Acute infections

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. 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 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.

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

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

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.

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 vivo 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

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⁾

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.