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Are there spirochetes in the brain in more than 90 percent of Alzheimer's Disease cases?

Abstract

Alzheimer's disease - a neurospirochetosis

Introduction

Borrelia burgdorferi (Lyme Disease)

Analysis

Causal relationship

Mechanisms

IRON IS BAD NEWS?

Koch's and Hill's postulates

Conclusions

References

Camp Other

Re-evaluation of the AIDS Dogma

The Cost of Alzheimer's

A Commentator wrote:

This is major.

Finally someone is investigating what the Lyme community has known for years. Alzheimer's can be caused by a bacterial infection -- Specifically Chronic Lyme Disease.

[For more on the impact of infection on human aging, see "Microbial Origin of the Gummy Substance of Fujita and Ging"

www.avonhistory.org/bug/gum.htm]

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lymesentinel.blogspot.com/2011/08/alzheimers-disease-neurospirochetosis.html

The Lyme Disease Sentinel Blog

Sunday, August 7, 2011

ALZHEIMER'S DISEASE: A NEUROSPIROCHETOSIS

Is there a direct connection between spirochetes (including the lyme spirochete) and Alzheimer's and or other forms of dementia? There is a huge rise in the cases of Alzheimer's disease and this is not just due to an aging population because Alzheimer's is striking people at much younger ages.

There is also a corresponding exponential rise in the number of cases of Lyme disease. Many people who harbor the Lyme disease spirochete do not even know they are infected. People with healthy immune systems may ward off a symptomatic case of Lyme until aging produces a weakening of the immune system where symptoms then become evident.

In many cases Lyme disease is underdiagnosed and undertreated. It is called The Great Imitator -- like its close cousin Syphilis -- it can mimic many different conditions.

It is imperative that we begin to look for the causes of Alzheimer's and not just treat the symptoms!! Of course there is never much of a profit in a cure or in prevention, which is one of the main reasons that important studies, such as the one below, often are not acted upon.

Let's be wise and realize that researching for the true benefit of others does not have to take anything "good" away from ourselves. We don't have to take away health or money from others in order for us to have what we need personally for a healthy prosperous life. This is a different perspective, an older one that we have been drawn away from -- but it is a better perspective -- and it can work.

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www.jneuroinflammation.com/content/8/1/90/abstract

Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria.

By Judith Miklossy

Correspondence: Judith Miklossy judithmiklossy@bluewin.ch

Journal of Neuroinflammation 2011, 8:90 doi:10.1186/1742-2094-8-90

Journal of Neuroinflammation, 2011 Aug 4;8(1):90.

dx.doi.org/10.1186/1742-2094-8-90

Published: 4 August 2011

Abstract (provisional):

It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis. Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum (syphilis), could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (Alzheimer's Disease).

Here, we review all data available in the literature on the detection of spirochetes in Alzheimer's Disease and critically analyze the association and causal relationship between spirochetes and Alzheimer's Disease following established criteria of Koch and Hill.

The results show a statistically significant association between spirochetes and Alzheimer's Disease ...

When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of Alzheimer's Disease cases.

Borrelia burgdorferi (Lyme Disease) was detected in the brain in 25.3% of Alzheimer's Disease cases analyzed and was 13 times more frequent in Alzheimer's Disease compared to controls.

Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi (Lyme Disease) were detected using species specific PCR and antibodies. Importantly, co-infection with several spirochetes occurs in Alzheimer's Disease.

The pathological and biological hallmarks of Alzheimer's Disease were reproduced in vitro. The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and Alzheimer's Disease.

Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of Alzheimer's Disease a comprehensive entity. As suggested by Hill, once the probability of a causal relationship is established prompt action is needed.

Support and attention should be given to this field of Alzheimer's Disease research. Spirochetal infection occurs years or decades before the manifestation of dementia. As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.

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Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria.

Journal of Neuroinflammation 2011, 8:90 doi:10.1186/1742-2094-8-90

Judith Miklossy (judithmiklossy@bluewin.ch)

ISSN 1742-2094

Article type Review

Submission date 16 May 2011

Acceptance date 4 August 2011

Publication date 4 August 2011

Article URL

www.jneuroinflammation.com/content/8/1/90

This peer-reviewed article was published immediately upon acceptance. It can be downloaded, printed and distributed freely for any purposes ...

Articles in JNI are listed in PubMed and archived at PubMed Central.

This is an open access article distributed under the terms of the Creative Commons Attribution License

creativecommons.org/licenses/by/2.0

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria.

By Judith Miklossy

International Alzheimer Research Center, Prevention Alzheimer Foundation, Martigny-Combe, Switzerland.

Abstract (See above)

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Introduction

The recognition that pathogens can produce slowly progressive chronic diseases has resulted in a new concept of infectious diseases. The pioneering work of Marshall and Warren has established that Helicobacter pylori (H. pylori) causes stomach ulcer [1]. Also the etiologic agent of Whipple's disease was revealed to be another bacterium, Tropheryma whippeli.

Recent reports have documented that infectious agents also occur in atherosclerosis, cardio- and cerebrovascular disorders [2-10], diabetes mellitus [11- 16], chronic lung [17-20] and inflammatory bowel diseases [1, 21-25], and various neurological and neuropsychiatric disorders [26-31].

Nearly a century ago, Fischer, Alzheimer and their colleagues [32, 33] discussed the possibility that microorganisms may play a role in the formation of senile plaques. Historic data indicate that the clinical and pathological hallmarks of syphilitic dementia in the atrophic form of general paresis, caused by chronic spirochetal infection, are similar to those of Alzheimer's Disease.

There is an increasing amount of data that indicates that spirochetes are involved in the pathogenesis of Alzheimer's Disease. This review presents historic and new data related to the involvement of spirochetes in Alzheimer's Disease. The goal was to critically analyze the association and causality between spirochetes and Alzheimer's Disease, based on the substantial amount of data available and on established criteria of Koch [34, 35] and Hill [36]

Pathological hallmarks and pathogenesis of Alzheimer disease

Alzheimer's Disease is the most frequent cause of dementia and is characterized by a slowly progressive decline of cognition and memory. Alzheimer described the characteristic cortical senile plaques and neurofibrillary tangles in the brain of a 51-year-old woman who suffered from presenile dementia [37].

Recently, it was pointed out that the presenile form, with onset before age 65, is identical to the most common form of senile dementia [38, 39]. Therefore today the term Alzheimer's Disease is used for the designation of both presenile and senile cases.

The pathological hallmarks of Alzheimer's Disease are progressive brain atrophy and the accumulation of cortical senile plaques and neurofibrillary tangles. A fibrillary amyloid substance is deposited in senile plaques, formed by the aggregation of the 4.2-kD amyloid beta peptide (amyloid beta peptide).

Amyloid beta peptide is derived by proteolytic cleavage from a transmembrane amyloid beta precursor protein (amyloid beta peptidePP). Neurofibrillary tangles contain paired helical filaments (PHFs), and the major component of PHFs is the microtubule associated protein tau. Granulovacular degeneration is another characteristic alteration of neurons in Alzheimer's Disease.

The origins of amyloid beta peptide deposition, neuronal tangle formation and granulovacuolar degeneration still remain unclear. Various hypotheses were proposed to explain the pathogenesis of Alzheimer's Disease [40, 41].

Mutations in amyloid beta peptidePP, presenilin 1 and presenilin 2 genes are implicated in inherited, early onset Alzheimer's Disease, but the frequency of familial cases is very low [42]. The epsilon 4 allele of apolipoprotein E (ApoE4) was revealed to be a risk factor for Alzheimer's Disease [43].

Polymorphisms of various genes, including numerous inflammatory genes [44] are associated with Alzheimer's Disease. The AlzGene database --

www.alzgene.org

assembles and organizes the increasing number of Alzheimer's Disease related susceptibility genes [45]. It provides a comprehensive, unbiased and regularly updated data on genetic studies performed in Alzheimer's Disease, including meta-analyses for various polymorphisms related to Alzheimer's Disease.

The relationship between the two major biological markers of Alzheimer's Disease -- amyloid beta peptide and hyperphosphorylated tau -- is not clear. That the soluble form of amyloid beta peptide and tau strongly interact [46] and that amyloid beta peptidePP is also expressed in neurofibrillary tangles [47] suggest that these apparently different pathologies are linked in Alzheimer's Disease.

The critical role of chronic inflammation in Alzheimer's Disease is now widely recognized. The important role of neuroinflammation and the importance of IL-1 signaling were first documented by McGeer, Rogers and Griffin [48-50]. Cellular and molecular components of the immune system reactions including the membrane attack complex (MAC, C5b-9) are associated with Alzheimer's Disease cortical lesions [51-54] and non-steroidal anti-inflammatory drugs (NSAIDs) reduce the risk of 55-80% for Alzheimer's Disease [55-57].

The clinical and pathological hallmarks of Alzheimer's Disease are similar to those of the atrophic form of general paresis.

Historic observations show that the clinical and pathological hallmarks of Alzheimer's Disease are similar to those occurring in the atrophic form of general paresis [58, 59]. Noguchi and Moore [60] by showing the presence of T. pallidum (syphilis) in the cerebral cortex of patients with general paresis provided the conclusive evidence that T. pallidum (syphilis) is responsible for slowly progressive dementia, cortical atrophy and local amyloidosis in the atrophic form of this chronic bacterial infection.

This form of general paresis is characterized by a diffuse, predominantly frontotemporal cortical atrophy. The characteristic pathological features comprise severe neuronal loss, reactive microgliosis and astrocytosis. Spirochetes form plaque-like cortical masses or colonies [61, 62]. Pacheco e Silva [61, 62] by analyzing the brains of more than 60 patients with atrophic general paresis reported that the number of spirochetes and spirochetal plaques increased with the severity of cortical atrophy.

The morphology and distribution of T. pallidum (syphilis) colonies are identical to those of senile plaques. Spirochetes are more numerous in the hippocampus and frontal cortex [61, 62] and accumulate without accompanying lymphoplasmocytic infiltrates. Another characteristic feature of the atrophic form of general paresis is the accumulation in the brain of "paralytic iron" [63].

Neurofibrillary tangles and amyloid deposition both occur in dementia paralytica [59, 64-66]. Recent analysis of archival brain material of clinically and pathologically confirmed general paretic cases revealed that the local amyloid deposit in general paresis, as in Alzheimer's Disease, consists of amyloid beta peptide [67].

Association of spirochetes and Alzheimer's disease

That dementia associated with cortical atrophy and microgliosis also occurs in late stages of Lyme disease [68-73] caused by Borrelia burgdorferi (Lyme Disease) (B. burgdorferi), suggested that various types of spirochetes in an analogous way to T. pallidum (syphilis) might cause dementia and brain pathology similar to Alzheimer's Disease.

Various Borrelia and Treponema species from the family Spirochaetaceae are responsible for diverse human diseases. From 36 known Borrelia species 12 cause Lyme disease or other borreliosis, which is transmitted by the bite of infected ticks.

Relapsing fever is caused by nearly 20 species of Borrelia recurrentis and is transmitted by ticks and lice [74, 75]. Near 60 diverse Treponema species were identified in subgingival pockets in human periodontal diseases [76, 77]. These periodontal pathogen spirochetes comprise Treponema denticola, Treponema socranskii, Treponema pectinovorum, Treponema amylovorum, Treponema lecithinolyticum, Treponema maltophilum and Treponema medium.

Treponema vincentii causes necrotizing fusospirochetal disease called Vincent angina. Many other Treponema species are present in the human genital mucosa. From the family Brachyspiraceae, two species of the genus Brachyspira (B.), i.e. B. aalborgi and B. (Serpulina) pilosicoli are responsible for human intestinal spirochetosis [78, 79]. Spirochetes of the genus Leptospira, family Leptospiraceae, cause human leptospirosis.

Detection of all types of spirochetes

To verify the hypothesis that several types of spirochetes may be involved in Alzheimer's Disease, 147 Alzheimer's Disease cases and 37 controls were analyzed using neutral techniques, which recognize all types of spirochetes.

In an initial study, helically shaped microorganisms were observed in 14 Alzheimer's Disease cases in the cerebrospinal fluid (CSF), blood and cerebral cortex [70]. They were isolated from the cerebral cortex, and cultivated from the blood in a modified Noguchi medium, which enables the cultivation of anaerobic spirochetes. They were absent in age-matched controls, which were without any Alzheimer's Disease-type cortical changes [70].

In three Alzheimer's Disease cases, spirochetes were also cultivated from the cerebral cortex in a synthetic Barbour- Stoenner-Kelly II (BSK II) medium [70]. Further scanning electron microscopy and atomic force microscopy analyses defined that these helically shaped microorganisms possess endoflagella and taxonomically belong to the order Spirochaetales [80].

Spirochetes were detected in the brains of 8 Alzheimer's Disease patients derived from another laboratory and in the blood of 5 living patients with Alzheimer's Disease-type dementia [81].

In addition to dark field, atomic force, electron and immune-electron microscopy analyses, immunohistochemical detection of spirochetes was also performed using spirochete and bacterial peptidoglycan (PGN) specific antibodies, and by using the nonspecific DNA marker 4',6-Diamidine-2'-phenylindole dihydrochloride (DAPI) and species-specific DNA as revealed by in situ hybridization (ISH) [70, 80-86].

Peptidoglycan is the building block of the cell wall of virtually all Eubacteria, including spirochetes, however, Mycoplasma and Chlamydia, which lack bacterial cell wall, do not show detectable peptidoglycan [87, 88].

The morphology of helically shaped microorganism detected by spirochete or peptidoglycan specific antibodies is identical [compare Fig. seven G and H of reference 89]. peptidoglycan- immunoreactive helically shaped spirochetes were detected in the brains in 32 definite Alzheimer's Disease cases and in 12 cases with mild or moderate Alzheimer's Disease-type cortical changes [87, 88].

Spirochetes were observed in senile plaques, neurofibrillary tangles, curly fibers and in the wall of cortical or leptomeningeal arteries exhibiting amyloid deposits [70, 80-82]. Spirochete and peptidoglycan specific antigens were co-localized with amyloid beta peptide [83, 85].

Control brains without Alzheimer's Disease-type cortical changes were negative [70, 83-85]. These observations have suggested that various types of spirochetes of the order Spirochaetales, might cause dementia and contribute to the pathogenesis of Alzheimer's Disease.

McLaughlin et al., [90] did not find spirochetes by dark field and electron microscopy in the brains of 7 Alzheimer's Disease cases tested. They observed spirochetes in the blood in one of 22 clinically diagnosed Alzheimer's Disease patients (Table 1). The spirochete illustrated by the authors corresponds to a regularly spiral vegetative form.

It is not clear, whether the atypical, pleomorphic spirochete forms, which are common in blood and in infected tissues [89, 91-93] were considered or not in this study. The authors have suggested that the spirochete observed could correspond to oral Treponema.

In all these studies, which detected spirochetes using neutral techniques, 680 brain and blood samples were analyzed. In Alzheimer's Disease, more than 91.1% (451/495) of the samples were positive, while the 185 control samples were all negative.

Periodontal pathogen spirochetes

Oral anaerobic Treponema (T) spirochetes are predominant periodontal pathogens, which are highly prevalent in the population. Several of them revealed to be invasive in vivo and in vitro [94, 95]. Six different periodontal pathogen spirochetes, specifically, T. denticola, T. pectinovorum, T. vincenti, T. amylovorum, T. maltophilum, T. medium and T. socranskii were detected in the brains of Alzheimer's Disease patients using species specific PCR.

At least one oral Treponema species was detected in 14 of 16 Alzheimer's Disease cases, and in 4 of 18 controls [96]. Species-specific antigens of T. pectinovorum and T. socranskii were observed in 15 Alzheimer's Disease and in 7 controls (P<0.001).

Six different Treponema species were detected in the brain in one Alzheimer's Disease patient, five species in four, four or three species each in one, and one species in seven Alzheimer's Disease cases. Of the four controls with Treponema spirochetes, one had two Treponema species and three one species each.

The number of diverse Treponema species was significantly higher in the brains of Alzheimer's Disease patients compared to controls [96]. Treponema antigens were detected both in the hippocampus and frontal cortex. These important results, as proposed earlier [70, 80-82], indicate that periodontal pathogen spirochetes in an identical way to T. pallidum (syphilis) have the ability to invade the brain, persist in the brain and cause dementia. They also indicate that co- infection by several spirochetes occurs in Alzheimer's Disease. These findings are in agreement with recent observations showing an association between periodontal diseases and Alzheimer's Disease [97].

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Borrelia burgdorferi (Lyme Disease)

B. burgdorferi (Lyme Disease) was first cultivated from the brain in two Alzheimer's Disease patients by MacDoald and Miranda [98] and MacDonald [99] and in 3 definite Alzheimer's Disease cases by Miklossy [85] (Table 1). Extensive characterization of the cultivated spirochetes confirmed, that the morphological, histochemical and immunohistochemical properties of these spirochetes are identical to those of B. burgdorferi (Lyme Disease) [85-86].

Electron microscopic analysis demonstrated that they possess 10-15 endoflagella representative of B. burgdorferi (Lyme Disease) species. 16S rRNA gene sequence analysis definitely identified the cultivated spirochetes as B. burgdorferi (Lyme Disease) sensu stricto (s. s.) [85]. In two of these Alzheimer's Disease cases post mortem serological analyses of blood and cerebrospinal fluid (CSF) have revealed a positive serology for B. burgdorferi (Lyme Disease) fulfilling the diagnostic criteria of the Center for Disease Control (CDC).

B. burgdorferi (Lyme Disease) specific antigens and genes were detected in the brains of these three Alzheimer's Disease patients where B. burgdorferi (Lyme Disease) was cultivated. Neurofibrillary tangles were also immunoreactive with specific anti-B. burgdorferi (Lyme Disease) antibodies and Borrelia antigens were co-localized with amyloid beta peptide.

Using in situ hybridization (ISH) B. burgdorferi (Lyme Disease) specific OspA and flagellin genes were detected in senile plaques and in a number of neurofibrillary tangles [85].

Importantly, the cortical distribution of spirochete masses or colonies was identical to that of senile plaques. The pathological changes observed in the brain were similar to those occurring in the atrophic form of general paresis and in Alzheimer's Disease.

B. burgdorferi (Lyme Disease) specific antigens were observed in the brain in an additional Alzheimer's Disease patient with concurrent Lyme neuroborreliosis [70]. Using species-specific PCR, B. burgdorferi (Lyme Disease) DNA was detected in the brains in 5 of 16 Alzheimer's Disease patients and in one of 18 controls [96]. In these 6 positive cases (5 Alzheimer's Disease and 1 control) B. burgdorferi (Lyme Disease) co-infected with oral Treponema spirochetes.

B. burgdorferi (Lyme Disease) specific DNA was detected by PCR in the brain of an additional patient with concurrent Alzheimer's Disease and Lyme neuroborreliosis [100] and in the hippocampus in 7 of 10 pathologically confirmed definite Alzheimer's Disease cases using PCR or ISH [101, 102] (Table 1).

Pappolla et al., [103] ... concluded that the possibility of a different spirochete in Alzheimer's Disease not detectable by their methods could not be excluded, indicating that they clearly considered the possibility that several types of spirochetes may be involved in Alzheimer's Disease.

Indeed, the goal of initial studies was not to show the involvement of B. burgdorferi (Lyme Disease) alone in Alzheimer's Disease but that of the involvement of various types of spirochetes of the order Spirochaetales, including B. burgdorferi (Lyme Disease), oral, intestinal and other, yet uncharacterized spirochetes [70, 80-84, 86].

The title of the initial report, "Alzheimer's disease - A spirochetosis?", clearly indicates this goal [70] ...

The frequency ... of positive blood serology for B. burgdorferi (Lyme Disease) is about 8 times higher in Alzheimer's Disease ...

This is in harmony with the findings that in a statistically significant proportion of the Alzheimer's Disease population analyzed (25.3 %) B. burgdorferi (Lyme Disease) was detected in the brain.

It is also noticeable that in all those studies, which show the involvement of B. burgdorferi (Lyme Disease) in Alzheimer's Disease, the patients had a positive serology for B. burgdorferi (Lyme Disease) and/or this spirochete was cultivated from the brain in BSK medium [70, 85, 98, 99] or species-specific DNA was detected in the brain [96] indicating that these Alzheimer's Disease patients suffered from Lyme neuroborreliosis ...

In future studies, to consider that several types of spirochetes can co-infect in Alzheimer's Disease [96] and that spirochetes frequently exhibit pleomorphism in host tissues [89] is also essential. In view of an infectious origin of Alzheimer's Disease the use of appropriate healthy control population without Alzheimer's Disease-type cortical changes and without other neuro-psychiatric disorders is also essential.

Taken together, these observations derived from various laboratories show that several types of spirochetes can infect the brain in Alzheimer's Disease and co-infection with several types of spirochetes occurs. As expected, the frequency of periodontal pathogen spirochetes is higher compared to that of B. burgdorferi (Lyme Disease) ...

The significantly higher frequency of B. burgdorferi (Lyme Disease) in the brain of Alzheimer's Disease patients, the high risk factor and the results of the multifaceted analysis in three Alzheimer's Disease patients with concurrent Lyme neuroborreliosis, where B. burgdorferi (Lyme Disease) was cultivated from the brain and species specific antigens and DNA were present in the cerebral cortex show that B. burgdorferi (Lyme Disease) is involved in the pathogenesis of a subset of Alzheimer's Disease cases [85].

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Analysis of the association of spirochetes and Alzheimer's Disease

Based on the substantial data available in the literature, contingency tables were used to analyze the strength of the association between spirochetes and Alzheimer's Disease. Fisher test was used to assess whether the difference between the occurrence of spirochetes in Alzheimer's Disease and controls is statistically significant. Odds ratio (OR) and 95% confidence interval (CI) values were also computed.

If in the control group the number of positive cases was 0 in order to calculate odds ratio and 95% confidence interval 1 positive control case was added (Table 1).

In those studies where all types of spirochetes were detected employing neutral techniques (Table 1, Fig. 1), spirochetes were observed in the brain in 90.1% (64/71) of Alzheimer's Disease cases and were absent in controls without any Alzheimer's Disease-type changes (Table 1). The difference was significant (P = 4.8. x 10 -18 ; odds ratio = 274, 95% confidence interval = 32-11345, Number = 102).

When cases with mild or moderate Alzheimer's Disease-type changes were also included as preclinical stages of Alzheimer's Disease, 91.5 % of the cases (76/83) were positive (P = 1 x 10 -19 ; odds ratio = 325, 95% confidence interval = 38-13440, Number = 114).

The difference remains significant when those cases were also included where spirochetes were analyzed in the blood (P = 1.1 x 10 -15 , odds ratio = 105, 95% confidence interval = 13-4329).

The association between periodontal pathogen spirochetes and Alzheimer's Disease was statistically significant as well (Table 1, Fig. 2). They were detected in the brain in 93.7% of Alzheimer's Disease and in 33.3% of control cases (P = 3.6 x 10 -4 ; odds ratio = 30; 95% confidence interval = 2.8-1364; Number = 34).

B. burgdorferi (Lyme Disease) (Table 1, Fig. 1) was observed 13 times more frequently in the brain in Alzheimer's Disease (19/75, 25.3%) compared to controls (1/52, 1.9%) (P = 2.9 x 10 -4 , odds ratio = 17; 95% confidence interval: 2 732; Number = 127).

The low prevalence of Lyme disease compared to Alzheimer's Disease is well reflected by the lower frequency (25.3%) of B. burgdorferi (Lyme Disease) compared to the higher, more than 90% frequency of all types of spirochetes detected with neutral techniques or the highly prevalent periodontal pathogen spirochetes.

When considering all studies (Table 1, Fig. 1) detecting all types of spirochetes and their specific species, their frequency was 8 times higher in the brain in Alzheimer's Disease (90/131 = 68.7%) compared to controls (6/71 = 8.45 %). The difference is statistically significant (P = 1.7 x 10 -17 ; odds ratio = 23; 95% confidence interval = 9-71, Number = 202).

The association remains strongly significant when the 12 cases with mild Alzheimer's Disease-type changes (P = 1.5 x 10 -19 , odds ratio = 26, 95% confidence interval = 10-80, Number = 214) or those cases where spirochetes were analyzed in the blood were also included (P = 1.5 x 10 -17, odds ratio = 20, 95% confidence interval = 8-60, Number = 247).

If considering errors, which may arise from those studies where the detection of spirochetes was restricted to B. burgdorferi (Lyme Disease) alone, without considering other spirochetes, the percentage of spirochetes in Alzheimer's Disease would be even higher than 68.7%. This is supported by the high percentage of spirochetes in studies where all types of spirochetes were detected using neutral techniques (90.1%) or where the highly prevalent periodontal pathogen spirochetes were analyzed (93.7%).

Taken together, these results show a strong, statistically significant association between spirochetes and Alzheimer's Disease and show that these microorganisms represent a strong risk for Alzheimer's Disease.

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Further experimental evidence for a causal relationship between spirochetes and Alzheimer's Disease

Additional studies have brought further evidence in support of a probable causal relationship between spirochetes and Alzheimer's Disease. For these experimental studies B. burgdorferi (Lyme Disease) was employed, as this spirochete can be cultivated in synthetic medium and maintained in pure culture.

When primary neuronal and glial cells and brain cell aggregates were exposed to B. burgdorferi (Lyme Disease) sensu stricto spirochetes (B. burgdorferi strain B31 and strains Alzheimer's DiseaseB1 and Alzheimer's DiseaseB2 cultivated from the brains of Alzheimer's Disease patients), Thioflavin S positive and amyloid beta peptide- immunoreactive "plaques" as well as tangle- and granular lesions similar to granulovacuolar degeneration were induced [107].

Spirochete induced amyloid beta peptide accumulation was identified by Western blot and the β-pleated sheet conformation of the amyloid in spirochete-induced plaques was detected in situ using Synchrotron InfraRed MicroSpectroscopy (SIRMS).

Borrelia induced tau phosphorylation and increased amyloid beta peptidePP levels represented additional experimental evidences that spirochetes are able to induce an Alzheimer's Disease-type host reaction [107].

Both, reference Borrelia spirochetes (B31) and those cultivated from the brains of Alzheimer's Disease patients (Alzheimer's DiseaseB1 and Alzheimer's DiseaseB2 strains) invaded neurons and glial cells and induced nuclear fragmentation, indicating that these spirochetes are invasive [89, 107].

They were located extra- and intracellularly. Their intracellular location indicates that they can be protected from destruction by the host immune reactions [70, 89, 107]. These results show that in an analogous way to T. pallidum (syphilis) they can persist in the brain and cause dementia, cortical atrophy and the pathological hallmarks of Alzheimer's Disease.

It is noteworthy that spirochetes frequently co-infect with other bacteria and viruses. Co-infection of T. pallidum (syphilis) with other bacteria, various Herpes viruses and Candida albicans was frequently observed in syphilis [91].

In Lyme disease, in addition to various co-infections transmitted by tick-bite (e.g. bartonellosis, ricketttsiosis, babesiosis etc.) B. burgdorferi (Lyme Disease) frequently co-infects with other pathogens, which are independent of the tick-bite, e.g. Clamydophyla pneumoniae (C. pneumonia) [108] and Herpes viruses [108-111].

Co-infection of spirochetes with C. pneumonia also occurs in a Lyme-like tick-borne disease in Brazil [112]. Intriguingly, C. pneumoniae [113, 114] and Herpes simplex type 1 (HSV-1) [115, 116] were also detected in the brain in Alzheimer's Disease, suggesting that similarly to Lyme disease and syphilis, concurrent infection with several pathogens may frequently occur in Alzheimer's Disease as well.

C. pneumoniae, H. pylori, periodontal pathogens, including T. denticola and Herpes viruses are also linked to atherosclerosis [2, 3, 7], cardiovascular disorders [4, 6, 117] and diabetes mellitus [16, 118-119], which indicate that these infectious agents, via hematogenous dissemination, may reach and infect various organs distant from the site of the primary infection.

In agreement with this view, epidemiological studies revealed a close association between periodontal diseases and these chronic disorders [120].

It is noteworthy that Alzheimer's Disease is not only associated with these chronic inflammatory disorders but with chronic periodontal disorders as well [121].

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Mechanisms involved in spirochete-host interaction and their similarities to Alzheimer's Disease

The strong neurotropism of spirochetes is well known. Spirochetes can invade the brain and generate latent, persistent infection [29, 63, 65]. In addition to hematogenous dissemination, they can spread via the lymphatics and along nerve fiber tracts [63, 91].

Accordingly, periodontal invasive spirochetes were detected along the trigeminal nerve and in trigeminal ganglia [96]. They might also propagate along the fila olfactoria and tractus olfactorius, which would be in harmony with the olfactory hypothesis [122- 124] and with previous observations showing that the olfactory tract and bulb are affected in the earliest stages of the degenerative process in Alzheimer's Disease [125].

Spirochetes attach to host cells through their surface components, including collagen-binding proteins, bacterial amyloids and pore forming proteins [126-131].

Through activation of plasminogen and factor XII, bacterial amyloids contribute to inflammation and modulate blood coagulation [132].

The innate immune system enables host cells to recognize spirochetes, execute proinflammatory defenses, and start adaptive immune responses. Pattern recognition receptors, located on the cell membrane of various cells, particularly on phagocytes and microglia recognize unique structures of spirochetes. The largest family of pattern recognition receptors is that of Toll-like receptors (Toll-like receptors).

Toll-like receptors are also present in the brain [133]. Macrophages and microglia activated through Toll-like receptor signaling secrete chemokines and cytokines and express various proinflammatory molecules for the removal of pathogens and affected cells.

Spirochetes and their surface lipoproteins activate Toll-like receptor signaling through CD14 [134-135]. As an example, tri- or di- acylated lipoproteins of B. burgdorferi (Lyme Disease) bind to lipopolysaccharide binding protein (LBP), which activates Toll-like receptor signaling through CD14 [136].

It is noteworthy, that in addition to spirochetal antigens and DNA, D-amino acids and bacterial peptidoglycan, two natural constituents of Prokaryotic cell wall unique to bacteria, were also detected in the brain in Alzheimer's Disease [83, 84, 137, 138].

Pattern recognition receptors are upregulated in the brain in Alzheimer's Disease, and Toll-like receptor2 and Toll-like receptor4 gene polymorphisms influence the pathology of Alzheimer's Disease [139, 140]. Activation of microglia with Toll-like receptors 2, 4 and 9 ligands markedly increases amyloid beta peptide ingestion in vitro [141].

Finally, stimulation of the immune system through Toll-like receptor9 in amyloid beta peptidePP (Tg2576) transgenic mice results in reduction of amyloid beta peptide deposits [142].

Once microorganisms are recognized, the activation of the innate immune system induces phagocytosis and bacteriolysis through the formation of the membrane attack complex (MAC, C5b9) [143-145] and promotes inflammatory responses.

Activation of the clotting cascade generates bradykinin, which increases vascular permeability. Spirochetes activate both the classic and alternative pathways and induce acute phase proteins.

Serum amyloid A (SAA) and C Reactive Protein (CRP) levels are elevated in T. pallidum (syphilis) and B. burgdorferi (Lyme Disease) infections [146, 147]. Through their ability to induce the production of tumor necrosis factor (TNF) by macrophages, spirochete lipoproteins play an important role in systemic and local inflammatory changes that characterize spirochetal infections [148].

In Alzheimer's disease, activated microglia that are designed to clean up bacteria and cellular debris surround senile plaques and extracellular neurofibrillary tangles [53].

Both the cellular and humoral components of the immune system reactions [48-53] and critical constituents of the classical and alternative complement pathways are associated with Alzheimer's Disease lesions [51, 52, 149].

Spirochetes are able to evade host defense mechanisms and establish latent and slowly progressive chronic infection. They employ a broad range of strategies to overcome antigenic recognition, phagocytosis and complement lysis.

Blockade of the complement cascade allows their survival and proliferation even in immune competent hosts. Complement resistant strains of B. burgdorferi (Lyme Disease) possess five Complement Regulatory Acquiring Surface Proteins (CRASPS), which bind to factor H (FH) and factor-H like protein-1 (factor-HL-1) of the alternative pathway [145, 150].

Binding to the surface of spirochetes host factor-H and factor-HL-1 promotes the formation of inactive iC3b from C3b preventing MAC lysis. B. burgdorferi (Lyme Disease) spirochetes possess a CD59-like complement inhibitory molecule as well [151], which by interacting with C8 and C9, inhibits binding of the opsonizing components C4b and C3b to MAC and consequently, prevents bacteriolysis [150].

Impaired complement lysis was also observed in T. pallidum (syphilis) infection [143].

B. burgdorferi (Lyme Disease) protects itself from destruction by the host adaptive immune system as well. It induces interleukin-12 (IL-12), a cytokine critical for driving cellular responses toward Th1 subset [152-154]. This shift retards antibody production by Th2 cells against the spirochete.

Intracellular survival of spirochetes also confers protection against destruction by the host defense reactions. Evasion of spirochetes will result in their survival and proliferation in the brain. Their accumulation in the cerebral cortex will lead to the formation of senile plaques, tangles and granulovacuolar-like degeneration as shown by historic observations in syphilis [61, 62] and by current observations and in vitro experiments reviewed here ...

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[IRON IS BAD NEWS?]

Accumulation in the brain of "paralytic iron" is characteristic in general paresis [59]. Free iron abolishes the bactericidal effects of serum and strongly enhances bacterial virulence [155-157]. It is necessary for bacterial growth and plays a pivotal role in infection and inflammation [155-157].

Iron increases the formation of reactive oxygen intermediates causing lipid peroxidation and subsequent oxidative damage of proteins and nucleic acids [155-157]. Iron, also accumulates in the brain in Alzheimer's Disease [155, 158-160].

The production of reactive oxygen and nitrogen intermediates by innate immune cells is an effective host-defense mechanism against microbial pathogens. Activation of macrophages and other host cells by bacteria or LPS, including spirochetes and their lipoproteins generates substantial amount of nitric oxide (NO) [157], which is critical in bacterial clearance [161].

Nitric oxide also plays a central role in Alzheimer's Disease [162].

Chronic bacterial infections (e.g. rheumatoid arthritis, leprosy, tuberculosis, syphilis, osteomyelitis) are frequently associated with amyloid deposition. Based on previous observations we have suggested that amyloidogenic proteins might be an integral part of spirochetes and could contribute to amyloid beta peptide deposition in Alzheimer's Disease [70].

Recent observations indeed showed that the BH (9-10) peptide of a beta-hairpin segment of B. burgdorferi (Lyme Disease) outer surface protein A (OspA) forms amyloid fibrils in vitro, similar to human amyloidosis [163, 164].

Recent observations also show that amyloid proteins constitute a previously overlooked integral part of the cellular envelope of many bacteria [163-168].

Bacterial amyloids have important biological functions and contribute to bacterial virulence and invasion of host cells [165, 166]. Genetic mutations occurring in Alzheimer's Disease (amyloid beta peptidePP, Presenilin 1 and 2) are related to the processing of amyloid beta peptidePP and result in increased production of Aβ 1-42 and Aβ 1-43 [169].

Amyloid beta peptidePP revealed to be a proteoglycan core protein [170] and is involved in the regulation of immune system responses and in T cell differentiation [171-173].

Recent observations showed that amyloid beta peptide is an innate immune molecule and belongs to the family of antimicrobial peptides AMPs [174], which are involved in innate immune responses. Consequently, genetic defects in amyloid beta peptidePP, PS-I and PS-II should be associated with an increased susceptibility to infection.

ApoE4, an important risk factor for Alzheimer's Disease, is also risk factor for infection and enhances increased expression of inflammatory mediators [175, 176].

Promoter polymorphisms in pro-inflammatory cytokine genes facilitate infections [177]. TNF-α plays a critical role in host defenses against infection [178, 179]. The influence of TNF-α on T. pallidum (syphilis) and B. burgdorferi (Lyme Disease) infections has been repeatedly reported [153, 180].

Human Leukocyte Antigen (HLA) gene polymorphism is a dominant marker of susceptibility to infection, including B. burgdorferi (Lyme Disease) infection [181]. TNF-α and HLA polymorphisms, which are risk factors for infection, substantially influence the risk of Alzheimer's Disease as well [182-184].

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Analysis of causal relationship between spirochetes and Alzheimer's Disease following Koch's and Hill's postulates

Koch's postulates were proposed to establish causal relationship between pathogens and specific diseases [34]. Following Koch's postulates I and II, the microorganism should be isolated from the affected tissue and grown in pure culture. Regarding Koch's postulates III and IV, the cultured microorganism should cause disease when introduced into a healthy host and must be re-isolated and identified as being identical to the original causative agent.

Spirochetes were cultivated from the brains of Alzheimer's Disease patients in a modified Noguchi medium and maintained in culture for about 1 month [70]. B. burgdorferi (Lyme Disease) was cultivated from the brains of 5 out of 8 Alzheimer's Disease patients who suffered from Lyme neuroborreliosis and was maintained and propagated in pure culture [70, 85, 89], which fulfills Koch's postulates I and II.

With respect to Koch's postulates III and IV the defining pathological and biological hallmarks of Alzheimer's Disease were reproduced in vitro not only in primary mammalian neuronal and glial cell cultures but in central nervous system organotypic cultures as well, which aim to replace in vivo studies [107].

B. burgdorferi (Lyme Disease) (strains B31, Alzheimer's DiseaseB1, Alzheimer's DiseaseB2) was also recovered in pure culture from infected cell cultures [89].

In vivo studies might bring further evidence with respect to Koch's postulates III and IV. Following Koch's postulates the causal relationship between B. burgdorferi (Lyme Disease) and dementia is much stronger, than in the case of T. pallidum (syphilis), which is known to cause dementia, but cannot be cultivated in pure culture.

Koch himself acknowledged that the application of his postulates to establish causality is sometimes difficult and suggested that his criteria should be used as guidelines [35]. Indeed, like T. pallidum (syphilis), several other bacteria and viruses cannot be grown in pure culture and based on his criteria to establish causality in chronic disorders is limited.

In order to address this question, new criteria were proposed by Hill [36]. A previous review [185], on the analysis of association of infectious agent with Alzheimer's Disease following Hill's criteria concluded that the "treatment of chronic infection may become an important part of Alzheimer's Disease prevention and therapy".

With respect to spirochetes only part of the historical and new data were included in this study. Therefore, based on the substantial data available on the detection of spirochetes in Alzheimer's Disease, we analyzed the probability of a causal relationship following Hill's nine criteria [36]:

1. Strength of the association

In agreement with Honjo et al. [185], the statistical analysis shows a significant association between spirochetes and Alzheimer's Disease (Table 1).

2. Consistency of the association

Following Hill, the consistency of the association demands whether the results were "repeatedly observed by different persons, in different places, circumstances and times? ".

In 14 studies [70, 80-85, 90, 96, 98-102] spirochetes were detected in Alzheimer's Disease. Various authors in diverse laboratories, in different countries, using different techniques have detected spirochetes in Alzheimer's Disease, fulfilling Hill's claim for the consistency of association.

In three studies [103-105], which failed to show the involvement of B. burgdorferi (Lyme Disease) in Alzheimer's Disease, evidence is lacking whether the Alzheimer's Disease patients had a positive serology for B. burgdorferi (Lyme Disease), as for this goal, the analysis of Alzheimer's Disease populations suffering from Lyme neuroborreliosis would be essential.

As mentioned by Pappolla et al. [103], the possibility of the involvement of other spirochetes in Alzheimer's Disease cannot be excluded.

In another study on the analysis of sero-prevalence of B. burgdorferi (Lyme Disease) in Alzheimer's Disease, due to the low incidence of Lyme dementia compared to Alzheimer's Disease can explain the negative result [106].

3, Specificity of the association

Spirochetes and spirochete specific antigens and DNA associated with lesions defining Alzheimer's Disease indicate the specificity of the association.

4. Temporality of the association

The temporal relationship of the association, is "... a question which might be particularly relevant with diseases of slow development... Have they already contracted it before?"

T. pallidum (syphilis) infection in the atrophic form of general paresis is a historical example of temporal relationship between spirochetal infection and slowly progressive dementia [29, 63, 65].

Spirochetes were detected in Alzheimer's Disease patients with early stages of plaque-, tangle- and curly fiber-formation [83, 84] indicating that infection takes place long before the diagnosis of dementia is made [70].

5. Biological gradient of the association

That spirochetes are able to form plaque-, tangle- and curly fiber-like lesions [70, 85, 107] and their number progressively increases in the brains of patients with mild, moderate [83, 84], and severe Alzheimer's Disease-type changes [70, 80-87] fulfill this condition.

6. Plausibility of the association

T. pallidum (syphilis) in the atrophic form of general paresis causes dementia, brain atrophy and amyloid beta peptide deposition similar to the pathological and biological hallmarks of Alzheimer's Disease [61, 62, 67, 85].

That Alzheimer's Disease-type pathological changes were also induced in vitro by B. burgdorferi (Lyme Disease) and were observed in the brains of patients with concurrent Alzheimer's Disease and Lyme neuroborreliosis indicate that chronic spirochetal infection can cause dementia.

7. Coherence of the association

As proposed by Hill, the cause-and-effect interpretation of the data should not seriously conflict with the generally known facts of the natural history and biology of the disease [36]. That a slow acting unconventional infectious agent acquired at an early age and requiring decades to become active may be involved in Alzheimer's Disease was never discarded [186, 187].

Fischer, Alzheimer and their colleagues discussed the possibility that microorganisms may play a role in the formation of senile plaques and described similarities in the clinical and/or pathological manifestations of Alzheimer disease and general paresis [32, 33, 58, 59, 67, 86].

Chronic spirochetal infection can cause slowly progressive dementia, cortical atrophy, chronic inflammation and amyloid beta peptide deposition, which are indistinguishable from those occurring in Alzheimer's Disease [29, 61, 62, 67, 85, 86].

Spirochete-host interactions result in various immune responses, free radicals, apoptosis and amyloid deposition, which are typical of Alzheimer's Disease [86]. The genetic defects occurring in Alzheimer's Disease can facilitate infection as well [for a review see 86].

Spirochetal infections cause cerebral hypoperfusion [188-190], cerebrovascular lesions and severely disturbed cortical capillary network [29, 191, 192], which are also important factors in the pathogenesis of Alzheimer's Disease [193-199].

As in Alzheimer's Disease, mixed forms of dementia due to cortical atrophy and vascular lesions frequently occur in neurospirochetoses [29, 63], further strengthening the coherence of the association.

All these observations indicate that, the association is in harmony with the natural history and biology of Alzheimer's Disease.

8. Experimental evidences

Following exposure of primary mammalian neuronal and glial cells and brain organotypic cultures to spirochetes, lesions similar to the defining pathological and biological hallmarks of Alzheimer's Disease were produced [107] representing experimental evidence in favor of a causal relationship between Alzheimer's Disease and spirochetes.

These experimental data [107, 89] indicate that as observed in syphilis [29, 61, 62] and Lyme neuroborreliosis [85, 89], the evasion of spirochetes can result in their survival and proliferation and the production of lesions similar to senile plaques, tangles and granulovacuolar-degenerations (Fig. 3).

Additional experimental data include transmission of amyloid beta peptide amyloidosis to experimental animals [200-203], the observations showing the immune regulatory function of APP [171-173], the antimicrobial properties of amyloid beta peptide [174] and the improvement in symptoms of Alzheimer's Disease patients following antibiotic treatment [204-208]. ...

9. Analogy of the association

The analogy of clinical and pathological hallmarks of Alzheimer's Disease to those of the atrophic form of general paresis and Lyme neuroborreliosis as revealed by historic observations and based on retrospective studies meets this condition [29, 33, 61, 62, 67, 85, 86].

Taken together, the analysis of historic and recent data available in the literature following Koch's and Hill's criteria is in favor of a causal relationship between neurospirochetosis and Alzheimer's Disease.

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Conclusions

Various types of spirochetes, including B. burgdorferi (Lyme Disease), and six periodontal pathogen spirochetes (T. socranskii, T. pectinovorum, T. denticola, T. medium, T. amylovorum and T. maltophilum) were detected in the brains of Alzheimer's Disease patients.

The pathological and biological hallmarks of Alzheimer's Disease, including increased amyloid beta peptidePP level, amyloid beta peptide deposition and tau phosphorylation were induced by spirochetes in vitro.

The statistical analysis showed a significant association between spirochetes and Alzheimer's Disease. The strongly significant association, the high risk factor and the analysis of data following Koch's and Hill's criteria, are indicative of a causal relationship between neurospirochetoses and Alzheimer's Disease.

Spirochetes are able to escape destruction by the host immune reactions and establish chronic infection and sustained inflammation.

In vivo studies with long exposure times will be necessary to efficiently study the sequence of events and the cellular mechanisms involved in spirochete induced Alzheimer's Disease-type host reactions and amyloid beta peptide- plaque, "tangle" and "granulovacuolar" formation.

The characterization of all types of spirochetes and co-infecting bacteria and viruses is needed, in order to develop serological tests for the early detection of infection.

The pathological process is thought to begin long before the diagnosis of dementia is made therefore, an appropriate targeted treatment should start early in order to prevent dementia.

Persisting spirochetal infection and their persisting toxic components can initiate and sustain chronic inflammatory processes through the activation of the innate and adaptive immune system involving various signaling pathways.

In the affected brain the pathogens and their toxic components can be observed, along with host immunological responses. The response itself is characteristic of chronic inflammatory processes associated with the site of tissue damage.

The outcome of infection is determined by the genetic predisposition of the patient, by the virulence and biology of the infecting agent and by various environmental factors, such as exercise, stress and nutrition.

The accumulated knowledge, the various views, and hypotheses proposed to explain the pathogenesis of Alzheimer's Disease form together a comprehensive entity when observed in the light of a persisting chronic inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection.

As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Similarly to syphilis, one may prevent and eradicate dementia in Alzheimer's Disease. The impact on healthcare costs and on the suffering of the patients would be substantial ...

Acknowledgements ...

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campother.blogspot.com/2011/08/paper-alzheimers-disease.html

Tuesday, August 9, 2011

Paper: Alzheimer's disease - a neurospirochetosis.

Camp Other wrote:

Miklossy has recently published a work on a probable causal relationship with infection with spirochetes in the brain and Alzheimer's disease which has many people talking ...

Comments:

These are my preliminary comments ...

This paper is one in a long line of research by Dr. Miklossy on the relationship between infection and Alzheimer's disease ...

I realize that a number of Lyme disease patients - especially those with persisting neurological symptoms - are probably reading the abstract and feeling somewhat nervous about their future potential for developing Alzheimer's disease ...

Once Miklossy outlined the statistical analysis of the studies and the correlation between the presence of pathogens in the brain and Alzheimer's disease, she continued with an outline of how the pathogenesis of spirochetal infection leads to the development of specific immunological responses and reactions within the brain. This part is the most difficult to summarize, but the intention is to show how similar the unfolding pathogenesis of spirochetal brain infections is to the development of Alzheimer's disease.

Later on, Miklossy shows how to apply Koch's Postulates and Hill's Postulates to the studies conducted, though there isn't a full cycle of re-infection or true xenodiagnosis done from the samples extracted. This is something I would like to see in a new study.

The notable part of the conclusion, for me, is this part:

"Spirochetes are able to escape destruction by the host immune reactions and establish chronic infection and sustained inflammation. In vivo studies with long exposure times will be necessary to efficiently study the sequence of events and the cellular mechanisms involved in spirochete induced Alzheimer's Disease-type host reactions and amyloid beta peptide-plaque, 'tangle' and 'granulovacuolar' formation.

The characterization of all types of spirochetes and co-infecting bacteria and viruses is needed, in order to develop serological tests for the early detection of infection. The pathological process is thought to begin long before the diagnosis of dementia is made therefore, an appropriate targeted treatment should start early in order to prevent dementia."

The basic message to take from this paper if you are a Lyme disease patient is that last sentence there:

"The pathological process is thought to begin long before the diagnosis of dementia is made. Therefore, an appropriate targeted treatment should start early in order to prevent dementia."

Regardless of the significance of the findings, early diagnosis and treatment of tickborne infections is paramount to reduce the risk of future problems. Something we all already knew.

My general thought about this meta-analysis is that more studies are needed and a larger collection of samples taken from Alzheimer disease patients need to be analyzed using similar means and methods. I think there is more that needs to be known about the relationship between any pathogenic invasion and the development of Alzheimer's disease.

Posted by Camp Other on Tuesday, August 09, 2011

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www1.biogema.de/WEK/312-Margulis-final.pdf

Google automatically generates html versions of documents as we crawl the web.

[A Call for a Re-evaluation of the AIDS Dogma]

SYMBIOSIS (2009) 47, 51 - 58

©2009 Balaban, Philadelphia/Rehovot

ISSN 0334-5114

Position paper.

Spirochete round bodies

Syphilis, Lyme disease & AIDS: Resurgence of "the great imitator"?

Lynn Margulis1*, Andrew Maniotis2, James MacAllister1, John Scythes3, Oystein Brorson4, John Hall1, Wolfgang E. Krumbein5, and Michael J. Chapman1 ...

Abstract

We advocate investigation of spirochete cyclical symbioses (e.g., Borrelia sp., Leptospira sp., Treponema sp.) given the newly established verification of a developmental history in these gram-negative motile helical eubacteria, both in pure culture and in mammals ...

Spirochete round bodies (also called cysts, L-forms and sphaeroplasts) can be induced by many types of unfavorable conditions (e.g., threats of starvation, desiccation, oxidation, penicillin and other antibiotics).

Reversion to familiar helical, motile active swimmers by placement of pure cultures into favorable environments in some cases can be controlled. These observations are supported by a European literature, especially Russian, apparently unknown to American medicine and medical research.

Keywords: ...

1. Introduction

At a small meeting, Spirochaete Co-evolution in the Proterozoic Eon: Ecology, symbiosis, and pathogenesis (an excursion into environmental immunology) organized by Prof. Dr. Wolfgang E. Krumbein and Prof. Lynn Margulis held in the Museum fur Naturkunde (Berlin, May 1 - 2, 2008) we scientists, medical researchers, historians and physicians endorsed this statement:

Powerful new techniques of microbiology, including molecular ecology and evolution inspire us to urge reinvestigation of the natural history of mammalian, tick-borne, and venereal transmission of spirochetes in relation to impairment of the human immune system.

We, the signatories of this paper, limit ourselves to four issues:

FIRST, that current medical discussions of two spirochetoses (spirochete-associated infirmities -- Lyme disease, syphilis) omit mention of "round bodies" or state that they have no clinical relevance (Feder et al., 2007).

Round bodies are viable, motile, slowly reproductive morphologies assumed by spirochetes when they are threatened by environmental insult such as changes in solution chemistry: acidity-alkalinity, salts, gas composition (i.e., oxygen, hydrogen sulfide); changes in chemical concentrations (i.e., antibiotics, antibodies, carbohydrates, amino acids, vitamins); or changes in viscosity or temperature.

Both starvation and threat of desiccation induce round body formation. Some cultures of spirochetes (e.g., Leptonema, Perfilievia, Dubinina et al., 2008) seem to persist more as round bodies than as typical spirochetes. Round bodies, often called by other names such as "cysts", granular bodies, L-forms, non-growing bodies, sphaero- plasts, vesicles, etc. revert to the active helical swimmers when conditions favorable to growth return (Fig. 1).

SECOND, that infections by spirochetes in humans, when seen in their evolutionary and ecological context, are examples of cyclical symbioses that have evolved over geologic time. Certain symbioses have been shown to be associated with viral-like particles capable of synthesis of reverse transcriptases (Fig. 2).

These are posited by Ryan (2007), based significantly on the work of Luis Villareal, to be part of the integration process between the symbiont partners (... human and spirochete) ...

THIRD, we caution that antibiotic treatment may be effective only in the earliest stages of these spirochetoses. Indeed antibiotics such as penicillin and its derivatives induce round body formation and quiescence of symptoms rather than cure.

Suspension of round bodies in growth media causes rapid, days to weeks, reversion to helical swimmers as the Norwegian investigators have shown (Fig. 3; Brorson and Brorson, 2004).

FOURTH, we question the accuracy of screening tests and clinical diagnoses for either of these infections, Treponema pallidum (the syphilis "germ") or Borrelia burgdorferi (the Lyme disease "germ").

Particularly vulnerable to misinterpretation are immunological tests in cases of reinfection, later secondary or tertiary syphilis.

2. Spirochetes: Past and Present

Most spirochete species live freely, are unrelated to any disease and therefore are unfamiliar to clinicians ...

Our interest, perhaps summarized around the question "What is the consequence of life's evolution on the Earth as a planet?" has led us to scientific investigation of spirochetes in nature. Our comments here are generated by an abundant international literature and years of our own work much of it on harmless spirochetes.

We have observed and occasionally isolated spirochetes from ponds rich in vegetation, digestive organs of marine mollusks (the "crystalline style" of oysters and clams) and intestines of wood-feeding termites and cockroaches. In these anoxic or low-oxygen habitats spirochetes swim and proliferate. Population densities often quickly reach over a thousand million per milliliter.

Margulis's laboratory explores an evolutionary hypothesis. She and her colleagues posit that a certain spirochete genome provided an ancestral component to the earliest nucleated cells (eukaryotes).

Spirochete remnant DNA hypothesized to be present in all nucleated organisms should be detectable in the proteomes of fully sequenced genomes.

Simply stated, spirochete ancestors of Perfilievia russae free-living spirochetes presented at the Berlin meeting by Galina Dubinina (Institute of Microbiology of the Russian Academy of Sciences, Moscow, Dubinina et al., 2008) by hypothesis are the closest co-descendants of the cytoskeleton of our nucleated cell lineage (Margulis et al., 2006).

We envision these (sulfide-oxidizing, 0.25 µm diameter spirochetes) are related to ancestors of cilia, sperm tails, haptonemes and myriad other organelles of motility in nucleated organisms.

If the evidence is correctly interpreted, spirochete remnants have dwelled in stable symbioses in eukaryotes since their origin in the Proterozoic eon over 1000 million years ago (mya) (Hall, 2008).

The most ancient intestinal spirochete symbiont in the fossil record is much younger (Miocene c. 20 mya). A Pillotina sp. large spirochete was discovered inside Mastotermes electrodominicus, a kalotermitid (dry wood-feeding termite) embedded in amber (Wier et al., 2002; 2007).

Intestinal spirochetes lived as symbionts in insects long before the appearance ... of any human animal on Earth.

Spirochetes are motile helical Gram-negative eubacteria. As heterotrophs, at optimal temperatures for growth, they require moisture and abundant food. Most ferment sugar in the absence of oxygen.

They form a cohesive taxon detectable by the DNA sequence that corresponds precisely to the 16 Svedberg-unit ribosomal RNA (16S rRNA) component of the small 30S ribosomal subunit.

Spirochetes with their Gram-negative cell walls and periplasmic (internal) flagella between their inner and outer membranes are distinctive at the level of thin section- electron microscopy (EM) ...

Borrelia burgdorferi (Lyme Disease) (4:8:4/5:10:5), or any other spirochete can be detected in three ways:

(1) morphology, especially active motility behavior in tissue,

(2) thin section transmission electron microscopy, and

(3) negative stain whole mount electron microscopy.

No reliable definitive tests for the presence of T. pallidum (syphilis) in patients exists short of quality high magnification observation of the spirochetes and/or their round bodies in affected tissue by an experienced expert microscopist. Reported cures of either infection, the syphilis Treponema or the Lyme disease Borrelia, lack this level of verification.

Spirochetoses (e.g., leptospiroses, yaws, syphilis, Lyme disease) are bacterial diseases correlated with continued presence in the body of specific spirochetes (i.e., obey Koch's postulates).

3. Chronic Infections as Symbioses

The likelihood that these two spirochete infections, syphilis and Lyme disease, correlate with the establishment of permanent human-spirochete symbioses soon after entry of the bacteria into tissue has been insufficiently investigated.

It is reported that reverse transcriptases and virus-like particles are generally abundant in cyclical symbioses and it is suggested that they may facilitate the integration of the association of the partners (Ryan, 2007).

Our intent is to improve and expand awareness of the relationship between spirochetoses and symptoms associated with immune suppression.

We posit that the spirochete disease syphilis persists in the human population where its signs and symptoms may be overlooked or misinterpreted for those of AIDS.

There may be many new drugs, but these two spirochetoses, syphilis and Lyme disease, are not new. Long-term association of symbiotic bacteria in animal tissue tends toward massive gene loss when compared to related bacteria that live freely in water, sand or mud.

The fact that Treponema pallidum (syphilis) and Borrelia burgdorferi (Lyme Disease) are no longer free-living and have lost many genes implies that these spirochetes have long co-evolved with mammals (and arthropods in the case of tick-borne Borrelia burgdorferi Lyme Disease) ...

4. Mistaken for Dead

An extensive round body (=cyst) literature exists in Russian, but has remained relatively unknown even to spirochete experts elsewhere. In many spirochetes formation and reversion of round bodies has been documented by video microscopy techniques ...

Both T. pallidum (syphilis) and Borrelia burgdorferi (Lyme Disease) are anaerobic heterotrophs that require complex organic food under anoxic conditions. They die if exposed to ambient oxygen. The round bodies, propagules that, until they revert to swimming helices, seem incapable of at least rapid growth by reproduction, form quickly.

Within less than an hour, under adverse conditions round bodies develop in large population numbers when the spirochete's needs are not met. They survive for extended periods of time. They revert to helical swimmer populations that grow vigorously when food, salt, temperature, acidity, media viscosity and other conditions become adequate ...

5. Spirochetoses and AIDS

Human tissue provides food and other conditions for growth for both Treponema pallidum (syphilis) and Borrelia burgdorferi (Lyme Disease) spirochetes. Electron micrographic samples, in principle, could verify the persistence of round bodies in patients with symptoms, including Alzheimer's-type dementia.

Examination of biopsies from AIDS patients or autopsies of brains from people who showed sudden personality disturbance could test the hypothesis.

Round body formation in the test tube is induced by penicillin especially in the presence of glycine (a protein amino acid, read "food"). This discovery formed the major contribution of the PhD dissertation (and accompanying patent application) of Andrei Belichenko (2006). Dr. Belichenko was a student of a well-known medical microbiologist Dr. Igor Bazikov ...

Far from eradicating syphilis, antibiotics are driving the disease underground and increasing the difficulty of detection. Although the incidence of disease has more than tripled since 1955, the chancre and secondary rash no longer are commonly seen ...

The ominous prospect of a widespread resurgence of the disease in its tertiary forms looms ahead" (Pereyra and Voller, 1970). We recommend studies to demonstrate or negate the hypothesis that relapse, grave illness or death may ensue from the reversion of round bodies to active spirochetes.

Please see bibliography, 254 references on 49 pages compiled by Joanna Rubel "Spirochetal Cysts, L-forms, and Blebs, Observations from 1905 to 2005", at

www.lymeinfo.net/medical/LDBibliography.pdf

A three-decade-long gap ushered in by the touted "cure of penicillin" separates physicians today from the bulk of medical literature on "the great imitator".

T. pallidum (syphilis) symbiosis may help explain the high correlation of the presence of viruses, pneumonias, other opportunistic infections and the general symptoms of immune suppression so well described in the "old syphilology" medical literature (Colman Jones

www.cbc.ca/ideas/features/Aids/aidsspin.html

) ...

T. pallidum (syphilis) spirochetes that cover themselves with human proteins to which people make antibodies (Radolf and Lukehart, 2006) cause "autoimmune diseases".

The vigorous antigenic response of early infection fades to the classical secondary-to-tertiary symptoms of paresis.

"PARESIS", a mnemonic, refers to a coherent and varying set of symptoms, a syndrome. "Personality disturbances, Affect abnormalities, Reflex hyperactivity, Eye abnormalities, Sensorium changes, Intellectual impairment and Slurred speech. PARESIS may begin with a dramatic delusional episode (e.g., Nietzsche January 1889 in the Turin Plaza; Margulis, 2004 and 2007).

However, over the years, dementia may alternate with periods of such clarity that there seems to have been a cure" (Hayden, 2003).

Since the research group of Luc Montagnier first described LAV "virus-like particles" (later called "HIV-1") from "Patient 1", a close connection has been shown between AIDS and a history of syphilis in multi-partner men (Barre-Sinoussi et al., 1983) ...

Chronic syphilitics and AIDS patients, those unmistakably ill and immune suppressed, do not succumb to HIV or syphilis directly. They die of reactivation tuberculosis (TB) and ubiquitous mycobacterium avium intracellulare (MAI group) diarrhea, and emaciation associated with refractory bowel infections in emaciated homosexuals and in immune compromised patients generally ...

Is it possible that the narrow focus on "HIV as the cause of AIDS", an example of scientific "misplaced concreteness" ... has facilitated missed diagnosis of syphilis? ...

Contrary to the statements on many official government and medical websites that "syphilis is easily curable by antibiotics", the disease is often refractory to antibiotic and other treatments except perhaps in very early immuno- responsive stages (Musher et al., 1990).

It has not been adequately shown that T. pallidum (syphilis) infection in its secondary and later stages is curable ...

We urge investigation into the extent to which undetected latent syphilis overlaps with AIDS. The correlation of a positive HIV test tends to indicate an enhanced likelihood of immune failure.

To date, all attempts to produce an effective HIV vaccine have failed. Robert Gallo characterized the failure of the latest STEP vaccine trial, as a "catastrophe".

Ronald C. Desrosiers, a molecular geneticist at Harvard University stated that "none of the products currently in the pipeline has any reasonable chance of being effective in field trials."

Anthony S. Fauci, head of the National Institute of Allergy and Infectious Diseases that sponsored the trial, comments, "There is something very, very peculiar going on in the vaccine trials. We've got to rethink these things" (Brown, 2008).

John Moore, an HIV virologist at Weill-Cornell Medical College stated "This was the first AIDS vaccine clinical trial in history where most people thought they'd at least see something positive" (Cohen, 2007) ...

We agree that spirochetoses need to be reevaluated. Is the situation better described as an obligate and ancient symbiosis where the bionts (spirochetes and humans) are integrated at the behavioral, metabolic and genetic level rather than a new viral infection such that HIV equals AIDS?

We think symbiosis analysis is appropriate here and in conclusion we advocate a necessary first step: We urge that the possible direct causal involvement of spirochetes and their round bodies in symptoms of immune deficiency be carefully and vigorously investigated.

Acknowledgements ...

[ rockcreekfreepress.tumblr.com/post/65407449/a-call-for-a-re-evaluation-of-the-aids-dogma

John Scythes, one of the researchers on the paper, reports that he has not found a single case of an immune suppressed patient (regardless of HIV status) who has died of complications of syphilis since the discovery of AIDS in the early 80s. The implications of this are staggering. It is simply not possible that syphilis stopped being fatal just as the new disease of AIDS came on the scene.

The researchers speculate that, because of its immune suppression effect and its ability to imitate other diseases, syphilis is being missed or misdiagnosed as AIDS. Now that improved tests for syphilis infection are available, the researchers urge a large scale investigation into the extent that this is happening.]

----------------

www.pnas.org/content/106/44/18656.long

Destruction of spirochete Borrelia burgdorferi (Lyme Disease) round-body propagules (RBs) by the antibiotic Tigecycline

ystein Brorsona, Sverre-Henning Brorsonb, John Scythesc, James MacAllisterd, Andrew Wiere,1 and Lynn Margulis ...

Abstract

Persistence of tissue spirochetes of Borrelia burgdorferi (Lyme Disease) as helices and round bodies (round-body propagules) explains many erythema-Lyme disease symptoms.

Spirochete round-body propagules (reproductive propagules also called coccoid bodies, globular bodies, spherical bodies, granules, cysts, L-forms, sphaeroplasts, or vesicles) are induced by environmental conditions unfavorable for growth ...

Molecular-microscopic techniques, in principle, can detect in animals (insects, ticks, and mammals, including patients) helices and round-body propagules of live spirochetes.

Genome sequences of B. burgdorferi (Lyme Disease) and Treponema pallidum (syphilis) spirochetes show absence of >75% of genes in comparison with their free-living relatives.

Irreversible integration of spirochetes at behavioral, metabolic, gene product and genetic levels into animal tissue has been documented.

Irreversible integration of spirochetes may severely impair immunological response such that they persist undetected in tissue.

We report in vitro inhibition and destruction of B. burgdorferi (Lyme Disease) (helices, round-body propagules = "cysts") by the antibiotic Tigecycline (TG; Wyeth), a glycylcycline protein-synthesis inhibitor (of both 30S and 70S ribosome subunits).

Studies of the pleiomorphic life history stages in response to Tigecycline of both B. burgdorferi (Lyme Disease) and Treponema pallidum (syphilis) in vivo and in vitro are strongly encouraged ...

We reexamine evidence and point to mainly Russian studies ignored in English scientific literature that spirochete round bodies (round-body propagules, also called coccoid bodies, globular bodies, spherical bodies, cysts, granules, L-forms, sphaeroplasts, or vesicles) are fully viable. round-body propagules are spherical, membrane-bounded structures that appear in pure cultures as they age in proportion to the disappearance of helical forms ...

Anglophone medical discussion of spirochetoses (spirochete-associated infirmities, such as Lyme disease or syphilis) omit mention of "round bodies" or state that they have no clinical relevance (2). Yet evidence abounds not only that round-body propagules are viable but also that they may locomote, grow, and reproduce ...

Penicillin, among many other "unfavorable growth conditions," induces round-body propagules (3, 6, 10 - 13, 15).

That penicillin does not cure either of the two "Great Imitators" (Lyme disease and syphilis) is widely accepted in Russian medical literature ... (16, 17) ...

Except for quality high magnification observation of spirochetes including their round-body propagules in affected tissue by an experienced microscopist ... no definitive tests for the presence of spirochetes in patients in late stages exist. Cures of Lyme disease or venereal treponeme infection (syphilis) lack this level of verification.

Spirochetoses (e.g., leptospiroses, yaws, syphilis, and Lyme disease) are bacterial diseases correlated with continued presence in the body of potentially identifiable spirochetes. They obey Koch's postulates.

[1. be found in all cases of the disease;

2. be isolated from the host;

3. cause the same disease when injected into a healthy host, and

4. then be found growing again in the newly infected host.]

The little-known history of Lyme borreliosis begins with the discovery of spiral bacteria in ticks by Dutton before the 1905 publications of Dutton and Todd (26) ... The spirochete bacteria were later named Borrelia duttoni.

Hindle (9) injected solutions of "granular forms" (i.e., round-body propagules) in the absence of motile helices (Borrelia duttoni) into mice to show that they caused symptoms of infection in the test animals.

Borrelia vincentii round-body propagules that had remained in their "granular" form for 31 months converted to helical motile spirochetes when transferred to fresh medium under conditions favorable for growth (8).

However, when other investigators failed to find propagules, ... the round-body propagules were declared to be dying spirochetes. Although terminologcal confusion (cysts, granules, round-body propagules, vesicles, etc.) exacerbated the problem, the dismissal of an entire scientific literature was unjustified (23).

The presence of the eubacterium spirochete Borrelia burgdorferi (Lyme Disease) in human tissue correlates with a syndrome of symptoms in people known to have experienced "erythema migrans," a mobile circular skin blemish related to a blood meal by immature ... [tick] nymphs that are the most active in transmission of the disease ...

Eggs hatch into small ticks that molt without metamorphosis into nymphs and later adults. Only 50% of those bitten who later test positive for Lyme borreliosis and present other symptoms like "Lyme arthritis" and neuroborreliosis actually develop the tell-tale ... coin-shaped rash at the site of the bite (27).

Symptoms vary greatly in severity, frequency, and persistence. When antibodies against tick-borne borreliosis ... are detected in patient blood, they are scored "Lyme disease borreliosis positive," but results are frequently negative despite infection (28).

An estimated 20,000 cases of Lyme disease are reported annually in the U.S., but the actual number is estimated to be closer to 200,000 cases per year.

In central Europe and Scandinavia, the disease is highly endemic. Cases of B. burgdorferi (Lyme Disease) in southern Sweden alone rose from 164 (in 1992) to 664 (in 2000) per 100,000 population (29). Over 100 strains of Borrelia sp. have been isolated from healthy ticks and grown in rich liquid medium that contains 6% mammalian serum cultured at elevated temperatures (30 - 36 °C).

At least three immunologically distinguishable strains have been claimed to transmit the tendency toward symptoms: Borrelia afzelii, B. burdorferi (Lyme Disease) sensu stricto, and Borrelia garinii.

Persistence of tissue spirochetes of B. burgdorferi (Lyme Disease) has been suggested since Dutton first reported them in the 19th century ...

Lyme borreliosis, with incidence that has increased in northern countries, becomes chronic and variable. The percentage of virulent strains has greatly increased in recent years (34). The site(s) of affected tissue or organ and the intensity, severity, frequency, and duration of symptoms are idiosyncratic. Clinical failures to eradicate all traces of symptoms ... have been widely reported in mainstream medical literature ...

We hypothesize that Lyme borrelioses is an old chronic bacterial symbiosis that tends toward necrotrophy in mammals. In healthy immature ticks, the spirochetes are seasonally transmitted by bite to vertebrates including seabirds, cervids, mice, rabbits, and humans.

Results ...

Telectron microscopy.

Spirochetes exposed to Tigecycline concentrations >0.006 μg/mL for 7 d had disintegrated; only a few empty membrane bounded round-body propagules were present ...

Discussion

Chronic spirochete infections in humans ... are examples of symbioses that have evolved over geologic time. Symbiotic relationships are characterized by numerous reverse transcriptases and viral-like particles that are posited to be part of the integration process between the symbionts (e.g., human and spirochete) (36, 37).

Our results are consistent with the idea that antibiotic treatment is effective only in the earliest stages of Lyme borreliosis. Antibiotics such as penicillin and its derivative doxycycline induce round body formation and quiescence of symptoms rather than cure. Suspension of round bodies in growth media causes rapid reversion to helical swimmers even in a few days (3 - 5).

The treatment of spirochetoses, specifically borrelioses, requires knowledge of the natural history, including pleiomorphy, of the borrelia spirochetes in their environmental context ...

Study and clinical trials of Tigecycline, a glycylcycline 30S and 70S ribosomal inhibitor of protein synthesis, ... on spirochetoses (e.g., Lyme disease, syphilis, and perhaps multiple sclerosis) are warranted ...

This broad-spectrum antibiotic is not affected by the kinds of problems of resistance encountered in tetracycline therapies ...

Morphological analyses of Miocene amber 20 million years old revealed an intestinal spirochete. This large Pillotina sp. was detected by transmission electron microscopy in a Mastotermes electrodominicus (family Mastotermitidae, wood-feeding termite) from a Dominican Republic mine.

The well-preserved fossil (43) and live observations (44) indicate that spirochetes lived on Earth as healthy symbionts in insects long before the appearance ... of any australopithecine of the genus Homo. Clearly spirochete - animal tissue symbioses precede by millions of years the spirochete-induced tissue necrotrophy associated with diseased states, i.e., spirochetoses of Lyme disease or syphilis.

Mainly Russian studies ignored in English literature show that many "unfavorable conditions" including penicillin do not injure round bodies and therefore fail to cure the "Great Imitators," either Lyme borreliosis or syphilis ... Little, if any, evidence for cure of late Lyme borreliosis exists in the scientific literature ...

Investigation to seek Borrelia burgdorferi (Lyme Disease), other borrelias and treponemes in lymph, joints, brain, eyes, etc. where pathology is asserted to "be caused by autoimmune disease" such as multiple sclerosis, is advocated.

To avoid perpetuation of underdiagnoses, misdiagnoses, and inappropriate therapies, the borrelia spirochetes, whether as helices or round-body propagules, can and should be DIRECTLY identified in tissue. Very ill patients are likely to be afflicted simultaneously by more than one kind (strain or species) of these symbiotic spirochetes.

The in vitro inhibition, even destruction, of B. burgdorferi (Lyme Disease) (helices, round-body propagules) by the antibiotic Tigecycline augurs well for a possibility of a Lyme disease cure.

Tigecycline deserves immediate scientific attention. The in vitro effects here of Tigecycline on borrelia life history stages help predict successful in vivo results both in laboratory animals and patients.

Failure to understand chronic diseases, in this case Lyme borreliosis, as a manifestation of permanent genetically integrated symbionts where disease symptoms are expressions of symbiogenesis to which many aspects of the vertebrate immune system respond, generates tragedy and even death due to ignorance ...

The borrelia - human physical association of Lyme disease, as a spirochete symbiosis, ought to be recognized as a coevolved eubacterial - acarid - mammalian association highly integrated on several levels: the genetic, gene product (RNA, protein, coenzyme), metabolic (metabolites, ion flow, water balance), and behavioral ...

This wider view of Lyme borreliosis, coupled with the efficacy of Tigecycline for inhibition and destruction of the pleiomorphic stages, especially the round-body propagules in vitro, provides a call to action to test this antibiotic in a clinical setting ...

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www.pbs.org/newshour/bb/politics/july-dec11/newtgingrich_09-29.html

NEWSHOUR TRANSCRIPT of Newt Gingrich on Jobs, Brain Research ..., 9-29-11

SUMMARY

After unveiling his "21st Century Contract with America," former House Speaker Newt Gingrich spoke with Judy Woodruff about his policy proposals ...

Transcript

JUDY WOODRUFF: ... Former Speaker Newt Gingrich, thank you for talking with us.

NEWT GINGRICH: Good to be with you.

JUDY WOODRUFF: ... I know you're interested in additional research on the human brain. Would that entail more money to the National Institutes of Health, the NIH, to do that kind of research?

NEWT GINGRICH: Well, I'm not sure whether it would go to the National Institutes of Health ...

In Alzheimer's alone, we're expected to spend between now and 2050 about $20 trillion, public and private combined. That's one and a half times the current federal debt. So sometimes, when people are looking for ways to help save dramatic amounts of money, they ought to look to breakthroughs to improve things, not just ways to cut things ...

When I talk to brain scientists, they believe, if we could simply slow down the onset of Alzheimer's by five years, we'd save somewhere between $8 trillion and $10 trillion. That's almost the entire size of the current national debt ...

When you do brain science, you're also doing autism, Parkinson's, mental health, systems of learning. It's an enormous opportunity area that we're currently underfunding and, frankly, not managing very well ...

JUDY WOODRUFF: Well, Newt Gingrich, we thank you for talking with us today. We appreciate it.

[For more on the impact of infection on human aging, see "Microbial Origin of the Gummy Substance of Fujita and Ging"

www.avonhistory.org/bug/gum.htm]

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