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Table of Contents

  • Acute vs. chronic infections
  • Disabled immune response increases susceptibility to acute infections
  • Acute infections predispose to chronic diseases
  • Certain treatments for acute infections can predispose to chronic disease
  • Vitamin D and acute infections
  • Targeting chronic microbes may decrease susceptibility to acute infections
  • Acute respiratory infections
Acute infections

Related articles: Antibiotics under special circumstances, Effects of bacteria and viruses on their human host, Successive infection and variability in disease

The white blood cell count rises in cases of infection, steroid use and other conditions.

The immune system responds to cues in the microenvironment to make acute and chronic adaptations in response to inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. and injury. The therapeutic significance of adenosine-mediated effects on the immune system is discussed here. 1)

The term acute infection is used to refer to microbe living inside a host for a limited period of time, typically less than six months. However, an abundance of research has emerged suggesting that acute infections have long-lasting effects, predisposing a person to later onset of chronic diseases.

The purpose of the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. is to rehabilitate the immune response and improve the mix of microbes in the human body. In theory, this would free the immune response to target acute infections. Anecdotal reports from physicians and patients suggest that the MP is effective in this manner. To date, there have been no reports of tuberculosis or AIDS among MP patients.

Acute vs. chronic infections

Related section: Can chronic infections really cause disease?

When compatible high dose ABx is required for Acute bacterial infection see short term non MP antibiotic treatment in acute infection.

Acute infections Chronic infections
Terms early, acute late, chronic, fastidious, latent; an important type of chronic infection is the 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.
Duration lasts no more than six months (although, as we'll see below, the effects of acute infections can be long-lived) lasts more than six months
Rate of growth fast - reproduce over the course of days slow – may take several weeks to reproduce; build up over the course of decades (for example, the velocity of DNA replication fork progression for Mycoplasma reproduces ten times slower than Escherichia coli2))
Ease of study present their own problems but more recognized and studied relatively difficult – fewer markers, more challenging to infer causation

Note that it is commonplace for a given species to morph between forms.

Disabled immune response increases susceptibility to acute infections

Certainly the exposure to and acquisition of new bacteria plays a role in the development of disease, but these factors don't account for everything. Diseases appear to strike randomly if for no other reason than their massive incidence and mortality. But, a close look at the evidence suggests that diseases tend to strike those who are most vulnerable. This is true even for acute infections such as the Black Death, the deadliest known epidemic in human history. The results of one analysis of 14th century skeletal remains found that “the Black Death did not kill indiscriminately - that it was, in fact, selective with respect to frailty….”3)

During the SARS epidemic, those who were succumbing were people with weakened immune systems, especially diabetics and healthcare workers.4) With the recent Escherichia coli O157:H7 epidemic, there appears to be a demographic pattern of patients who are likely already heavy carriers of a pathogenic microbiotaThe bacterial community which causes chronic diseases - one which almost certainly includes multiple species and bacterial forms.. Remember that, like SARS, a lot more people are getting infected than those who actually fall ill and can't recover.

Trevor Marshall, PhD

According to the Marshall PathogenesisA description for how chronic inflammatory diseases originate and develop., “frailty” could just as easily refer to the strength of immune response. It is the absence of a robust immune response which is the primary contributing determinant in whether someone gets sick with chronic illness or someone remains healthy.

Bacterial pathogens themselves can make a human host more hospitable to their growth and reproduction by secreting substances like the sulfonolipid capnine, which bind and block the Vitamin D ReceptorA nuclear receptor located throughout the body that plays a key role in the innate immune response., a nuclear receptorIntracellular receptor proteins that bind to hydrophobic signal molecules (such as steroid and thyroid hormones) or intracellular metabolites and are thus activated to bind to specific DNA sequences which affects transcription. that controls the innate immune response. Over time, bacteria succeed in suppressing the immune response through a gradual process known as successive infection. In the absence of intervention, successive infectionAn infectious cascade of pathogens in which initial infectious agents slow the immune response and make it easier for subsequent infections to proliferate. is something of an inevitability as everyone who lives long enough will take on the aches, pains, memory loss, and other symptoms that are the hallmark of chronic disease.

Bacteria are allowed to further proliferate when a person consumes any number of immunosuppressive foods, drugs, supplements and other substances. These substances include: immunosuppressants, beta-lactam antibiotics such as penicillin, corticosteroids, and foods and supplements containing high levels of vitamin D. The consumption of such substances is at historical levels and may be largely responsible for the recent spike in chronic disease incidence.

Acute infections predispose to chronic diseases

There is broad support for the conclusion that early infections, especially acute infections, predispose a person to later onset of chronic diseases, diseases which are likely caused by chronic microbial infections. In a 2004 Science paper, Finch and Crimmins proposed that early infection burdened survivors with a “cohort morbidity phenotype,” which they carry with them throughout their lives.5)

Microbial infections make the body a more hospitable environment for other infections via two primary means: affecting both human host-cell pathways and the expression of human genes. This effect has been documented in a range of clinical and laboratory-based studies. O'Connor and team at the Centers for Disease Control and Prevention state, “At least 13 of 39 recently described infectious agents induce chronic syndromes.”6) The section Successive infection: early infections predispose a person to later chronic disease lists at least a dozen such examples.

Certain treatments for acute infections can predispose to chronic disease

A variety of conventional treatments address acute infections with no eye towards their effect on chronic microbes:

  • corticosteroidsA first-line treatment for a number of diseases. Corticosteroids work by slowing the innate immune response. This provides some patients with temporary symptom palliation but exacerbates the disease over the long-term by allowing chronic pathogens to proliferate. – In a 2011 Lancet study, Dutch researchers concluded that patients with community-acquired pneumonia appear to recovery quickly in the hospital when treated with dexamethasone, a corticosteroidA first-line treatment for a number of diseases. Corticosteroids work by slowing the innate immune response. This provides some patients with temporary symptom palliation but exacerbates the disease over the long-term by allowing chronic pathogens to proliferate., in addition to the standard regimen of antibiotics.7) The statistically significant benefit: approximately 24 hours. While the researchers concluded that “serious adverse events were rare,” patients were observed for all of a week – certainly not long enough to measure the effect an immunosuppressant has on chronic microbes. A follow up study of sufficient time would surely show something different.
  • beta-lactam antibiotics – Beta-lactam antibiotics such as ceftazidime for Psuedomonas aeruginosa induce microbes to shed their cell walls, producing “viable monsters.”8)
  • antibiotics – High-dose antibiotics used to control inflammation would likewise show a short-term benefit and long-term harm. Note that the Marshall Protocol uses pulsed low-dose antibiotics so as to avoid this problem.

It remains unclear how most standard treatments for acute infections affect the immune response. This is especially true of antibiotics, the primary action of which may be, unexpectedly, to target the body's nuclear receptorsIntracellular receptor proteins that bind to hydrophobic signal molecules (such as steroid and thyroid hormones) or intracellular metabolites and are thus activated to bind to specific DNA sequences which affect transcription..

Many of the antivirals, antibacterials, etc., do not do the same thing in vivoA type of scientific study that analyzes an organism in its natural living environment. as medicine expects them to, and the lack of discrimination between immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. and immunosuppression in early stages of treatment may well determine which of the more serious cases proceed towards death.

Trevor Marshall, PhD

Vitamin D and acute infections

Some have speculated that vitamin D is protective against acute infections, but this has not been supported by the evidence.

  • A 2009 systematic review examined 13 studies examining vitamin D for treatment or prevention of infectious diseases in humans. The authors concluded (in the euphemistic fashion characteristic of many pro-vitamin D studies) that vitamin D was ineffective: “On the basis of studies reviewed to date, the strongest evidence supports further research into adjunctive vitamin D therapy for tuberculosis, influenza, and viral upper respiratory tract illnesses.”9)
  • Shaman et al. found that they could not use serum concentration of the vitamin D metabolite 25-DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver. in a model for seasonal changes in infection.10)

Targeting chronic microbes may decrease susceptibility to acute infections

The purpose of the Marshall Protocol is to rehabilitate the immune response and improve the mix of microbes in the human body. In theory, this would free the immune response to target acute infections. Anecdotal reports from physicians and patients suggest that the MP is effective in this manner. To date, there have been no reports of tuberculosis or AIDS among MP patients.

Acute respiratory infections

Main article: Acute respiratory infections

Related articles: Acute infections, Effects of bacteria and viruses on their human host

While it is certainly possible to contract an acute respiratory infection while on the Marshall Protocol, many symptoms of immunopathology mimic those of an acute respiratory infection. Adjusting one's antibiotics or olmesartan (Benicar)Medication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. can sometimes help a patient distinguish between the two. The MP tends to make no difference to the course of a common cold. Patients with acute respiratory infections can manage their infections with antiviral agents as well as medicines which palliate symptoms.

“It seems COVID-19 is probably not Pneumonia at all, the microbe attacks the HEME of red blood cells, destroying their ability to absorb oxygen and carbon dioxide so that gently applied supplementary pure oxygen will be an important part of treatment.”

vide: importance of HEME at the 12 minute mark

→ Read more...

acute infections, Pathogenesis, Microbes in the human body

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

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  • https://www.marshallprotocol.com/view_topic.php?id=3837&forum_id=32&jump_to=86100#p86100 f170

There is also very little evidence that vitamin D affects the course of human TB infection. Experiments have not been done in cells, mice or humans to evaluate the effect of vitamin D on influenza virus. At this time it would be premature to claim that vitamin D has an effect on TB, influenza or any other infection.11)

Measles may protect kids against allergies

https://www.reuters.com/article/healthNews/idUSTRE5236HS20090304

There was no correlation with immunization, just with catching the actual disease. Kids who had been immunized and still caught measles (about 11% of the them) received the same benefit as kids who had never been immunized. The disease was what modified the allergies

..Trevor..

12)

Measles makes the cells more susceptible to a secondary infection

Measles Virus-induced Immunosuppression

“MV infection, while inducing lifelong immunity, also suppresses the immune system leading to an increase in susceptibility to other, secondary infections (24, 67, 91). In vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory. research has shown that MV infection of cell cultures makes the cells more susceptible to a secondary bacterial invasion (13) ”

PLoS One. 2009 Dec 31;4(12):e8540. Streptococcus pneumoniae coinfection is correlated with the severity of H1N1 pandemic influenza.13)

Palacios G, Hornig M, Cisterna D, Savji N, Bussetti AV, Kapoor V, Hui J, Tokarz R, Briese T, Baumeister E, Lipkin WI. Center for Infection and Immunity, Mailman School of Public Health, Columbia University, New York, New York, USA. [email protected] Abstract BACKGROUND: Initial reports in May 2009 of the novel influenza strain H1N1pdm estimated a case fatality rate (CFR) of 0.6%, similar to that of seasonal influenza. In July 2009, however, Argentina reported 3056 cases with 137 deaths, representing a CFR of 4.5%. Potential explanations for increased CFR included virus reassortment or genetic drift, or infection of a more vulnerable population. Virus genomic sequencing of 26 Argentinian samples representing both severe and mild disease indicated no evidence of reassortment, mutations associated with resistance to antiviral drugs, or genetic drift that might contribute to virulence. Furthermore, no evidence was found for increased frequency of risk factors for H1N1pdm disease. METHODS/PRINCIPAL FINDINGS: We examined nasopharyngeal swab samples (NPS) from 199 cases of H1N1pdm infection from Argentina with MassTag PCR, testing for 33 additional microbial agents. The study population consisted of 199 H1N1pdm-infected subjects sampled between 23 June and 4 July 2009. Thirty-nine had severe disease defined as death (n = 20) or hospitalization (n = 19); 160 had mild disease. At least one additional agent of potential pathogenic importance was identified in 152 samples (76%), including Streptococcus pneumoniae (n = 62); Haemophilus influenzae (n = 104); human respiratory syncytial virus A (n = 11) and B (n = 1); human rhinovirus A (n = 1) and B (n = 4); human coronaviruses 229E (n = 1) and OC43 (n = 2); Klebsiella pneumoniae (n = 2); Acinetobacter baumannii (n = 2); Serratia marcescens (n = 1); and Staphylococcus aureus (n = 35) and methicillin-resistant S. aureus (MRSA, n = 6). The presence of S. pneumoniae was strongly correlated with severe disease. S. pneumoniae was present in 56.4% of severe cases versus 25% of mild cases; more than one-third of H1N1pdm NPS with S. pneumoniae were from subjects with severe disease (22 of 62 S. pneumoniae-positive NPS, p = 0.0004). In subjects 6 to 55 years of age, the adjusted odds ratio (OR) of severe disease in the presence of S. pneumoniae was 125.5 (95% confidence interval [CI], 16.95, 928.72; p<0.0001). CONCLUSIONS/SIGNIFICANCE: The association of S. pneumoniae with morbidity and mortality is established in the current and previous influenza pandemics. However, this study is the first to demonstrate the prognostic significance of non-invasive antemortem diagnosis of S. pneumoniae infection and may provide insights into clinical management. PMID: 20046873

===== References =====

1) , 9) Syntax error [pubmed plugin] 2) Seto S, Miyata M. Cell reproduction and morphological changes in Mycoplasma capricolum. J Bacteriol. 1998 Jan;180(2):256-64. doi: 10.1128/JB.180.2.256-264.1998.[PMID: 9440514] [PMCID: 106880] [DOI: 10.1128/JB.180.2.256-264.1998] 3) DeWitte SN, Wood JW. Selectivity of black death mortality with respect to preexisting health. Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1436-41. doi: 10.1073/pnas.0705460105. Epub 2008 Jan 28.[PMID: 18227518] [PMCID: 2234162] [DOI: 10.1073/pnas.0705460105] 4) Lai ST. Treatment of severe acute respiratory syndrome. Eur J Clin Microbiol Infect Dis. 2005 Sep;24(9):583-91. doi: 10.1007/s10096-005-0004-z.[PMID: 16172857] [PMCID: 7088345] [DOI: 10.1007/s10096-005-0004-z] 5) Finch CE, Crimmins EM. Inflammatory exposure and historical changes in human life-spans. Science. 2004 Sep 17;305(5691):1736-9. doi: 10.1126/science.1092556.[PMID: 15375259] [DOI: 10.1126/science.1092556] 6) O'Connor SM, Taylor CE, Hughes JM. Emerging infectious determinants of chronic diseases. Emerg Infect Dis. 2006 Jul;12(7):1051-7. doi: 10.3201/eid1207.060037.[PMID: 16836820] [PMCID: 3291059] [DOI: 10.3201/eid1207.060037] 7) Meijvis SCA, Hardeman H, Remmelts HHF, Heijligenberg R, Rijkers GT, van Velzen-Blad H, Voorn GP, van de Garde EMW, Endeman H, Grutters JC, Bos WJW, Biesma DH. Dexamethasone and length of hospital stay in patients with community-acquired pneumonia: a randomised, double-blind, placebo-controlled trial. Lancet. 2011 Jun 11;377(9782):2023-30. doi: 10.1016/S0140-6736(11)60607-7. Epub 2011 Jun 1.[PMID: 21636122] [DOI: 10.1016/S0140-6736(11)60607-7] 8) Mattman, L.H. (2000). Cell wall deficient forms. Third edition, p. 84. 10) Shaman J, Jeon CY, Giovannucci E, Lipsitch M. Shortcomings of vitamin D-based model simulations of seasonal influenza. PLoS One. 2011;6(6):e20743. doi: 10.1371/journal.pone.0020743. Epub 2011 Jun 3.[PMID: 21677774] [PMCID: 3108988] [DOI: 10.1371/journal.pone.0020743] 11) Bruce D, Ooi JH, Yu S, Cantorna MT. Vitamin D and host resistance to infection? Putting the cart in front of the horse. Exp Biol Med (Maywood). 2010 Aug;235(8):921-7. doi: 10.1258/ebm.2010.010061.[PMID: 20660091] [PMCID: 3138330] [DOI: 10.1258/ebm.2010.010061] 12) Siegler RL, Pavia AT, Christofferson RD, Milligan MK. A 20-year population-based study of postdiarrheal hemolytic uremic syndrome in Utah. Pediatrics. 1994 Jul;94(1):35-40.[PMID: 8008534] 13) Palacios G, Hornig M, Cisterna D, Savji N, Bussetti AV, Kapoor V, Hui J, Tokarz R, Briese T, Baumeister E, Lipkin WI. Streptococcus pneumoniae coinfection is correlated with the severity of H1N1 pandemic influenza. PLoS One. 2009 Dec 31;4(12):e8540. doi: 10.1371/journal.pone.0008540.[PMID: 20046873] [PMCID: 2795195] [DOI: 10.1371/journal.pone.0008540] home/pathogenesis/microbiota/acute_infections.txt · Last modified: 09.14.2022 by 127.0.0.1 © 2015, Autoimmunity Research Foundation. All Rights Reserved.

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