Archive for the ‘Alzheimer’s’ Category

Detecting Borrelia Spirochetes: A Case Study With Validation Among Autopsy Specimens  Go here for full study.  Excerpts below:

Front. Neurol., 10 May 2021 |

Detecting Borrelia Spirochetes: A Case Study With Validation Among Autopsy Specimens

The complex etiology of neurodegenerative disease has prompted studies on multiple mechanisms including genetic predisposition, brain biochemistry, immunological responses, and microbial insult. In particular, Lyme disease is often associated with neurocognitive impairment with variable manifestations between patients. We sought to develop methods to reliably detect Borrelia burgdorferi, the spirochete bacteria responsible for Lyme disease, in autopsy specimens of patients with a history of neurocognitive disease. In this report, we describe the use of multiple molecular detection techniques for this pathogen and its application to a case study of a Lyme disease patient. The patient had a history of Lyme disease, was treated with antibiotics, and years later developed chronic symptoms including dementia. The patient’s pathology and clinical case description was consistent with Lewy body dementia. B. burgdorferi was identified by PCR in several CNS tissues and by immunofluorescent staining in the spinal cord.

These studies offer proof of the principle that persistent infection with the Lyme disease spirochete may have lingering consequences on the CNS.


Neuroborreliosis can occur in up to 15% of patients with Lyme disease, affecting both the central nervous system (CNS) and peripheral nervous system (PNS). The disease of the nervous system can become chronic and debilitating. Prior studies of persistent post-treatment Lyme encephalopathy demonstrated both immune activation in CSF and serum and metabolic and blood flow deficits in the CNS (13). While the persistence of the pathogen after antibiotic treatment in humans remains controversial, animal studies have clearly demonstrated its occurrence (48). Evidence from experiments performed in mice, dogs and primates have shown that intact spirochetes can persist in the mammalian host after the administration of antimicrobial drugs, and that they can be metabolically viable (9). Studies in vitrohave demonstrated that persister Borrelia develop stochastically in the presence of microbiostatic antibiotics and that tolerance is enabled by slowed growth (10, 11).

We have recently demonstrated both inflammation and persistence of Borrelia in the CNS and PNS of doxycycline-treated rhesus macaques that were infected with the Lyme disease pathogen (9, 12). In humans, persistence has been studied early after treatment and in Post-Treatment Lyme Disease (PTLD) patients. In one study, skin biopsies were taken from the erythema migrans (EM) lesion and after treatment (~2 mo later). Approximately 1.7% of these were culture-positive and confirmed as the same strain (13, 14). Human xenodiagnoses were also performed in a more recent study. Larval ticks were placed on patients who had EM (early stage) or PTLDS (15). Tick samples were evaluated by PCR and culture; of the 23 patients on whom ticks fed and were recovered, 19 were negative, 2 were indeterminate, and 2 were positive by PCR (1 patient with EM and 1 with PTLDS). Two other studies have indicated that the spirochetes could be cultured from late stage Lyme patients, yet the cultures took many weeks and rounds of subculturing without active growth (16, 17). Thus, in the absence of a reliable detection system, persistent infection in humans remains difficult to assess. One means to address this issue is to interrogate patient tissue for persistent pathogen through the analysis of post-mortem specimens.

In this report, we describe the use of multiple overlapping techniques, including immunofluorescence assay (IFA), RNA in situ hybridization (RNAscope), and PCR for detection of Borrelia spirochetes in post-mortem tissues. As example, we describe the detection of B. burgdorferiin the brain tissue of a post-mortem donor from the brain repository of the Lyme and Tick-Borne Diseases Research Center at the Columbia University Irving Medical Center. This individual had a history of Lyme disease that appeared to have been successfully treated with antibiotics; 4 years later developed a neurodegenerative disorder leading to dementia.

Case Study Description

This 69 year old woman (Patient 12,577) contracted Lyme disease at age 54 with a well-documented erythema migrans rash accompanied by a severe headache, joint pains and a fever of 104; convalescent serologies were positive on ELISA and both IgM and IgG Western blots. Treatment with doxycycline for 10 days led to symptom resolution. Two years later, a sleep behavior disorder emerged. Four years later, cognitive problems (processing speed, mental tracking, and word-finding) emerged and gradually worsened. Other symptoms included photophobia, paresthesias, fasciculations, and myoclonic jerks. Neurocognitive testing revealed deficits in visuospatial skills and executive functions with preservation of verbal skills, suggesting a neurodegenerative process. Brain Magnetic Resonance Imaging with and without contrast showed mild atrophy and non-specific scattered white matter hyperintensities without enhancement. Brain Single Photon Emission Computed Tomography scans showed decreased perfusion in the right posterior parietal and temporal lobes. Serum was negative or normal for erythrocyte sedimentation rate, c-reactive protein, antinuclear antibody, and thyroid stimulating hormone. PCR assays of blood for Bartonella henselae, Babesia microti, and Borrelia burgdorferi were negative. Serum C6 ELISA was negative but Lyme IgG Western blot was positive with 9/10 bands. Treatment with IV ceftriaxone at age 60 for 8 weeks led to 60% improvement in cognition and interpersonal engagement; oral amoxicillin 500 mg three times daily was continued for 6 months after the IV treatment. The initial improvement was not sustained and subsequent antibiotic therapy with minocycline was of no clear benefit; gradually her visual spatial skills and executive functions deteriorated further, and anxiety worsened. Serum IgG Western blot continued to be positive. At age 62, a cerebrospinal fluid study demonstrated 4 CSF IgG bands on Lyme Western blot; unfortunately, because CSF and serum ELISA studies were not conducted, intrathecal Bb specific antibody production could not be assessed. Other CSF studies were unremarkable including absence of pleocytosis or elevated protein, absence of P-tau elevation, Venereal Disease Research Laboratory assay, Acid-Fast bacteria, fungi, and negative Herpes Simplex Virus and Epstein-Barr Virus PCRs. A second brain MRI showed periventricular and subcortical T2 hyperintensities possibly due to “small vessel ischemia or demyelinating disorders like Lyme disease.” Fluorodeoxyglucose-Positron Emission Tomography scan showed “diffuse cortical hypometabolism, worse in the posterior parietal and temporal lobes, with sparing of the sensory motor cortex and visual cortex bilaterally—findings consistent with Alzheimer’s disease.” The extensive workup at that time led to the diagnoses of both a REM behavioral disorder with verbalizations and movements and a neurodegenerative dementia characterized by expressive aphasia, visual agnosia, anomia, deficits in executive function and calculation, and mild memory problems. Eventually, she developed severe oral dystonia, making feeding progressively more difficult; she died 15 years after the initial infection with B. burgdorferi. Early and severe movement disorders, REM behavioral disorder, paranoia, and personality changes all favored a clinical diagnosis of dementia with Lewy bodies.

Human Control Tissues

Tissue blocks from various regions of seven specimens from brains of deceased Macedonian residents that were housed in the Macedonian/New York State Psychiatric Institute Brain Collection were used as controls. Though none had a clinical history of Lyme disease based on interview with the surviving family members, Borrelia is endemic in Macedonia. These brain tissues were probed in the same manner as the human case study with IFA and PCR-based detection methods.


The Case Study Pathology Is Characteristic of Dementia With Lewy Bodies (DLB)

The fresh brain weighed 996 g and appeared atrophic Coronal sections through the left cerebral hemisphere and brain stem revealed mild enlargement of the lateral ventricle, particularly the temporal horn. The substantia nigra was normally pigmented or nearly so. Microscopically, nigral and cortical Lewy bodies, were seen with hematoxylin and eosin stain (H&E, Figures 4A,B). Immunohistochemistry (IHC) for α-synuclein (clone 42, BD Transduction Laboratories) showed numerous immunoreactive Lewy bodies and fibers in substantia nigra, hippocampal formation and neocortex, Figures 4C–E). IHC for hyperphosphorylated tau (monoclonal antibody AT8; ThermoFisher) revealed intense staining of many limbic neurofibrillary tangles and neuropil threads (Braak stage 2–3, Figure 5), and of occasional neurofibrillary tangles in neocortex, but senile plaques were extremely rare, and each contained only a few fibrils (Figure 5). H&E showed prominent thickening of small blood vessels in gray and white matter, extensive mineralization of pallidal vessels, and rare microglial nodules in the hippocampal formation. Immunohistochemistry for Iba-1 (Wako), CD68 (clone KP1, Dako), and CD163 (clone EDHu-1; Bio-Rad) showed moderate numbers of activated microglia and large numbers of macrophages in hippocampal formation and spinal cord (Figure 6). In summary, we see DLB accompanied by features of Alzheimer’s disease, a common presentation.


Two reasons exist for the interrogation of autopsy specimens for the Lyme disease spirochete. First, in patients with a known history of Lyme disease and a record of antibiotic treatment, the potential for treatment to fail in eradicating the infection can be evaluated. Notably, a detailed patient history, including history of possible second B. burgdorferiinfection and treatment non-compliance, is necessary. Given the difficulty in recovering organisms from living people, looking at post-mortem tissue can provide some resolution on the issue of persistence. Secondly, patients such as the one presented here, can manifest neurological disease that may or may not be related to infection. Here, the patient developed dementia with Lewy body pathology. While availability of tissue may be a challenge, the role of Borrelia burgdorferiin the etiology of chronic neurological disease, can be studied as a “proof of principle.”

Our study confirms that Borrelia burgdorferi was detected in the brain and spinal cord tissue of this patient with a history of previously treated Lyme disease. These results however do not clarify whether the Borrelia infection had anything to do with her progressive neurodegenerative disorder. It is possible this is an unrelated incidental finding or that there is a relationship between CNS infection with Bb and the development of a neurodegenerative dementing disorder.

Previous studies suggest that Borrelial spirochetes can start invading the nervous system during early stages of the infection resulting in meningeal seeding (29), and this later leads to neuroborreliosis. To define the pivotal neurological deficits, a study in Europe examined the clinical manifestations of 68 patients hospitalized for neuroborreliosis. Meningitis was found to be one of the least frequent conditions, present in 6% of the patients (30), whereas cranial neuritis was the most frequent (25%). The clinical Lyme case presented here was documented with meningismus at the time of the EM rash, supporting the possibility of mild meningitis at early infection. Bacterial meningitis leading to cognitive impairment was well-studied in Treponema pallidum in relation to dementia (31). B. burgdorferi infection has also been associated with mild (32) to severe (33) cognitive deficits. In the endemic areas of Lyme disease, Borrelia infections as a possible cause of cognitive impairment has to be carefully considered.

Neurotropic viruses have been associated with neurodegenerative syndromes, as have spirochetal infections (3438). Precedence for an association between B. burgdorferi infection, specifically, and dementia exist (3842), however there are also reports that have failed to link B. burgdorferi to AD (43). Evidence that amyloid plaques may have a functional protective role in combatting microbial infection has also come to the fore (44). Evidence that Borrelia can induce amyloid production is suggestive of a possible mechanism for development of AD (4547).

To comprehensively evaluate the possible role of Borrelia in dementia (Alzheimer’s and LB), 20 patients were identified from a total of 1,594 patients who were seen for dementia, who had positive intrathecal anti-Borrelia antibody index (AI), indicative of past or present Lyme disease (48). Among these 20 patients, 7 patients with neuroborreliosis dementia showed stability or mild improvement in their cognitive functions after treatment with ceftriaxone, and the others showed progressive worsening despite antibiotic treatment (48). The individual in our clinical case reported 60% cognitive improvement after the antibiotic treatment. However, this improvement was not sustained and cognition gradually worsened, a finding consistent with a previous study demonstrating cognitive functional deficits in treated Lyme neuroborreliosis patients (49). The possible anti-inflammatory effects of antibiotic cannot be discounted (50).

A recent study aimed at testing the hypothesis that polymicrobial infections contribute to Alzheimer’s disease was conducted. Brain sample tissues were probed for B. burgdorferi using a commercially available monoclonal antibody (43). However, this study was unable to demonstrate the presence of Borrelia spirochetes in the tissue samples. The possibility exists that this could be due to the selection of antibody. The polyclonal used exhibited some cross-reactivity to fungal structures and the monoclonal antibody may have targeted an antigen (OspA) that is downregulated as spirochetes migrate from tick to mammalian host. Studies have shown that the expression of the OspA is abundant on the surface of bacteria when residing in tick midguts, but its expression is repressed during host infections (51). However, there are studies showing the expression of OspA in one-third of the spirochetes inoculated in mice and in cerebrospinal fluid of early neurologic Lyme disease (52, 53), suggesting that OspA might not be an ideal choice in the interpretation of the analysis of a study. In a recent study from our laboratory, we were able to identify B. burgdorferi with a monoclonal antibody to OspA in some tissues (e.g., heart) but not others, where they were positively identified with polyclonal antibodies instead (12). Anti-OspA in combination with anti-Flagellin may be an exemplary choice in the analysis of either nucleic acid data or IFA, as these two proteins constitute one-third of the total protein content of a spirochete during early Lyme disease (54, 55). The gene expression profile of long-term persisters within a host is as yet unknown.

Recently, another study was published in which Borrelia spirochetes appeared to be present in the form of biofilms in human brain specimens of a chronic Lyme disease case. This study refers to the usage of a monoclonal antibody that is specific for B. burgdorferi sensu stricto (56), yet there was no reference to a commercial source or a research laboratory. The methodology section of the paper cites articles that used a conjugated version of rabbit-polyclonal antibodies which target Borrelia spirochetes. The study neglected to include controls testing cross-reactivity of the antibodies used, so it is difficult to determine the validity of the IFA and to repeat the assay. The authors, however, indicated that Borrelia sequences were identified from the tissues through metagenomics sequencing.

In the study reported here, we used primers that target internal transcribed spacer region (ITS) of the bacterial ribosomal RNA. Although the protein coding regions often have a higher specificity compared to ribosomal markers (57), low PCR amplification, integrity of the tissue sample, and low copy number eliminated them as candidates for the PCR assay of our human autopsy specimens. Previously, 16S rRNA gene was utilized for rapid detection and identification of Borrelia species considering its ubiquity among all the members of the Borrelial genus and almost all bacteria (58). However, this 16S rRNA gene would be very difficult to differentiate between species of Borrelia because of its high sequence similarity. To differentiate Borrelia burgdorferi from other species, we utilized nested PCR. According to a BLAST search, these primers matched 100% with different isolates of B. burgdorferiand didn’t align with any other bacteria or host species except, the Borrelia species finlandensis. According to a recent study in which 7,292 clinical specimens were tested for Borrelia species in US patients, five different species of Borrelia were identified and the species finlandensis was not one of them (59). Most recently, a group that analyzed the microbiomes of ticks collected from the states of New York and Connecticut identified only two Borrelia species, B. burgdorferi and B. miyamotoi, in adult Ixodes scapularis ticks (60). Out of 197 ticks that were analyzed, B. burgdorferi was detected in 111 (56.3%) of the individual ticks and B. miyamotoi in 10 (5.07%) ticks. Among these 10 ticks, seven ticks harbored both species (60). Considering the geographical location and the environment of the Lyme case used in this study and the tick microbiome study, designing primers that are sensitive and specifically detect B. burgdorferi was of utmost importance.

Given the disparity in findings over multiple studies, having multiple methodologies to evaluate specimens for Bb should significantly strengthen any results. Studies suggesting a role for Bb in dementia have been published previously by (38, 46, 47, 61, 62), but negative findings for Borrelia spirochetes have also been reported by others as mentioned above (43, 63). Our studies here represent a major improvement in methodology– both in terms of microbial probing techniques and in numbers of brain samples.

In this report, we provide methodology which succeeded in identifying persistent Borrelia in the CNS of a deceased woman with a history of Lyme disease. This patient did not meet full diagnostic criteria for neuroborreliosis, as it was never demonstrated that she had B. burgdorferi– specific intrathecal antibody production, nor did her CSF show lymphocytosis. While she did have 4 IgG Bb-specific IgG bands in her CSF when assessed by Western blot, specific intrathecal production which requires a comparison of serum and CSF by a diagnostic ELISA was never assessed. The lack of CSF lymphocytosis may reflect the prior extensive antibiotic therapy. Our molecular results however confirm B. burgdorferi invasion of the central nervous system. An earlier lumbar puncture at the time of the initial cognitive decline and prior to the intravenous antibiotic therapy may have confirmed the diagnosis of neuroborreliosis; this case highlights the clinical importance of CSF studies before initiating antibiotic therapy for presumed neurologic Lyme disease. Her initial good response to the IV ceftriaxone suggests a microbial infection was being treated, or that inflammation was dampened. The decline thereafter suggests either that persister Borrelia were present that are now known not to remit with standard antibiotic therapy (6, 12), that an irreversible neurodegenerative process had been triggered by the prior B. burgdorferi infection, or that an unrelated neurodegenerative disorder was present at the same time as the presumed B. burgdorferi CNS infection.

A prior case series of patients who developed chronic neurologic Lyme disease in the United States (64) noted that encephalopathy may emerge months to many years after treated erythema migrans and that about 22% of these patients with late neurologic manifestations show an initial improvement in cognition after intravenous ceftriaxone therapy that is followed months later by relapse. Our patient demonstrated severe headache at the time of the EM rash which suggests meningeal inflammation, a symptom profile also reported by 41% of the patients at initial infection in the case series of patients who later developed chronic neurologic Lyme disease. Notably, our patient did have a good response to the antibiotic treatment only to develop a sleep disorder 2 years later and a cognitive disorder 4 years later.

This patient’s neurodegenerative disorder demonstrated clinical (REM behavior disorder, visuospatial, and attention problems) and neuropathologic features of a Lewy Body Dementia. The case report raises the question of whether B. burgdorferi may play a role in the development of Lewy body dementia. Future studies will be directed at testing more affected subjects and more control subjects in order to substantiate or refute this possible link.


For more:

Lyme & Memory Loss

What causes memory loss specifically? And what does it feel like to experience it?

My long-term memory has always been sharp as a tack. I can repeat verbatim a conversation that happened two decades ago; I can tell you what a friend was wearing on the first day of third grade; I know what I ate at the restaurant my family went to on the last night of a vacation we took when I was in high school. People say, “It’s incredible that you can remember so much,” to which I often respond, “Just don’t ask me what I had for breakfast.”

The joke gets a good laugh, but it’s actually a serious matter: despite my unusually strong long-term memory, my short-term memory has been affected by the tick-borne illnesses Lyme disease, babesiosis, and ehrlichiosis. Some evenings I truly couldn’t tell you what I had for breakfast, and other times I need to look at my calendar to remember what I did that day. Once jogged, the memory comes back to me like a slow Google search, but the hang time between someone asking me about my day and my response can be embarrassingly long.

What causes memory loss specifically? And what does it feel like to experience it?

Though our central nervous systems are generally protected by the blood brain barrier, Lyme bacteria (spirochetes) are sneaky and smart, and can spiral their way across the border. Once that security breach occurs, a patient may experience “Lyme brain”, which can manifest as brain fog, word or song iteration, depression and anxiety, tremors, mini-seizures, headaches, burning extremities and memory loss.

As described in the book Conquering Lyme Disease: Science Bridges the Great Divide by Brian A. Fallon, MD and Jennifer Sotsky, MD, “Lyme disease can directly affect brain and sensorium in multiple ways: via direct infection, immune system effects, changes in neurotransmitter balance, and altered neural pathways.” Inflammation in the brain, as well as impaired oxygen flow to the brain as is often seen with babesiosis, can impact cognitive function. Drs. Fallon and Sotsky write that short-term memory problems are one of the most common cognitive effects of neurological Lyme disease. The book includes images of low blood flow in the brain of patients with memory impairment after Lyme disease (referred to as post-treatment Lyme encephalopathy).

In her book Lyme Brain, Nicola McFadzean Ducharme, ND, references studies in which Borrelia burgdorferi spirochetes were found in the brains of Alzheimer’s patients. While many Alzheimer’s patients don’t have Lyme, and many Lyme patients won’t develop Alzheimer’s, the studies show both how easily Lyme bacteria can cross the blood brain barrier, and how easily their presence can be misdiagnosed as dementia or Alzheimer’s when a chief symptom is memory loss.

The extent to which a patient’s memory is affected depends largely on their response to treatment.

When I started antibiotic therapy, some of my neurological systems worsened at first, as I experienced Herxheimer reactions, and the antibiotics chased those clever spirochetes deeper into my brain. After a couple months, my brain fog decreased, I had better concentration, and my memory improved. Sticking to an anti-inflammatory diet and taking supplements to help rid my brain of neurotoxins also helped. I learned to pace myself and to stay away from overstimulating activities (like big movie theaters or fireworks shows) that rile up my neurological symptoms, including memory loss.

Luckily, my long-term memory was never affected, which is a blessing as a writer. But while my short-term memory problems have improved, they are not fully gone. I especially notice them now when I am over tired or over worked. During those periods, I might leave someone a voicemail in the morning and then leave a similar message later in the day, forgetting about the first. I find myself asking friends, “Did I already tell you this story?” I’m hyper-aware of the deficit, but friends and family assure me that my lapses are relatively infrequent. Rest, quiet time away from screens, and relaxation usually have me back in “working order” in just a couple days.

If you are in an acute stage of neurological tick-borne illness, it’s possible that you’ve read this post and forgotten what it said; that you lost track of where you were whiling reading; or that you’ll tell someone about what you read more than once. Know that you’re not alone, and that with proper treatment through a Lyme Literate Medical Doctor (LLMD) and good self-care, a time will come when everything will seem much clearer.

[1] Fallon, Brian A., MD and Sotsky, Jennifer, MD. Conquering Lyme Disease: Science Bridges the Great Divide. New York: Columbia University Press (2018), 314.

[1] McFadzean Ducharme, Nicola, ND. Lyme Brain. California: BioMed Publishing Group, LLC (2016), 15-16.

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Opinions expressed by contributors are their own.

Jennifer Crystal is a writer and educator in Boston. Her memoir about her medical journey is forthcoming. Contact her at

COVID-19 RNA Based Vaccines & The Risk of Prion Disease

Microbiology & Infectious Diseases

COVID-19 RNA Based Vaccines and the Risk of Prion Disease  

J. Bart Classen, MD*

Classen Immunotherapies, Inc., 3637 Rockdale Road, Manchester, MD 21102, E-mail:

Citation: Classen JB. COVID-19 RNA Based Vaccines and the Risk of Prion Disease. Microbiol Infect Dis. 2021; 5(1): 1-3. 


J. Bart Classen, MD, Classen Immunotherapies, Inc., 3637 Rockdale Road, Manchester, MD 21102, Tel: 410-377-8526.

Received: 27 December 2020; Accepted: 18 January 2021


Development of new vaccine technology has been plagued with problems in the past. The current RNA based SARS- CoV-2 vaccines were approved in the US using an emergency order without extensive long term safety testing. In this paper the Pfzer COVID-19 vaccine was evaluated for the potential to induce prion-based disease in vaccine recipients. The RNA sequence of the vaccine as well as the spike protein target interaction were analyzed for the potential to convert intracellular RNA binding proteins TAR DNA binding protein (TDP-43) and Fused in Sarcoma(FUS) into their pathologic prion conformations.

The results indicate that the vaccine RNA has specific sequences that may induce TDP-43 and FUS to fold into their pathologic prion conformations. In the current analysis a total of sixteen UG tandem repeats (ΨGΨG) were identifed and additional UG (ΨG) rich sequences were identifed. Two GGΨA sequences were found. Potential G Quadruplex sequences are possibly present but a more sophisticated computer program is needed to verify these.

Furthermore, the spike protein, created by the translation of the vaccineRNA, binds angiotensin converting enzyme 2 (ACE2), a zinc containing enzyme. This interaction has the potential to increase intracellular zinc. Zinc ions have been shown to cause the transformation of TDP-43 to its pathologic prion configuration. The folding of TDP-43 and FUS into their pathologic prion conformations is known to cause ALS, front temporal lobar degeneration, Alzheimer’s disease and other neurological degenerative diseases. The enclosed finding as well as additional potential risks leads the author to believe that regulatory approval of the RNA based vaccines for SARS-CoV-2 was premature and that the vaccine may cause much more harm than benefit.


Important excerpt from the summary:

Many have raised the warning that the current epidemic of COVID-19 is actually the result of an bioweapons attack released in part by individuals in the United States government [10,11]. Such a theory is not far fetched given that the 2001 anthrax attack in the US originated at Fort Detrick, a US army bioweapon facility. Because the FBI’s anthrax investigation was closed against the advice of the lead FBI agent in the case, there are likely conspirators still working in the US government. In such a scenario the primary focus of stopping a bioweapons attack must be to apprehend the conspirators or the attacks will never cease. Approving a vaccine, utilizing novel RNA technology without extensive testing is extremely dangerous. The vaccine could be a bioweapon and even more dangerous than the original infection.

5 doctors state the injections are bioweapons & what you can do about it. (This was never a viral illness but blood poisoning due to a spike protein. The injections are NOT “vaccines” but cause YOU to manufacture spike proteins – perhaps indefinitely – the very thing causing illness. Those getting the injections are now transmitting this spike protein to those foregoing the injections.  Those getting the shots should be quarantined.) A lot is unknown.  (Within the 5 doctors link, Dr. Lee Merritt speaks about this “prion” disease within)

In-Depth Look at the Dangers of Mold Toxicity

In-Depth Look at the Dangers of Mold Toxicity


By Holtorf Medical Group

Mold is a type of fungus that grows in the form of multicellular filaments called hyphae. There are tens of thousands of mold species that have evolved to survive harsh conditions. Mold reproduces by means of small, lightweight spores that travel through the air. These spores contain toxic chemicals called mycotoxins that can be inhaled and lead to mold toxicity.

Mold toxicity is a very prevalent and underdiagnosed condition that can consist of a variety of symptoms. Although anyone can suffer from mold toxicity, 25% of the population is particularly vulnerable due to a genetic predisposition that inhibits the clearance of biotoxins.

Learn about sources of mold, how mold affects the body, and more below.


Because mold grows on organic matter, it is an increasingly common part of our environment and people can be exposed in a variety of ways. Mold is able to feed on the moisture and warmth of its surroundings, leading to the release of mold spores and volatile organic compounds (VOCs). In fact, research suggests that mold can surface anywhere after just two days of moisture exposure.

Outdoor sources of mold include:

  • Stagnant water sources
  • Forests, beaches
  • Playgrounds
  • Sidewalks

Unfortunately, mold is also commonly found indoors, which is typically more harmful as mold spores can accumulate in higher concentrations due to a lack of airflow. Mold spores can enter homes, schools, and workplaces by attaching to clothing, shoes, or pets. Additionally, homes in climates where it frequently rains or that reside near the water are more likely to develop mold as they are exposed to moisture more often. It is common for mold to be found in damp bathrooms, basements, carpets, tiles, drywall, washing machines, and dishwashers. Some of the most common varieties of indoor mold are Aspergillus, Cladosporium, and Stachybotrys atra, all of which are considered black mold.

There is a growing number of health problems caused by mold inhalation. This is thought to be, in part, due to the rise of people living in urban areas. Researchers at Hospital General Universitario Gregorio Maranon in Spain reported that Aspergillus spores in outdoor air are more common in urban than rural settings in the province of Madrid. The continuing rise in global population has also pushed more people into environments that are likely to breed mold such as coastal and riparian floodplains, other bottomlands, and hurricane-prone areas.

Other mold risk factors are on the rise due to poor building practices that have been accepted for convenience. For instance, poorly built roofs leave behind rainwater that fosters mold growth. It is also common for venting clothes dryers to be located in a spot where they direct moisture to vulnerable areas inside homes. Additionally, modern homes often have tighter building envelopes, slowing the escape of water vapor and allowing it to become trapped and grow mold.

It is important to note that the same conditions that allow for mold growth also foster bacteria, MVOCs, beta-glucans, live or dead spores, fungal fragments, endotoxins, dust mites, cockroaches, and other pests. This combination of toxins can trigger an immune response and exacerbate chronic illnesses.

How Mold Affects the Body

Fungal secondary metabolites or mycotoxins affect numerous bodily functions mainly through triggering an immune response that leads to chronic inflammation. Mycotoxins impact both the innate immune system (the first line of defense against invading pathogens) and the adaptive immune response (specified immune response that eliminates certain pathogens and prevents their growth).

Mycotoxins such as aflatoxins and ochratoxins (which are produced from Aspergillus) as well as fumonisins (produced by Fusarium) have immunomodulatory properties. Consequently, these mycotoxins alter the body’s inflammatory response. Specifically, they target the functionality and production of cytokines, macrophages, and neutrophils.

Mycotoxins bind with cytokines, leading to an increase in clot formation and arterial blockages. This can lead to headaches, muscle aches, lack of temperature regulation, and brain fog. Increased cytokine levels then trigger action from white blood cells such as macrophages and neutrophils. This inflammatory immune response can restrict blood flow and reduce the amount of oxygen transported to tissues, resulting in fatigue, shortness of breath, and muscle cramps.

Another contributing aspect to the chronic inflammation experienced with mold toxicity is due to the way in which mycotoxins impair the white blood cell’s regulation cytokines, which leads to an increase in infections and a slower recovery from these infections.

Moreover, some mycotoxins inhibit the production of messenger cells, leukotriene B4, by targeting the enzyme, LTA4 hydrolase. This interrupts communication between the immune cells and minimizes the body’s defense mechanism. Because the first line of defense is impaired, it is difficult to develop adaptive immunity and eliminate the mycotoxins. As a result, the body is likely to experience chronic inflammation and a host of other issues.

Respiratory Impact

Mold enters the body through the skin and through inhalation, making respiratory function a primary target of mold. Once inhaled, mold can quickly colonize the lungs and sinuses as they are optimal growing conditions. This leads to the continual release of mycotoxins. Moreover, biofilms can form around the mold colonies, protecting them from the body’s immune system.

The sinuses are particularly susceptible to mold colonies and many species of Aspergillus have been identified in the sinuses of those with chronic sinus inflammation. Aspergillosis is known to be able to colonize in the lungs of both humans and animals, which causes invasive fungal infections. Because of the respiratory tract’s susceptibility to mold, mold exposure often mirrors allergy symptoms such as coughing, runny nose, sneezing, itchy eyes, and asthma.

Neurological Impact

Once mycotoxins are inhaled, they are stored in the body’s fatty tissue. Given that the brain is approximately 60% fat, mold toxicity can have profound neurological effects. Mycotoxins trigger an inflammatory immune response and this inflammation in the brain can impair cognitive function and lead to symptoms such as fatigue, memory loss, headaches, insomnia, dizziness, anxiety, depression, and more.

Chronic inflammation in the brain, especially when caused by toxins, can cause long-lasting damage. This is because when the brain is in a chronic state of inflammation, glial cells can no longer support neuron health and neural communication. When inflammation is present, glial cells change their cell morphology significantly and activate rapidly. These cells generate reactive oxygen species and release signals to trigger immune cells, which results in a continuation of the body’s inflammatory response. Over time, this leads to the degradation of tissue and of the blood–brain barrier and neurocognitive issues.

Alzheimer’s specialist, Dr. Bredson, MD, has found that one-third of Alzheimer’s Disease patients are considered “Inhalational Alzheimers,” which means their Alzheimer’s is a result of chronic inflammation caused by mold or other toxins. Other diseases that can be caused by mycotoxins include: ADHD, migraines, Parkinson’s, Chronic Fatigue Syndrome, and more.

The Role of Mold in Lyme Disease and Chronic Illness

Mold has a significant negative impact on the immune system, making those with chronic illnesses such as Lyme disease more at risk for developing serious health issues.

Because those with a chronic illness often have a weakened immune system, their body is less likely to be able to fight off mold spores and toxins. When the mold then begins to colonize in the body, patients experience chronic mycotoxin exposure, which reduces the body’s ability to fight infection due to mycotoxins immuno-suppressant effect. Thus, the body’s weakened immune system is forced to fight the chronic illness in addition to mycotoxins, leading to a worsening of symptoms associated with both conditions. Additionally, mold exposure and toxicity elicit an inflammatory response, which worsens chronic conditions such as Lyme, Fibromyalgia, gut dysfunction, and more.

Warning Signs of Mold Toxicity

Mold illness can cause a wide variety of symptoms. Often, it is only the respiratory symptoms that are recognized but it is important to be aware of its profound effects:

  • Fatigue
  • Anxiety
  • Depression
  • Light sensitivity
  • Headaches
  • Blurred vision
  • Dizziness
  • Vertigo
  • Brain fog
  • Memory loss (typically short-term)
  • Chronic congestion or sinus infections
  • Coughing
  • Abdominal pain
  • Muscle pain and/or joint pain
  • Hormone deficiency
  • Adrenal dysfunction
  • Nose bleeds
  • Environmental sensitivity (chemical sensitivity)
  • Chronic colds, flus, acute infections
  • Nausea
  • Itchy/ red eyes
  • Insomnia
  • Night sweats
  • Temperature dysregulation
  • Weight gain
Seeking Treatment

For over a decade, there has been a consensus in the medical community that regular exposure to mold significantly increases people’s risk for disease. This public health hazard has still not been addressed with the concern it should be as governmental agencies, such as the Institute of Medicine report commissioned by the CDC and released in 2004, have concluded that the primary health concerns with mold are solely respiratory. However, mold can have long-lasting health effects, especially for those dealing with a chronic illness.

If you feel you are suffering from mold toxicity or would like to get tested, contact Holtorf Medical Group today. At Holtorf Medical Group, our physicians are trained to provide you with cutting-edge testing and innovative treatments to properly diagnose and treat your condition, optimize your health, and improve your quality of life.



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Are Infections Seeding Some Cases of Alzheimer’s Disease?

Are infections seeding some cases of Alzheimer’s disease?

A fringe theory links microbes in the brain with the onset of dementia. Now, researchers are taking it seriously.

Some scientists think that microbes such as the herpes simplex virus 1 (shown here on an epithelial cell) could trigger some cases of Alzheimer’s disease. Credit: SPL

Two years ago, immunologist and medical-publishing entrepreneur Leslie Norins offered to award US$1 million of his own money to any scientist who could prove that Alzheimer’s disease was caused by a germ.

The theory that an infection might cause this form of dementia has been rumbling for decades on the fringes of neuroscience research. The majority of Alzheimer’s researchers, backed by a huge volume of evidence, think instead that the key culprits are sticky molecules in the brain called amyloids, which clump into plaques and cause inflammation, killing neurons. (See link for article)



Important quote:

Several microbes have been proposed as triggers of Alzheimer’s, including three human herpes viruses and three bacteria: Chlamydia pneumoniae, a cause of lung infections; Borrelia burgdorferi, the agent of Lyme disease; and, most recently, Porphyromonas gingivalis, which leads to gum disease. In theory, any infectious agent that can invade the brain could have this trigger role (there’s no good evidence, however, that SARS-CoV-2, the virus behind COVID-19, has this ability).

It’s also sad that Alzheimer’s research has been pigeon-holed for so long:,

This article contains Norrins’ paper in the comment section. The article above states there are 40 studies in the cue vying for the 1 million cash prize in March, when the challenge results will be announced: