-1992 and 2004-2005. Preliminary studies suggest that the influenza HA induces anti-GM(1) antibodies. CONCLUSIONS: Influenza vaccines contain structures that can induce anti-GM(1) antibodies after inoculation into mice. Further research into influenza vaccine components that elicit anti-ganglioside responses and the role played by these antibodies (if any) in vaccine-associated GBS is warranted.

PMID: 18522505

Patients with GBS develop anti-ganglioside antibodies that are implicated in the pathogenesis of this disease. Antibodies to a number of different complex gangliosides, includingGM1,GD1a, GD3, GT1a, and GQ1b, can be detected in patients with GBS [10]. Infections with several agents are associated with the development of GBS [11], and Campylobacter jejuni, a common cause of bacterial gastroenteritis, is one of the most frequently identified bacterial pathogens associated with the development of GBS [12]. It has been deduced that the development of GBS after C. jejuni infection is the result of molecular mimicry between the bacterial surface lipooligosaccharide (LOS) expressing ganglioside-like epitopes and relevant targets in peripheral nerves

PMS: https://www.ncbi.nlm.nih.gov/pubmed/17468538?dopt=Abstract

I just got the all clear from CNS Vasculitis in less than 2 years and I would like that to show in the MPKB for the benefit of any Savvy vasculitis members who come across, I write periodically on the Savvy chat site about the protocol though I haven't seen any evidence of people taking notice except Lew newmark who wrote about it here:- https://mlcss.com/2010/10/13/the-keith-waterhouse-interview-part-three/

Rheumatology (Oxford, England). 2010 Dec 11;> Bacterial DNA motifs trigger ANCA production in ANCA-associated vasculitis in remission.

Tadema H, Abdulahad WH, Lepse N, Stegeman CA, Kallenberg CG, Heeringa P

Objectives. CpG motifs, which are highly prevalent in bacterial DNA, have been shown to trigger the production of ANCA in vitro by B lymphocytes from patients with active ANCA-associated vasculitis (AAV). Staphylococcus aureus is associated with relapses in AAV, and CpG motifs from staphylococcal DNA may trigger ANCA production in AAV patients in remission. We investigated the presence of ANCA-producing B lymphocytes during quiescent disease and tested the capacity of these cells to produce ANCA in response to CpG. Methods. Expression of Toll-like receptor 9 (TLR9) by B lymphocytes from AAV patients and controls was assessed. Peripheral blood mononuclear cells were isolated from 23 PR3-ANCA and 15 MPO-ANCA patients (33 quiescent, 5 active disease) and 14 healthy controls, and cultured for 12 days in the presence of cytosine-phosphate-guanine oligodeoxynucleotide (CpG-ODN) and IL-2. B-lymphocyte activation, differentiation, immunoglobulin production and in vitro ANCA production were studied. Results. TLR9 expression by B lymphocytes was comparable in AAV patients and controls. B lymphocytes were activated and differentiated towards a plasma cell phenotype in response to CpG-ODN and IL-2. ANCA were produced in vitro by 13 out of 23 PR3-ANCA patients and 3 out of 15 MPO-ANCA patients. Conclusions. We conclude that ANCA-producing B lymphocytes can be present in the peripheral blood of AAV patients during remission. These autoreactive B lymphocytes are triggered by CpG-ODN and IL-2 to produce ANCA in vitro. CpG motifs may trigger the production of ANCA in vivoA type of scientific study that analyzes an organism in its natural living environment., contributing to the development of relapses in AAV.

PMID: 21149241

In a study of bacteria inhabiting healthy women’s vaginas, Jacques Ravel of the University of Maryland School of Medicine in Baltimore and his colleagues found that each woman had one of five major communities of micro­organisms. Four of the communities were dominated by types of Lactobacillus, bacteria like those found in yogurt that are well-known for making infection-fighting lactic acid, the researchers reported in the March 15 Proceedings of the National Academy of Sciences.

But the fifth group of bacteria contained few lactobacilli, which usually signals an infection. “If you were to give those samples to a physician, they would probably say the women were sick and had bacterial vaginosis,” Ravel says. In fact, the women were perfectly healthy. Some researchers think that what bacteria do is far more important than which bacteria colonize the body. In this case, even though most of the bacteria in the fifth group weren’t Lactobacillus, the microbes still made plenty of lactic acid that could ward off serious infections.

From: Phillyguy Date: 2011-05-10 13:23:42 Reply: https://www.marshallprotocol.com/reply.php?topic_id=13412

Korean J Urol. 2011 vol. 52(3) pp. 194-9

Detection of nanobacteria in patients with chronic prostatitis and vaginitis by reverse transcriptase polymerase chain reaction.

Kim TH, Kim HR, Myung SC

We found that conventional RT-PCR for NB was rapid, simple, low in cost, and easily available for the detection of NB, and that NB may be a possible etiological factor for vaginitis and CP/CPPS. The prevalence of U. urealyticum among the four patients with NB coinfection was 75%; the presence of U. urealyticum might therefore raise suspicion for nanobacterial infection.

Affiliation: Department of Urology, Chung-Ang University College of Medicine, Seoul, Korea.

From: ChrisMavo Date: 2011-05-10 13:29:58 Reply: https://www.marshallprotocol.com/reply.php?topic_id=13412

Can someone explain what they mean by nanobacteria? This is the first time I've seen this term used for bacteria. Could this be the first indication of a whole new category of bacteria that has not been uncovered yet? Are these nanobacteria the main component of what we call the microbiota?

So many questions… sorry!

From: Bane Date: 2011-05-10 14:14:45 Reply: https://www.marshallprotocol.com/reply.php?topic_id=13412

ChrisMavo wrote: Can someone explain what they mean by nanobacteria?

“Nanobacteria (NB) are newly discovered infectious agents of 100-500 nm in size with a 16S ribosomal RNA (rRNA) gene sequence and slow growth and a doubling time of about 3 days. They are fastidious and difficult to culture but can be detected with standard microbiological methods”


High levels of Epstein–Barr virus in COPD


COPD is related to the EBV Virus, which may potentiate other Viruses/Pathogens:

Thus, chronic EBV infection may lead to impaired interferon-γ production and, in turn, a reduced innate immune response characterised by recurrent viral and bacterial infection.

Also interesting is that people with COPD have high amounts of the bacteria pseudomonas, plus other bacterias. When one smokes, it is like injecting pathogens into the blood stream, via the lungs.




Fifteen different classes of bacteria and a broad range of potentially pathogenic organisms were detected in all cigarette samples. Most notably, we detected Acinetobacter, Bacillus, Burkholderia, Clostridium, Klebsiella, Pseudomonas aeruginosa, and Serratia in ≥ 90% of all cigarette samples. Other pathogenic bacteria detected included Campylobacter, Enterococcus, Proteus, and Staphylococcus. No significant variability in bacterial diversity was observed across the four different cigarette brands.


Previous studies have shown that smoking is associated with colonization by pathogenic bacteria and an increased risk of lung infections. However, this is the first study to show that cigarettes themselves could be the direct source of exposure to a wide array of potentially pathogenic microbes among smokers and other people exposed to secondhand smoke. The overall public health implications of these findings are unclear at this time, and future studies are necessary to determine whether bacteria in cigarettes could play important roles in the development of both infectious and chronic respiratory diseases.

From: LeeDate: 2011-11-01 07:44:01 Reply: https://www.marshallprotocol.com/reply.php?topic_id=13718

When I tested positive for EBV the doc said I had the highest titers they had even seen in that clinic ….:shock: I am a non-smoker DX- Sarcoidosis with COPD and emphysema. Lee

From: eClaire Date: 2011-11-01 11:07:07 Reply: https://www.marshallprotocol.com/reply.php?topic_id=13718

I have COPD and had two different strains of EBV in the late 90s alone. Who knows when I was younger? I doubt I was ever tested.

I was raised by smokers. The COPD came to light when having some sort of cardiogram… the person had trouble seeing my heart because of my damaged lungs. She said my lungs looked like that of someone who was a heavy smoker or had had very bad asthma throughout life. This much I know: when my immune system would go on a tear related to tobacco smoke, VOCs in paint, allergy to cats, etc., my lungs would produce an oatmeal like substance and sometimes I'd stay awake steaming my lungs because it felt like I had to focus on breathing to get oxygen. Even my allergist was puzzled by what my lungs produced when I was in this state.

Anaerobe. 2011 Aug;17(4):191-5. Epub 2011 Mar 3.Molecular methods to describe the spectrum and dynamics of the vaginal microbiota. Fredricks DN. Source Fred Hutchinson Cancer Research Center, Vaccine and Infectious Disease Division, Seattle, WA 98109-1024, USA. dfredric@fhcrc.org Abstract The human vagina hosts a collection of microbes that is distinct from other human surfaces and mucosal sites, with reduced microbial diversity that is likely driven by the acidic environment. The microbial ecosystem of the vagina is dominated by lactobacilli in women without bacterial vaginosis (BV), and is characterize by increased species richness, diversity, and evenness in women with BV. The use of molecular, cultivation-independent methods to describe the bacterial biota of the human vagina has revealed many novel putative anaerobes in women with BV, and has demonstrated the almost ubiquitous nature of Lactobacillus iners which is found in most women regardless of BV status. A variety of molecular tools are being employed to study the vaginal microbiota, and each approach has distinct advantages and disadvantages that are reviewed. Longitudinal studies have demonstrated that the vaginal microbiota can be highly dynamic, with dramatic shifts in bacterial composition and concentrations in response to numerous endogenous and exogenous factors. Copyright © 2011 Elsevier Ltd. All rights reserved. PMID: 21376827

Sperandio V, Torres AG, Jarvis B, Nataro JP, Kaper JB. Bacteria-host communication: the language of hormones. Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8951-6. doi: 10.1073/pnas.1537100100. Epub 2003 Jul 7.
[PMID: 12847292] [PMCID: 166419] [DOI: 10.1073/pnas.1537100100]
Shrout JD, Tolker-Nielsen T, Givskov M, Parsek MR. The contribution of cell-cell signaling and motility to bacterial biofilm formation. MRS Bull. 2011 May 1;36(5):367-373. doi: 10.1557/mrs.2011.67.
[PMID: 22053126] [PMCID: 3204577] [DOI: 10.1557/mrs.2011.67]
Jakobsen TH, Tolker-Nielsen T, Givskov M. Bacterial Biofilm Control by Perturbation of Bacterial Signaling Processes. Int J Mol Sci. 2017 Sep 13;18(9):1970. doi: 10.3390/ijms18091970.
[PMID: 28902153] [PMCID: 5618619] [DOI: 10.3390/ijms18091970]
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