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home:pathogenesis:evidence_bacteria [03.26.2016] – [Evolutionary evidence] swopped order last 2 sentence sallieqhome:pathogenesis:evidence_bacteria [01.13.2020] – [Other evidence] sallieq
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 ===== Other evidence ===== ===== Other evidence =====
  
-There is also the following types of evidence, the first three of which are noted in a [[http://www.medicinejournal.co.uk/article/S1357-3039(06)00185-X/abstract|1998 article]] and 2005 paper(({{pubmed>long:9779355}})) by David Relman and David Fredricks:+There is also the following types of evidence, the first three of which are noted in a [[http://www.medicinejournal.co.uk/article/S1357-3039(06)00185-X/abstract|1998 article]] and 2005(({{pubmed>long:9779355}})) paper by David Relman and David Fredricks:
   * **Clinical features** – Chronic diseases often share the same clinical presentation as those of known infectious diseases including fever and leucocytosis (an elevated number of white cells in the blood).   * **Clinical features** – Chronic diseases often share the same clinical presentation as those of known infectious diseases including fever and leucocytosis (an elevated number of white cells in the blood).
   * **Histology** – The inflammation of affected tissues in a chronic disease is very similar to inflammation caused by infection of characteristic microbial structures. [[http://en.wikipedia.org/wiki/Granuloma|Granuloma]] (an organized collection of immune cells) are widely agreed to be precipitated by infectious diseases such as tuberculosis, leprosy, histoplasmosis, cryptococcosis, blastomycosis, coccidioidomycosis and syphilis.(({{pubmed>long:14527294}})) However, a number of researchers continue to assume that certain chronic diseases such as sarcoidosis and Crohn's disease are not caused by infection even though they present with granuloma which are similar to those found in diseases known to be infectious. In fact, a Japanese team showed that one could use //Propionibacterium acnes// in mice to induce lung granuloma mimicking sarcoidosis.(({{pubmed>long:20424662}}))   * **Histology** – The inflammation of affected tissues in a chronic disease is very similar to inflammation caused by infection of characteristic microbial structures. [[http://en.wikipedia.org/wiki/Granuloma|Granuloma]] (an organized collection of immune cells) are widely agreed to be precipitated by infectious diseases such as tuberculosis, leprosy, histoplasmosis, cryptococcosis, blastomycosis, coccidioidomycosis and syphilis.(({{pubmed>long:14527294}})) However, a number of researchers continue to assume that certain chronic diseases such as sarcoidosis and Crohn's disease are not caused by infection even though they present with granuloma which are similar to those found in diseases known to be infectious. In fact, a Japanese team showed that one could use //Propionibacterium acnes// in mice to induce lung granuloma mimicking sarcoidosis.(({{pubmed>long:20424662}}))
   * **Treatment response** –  Whatever the chronic inflammatory condition, patients on the Marshall Protocol invariably experience the tell-tale immunopathological reaction, which can only be described as a bacterial die-off reaction. Though a number of other antibacterial treatments are ultimately less effective than the MP, patients also respond to these. Even high-dose antibiotics, which has a well-deserved reputation for being ineffective over the long term, do cause fundamental changes in disease symptoms of supposedly non-infectious diseases.   * **Treatment response** –  Whatever the chronic inflammatory condition, patients on the Marshall Protocol invariably experience the tell-tale immunopathological reaction, which can only be described as a bacterial die-off reaction. Though a number of other antibacterial treatments are ultimately less effective than the MP, patients also respond to these. Even high-dose antibiotics, which has a well-deserved reputation for being ineffective over the long term, do cause fundamental changes in disease symptoms of supposedly non-infectious diseases.
   * <html><span id="microbepopulations"></span></html>**Microbe populations** – Bacteria populations in patients with a given chronic disease have been shown to be different compared to those found in controls. Patients with autism have different bacteria in their gastrointestinal tract(({{pubmed>long:16157555}})) (({{pubmed>long:15459553}})) than do healthy infants as do those babies who later in life become obese or overweight.(({{pubmed>long:18326589}})) A team at Washington University has shown that the types of microbes in obese humans and mice are different when compared to those of normal weight; obese humans and mice have a 50% relative reduction in the abundance of Bacteroidetes and a proportional increase in Firmicutes.(({{pubmed>long:16033867}})) The team further showed that when the chronic disease obesity is decreased in humans through a low-calorie diet, the relative proportion of microbes changes.(({{pubmed>long:17183309}})) Finally, the group showed that obesity is transmissible: Ley et al took germ-free mice of normal weight, colonized their guts with an "obese microbiota", and found a significantly greater increase in total body fat than those mice colonized with a "lean microbiota."(({{pubmed>long:17183312}}))   * <html><span id="microbepopulations"></span></html>**Microbe populations** – Bacteria populations in patients with a given chronic disease have been shown to be different compared to those found in controls. Patients with autism have different bacteria in their gastrointestinal tract(({{pubmed>long:16157555}})) (({{pubmed>long:15459553}})) than do healthy infants as do those babies who later in life become obese or overweight.(({{pubmed>long:18326589}})) A team at Washington University has shown that the types of microbes in obese humans and mice are different when compared to those of normal weight; obese humans and mice have a 50% relative reduction in the abundance of Bacteroidetes and a proportional increase in Firmicutes.(({{pubmed>long:16033867}})) The team further showed that when the chronic disease obesity is decreased in humans through a low-calorie diet, the relative proportion of microbes changes.(({{pubmed>long:17183309}})) Finally, the group showed that obesity is transmissible: Ley et al took germ-free mice of normal weight, colonized their guts with an "obese microbiota", and found a significantly greater increase in total body fat than those mice colonized with a "lean microbiota."(({{pubmed>long:17183312}}))
-  * **[[home:diseases:co-infections|Co-infections]]** - Persistent co-infections, including fungi and viruses, are generally a sign of disease driven by infection. According to the Marshall Pathogenesis, these co-infections are able to proliferate because such chronic infections are able to slow the innate immune response. The presence of co-infections able to persist because the host is immunocompromised is common across all chronic disease types.  For example, a wide range of pathogens - at least have been found in the granuloma of sarcoidosis patients. According to Nicolson: "A large subset of ASD [autism spectrum disorder] patients shows evidence of bacterial and/or viral infections." (({{pubmed>long:17265454}}))  He reports that his team found conclusive evidence of Mycoplasma ssp., Chlamydia pneumoniae, and human herpes virus-6 coinfections in ASD patients. +  * **[[home:diseases:co-infections|Co-infections]]** - Persistent co-infections, including fungi and viruses, are generally a sign of disease driven by infection. According to the Marshall Pathogenesis, these co-infections are able to proliferate because such chronic infections are able to slow the innate immune response. The presence of co-infections able to persist because the host is immunocompromised is common across all chronic disease types.  For example, a wide range of pathogens - at least have been found in the granuloma of sarcoidosis patients. According to Nicolson: "A large subset of ASD [autism spectrum disorder] patients shows evidence of bacterial and/or viral infections." (({{pubmed>long:17265454}}))  He reports that his team found conclusive evidence of Mycoplasma ssp., Chlamydia pneumoniae, and human herpes virus-6 co-infections in ASD patients. 
 [{{ :home:pathogenesis:microbiota:gestationalage.gif|**Newer cultivation techniques have associated bacterial count in a pregnant woman's amniotic fluid with age at delivery.** This data strongly suggests a causative role for pathogenic bacteria in premature delivery. Source: [[http://www.ncbi.nlm.nih.gov/pubmed/18725970|DiGulio et al.]]}}] [{{ :home:pathogenesis:microbiota:gestationalage.gif|**Newer cultivation techniques have associated bacterial count in a pregnant woman's amniotic fluid with age at delivery.** This data strongly suggests a causative role for pathogenic bacteria in premature delivery. Source: [[http://www.ncbi.nlm.nih.gov/pubmed/18725970|DiGulio et al.]]}}]
   * **Failure of lifestyle interventions** – It has been widely hypothesized that lifestyle factors, including a poor diet and a lack of exercise, are the primary driver behind increased rates of chronic disease. For example, the World Health Organization [[http://www.who.int/dietphysicalactivity/publications/facts/obesity/en/|has termed]] "an obesity epidemic," but even the most ambitious obesity intervention programs, which have gone to great lengths to increase rates of exercise and improve eating habits of a population, have been failures. One 1999 $200,000 NIH-funded intervention, known as the Pathways program, was performed on two groups of children. Pathways involved a substantial increase in physical education programs, classes about nutrition, significant reduction in fat and calorie content of all school meals, and several other health related measures - and all as part of a randomized controlled trial, the gold standard in studies. The primary goal of the study was to reduce the rate of body fat in the intervention group, but after the three-year intervention the percent of body fat in both groups was essentially identical. The researchers were unable to explain the failure of their intervention.(({{pubmed>long:14594792}})) Other such trials for obesity have been equally unsuccessful.(({{pubmed>long:17028105}}))   * **Failure of lifestyle interventions** – It has been widely hypothesized that lifestyle factors, including a poor diet and a lack of exercise, are the primary driver behind increased rates of chronic disease. For example, the World Health Organization [[http://www.who.int/dietphysicalactivity/publications/facts/obesity/en/|has termed]] "an obesity epidemic," but even the most ambitious obesity intervention programs, which have gone to great lengths to increase rates of exercise and improve eating habits of a population, have been failures. One 1999 $200,000 NIH-funded intervention, known as the Pathways program, was performed on two groups of children. Pathways involved a substantial increase in physical education programs, classes about nutrition, significant reduction in fat and calorie content of all school meals, and several other health related measures - and all as part of a randomized controlled trial, the gold standard in studies. The primary goal of the study was to reduce the rate of body fat in the intervention group, but after the three-year intervention the percent of body fat in both groups was essentially identical. The researchers were unable to explain the failure of their intervention.(({{pubmed>long:14594792}})) Other such trials for obesity have been equally unsuccessful.(({{pubmed>long:17028105}}))
   * **[[transmission|Transmission of disease through blood, bone marrow, organs or other tissues]]** – Organs and tissue from sarcoidosis patients have been known to cause sarcoidosis in the transplanted recipients.(({{pubmed>long:12002380}})) (({{pubmed>long:7951107}})) (({{pubmed>long:11607780}}))   * **[[transmission|Transmission of disease through blood, bone marrow, organs or other tissues]]** – Organs and tissue from sarcoidosis patients have been known to cause sarcoidosis in the transplanted recipients.(({{pubmed>long:12002380}})) (({{pubmed>long:7951107}})) (({{pubmed>long:11607780}}))
   * **Disease appearing in tattoos** – Over the last 40 years, there have been numerous reports of patients developing skin cancer in their tattoos including melanoma, basal cell carcinomas, squamous cell carcinomas, and keratoacanthomas.(({{pubmed>long:18617744}})) Also, the literature contains multiple reports of sarcoidosis patients developing skin lesions within tattoos. According to one researcher, this is "a well-recognized occurrence in patients with sarcoidosis."(({{pubmed>long:16027303}})) That a tattoo procedure could induce this kind of reaction strongly suggests that diseases such as cancer and sarcoidosis are caused by the introduction of infectious pathogens through contaminated needles.    * **Disease appearing in tattoos** – Over the last 40 years, there have been numerous reports of patients developing skin cancer in their tattoos including melanoma, basal cell carcinomas, squamous cell carcinomas, and keratoacanthomas.(({{pubmed>long:18617744}})) Also, the literature contains multiple reports of sarcoidosis patients developing skin lesions within tattoos. According to one researcher, this is "a well-recognized occurrence in patients with sarcoidosis."(({{pubmed>long:16027303}})) That a tattoo procedure could induce this kind of reaction strongly suggests that diseases such as cancer and sarcoidosis are caused by the introduction of infectious pathogens through contaminated needles. 
-  * **Disease appearing in scars** – There are several case reports of sarcoidosis lesions forming within scars, which are especially susceptible to infection. That these granuloma often take long periods of time to be realized corresponds with the growth rate of the slow-growing chronic pathogens which the Marshall Pathogenesis implicates in chronic disease.(({{pubmed>long:17243430}})) According to one report, a patient developed sarcoid granuloma fully 50 years after his initial injury.(({{pubmed>long:19094856}})) Sorabee //et al// write(({{pubmed>long:15640432}})) that in addition to reactivation of scars obtained from previous wounds, scar sarcoidosis has been reported at the sites of previous intramuscular injections, blood donation venepuncture sites, scars of herpes zoster,(({{pubmed>long:10086879}})) sarcoidosis on ritual scarification,(({{pubmed>long:2917808}})) and at the sites of allergen extracts for desensitisation.(({{pubmed>long:1458650}})) +  * **Disease appearing in scars** – There are several case reports of sarcoidosis lesions forming within scars, which are especially susceptible to infection. That these granuloma often take long periods of time to be realized corresponds with the growth rate of the slow-growing chronic pathogens which the Marshall Pathogenesis implicates in chronic disease.(({{pubmed>long:17243430}})) According to one report, a patient developed sarcoid granuloma fully 50 years after his initial injury.(({{pubmed>long:19094856}})) Sorabee //et al// write that in addition to reactivation of scars obtained from previous wounds(({{pubmed>long:15640432}})), scar sarcoidosis has been reported at the sites of previous intramuscular injections, blood donation venepuncture sites, scars of herpes zoster,(({{pubmed>long:10086879}})) sarcoidosis on ritual scarification,(({{pubmed>long:2917808}})) and at the sites of allergen extracts for desensitisation.(({{pubmed>long:1458650}})) 
   * **Absence of an effect for most chemicals thought to be toxic** – In contrast to infectious agents, little evidence implicates typical doses of dietary chemicals as primary causes of human cancer. Paul Ewald, PhD has concluded that humans have evolved effective flexible enzymatic systems for degrading potentially carcinogenic chemicals.(({{pubmed>long:9255573}})) Even aflatoxins, which are one of the most carcinogenic of dietary constituents, may exert their negative effects largely in conjunction with viral infection.(({{pubmed>long:9270015}}))   * **Absence of an effect for most chemicals thought to be toxic** – In contrast to infectious agents, little evidence implicates typical doses of dietary chemicals as primary causes of human cancer. Paul Ewald, PhD has concluded that humans have evolved effective flexible enzymatic systems for degrading potentially carcinogenic chemicals.(({{pubmed>long:9255573}})) Even aflatoxins, which are one of the most carcinogenic of dietary constituents, may exert their negative effects largely in conjunction with viral infection.(({{pubmed>long:9270015}}))
   * **Difficulty distinguishing autoimmune disease from infectious disease** – Although they have identified a signature that distinguishes healthy individuals from sarcoidosis or tuberculosis patients, the biosignatures of both diseases are nevertheless very similar. According to the [[http://www.mpg.de/5771449/biosignatures_tuberculosis_sarcoidosis|Max Planck Institute]], it is almost impossible to distinguish between tuberculosis and sarcoidosis with just a single signature. A set of different biosignatures is better suited for distinguishing in a first step between diseased and healthy individuals and, in a further step, between the specific diseases.   * **Difficulty distinguishing autoimmune disease from infectious disease** – Although they have identified a signature that distinguishes healthy individuals from sarcoidosis or tuberculosis patients, the biosignatures of both diseases are nevertheless very similar. According to the [[http://www.mpg.de/5771449/biosignatures_tuberculosis_sarcoidosis|Max Planck Institute]], it is almost impossible to distinguish between tuberculosis and sarcoidosis with just a single signature. A set of different biosignatures is better suited for distinguishing in a first step between diseased and healthy individuals and, in a further step, between the specific diseases.
home/pathogenesis/evidence_bacteria.txt · Last modified: 09.14.2022 by 127.0.0.1
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