Home

Differences

This shows you the differences between two versions of the page.

Link to this comparison view

Both sides previous revisionPrevious revision
Next revision
Previous revision
home:pathogenesis:microbiota:acute_infections [01.12.2020] sallieqhome:pathogenesis:microbiota:acute_infections [09.14.2022] (current) – external edit 127.0.0.1
Line 3: Line 3:
  
 <relatedarticles>  <relatedarticles> 
-[[home:othertreatments/antibacterials/takingnonmpantibiotics]], [[home:pathogenesis:successive_infection|Successive infection and variability in disease]]+[[home:othertreatments/antibacterials/takingnonmpantibiotics]], [[home:pathogenesis/microbiota/interaction|Effects of bacteria and viruses on their human host]], [[home:pathogenesis:successive_infection|Successive infection and variability in disease]]
  </article>  </article>
  
Line 9: Line 9:
 The white blood cell count rises in cases of infection, steroid use and other conditions. 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 inflammation and injury. The therapeutic significance of adenosine-mediated effects on the immune system is discussed here.  (({{pubmed>long:21586357 }})) +The immune system responds to cues in the microenvironment to make acute and chronic adaptations in response to inflammation and injury. The therapeutic significance of adenosine-mediated effects on the immune system is discussed here.  (({{pmid>long:21586357 }})) 
  
 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 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 Protocol is to stimulate 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.+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 vs. chronic infections ===== ===== Acute vs. chronic infections =====
Line 25: Line 25:
 |**Terms**  |early, acute       |late, chronic, fastidious, latent; an important type of chronic infection is the l-form        | |**Terms**  |early, acute       |late, chronic, fastidious, latent; an important type of chronic infection is the l-form        |
 |**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      | |**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 coli//(({{pubmed>long:9440514}})))      |+|**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 coli//(({{pmid>long:9440514}})))      |
 |**Ease of study** |present their own problems but more recognized and studied    |relatively difficult – fewer markers, more challenging to infer causation   | |**Ease of study** |present their own problems but more recognized and studied    |relatively difficult – fewer markers, more challenging to infer causation   |
  
Line 37: Line 37:
 ===== Acute infections predispose to chronic diseases===== ===== 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.(({{pubmed>long:15375259}}))+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.(({{pmid>long:15375259}}))
  
-Microbial infections make the body a more hospitable environment for other infections via two primary means: affecting both [[home:pathogenesis:microbiota#bacteria_affect_host-cell_pathways|human host-cell pathways]] and the [[home:pathogenesis:microbiota#bacteria_affect_human_genes_and_gene_expression|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."(({{pubmed>long:16836820}})) The section [[home:pathogenesis:successive_infection#successive_infectionearly_infections_predispose_a_person_to_later_chronic_disease|Successive infection: early infections predispose a person to later chronic disease]] lists at least a dozen such examples.+Microbial infections make the body a more hospitable environment for other infections via two primary means: affecting both [[home:pathogenesis:microbiota#bacteria_affect_host-cell_pathways|human host-cell pathways]] and the [[home:pathogenesis:microbiota#bacteria_affect_human_genes_and_gene_expression|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."(({{pmid>long:16836820}})) The section [[home:pathogenesis:successive_infection#successive_infectionearly_infections_predispose_a_person_to_later_chronic_disease|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===== ===== 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: A variety of conventional treatments address acute infections with no eye towards their effect on chronic microbes:
-  * **corticosteroids** – In a 2011 //Lancet// study, Dutch researchers [[http://www.drugs.com/news/corticosteroids-may-speed-pneumonia-recovery-some-31677.html|concluded]] that patients with community-acquired pneumonia appear to recovery quickly in the hospital when treated with dexamethasone, a corticosteroid, in addition to the standard regimen of antibiotics.(({{pubmed>long:21636122}})) 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. +  * **corticosteroids** – In a 2011 //Lancet// study, Dutch researchers [[https://www.drugs.com/news/corticosteroids-may-speed-pneumonia-recovery-some-31677.html|concluded]] that patients with community-acquired pneumonia appear to recovery quickly in the hospital when treated with dexamethasone, a corticosteroid, in addition to the standard regimen of antibiotics.(({{pmid>long:21636122}})) 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."((Mattman, L.H. (2000). //Cell wall deficient forms.// Third edition, [[http://books.google.com/books?id=mincr2Hi81UC&pg=PA23&vq=penicillin&dq=beta-lactam+lida+mattman+cell+wall+deficient&source=gbs_search_s&cad=0#PPA82,M1|p. 84]].)) +  * **beta-lactam antibiotics** – Beta-lactam antibiotics such as ceftazidime for //Psuedomonas aeruginosa// induce microbes to shed their cell walls, producing "viable monsters."((Mattman, L.H. (2000). //Cell wall deficient forms.// Third edition, [[https://books.google.com/books?id=mincr2Hi81UC&pg=PA23&vq=penicillin&dq=beta-lactam+lida+mattman+cell+wall+deficient&source=gbs_search_s&cad=0#PPA82,M1|p. 84]].)) 
   * **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.   * **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.
  
Line 59: Line 59:
  
 Some have speculated that vitamin D is protective against acute infections, but this has not been supported by the evidence. 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."(({{pubmed>long: 19491064}})) +  * 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."(({{pmid>long: 19491064}})) 
-  * Shaman //et al.// found that they could not use serum concentration of the vitamin D metabolite 25-D in a model for seasonal changes in infection.(({{pubmed>long:21677774}}))+  * Shaman //et al.// found that they could not use serum concentration of the vitamin D metabolite 25-D in a model for seasonal changes in infection.(({{pmid>long:21677774}}))
  
  
Line 74: Line 74:
 {{tag>acute_infections Pathogenesis Microbes_in_the_human_body}} {{tag>acute_infections Pathogenesis Microbes_in_the_human_body}}
  
 +<nodisp>
 ===== Notes and comments ===== ===== Notes and comments =====
  
Line 82: Line 83:
  
  * Legacy content  * Legacy content
-  * http://www.marshallprotocol.com/view_topic.php?id=3837&forum_id=32&jump_to=86100#p86100 f170 +  * https://www.marshallprotocol.com/view_topic.php?id=3837&forum_id=32&jump_to=86100#p86100 f170 
   *    * 
  
  
-<blockquote>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.(({{pubmed>long:20660091}}))+<blockquote>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.(({{pmid>long:20660091}}))
  
 </blockquote> </blockquote>
Line 93: Line 94:
 Measles may protect kids against allergies Measles may protect kids against allergies
  
-http://www.reuters.com/article/healthNews/idUSTRE5236HS20090304+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  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 
Line 101: Line 102:
  
  
-(({{pubmed>long:8008534}}))+(({{pmid>long:8008534}}))
  
 Measles makes the cells more susceptible to a secondary infection Measles makes the cells more susceptible to a secondary infection
  
-[[http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=pmd&part=A2876#A2876|Measles Virus-induced Immunosuppression]]+[[https://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=pmd&part=A2876#A2876|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 vitro research has shown that MV infection of cell cultures makes the cells more susceptible to a secondary bacterial invasion (13) " "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 vitro research has shown that MV infection of cell cultures makes the cells more susceptible to a secondary bacterial invasion (13) "
  
 <blockquote>PLoS One. 2009 Dec 31;4(12):e8540. <blockquote>PLoS One. 2009 Dec 31;4(12):e8540.
-Streptococcus pneumoniae coinfection is correlated with the severity of H1N1 pandemic influenza.(({{pubmed>long:20046873}}))+Streptococcus pneumoniae coinfection is correlated with the severity of H1N1 pandemic influenza.(({{pmid>long:20046873}}))
  
  
Line 124: Line 125:
  
  
-===== References =====+===== References =====</nodisp> 
home/pathogenesis/microbiota/acute_infections.txt · Last modified: 09.14.2022 by 127.0.0.1
© 2015, Autoimmunity Research Foundation. All Rights Reserved.