I found this Sott comment most interesting - relating to the article,
One benefit of a higher internal body temperature is an increased ability to fight off viral infection, and in the first half of the 20th century mainstream medicine acknowledged its benefits and practised it in the form of
pyrotherapy.
From wiki:
Pyrotherapy (
artificial fever) is a method of treatment by raising the
body temperature or sustaining an elevated body temperature using a
fever. In general, the body temperature was maintained at 41 °C (105 °F).
[1] Many diseases were treated by this method in the first half of the 20th century. In general, it was done by exposing the patient to hot baths, warm air, or (electric) blankets. The technique reached its peak of sophistication in the early 20th century with
malariotherapy, in which
Plasmodium vivax, a causative agent of
malaria, was allowed to infect already ill patients in order to produce intense fever for therapeutic ends. The sophistication of this approach lay in using
effective anti-malarial drugs to control the
P. vivax infection, while maintaining the fever it causes to the detriment of other, ongoing, and then-incurable infections present in the patient, such as late-stage
syphilis. This type of pyrotherapy was most famously used by psychiatrist
Julius Wagner-Jauregg, who won the
Nobel Prize for Medicine in 1927 for his elaboration of the procedure in treating neurosyphilitics.
[2]
Wagner-Jauregg’s 1917 treatment method, also known as
malariotherapy, involved the introduction of
Plasmodium vivax malaria via injection into patients with advanced stages of
syphilis.
[2] Advanced syphilitic infection
can invade the brain causing
neurosyphilis, affecting neural performance and function, which can in turn lead to
general paresis of the insane (GPI), a severely debilitating mental disorder. Doing so induced high-grade (103 °F, 39.4 °C or above) fever that was easily sustainable to eradicate
invading spirochaetal bacterium Treponema pallidum, the pathogen responsible for syphilitic infection.
[2][3] Successive rounds of treatment were required to fully eradicate the infectious bacteria, while simultaneously
using quinine to treat the malaria infection.
[2] Management of the fevers was risky as malaria fevers can sometimes cause death, but syphilis was a proliferate and terminal disease at the time with no other viable treatment.
[2] This procedure was used to treat syphilis until
penicillin was found to be a safer, more effective measure in the 1940s.[3]
In 1921, Wagner-Jauregg reported impressive success and many other physicians attempting malaria induced pyrotherapy made similar claims.
[6] Later analyses have shown this might not have been true since approximately 60% would relapse within 2 years and 3–20% have died from the resulting fevers.
[6]
First of all, this shows that quinine was the effective anti-malarial drug of the day and that high-grade fever was effective in eradicating invading spirochaetal bacterium. So I'm thinking of the mRNA injection-producing spike proteins and how some of these create prions (over-simplifying here) that can result in Creutzfeldt-Jakob disease. Here's some more info from a dentistry article:
Viruses are an extremely important component of periodontal disease, both in its initiation and in the ongoing promotion of the attack process. Viruses that initially stem from the mouth also may have much wider systemic impacts.
Several years ago, Jorgen Slots, DDS, PhD, a professor of dentistry at the University of Southern California, reported that herpesviruses [both Epstein-Barr virus type 1 (EBV-1) and human cytomegalovirus (HCMV)] are some of the unrecognized major viruses implicated1 in periodontal attack. Unfortunately, when one transitions from the study of bacteria to consideration of viruses, most dentists cringe, since the profession has the least training in comprehending that submicroscopic world.
Herpesviruses are a leading cause of human viral diseases. There are 9 herpesvirus types known to infect humans: herpes simplex viruses (HSV-1 and HSV-2), varicella-zoster virus (chicken pox and shingles), Epstein-Barr virus (EBV or HHV-4), human cytomegalovirus (HCMV or HHV-5), human herpesvirus (HHV-6A, HHV-6B, and HHV-7), and Kaposi’s sarcoma-associated herpesvirus (KSHV)2.
Ruth F. Itzhaki, PhD, MSc, MA3, demonstrated that the herpes simplex virus type 1 (HSV1), the same virus that causes cold sores in the mouth, is present in the elderly human brain. Once HSV1 infects the epithelial cells of the mucous membranes of the face, it secondarily infects sensory nerve terminals. After it enters the neuron, HSV1 moves to the neuronal cell body in the trigeminal ganglion, located at the base of the skull adjacent to the brain stem.
HSV1 remains in the ganglion in a latent form until reactivation, when the newly synthesized virus is retrograde transported more peripherally4, eventually leading to visible outbreaks such as on the lip. In older subjects, this highly prevalent virus reactivates and enters the brain by way of the peripheral nervous system or the olfactory route5. Though it becomes latent in the brain, it periodically reactivates in association with stressors such as systemic infection and immunosuppression.
Spirochetes, HSV1, Beta Amyloid, and Systemic Diseases
Pathogen-induced inflammation and central nervous system accumulation of beta amyloid (Aβ) (Figure 1) damages the blood-brain barrier, which contributes to the pathophysiology of Alzheimer’s disease (AD)6. Data for both
Chlamydophila pneumoniae and spirochetes7,8 shows a high prevalence of these pathogens in AD brains only, suggesting that secondary
C pneumoniae and/or spirochete infection of the brain may occur after preliminary HSV1 and other co-factors have already initiated AD pathogenesis9.
Figure 3. The icosahedral capsid in the herpes simplex virus resembles the bacteriophage capsid.
Aside:
Bacteriophages inject virus particles into
spirochetes. Viruses also may be involved
Creutzfeldt-
Jakob disease (
CJD) despite its earlier connection with . . .
Bacteriophages inject virus particles into spirochetes. Viruses also may be involved Creutzfeldt-Jakob disease (CJD) despite its earlier connection with prion accumulation. CJD is more commonly known as the human form of "mad cow disease" [bovine spongiform encephalopathy (BSE)]. This devastating degenerative neurological disorder is untreatable and inevitably fatal.
Protect Your Patients and Practice from Prions, Viruses, and Systemic Disease
Review article relating periodontal disease to Alzheimer's disease, diabetes and Creutzfeldt–Jakob disease (CJD)
Since spirochetes can invade all tissues of the body via circulatory pathways10, they may be the instigators of the inflammation that damages the lining of blood vessels and possibly deteriorates the blood brain barrier11. Spirochetes also can take the trigeminal nerve pathway to the brain. Thus, the activation of the already present latent HSV1 by spirochetes in the brain could represent the final step in a series of infections leading to full blown Alzheimer’s disease.
Amyloid plaques, the hallmark of AD, contain fibrillar Aβ (Figure 2). HSV1 has been implicated as a risk factor for AD and found to co-localize within Aβ plaques. Aβ peptides represent anti-infective peptides that protect against neurotropic virus infections such as HSV1 (Figure 3). The Aβ peptide may protect against latent herpes viruses and other infections. This antimicrobial property may explain why Aβ plaque formation plays a pathogenic role in the progression of the sporadic form of AD because it is reacting to an infection12,13.
Very recent research has shown that Aβ plaque in AD is an active biofilm of viable
Borrelia spirochetes in Alzheimer’s disease patients. Alan MacDonald, MD, presented compelling evidence from brain tissue harvested from deceased Alzheimer’s patients. In his 37-minute video14,
Borrelia Chronic Brain Infections and Development of Alzheimer’s Disease, MacDonald used specific DNA marker probes to ascertain the presence of
Borrelia burgdorferi spirochetes (implicated in Lyme disease).
Figure 4. There are key differences between a normal prion and the variant folded-over pathogenic form.
Figure 5. The icosahedral capsid in the bacteriophage resembles the herpes virus capsid.
According to MacDonald, 100% of the samples tested demonstrated that active biofilms of various forms of
Borrelia were enveloped within Aβ. For the first time, MacDonald demonstrated the spore-like role of granular forms of
borrelia as viable, virulent pathogens, distinct from the easily recognized spiral corkscrew shaped forms. He identified round body forms of spirochetes in the evolution of AD. All these forms live within active biofilm communities previously characterized as undefined, dead, brown-appearing lesions called Aβ plaques.
Alzheimer’s, Diabetes, and CJD
Growing evidence is showing that diabetes and AD are concurrent entities. Plaques containing fibrillar Aβ deposits associated with dying cells and inflammatory processes are hallmark pathological features in AD and diabetes15,16. The accumulation of Aβ within islet β-cells is a major pathological feature of the pancreas in patients with chronic diabetes.
[see previous aside]
CJD is characterized by the presence of a deformed protein called a prion. There is controversy as to how the disease progresses. The explanation most commonly accepted is that a defective prion replicates by converting its properly folded counterparts in the host to the same misfolded structure it possesses, or “prion only theory”17.
However, Laura Manuelidis, MD,18 proposed that virus particles cause CJD.19 Manuelidis claimed that although much work remains to be done, there is a reasonable explanation that viral particles cause the transformation of the prion that is the hallmark of CJD.
It is likely that all the various versions of an abnormal prion are the result of infection by an exogenous and stable viral particle and are a consequence of the neurodegenerative disease process rather than its cause. Abnormal prions are present in extremely small amounts in accessible tissues or body fluids such as blood, urine, saliva, and cerebrospinal fluid20,21.
CJD causes tissue to degenerate rapidly. As the disease destroys the brain, holes in the neural structures develop that resemble a sponge in appearance. Viruses incorporating their DNA elements into the host DNA can reprogram the prion protein synthesis mechanism to produce “mutant” prions.
Prion disease epidemics, which have demonstrated unpredictable recurrence, are of significant concern for animal and human health. Furthermore, chronic wasting disease (CWD) is a relatively new and burgeoning prion epidemic in deer, elk, and moose (members of the cervid family) and may be related to the human prion versions22,23.
This perspective on possible links between CJD and viral pathogens causes us to question if other neurologic diseases causing similar brain damage also may by caused by viruses. AD, multiple sclerosis, autism, Parkinson’s disease, amyotrophic lateral sclerosis, and other neurological entities display similar brain damage.
FULL ARTICLE
Ok - so after all of the above -
which really brings alien invasion to mind - I'm wondering if that now outmoded medical treatment of pyrotherapy could be useful for some instances of Covid or even CJD?
Learning is fun - or pattern recognition gone amuck . . .
