Lawrence Broxmeyer, MD

We looked forward to Lowry’s “Alzheimer's disease: protective effects of Mycobacterium vaccae, a soil-derived mycobacterium with anti-inflammatory and anti-tubercular properties, on the proteomic profiles of plasma and cerebrospinal fluid in rats” publication in the Journal of Alzheimer’s Disease [1] as an often-overlooked possibility towards Alzheimer’s disease (AD) genesis.
The thought that AD might be of a mycobacterial etiology has recently gained traction, but has been too little expressed. Mawanda and Wallace simply cite that “amyloidopathy—a condition characterized by elevated levels of serum amyloid and by amyloid deposition and aggregation in tissues—is a frequent occurrence in several acute and chronic systemic inflammatory conditions, especially chronic infections like tuberculosis.” [2]. Several studies have already shown a “neuroprotective affect” using anti-mycobacterial antibiotics [3,4], and evidence suggests that patients aged 50-64 with infection with M. tuberculosis have a significantly higher risk of dementia [5].

An “urgent notice” from the Wuhan Health Commission warning of “successive cases of unknown pneumonia” was also leaked and posted online on 30 December 2019. The statement ordered hospitals to “strengthen responsible leadership” and ensure that no one “disclose information to the public without authorization.” Under growing pressure regarding this “unknown pneumonia”, the following day the Health Commission said researchers were investigating 27 cases of viral pneumonia, its first official notice. How did they know it was a virus? They didn’t.

I pazienti affetti da Coronavirus sono in larga parte asintomatici e vengono ospedalizzati per la comparsa di problematiche febbrili, respiratorie,… giungono comunque all'attenzione dei sanitari quando il quadro infettivo è conclamato. La prima cosa che viene effettuata in caso di sospetta infezione è il tampone naso-faringeo per il quale però non sussistono prove riscontrabili che effettivamente riscontri l'RNA di un virus, sia esso coronavirus o qualsiasi altro.

With Lawrence Broxmeyer MD, by exclusive interview One source reports 80.9% of newly infected COVID-19 coronavirus patients were asymptomatic (no symptoms) in the early stage of their infection. Among these individuals who are asymptomatic there is a 47% chance of a false positive coronavirus test (the test said they are infected, but they really aren't). There just has to be a reason why 47% of tests for COVID-19 coronavirus are false positive. If not coronavirus, then what? Dr. Lawrence Broxmeyer, a long-time disease investigator and skeptic of modern assumptions regarding the origins of infectious disease, postulates that a small and prevalent mycobacterium that causes 1.7 million deaths a year, is the origin of the infection, hospitalizations and deaths attributed to a newly mutated coronavirus, now identified as COVID-19. According to Dr. Broxmeyer, COVID-19 may be nothing more than a passenger virus while the mycobacterium commonly known as tuberculosis, is wreaking all the damage in the lungs in the current epidemic that is holding the world in a news media-created grip of terror. Cause and effect have not been proven. Tuberculosis: the great masquerader Mycobacteria tuberculosis is the great masquerader. Just type in "tuberculosis" and "masquerade" into your web browser and see how many maladies TB pretends to be. The TB mycobacterium has fooled doctor after doctor. And it may be fooling the entire world now. Mycobacteria tuberculosis (TB) acts like a virus. It is a seasonal infection peaking in winter just like cold and flu viruses. While the TB mycobacterium is spread throughout the year, it is only when vitamin D levels are low and the immune system weak that it produces symptoms. It is a cell-wall deficient germ that appears like a virus under a microscope. It attacks the lungs, resulting in inflammation that essentially drowns infected patients who cannot breathe, just like COVID-19 coronavirus is said to do. Demographic evidence Now further circumstantial demographic evidence appears to correlate with the mycobacterial origins of the current lung disease pandemic that is said to have spread geographically via airplane travel from its epicenter in China to a long list of other countries. Nowadays, TB is largely a disease of poverty and malnutrition. The COVID-19 coronavirus epidemic in China occurred while China had been battling a rampant TB outbreak for many months.

BULLET-POINT SUMMARY:

• Antivirals did not play a significant role in helping curb previous coronavirus outbreaks — SARS and MERS largely went away on their own, through public health measures that helped contain the spread.
• Present coronavirus trials using antivirals have to this point on the whole proved either inconclusive or disappointing.
• Azithromycin, an antibiotic with no antiviral activity whatsoever, is proving quite efficacious in treating the disease behind the “COVID-19” pandemic. Azithromycin is a first-line drug against Mycobacterium avium, which can simulate obstructive lung disease, and every other sign or symptom of COVID-19 documented to date.  In addition azithromycin is a second or third-line drug against drug-resistant Mycobacterium tuberculosis.
• There was and still is a Pandemic going on in the world which dwarfs coronavirus. A Pandemic which kills one person every 21 seconds. A pandemic which in 2018 alone killed at least 1.5 million people annually. A mycobacterial pandemic, from Mycobacterium tuberculosis.
• In the United States, pulmonary Mycobacterium avium complex (MAC) disease or “fowl tuberculosis” is more common than tuberculosis
• Furthermore, Mycobacterium avium complex is now the leading mycobacterial cause of chronic pneumonia in the United States.
• Infections due to non-tuberculous mycobacteria (NTM) such as Mycobacteria avium are increasing worldwide, and are particularly important to take into account when considering a zoonosis, which COVID-19 was originally thought to be.
• Not only does the drug hydroxychloroquine inhibit intracellular TB, but it acts synergistically against mycobacterial disease when combined with certain antimycobacterials. Azithromycin is also used as an antimycobacterial.
• The BCG tuberculosis vaccine is currently the focus of an international 4 country study to combat the Coronavirus pandemic.
• In the present Coronavirus pandemic, tubercular infection is by far the most common co-morbidity or underlying condition.
• A Recent preliminary Chinese study shows that tubercular infection likely increases susceptibility to SARS-CoV-2, and also increases COVID-19 severity.

Bullet Point Summary:
• The community of Chinese people in Italy has grown rapidly in the past ten years. Official statistics indicate there are at least 320,794 Chinese citizens in Italy. Milan, in Northern Italy where COVID-19 first struck, has the largest Chinese population in Italy.
• Before there was a COVID-19 Coronavirus, there was and still is a tuberculosis global Pandemic, a Pandemic which presently kills someone approximately every 21 seconds — about 1.5 million or more in 2018 alone [ https://www.tballiance.org/why-new-tb-drugs/global-pandemic]. It is still treatable, but only if looked for and considered.  By 2013, Faccini et al reported in Emerging Infectious Diseases, an outbreak of tuberculosis, Beijing strain, in a primary school in Milan, Italy which was eventually traced to include 15 schoolchildren with active TB and 173 with latent infection.
• The coronavirus, AKA Covid-19, first appeared in Lombardy and Veneto. [See Map Figure 1]. Italy's first victim was a 76-year-old woman who was found dead at her home 50 km. (30 miles) south of Milan, in Lombardy, on Thursday, March 12, 2020 and tested positive for the coronavirus. A 78-year-old man died of the infection in a hospital near Padua, in Veneto, during the next evening.
• Traditionally, Italy has a low incidence of tuberculosis (TB); and in 2008, the incidence of notified cases was only 7.6/100,000 population. Yet even by 2009, in Milan, the largest urban area and the birthplace of Italian COVID-19, in Lombardy, the incidence climbed steeply to 20.44/100,000 population. By 2019, Cuomo et al attributed this to rising immigration patterns.
• With the sharp increase in tuberculosis statistics, the basis of what would happen to Northern Italy had been laid, the tripling of an “underlying” tubercular medical condition that could provide fertile grounds to foster a second pandemic pathogen. But what would happen next in Northern Italy was an event that no one could have foreseen.
• On January 22nd, 2020, Customs authorities from the Guardia di Finanza in the northern Italian city of Padua seized and burnt nearly 10 tons of Chinese pig meat, potentially infected with African swine fever. By the end of 2019, half of China’s swine herd —250 million pigs, were dead. Padua is located in the Veneto region of Italy. The coronavirus, AKA Covid-19, first appeared in Lombardy (Milan) and Veneto (Padua). Swine fever is deadly among pigs, though it poses no risk to humans.
• But if Italy thought it had incinerated its problems away by burning tainted Chinese pig meat, much of which probably originated from Wuhan’s vast pig reservoir, it had another thought coming. Now, infectious particles were circulating through the air of Northern Italy. Furthermore, if Swine fever posed no risk to humans, what did pose a risk is a common disease in pigs called Mycobacterium avium (AKA MAC or fowl tuberculosis), a non-tubercular mycobacteria (NTM). In one study, the incidence of Mycobacterium avium (fowl tuberculosis) in a pig population was an astonishing 81%. As reported by some workers, M. avium isolates from swine represent a major threat to human beings. And the similarity of the IS1245 RFLP [restriction fragment length polymorphism (RFLP)] patterns of the human and porcine isolates indicated a close genetic relatedness, suggesting that M. avium is transmitted between pigs and humans. Such M. avium infection can occur wherever the right “underlying pulmonary conditions” exist, which can be an event as simple as a childhood or reactivated tubercular infection, or merely tying up the lungs with an excess of dust or particulate matter.
• Thus, just before the event attributed to COVID-19 in Northern Italy began, a deadly combination of rising TB rates followed by the introduction of porcine [from pigs] M. avium [also called fowl tuberculosis] into the environment would eventually first bring the Italian Northern provinces, and then the entire peninsula to its knees. This precise series of events led to the Great Pandemic of 1918 at Fort Funston and the Chinese episode at Wuhan, a major player in China’s pig industry.
• Mycobacterium avium complex (MAC) or mycobacterium avium is a poorly understood disease which fulfills almost all of those characteristic signs and symptoms attributed to the latest “novel” Coronavirus.  In general Mycobacterium avium is a milder disease then Mycobacterium tuberculosis. The most common type of nontuberculous mycobacterial lung infection that causes pulmonary disease in the United States are due to the group of bacteria in the M. avium complex (MAC).
• When it appears in the lungs, Mycobacterium avium favors an older population with an underlying condition. As with COVID-19, not all people with a nontuberculous mycobacterial lung infection such as M. avium need to be treated.  On the other hand, if it disseminates or spreads systemically, the patient can present with fever or high fever, diarrhea, fatigue, shortness of breath, chronic or recurrent sore throat and cough……….most of which have been reported in Coronavirus patients.
• Non-tubercular-mycobacteria (NTM) such as Mycobacterium avium can be asymptomatic or can cause symptoms similar to tuberculosis, such as cough, fever, fatigue, and weight loss.
• It is projected that the present Italian outbreak and outbreaks worldwide will follow the timetable of Yang’s Wuhan study, which describes an annual TB surge in Wuhan as being fueled by increased transmission in the winter; peaking in March, with a second smaller peak in September.

BULLET POINT SUMMARY
 COVID‐19 Coronavirus is as much an ecological disaster as it is a medical
one. Initially it appears to be a unique experience centered in Wuhan,
China. It emanates from an environment of incinerated pig waste, airborne
particles, and low vitamin D blood levels in winter, and weakened immune
systems, particularly among smokers, drinkers and the elderly.
 It is believed both the Spanish flu of 1918 and the COVID‐19 coronavirus
began as zoonotic (animal to human) infections. Not from bats as first
reported in the Wuhan COVID‐19 outbreak, but rather from pigs, and pig
waste.
 The 1918 Spanish flu pandemic began in the midst of an infectious pig
slaughter of undiscovered cause, a few hundred miles from Camp Funston,
what is Fort Riley today. Similarly, the outbreak of the COVID‐19
coronavirus outbreak began in the Wuhan, China area in the wake of a
massive kill‐off of pigs who were dying from African Swine Flu.
 Viral outbreaks arise in winter, but so does tuberculosis.
 Some types of mycobacteria do not have cell walls and can mimic the
appearance of a virus under the microscope.
 Antibiotics cannot be used for viruses. If a virus, then why aren’t antiviral
drugs working but antibiotics are?
 COVID‐19 coronavirus may just be a “passenger virus,” not the primary
microbial organism that kills by filling the lower lungs with fluid.
 Both the current Wuhan COVID‐19 coronavirus and tubercular
mycobacteria do not tend to infect or cause serious disease in young
children roughly 5‐12 years of age.
 Fear of the COVID‐19 coronavirus may be misplaced. More people are
killed by Mycobacterium tuberculosis (1.7 million) in a year than the few
who have been infected (~80,000) or have died (less than 2000) of the
COVID‐19 coronavirus.
 It is projected that the "COVID‐19 Coronavirus" will peak worldwide in
March and then return in a second but lesser peak in September, in
accordance with Yang’s Wuhan study from 2004 to 2013, describing the
annual TB surges in Wuhan, China.

History has a tendency to repeat itself, and pandemics/epidemics are no exception. Case in point, the common ground between the present “novel” 2019 coronavirus (AKA COVID-19), the SARS (Severe Acute Respiratory Syndrome) and MERS (Middle East respiratory syndrome) outbreaks before that, and the Great Pandemic of 1918, long ago. The
present COVID-19, did not occur in a vacuum. By December of 2018, Liu et al., proclaimed tuberculosis to be an epidemic throughout China, an epidemic which still rages on. China harbors the second largest burden of tuberculosis in the world ̶ a disease which often begins with flu-like symptoms, and a disease whose bacilli are laden with RNA bacterial
viruses called mycobacteriophages. Quietly, by 2016, the World Health Organization acknowledged that despite advances, the TB bacillus, which Koch was forced to refer to as “the TB virus”, is once again the deadliest pathogen in the world. Here we compare all 4 pandemics/epidemics with some surprising results and similarities.

A 2018 study by Tricco., et al. ranking the safety and effectiveness of the four leading drugs now taken to enhance concentration, memory, alertness and moods in, found that donepezil (Aricept®) was most likely to effectively improve cognition in patients with Alzheimer's dementia. However, patients who took donepezil were more likely to experience side effects including nausea, vomiting and diarrhea than those who received a placebo, according to the study, published online in the Journal of the American Geriatrics Society [1]. And an earlier study showed that almost 19% of patients in an Aricept 23 mg daily group discontinued treatment due to side effects [2]. The fact is that as for all conventional drugs used in Alzheimer's treatment-only a small percentage of AD victims are helped by them. Yet, in both the case of FDA approved and alternative treatments presently available, much can be gleaned by scrutinizing which pathogen or pathogens the bulk of their activity is directed towards. It seems that several compounds said to have effects upon the neuronal systems in Alzheimer's may also exert influence through other mechanisms, such as antimicrobial actions.

Alois Alzheimer might have mentioned plaques and tangles in a single short paper on pre-senile dementia in 1907, but it was the co-discover of Alzheimer's disease (AD), Oskar Fischer, who in that same year far more extensively reported neuritic plaque in 12 cases of senile dementia, a condition which he and many others refused to differentiate from Alzheimer's " pre-senile " dementia. Fischer, Alzheimer's great rival, speculated that for the most part these plaques, found only in senile demented patients, caused their dementia. Moreover, Fischer felt such cerebral plaque to be the result of an infection and was very specific as to the sort of infection that might be involved. He felt that he had spotted, throughout his brain autopsies, a tubercular-like Actinobacteria then called Streptothrix (Actinomycosis), often and repeatedly confused with the filamentous cell-wall-deficient forms of the tubercular bacilli. At this point for Fischer, this was the possible infectious cause of AD. To be sure, Oskar Fischer was the first on record to suggest that chronic infection might be causative for what we today call AD. Fischer's infectious view never gained immediate popularity, although today, more than a century later, a volume of data supporting such an approach has begun to accumulate. But was Fischer's specific microbe on the right track to discovering the cause of AD to begin with? Documents uncovered since then seem to suggest that he was considerably closer than anyone else—either then or since. In June of 2017, a University of Bristol study in the UK found a 5 to 10-fold increase in Actinobacteria (order Actinomycetales) population in postmortem AD brains compared with controls [1]. Oskar Fischer's Steptothrix was an Actinobacteria as well, as was the filamentous tuberculosis that Streptothrix was so often mistaken for. But specifically, the Bristol group found an Actinobactor called Propionibacterium acnes (P. Acnes) in autopsied AD brains—a common organism, traditional felt to be non-pathogenic and commonly found on our skin which can

The word Influenza comes from mid–18th century Italian and literally means ‘influence’. Similar to how the coronavirus was once best known to cause the common cold, in 1918 Influenza was felt to be so benign a disease that it was not reportable in the United States. And it was not until 1933 that Influenza was “discovered”. So just what was causing the deaths in 1918? And why did the corona “virus” turn so deadly so quickly? Before we can be certain of anything, these questions need to be answered. But to this point, they have not been answered. In the meantime, during both events there was a deadly pandemic of tuberculosis going on, a pandemic which even in 2020 kills one person every 21 seconds for a total of at least 1.5 to 1.8 million dead in 2018 alone. Yet Robert Koch, TB’s discoverer, was repeatedly forced to call it a virus, to assuage other authorities of his time. And, as we shall soon see, the concept that only a new and virulent strain of a virus can be so infectious and kill so quickly is not only fallacious, but dangerous -and completely at odds with what used to be called the acute form of “galloping consumption” [tuberculosis] which did and still can kill in a matter of hours, days or weeks.
“Viral” influenza was informally first mentioned as being behind America’s 1918 influenza pandemic not by a direct study of the disease in humans, but rather from studies on animal diseases. In 1918, J.S. Koen, a veterinarian, observed a disease killing thousands of pigs which he believed to be the same disease as the now infamous influenza Pandemic of 1918. He felt that it was a virus. It was solely his belief. Yet new evidence and older historical findings bring up the possibility that influenza doesn’t originate from a virus –despite the indefatigable efforts, up to the present, of flu enthusiasts to viralize the 1918-19 pandemic. (Burnet F, Clark E. 1942) (Morens DM, Taubenberger JK. 2009). As we shall see, such efforts on the part of viral devotees are nothing new, and began in force with scant evidence in Great Britain during the 1st World War, also known as the Great War.

Alois Alzheimer might have mentioned plaques and tangles in a single short paper on pre-senile dementia in 1907 but it was the co-discover of Alzheimer's disease, Oskar Fischer, who in that same year far more extensively reported neuritic plaque in 12 cases of senile dementia, a condition which he and many others refused to differentiate from Alzheimer's " pre-senile " dementia. Fischer, Al-zheimer's great rival, speculated that for the most part these plaques, found only in senile demented patients, caused their dementia. Moreover, Fischer felt such cerebral plaque to be the result of an infection and was very specific as to the sort of infection that might be involved. He felt that he had spotted, throughout his Alzheimer's brain autopsies, a tubercular-like Actinobacteria then called Streptothrix (Actinomycosis), often and repeatedly confused with the filamentous cell-wall-deficient (CWD) forms of the tubercular bacilli. At this point for Fischer, this was the possible infectious cause of Alzheimer's. To be sure, Oskar Fischer was the first on record to suggest that chronic infection might be causative for what we today call Alzheimer's disease. Fischer's infectious view never gained immediate popularity, although today, more than a century later, a volume of data supporting such an approach has begun to accumulate. But was Fischer's specific microbe on the right track to discovering the cause of Alzheimer's to begin with? Documents uncovered since then seem to suggest that he was considerably closer than anyone else –either then or since.

In May, 2017, a Norwegian study done by Berstad and Berstad threw its support behind revitalizing of the hypothesis that with regard to Parkinson's disease (PD), the preponderance of convincing evidence points to a chronic infectious cause – not viral and most likely of the family Actinomycetales of which tuberculosis and the mycobacteria are premier members. The Berstads concluded that in accordance with such thoughts and despite the diagnostic challenges ahead, that further studies in human brain tissue from PD patients to detect such an underlying infectious cause were warranted. Such thoughts are really nothing new, and have been in circulation since James Parkinson mentioned this same infectious cause in An Essay on the Shaking Palsy in which he was the first to describe " paralysis agitans " , a condition that would later be renamed Parkinson's disease by Jean-Martin Charcot. Here we review further evidence in support for this particular infectious cause of Parkinson's.

The history of coming to grips with what autism is and its etiology has been tortuous ― if not tortured. By 1908 the word autism was defined as a schizophrenic who was withdrawn or self-absorbed. Some decades later Leo Kanner decided that autism was based on children with “a powerful desire for aloneness.” In the 1960’s psychologist Bruno Bettelheim, picking up on another aspect of Kanner’s observations, thought autism was simply based upon mothers not loving their children enough. Then came the twin research studies which purported autism to be caused by genetics or biological differences in brain development. Yet the consensus that Autism is from an intrauterine infection had also been growing, bolstered more recently by Patterson’s and Fatemi’s studies. However, the question would still remain: which infection? This, of course, remains unknown. Until 1980 autism in the US is still called “childhood schizophrenia” and in some parts of the world, it still is. By the same token, there has been, for some time, an extensive body of medical literature which ties schizophrenia to chronic infection –some time before when Rzhetsky [5] in 2007, used a proof-of-concept bio-statistical analysis of 1.5 million patient records, finding significant genetic overlap in humans with autism, schizophrenia and tuberculosis. This lends an explanation as to why anti-tubercular drugs such as Seromycin have been so successful in NIH trials treating autism. Tracing the history of autism from John Langdon Down’s children, a subset of which were autistic, to the present, this paper also explains how the stealth pathogen hypothesized to be behind autism has evaded modern day diagnostics..

The word ‘cancer’ is of Latin derivation and means crab. By the turn of the 20th Century organized medicine had come to the conclusion that it was not a matter of whether infectious disease caused cancer, but which one. Then, in 1910, certain American medical powers did a 180-degree rotation –abruptly deciding that cancer was not caused by a microbe. This flew in the face of over two hundred years of research in which a cancer germ had been discovered and rediscovered. Of all the infectious possibilities for cancer, unquestionably the one class of microbes that has been long recognized to most consistently mimic and imitate ‘cancer’ at both clinical and tissue levels were the mycobacteria of the family Actinomycetales of which tuberculosis and leprosy are premier examples. The association of TB with carcinoma was initially described about 200 years ago by Bayle who considered the lung malignancy ‘cavitation cancereuse’ to merely be one of the various types of tuberculosis. Ever since, almost as if in reflex to the obvious –the potential association between TB and subsequent development of cancer has drawn active investigation. In a combined 2017 Cleveland Clinic/Case Western probe, Wang et al compared the microorganisms in breast tissue of 57 patients with breast cancer (the most common cancer in women worldwide), and 21 healthy individuals undergoing breast surgery for cosmetic purposes. Three out of the four pathogens they found in breast cancer tissue belonged to the order Actinomycetales.

Medline studies in the Parkinson's literature have cited a tuberculosis-like germ called Nocardia as being responsible for Parkinson's disease. Kohbata seemingly cemented a relationship between Nocardia and Parkinson's by finding serologic evidence in 20 of 20 Parkinson's patients, acknowledging that blood tests for Nocardia and the mycobacteria such as tuberculosis often cross-react, as they belong to the same order of bacteria, the Actinomycetales. Besides this difficulty in differentiation, a well-used medical school textbook of microbiology, Atlas, points out that even among experts, different observers may classify the same strain of bacteria as Nocardia or Mycobacterium tuberculosis. Parkinson's: Another Look is a theoretical text which presents compelling, well-documented evidence for an infectious cause for Parkinson's disease on historical, epidemiological, pharmacologic, microbiological, and biochemical levels. A supportive Norwegian study done by Berstad and Berstad in May of 2017 is also attached.

The TSE'S or transmissible spongiform enchephalopathies, include bovine spongiform encephalopathy (also called BSE or " mad cow disease "), Creutzfeldt– Jakob disease (CJD) in humans, and " scrapie " in sheep or goats (caprine spongiform encephalopathy). They remain a mystery, their cause still hotly debated. Current mad cow diagnosis lies solely in the detection of late appearing " prions " , an acronym for hypothesized, geneless, misfolded proteins, somehow claimed to cause the disease. Yet laboratory preparations of prions contain other things, which could include unidentified bacteria or viruses. And the only real evidence that prion originator Stanley Prusiner had in his original paper that the disease agent behind " Scrapie " in sheep and goats was devoid of DNA or RNA– was based upon the fact that he couldn't find any. Furthermore, the rigors of prion purification alone, might, in and of themselves, have killed any causative microorganism and Heino Dringer, who did pioneer work on their nature, candidly predicts " it will turn out that the prion concept is wrong. " Roels and Walravens as well as Hartly traced Mad Cow to Mycobacterium bovis. Moreover, epidemiologic maps of the origins and peak incidence of Mad Cow in the UK, suggestively match those of England's areas of highest bovine tuberculosis, the Southwest. The neurotaxic potential of bovine tuberculosis has for some time been well known. By 1911 Alois Alzheimer called attention to " a characteristic condition of the cortical tissue which Fischer referred to as 'spongy cortical wasting " in Alzheimer's disease (AD). But behind AD, Fischer suspected a microbe called Streptothrix which was constantly being mistaken and confused for tuberculosis. Our present investigation of the TSEs clearly shows cell-wall-deficient (CWD) tubercular mycobacteria present, verified by molecular analysis, ELISA, PCR and microscopy to cause spongiform encephalopathy.

Recent literature shows a controversial new push to tie microorganisms to Alzheimer's disease (AD). Study after study, in which scientists have injected human Alzheimer-diseased brain tissue into mice and other laboratory animals that later developed the disease have left little doubt that Alzheimer's disease (AD) arises from an infectious process. By 2013 Mawanda and Wallace's " Can Infections Cause Alzheimer's Disease " struck down some of the commonly entertained pathogens for AD such as herpes simplex virus type 1, Chlamydia pneumoniae, and several types of spirochetes. Instead they pointed to two prime suspects for Alzheimer's amyloid-beta deposition: " especially chronic infections like tuberculosis and leprosy. " To be sure, it was German neuropathologist Oskar Fischer of the Prague school of Neuropathology, Alzheimer's great rival, who was the first to suggest that infection might be causative for Alzheimer's. Fischer's credentials: he was the co-discoverer of Alzheimer's disease. His suspected germ was the Streptothrix, today classified as Actinomycetes, a rare central nervous system pathogen which at the time was so constantly and consistently mistaken for tuberculosis that Choppen-Jones suggested that TB be called tuberculomycosis. And Just ten years before Oskar Fischer found Actinomycosis-like forms in Alzheimer's cerebral plaque, Babèş and immunologist Levaditi reported in " On the Actinomycotic Shape of the Tuberculous Bacilli " that Fischer's typical Actinomyces-like clusters (Drüsen) with clubs appeared in the tissue of rabbits inoculated with tubercle bacilli beneath the dura mater of their brains. Investigators who supported and subsequenly followed up on Fischer's Alzheimer's germ are also discussed.

A growing body of health officials in Brazil are doubting that the Zika " virus " is responsible for the rise in birth defects in parts of that country. Zika, along with yellow fever, has been tossed into the family Flaviviruses; the Latin " flavus " meaning yellow. But unlike yellow fever, the vast majority of Zika's symptoms for the last 70 years have been mild to non-existent. Despite disseminations by the lay and scientific press, there are serious questions whether Zika causes microcephaly at all. If by March, 2016 the Brazilian Ministry of Health reported 2,197 suspected cases of microcephaly, only 11.48% of these were Zika-positive. Zika is widespread throughout Brazil and South and Central America, yet the bulk of microcephaly cases are confined to the costal tip of Northeastern Brazil. Furthermore, despite extensive testing, no known mosquito-borne arbovirus or any other virus has to this point been proven to cause Brazilian microcephaly. While Zika was being portrayed as " the most alarming health crisis to hit Brazil in decades " , tuberculosis and its related mycobacteria were quietly gaining a stranglehold and building an ecologic niche in the very Northeastern region being hit by epidemic microcephaly. Why was this important? With NE Brazilian microcephaly/Zika we are probably dealing with a mosquito-fuelled environmental zoonosis ― a disease that can be transmitted from animals to humans ― such as primates, and to a lesser extent birds (Mycobacterium avium), and rodents (Mycobacterium microti) , all mentioned in the Zika literature. Add to this the penchant of Brazilian's to illegally capture and keep mycobacterial-laden wild monkeys and exotic birds as pets or for revenue, and you have a potential zoonotic time-bomb ready to explode once the proper vectors presents themselves. Three mosquito vectors have been steadily populating Northeastern Brazil: namely Culex quinquefasciatus, the Aedes aegypti and the Aedes albopictus ― all of which have the capacity to transmit viral-like forms of the mycobacteria associated with HIV and through direct laboratory investigation with microcephaly. Perhaps it is time to rethink what's really behind Brazilian Microcephaly and other symptomatology from the " Zika " agent.

Mycobacterium avium causes disseminated infection in patients with acquired immune deficieny syndrome. Mycobacterium tuberculosis is a pathogen associated with the deaths of millions of people worldwide annually. Effective therapeutic regimens exist that are limited by the emergence of drug resistance and the inability of antibiotics to kill dormant organisms. The present study describes a system using Mycobacterium smegmatis, an avirulent mycobacterium, to deliver the lytic phage TM4 where both M. avium and M. tuberculosis reside within macrophages. These results showed that treatment of M. avium–infected, as well as M. tuberculosis–infected, RAW 264.7 macrophages, with M. smegmatis transiently infected with TM4, resulted in a significant time- and titer-dependent reduction in the number of viable intracellular bacilli. In addition, the M. smegmatis vacuole harboring TM4 fuses with the M. avium vacuole in macrophages. These results suggest a potentially novel concept to kill intracellular
pathogenic bacteria and warrant future development.

In 2014, Buehring reported that Bovine Leukemic Virus (BLV), a common oncogenic retrovirus of cattle, was present in some humans, primarily localized to the breast epithelium ― the very cell type from which most breast malignancies arise. By 2015, there appeared data (Buehring, 2015) supporting that as many as 37% of human breast cancer cases could be attributable to BLV exposure. But if recent estimates suggest over 83% of U.S. dairy operations are currently positive for BLV, they also show that approximately 68% are positive for cell-wall-deficient Mycobacterium avium subspecies paratuberculosis (MAP). Although tubercular lung infection has been said to cause 11 times the incidence of lung cancer as normal control subjects, it is its cell-wall-deficient (CWD) forms (also called L-forms) that have recently repeatedly been found through genetic analysis and appropriate stains in such cancer tissue ― suggesting that CWD tuberculosis or atypical tuberculosis " is likely to be involved in the occurrence or development of lung carcinoma ". A similar relationship between tubercular L-forms and the genesis of the very breast cancer addressed in the aforementioned BLV viral trials. This is not a coincidence. L-forms (CWD forms) predominate and are crucial to the survival of mycobacteria in vivo and they have been documented by fluorescence microscopy in all intracellular macrophage-grown M. tuberculosis observed. From its origin, the very concept of the " BLV leukemic virus" has been on shaky, unstable ground. In 1969, veterinarians Janice and Lyle Miller from the University of Wisconsin-Madison spotted C-shaped " virus-like " particles in cattle lymposarcoma insisting that these were similar to other C-type viruses " regarded as the cause of leukemia in other species. " But by 1978, scientists at Downstate reported atypical mycobacterial forms, including its preferred filterable virus-sized " L " or cell-wall-deficient (CWD) forms in not only leukemia but all other malignancies ― all having, as their common denominator the continuous presence of mycobacterial C-shaped forms. Tracing back to techniques similar to Miller and Millers original BLV study we found in the very lyophilized antigens present in commercial kits for the diagnosis of BLV (AgBLV), these very same CWD (cell-wall-deficient) mycobacteria and mycobacterial DNA in all BLV samples ― which when introduced into guinea pigs stimulated the same antibody as occurred when mycobacteria-infected internal organ homogenates themselves were injected into other guinea pigs. It is therefore assumed that the Bovine Leukemic Virus (BLV) is being mistaken for viral-like forms of cell-wall-deficient (CWD) atypical tubercular mycobacteria. Since latent tubercular infection, as well as the administration of BCG and tuberculin also results in persistent CWD forms, their possible role in carcinogenesis is also considered.

Recent literature shows a controversial new push to tie microorganisms to Alzheimer’s disease (AD) ― which despite the protests of some, is badly needed. Indeed there is a good chance that Alzheimer’s is caused by a microbe. Study after study, in which scientists have injected human Alzheimer-diseased brain tissue into mice and other laboratory animals that later developed the disease have left little doubt that Alzheimer’s arises from an infectious process. So the proper focus of the present debate regarding AD should not be ‘is there an infectious process or processes behind Alzheimer’s?’…….. but rather ‘which one?’ Clearly, whatever the infectious cause behind Alzheimer’s is, it must be a disease that is statistically widespread in the world today and that was also prevalent at the time of Dr. Alzheimer. Presently, in America alone, more than 5 million people, to varying degrees, have lost their memory or cognition to this challenging disease.

Specifically mentioned to this point as possible causes have been: [1] herpes simplex virus type 1 (HSV-I), [2] Chlamydia pneumoniae, and [3] several types of spirochetes. Also mentioned is [4] fungal infection in the AD brain as well.

Mawanda and Wallace’s review (2013) gave seven annotated references as to why Herpes Simplex virus type 1 (HSV-1) “remains questionable” as a cause for Alzheimer’s; nine studies referenced as to why there was “no evidence to suggest an association between Chlamydia pneumoniae infection and AD pathogenesis”; and six “rigorous studies which found no evidence to suggest that spirochetal B. Burgdorferi, is “causally linked to AD” Wallace also mentioned that although Riviere et al. found oral spirochetal Treponema, including T. denticola, T. pectinovorum, T. vincentii, T. amylovorum, T. maltophilum, T. medium, and T. socranskii in a significantly higher proportion of postmortem brain specimens from AD cases than controls. These results have, however, according to Mawanda and Wallace’s review, not been replicated.

As for fungal forms found in the Alzheimer’s brain, this is nothing new. Oskar Fischer, the co-discoverer of Alzheimer’s disease, saw such forms in 1907. But Fischer knew that they were related to Streptothrix, a germ with both bacterial and fungal properties often confused with tuberculosis. The disease actinomycosis was at one time referred to interchangeably with its older bacterial name, the “Streptotriches” (the plural form of Streptothrix). Fischer used such older nomenclature in describing certain forms he saw under his microscope. Furthermore, regarding the thick, black, club-shaped "Drüsen" in Oskar Fischer's 1907 drawing of senile plaque ― at the time, it was widely acknowledged that such drüsen could result from either infection with Streptothrix, now known as actinomycosis (aktinomycesdruse), a rare disease in humans, or tuberculosis, a disease that by 1882, as Alzheimer prepared to leave for Berlin for his medical education, was understood to be far and away the leading cause of infectious death in Europe. And just ten years before Oskar Fischer found Actinomycosis-like Streptothrix in Alzheimer’s cerebral plaque, Babèş and immunologist Levaditi reported in “On the Actinomycotic Shape of the Tuberculous Bacilli” that typical Actinomyces-like clusters [Drüsen] with clubs appeared in the tissue of rabbits inoculated with tubercle bacilli beneath the dura mater of their brains. Once introduced into the brain this way, reported Babes, TB bacilli not only branched out like the Actinomycosis such as Streptothrix, but they developed rosettes that were identical to the "drüsen" that Oskar Fischer spotted in Alzheimer’s plaque.

What Mawanda and Wallace did maintain however was the emerging evidence that supported an infectious pathogen and two prime suspects for Amyloid beta deposition to the extent that it was going on in Alzheimer’s. This article discusses one of them.

Every 72 seconds someone in America develops Alzheimer’s disease (AD). And it has been said that almost everyone living long enough will eventually show evidence of Alzheimer’s disease. Thus far its cause has remained elusive. Nevertheless, recently, study after study, in which scientists have injected human Alzheimer diseased brain tissue into mice and other laboratory animals that later developed the disease have left little doubt that Alzheimer’s arises from an infectious process, and the focus of debate seeming to be which particular disease. But clearly, it must be a disease that is not only statistically widespread in the world today, but that was also prevalent at the time of Dr. Alois Alzheimer. To be sure, it was German neuropathologist Oskar Fischer of the Prague school of Neuropathology, Alzheimer’s great rival, who was the first to suggest that infection might be causative for Alzheimer’s. Fischer’s credentials: he was the co-discoverer of Alzheimer’s disease and tirelessly did autopsies on the brains of patients with Alzheimer’s. Fischer’s infectious view never gained immediate popularity, although today, more than a century later, a volume of data supporting such an approach has begun to accumulate. But was Fischer’s specific microbe, a tubercular-like Streptothrix, on the right track to discovering the cause of Alzheimer’s to begin with? The evidence and events uncovered in this manuscript, including those of Babes, Chantemesse, Marinescu, Southard, Clouston and Schwartz  seems to suggest that he was considerably closer than anyone else ― either then or since.

IN PRESS

Every seventy-two seconds someone in America develops Alzheimer’s disease (AD). And it has been said that almost everyone living long enough will eventually show evidence of Alzheimer’s disease. Thus far its cause has remained elusive.

Nevertheless, recently, study after study, in which scientists have injected human Alzheimer diseased brain tissue into mice and other laboratory animals that later developed the disease have left little doubt that Alzheimer’s arises from an infectious process, the focus of debate seeming to be which particular disease. But clearly, it must be a disease that is not only statistically widespread in the world today, but that was also prevalent at the time of Dr. Alois Alzheimer.

To be sure, it was German neuropathologist Oskar Fischer of the Prague school of neuropathology, Alzheimer’s great rival, who was the first to suggest that infection might be causative for Alzheimer’s. Fischer’s credentials: he was the co-discoverer of Alzheimer’s disease and tirelessly did autopsies on the brains of patients with Alzheimer’s.

Fischer’s infectious view never gained immediate popularity, although today, more than a century later, a volume of data supporting such an approach has begun to accumulate. But was Fischer’s specific microbe on the right track to discovering the cause of Alzheimer’s to begin with? The evidence uncovered in this book seems to suggest that he was considerably closer than anyone else—either then or since.

In this volume, doctor and medical researcher Lawrence Broxmeyer presents a stunning hypothesis about the bacterial nature of Alzheimer’s disease, forgotten long ago. Immensely readable and enormously well-researched, this work of medical history should change the way we think about, diagnose, and treat this debilitating condition.

I f biotechnology describes the exploitation of living systems or their products towards biomedical processes, then few entities have a greater biotechnological potential than the use of bacteriophages to cure human illness. Many researchers studying infectious diseases have little doubt that phage therapy has a contribution to make and will achieve mainstream medical relevance in the 21st century. This would come not a moment too soon. Today multi‑drug‑resistant and "extremely" drug‑resistant forms of pathogens are reaching epidemic proportions and causing death on a global scale. But until recently, there seemed neither promise nor assurance that the use of such phage therapy would indeed kill pathogens intracellularly, in white blood cells, where they live and propagate; a necessary condition for cure. For this very reason many a National Institute of Health (NIH) grant application regarding phagotherapy had to be turned down. By late 2002, the question as to whether a ...

Acid-fast tuberculous mycobacterial infections are common in AIDS and are regarded as secondary "opportunistic infections." Could such bacteria play a primary role in the progression of HIV infection to immunodeficiency and full-blown clinical AIDS? In screening tests for HIV, there is frequent cross-reactivity between the gag and pol proteins of HIV in patients with certain mycobacterial infections, including tuberculosis. Could HIV itself be a virus-like cell-wall deficient form (CWD) of tuberculous mycobacteria? Do laboratory cultures of HIV contain "pure" virus, or are they contaminated with cellular proteins and/or proteins from other infectious agents? Is there a correlation between the molecular proteins of CWD mycobacteria and those proteins (such as gag and pol) that have been ascribed specifically to HIV? There are unanswered questions and controversy concerning the role of HIV “as the sole cause of AIDS.” This paper explores the possible role of acid-fast tuberculous mycobacteria as “primary agents” in AIDS.

The thought that tuberculosis and the mycobacteria could cause diabetes seems farfetched, but is not. The peculiar relationship and frequent association of diabetes mellitus and tuberculosis has been observed for more than 2000 years, yet the reason for this correlation is, to this day, not known. Before the discovery of insulin, a diagnosis of diabetes was a death sentence within 5 years, and the usual cause of that death was tuberculosis. Despite this, in the 5th century, tuberculosis was already being portrayed as a "complication" of diabetes, a view little changed to this day, parroting Root's original 1934 description of "a one-sided relationship": tuberculosis still seen as a common complication of diabetes, while diabetes is thought to be no more common among TB patients than in the population at large. To Nichol's, this was "not logically tenable" and in his study of 178 otherwise healthy, non-diabetic military men with tuberculosis at Fitzsimmons Army Hospital, one-third had abnormal glucose screening tests. But despite his findings and those of Reaud in New York and others, this was not being recognized elsewhere, and Nichols wanted to know why. Nichols concluded that the incidence of diabetes among tuberculosis patients was considerably underestimated and that in tuberculosis patients, diabetes develops quite commonly. Diabetes was easy to detect. Tuberculosis and the mycobacteria were not. The evidence for a mycobacterial cause of diabetes is mounting rapidly. Schwartz and Haas both linked Type-2 diabetes to tuberculosis. And the pancreatic islet amyloid deposits that they found as a by-product of systemic tubercular infection have recently been dissolved by rifampicin, a first line drug against tuberculosis. Engelbach spoke of "transitory" diabetes in TB and Karachunskii noted changes in carbohydrate metabolism in patients with tuberculosis which commonly led to insulin deficiency with persistent hyperglycemia. Furthermore, mycobacterial elements have been shown recently not only to cause "autoimmune" Type-1 diabetes in NOD (non-obese diabetic) mice, but act as a vaccine to stop the inevitable diabetes that would otherwise materialize. The documentation of patient cases where TB has preceded and come before the development of diabetes is extensive yet underplayed and both Lin's and Tsai's studies speak of tuberculosis complicated by diabetes. Diabetes has been around since the first century AD, in a perpetual state of coping and managing. It is time, it is long past time, to cure diabetes. But current models as to its cause are not equipping us to do so.

Medline studies in the Parkinson's literature have cited a tuberculosis-like germ called Nocardia as being responsible for Parkinson's disease. Kohbata seemingly cemented a relationship between Nocardia and Parkinson's by finding serologic evidence in 20 of 20 Parkinson's patients, acknowledging that blood tests for Nocardia and the mycobacteria such as tuberculosis often cross-react, as they belong to the same order of bacteria, the Actinomycetales. Besides this difficulty in differentiation, a well-used medical school textbook of microbiology, Atlas, points out that even among experts, different observers may classify the same strain of bacteria as Nocardia or Mycobacterium tuberculosis. Parkinson's: another look is a theoretical article which presents compelling, well-documented evidence for an infectious cause for Parkinson's disease on historical, epidemiological, pharmacologic, microbiological, and biochemical levels. A supportive Norwegian study done by Berstad and Berstad in May of 2017 is also attached.

The possibility of the age-related reemergence of foodborne Mycobacterium bovis (bovine tuberculosis) as a vector for Creutzfeldt-Jakob Disease (CJD or human Mad Cow Disease) and Mad Cow disease itself is real. The CDC reported last May of an outbreak of CJD linked to the consumption of meat contaminated "with the agent causing" bovine spongiform encephalopathy (BSE) in a New Jersey racetrack between the time frame 1995-2004. In the opinion of experts, ample justification exists for considering a similar pathogenesis for Alzheimer's, Creutzfeldt-Jakob and the other spongiform encephalopathies such as Mad Cow disease. In fact, Creutzfeldt-Jakob and Alzheimer's often coexist and at this point are thought to differ merely by time-dependent physical changes. A recent study links up to 13% of all "Alzheimer's" victims as really having Creutzfeldt-Jakob disease. Bovine tuberculosis, which includes Mycobacterium bovis and M. avium-intracellulare or paratuberculosis, is and has always been the most prevalent threat to the cattle industry, and the USDA reports that between 20% and 40% of US dairy herds are infected with paratuberculosis alone. The health risk for milk tainted with M. bovis has been known for decades and there was a time not so long ago when "tuberculin-tested" was printed on every milk container. Schliesser stated that meat from tuberculous animals may also constitute a significant risk of infection. At the turn of the 20th century 25% of the many US deaths from TB in adults were caused by M. bovis. Dairy products aside, when past and present meat consumption are factored in, there is three times the risk of developing Alzheimer's in meat eaters as opposed to vegetarians. The investigation into the causal trail for Creutzfeldt-Jakob, indistinguishable from Alzheimer's except for its shorter, lethal course might have grown cold where it not for Roel's and others who linked mad cow in cattle with M. bovis and related paratuberculosis on clinical, pathologic and epidemiological grounds. The southwest of the UK, the very cradle of British BSE and CJD outbreaks, saw an exponential increase in bovine tuberculosis just prior to it's spongiform outbreaks. All of this brings up the unthinkable: that Alzheimer's, Cruetzfeldt-Jackob, and Mad Cow Disease might just be caused by eating the meat or dairy in consumer products or feed. It is only appropriate therefore to explore the role of bovine TB and the atypical mycobacteria in Alzheimer's, JCD and Mad Cow disease and develop better serological surveillance for these pathogens.

Acid-fast tuberculous mycobacterial infections are common in AIDS and are regarded as secondary "opportunistic infections." According to the National Institute of Allergy and Infectious Diseases, TB is the major attributable cause of death in AIDS patients. Could such bacteria play a primary or causative role in AIDS? Certainly, In screening tests for HIV, there is frequent, up to 70%, cross-reactivity, between the gag and pol proteins of HIV and patients with mycobacterial infections such as tuberculosis. By 1972, five years before gays started dying in the U.S., Rolland wrote Genital Tuberculosis, a Forgotten Disease? And ironically, in 1979, on the eve of AIDS recognition, Gondzik and Jasiewicz showed that even in the laboratory, genitally infected tubercular male guinea pigs could infect healthy females through their semen by an HIV-compatible ratio of 1 in 6 or 17%, prompting him to warn his patients that not only was tuberculosis a sexually transmitted disease, but also the necessity of the application of suitable contraceptives, such as condoms, to avoid it. Gondzik's solution and date of publication are chilling; his findings significant. Since 1982 Cantwell et al found acid-fast bacteria closely related to tuberculosis (TB) and atypical tuberculosis in AIDS tissue. On the other hand molecular biologist and virologist Duesberg, who originally defined retroviral ultrastructure, has made it clear that HIV is not the cause of AIDS and that the so-called AIDS retrovirus has never been isolated in its pure state. Dr. Etienne de Harven, first to examine retroviruses under the electron, agrees. In 1993 HIV co-discoverer Luc Montagnier reported on cell-wall-deficient (CWD) bacteria which he called "mycoplasma" in AIDS tissue. He suspected these as a necessary "co-factor" for AIDS. Remarkably, Montagnier remained silent on Cantwell's reports of acid-fast bacteria which could simulate "mycoplasma" in AIDS tissue. Mattman makes clear that the differentiation between mycoplasma and CWD bacteria is difficult at best and cites Pachas's 1985 study wherein one mycoplasma was actually mistaken for a CWD form of a bacterium closely related to the mycobacteria. It is important to realize that the statement "HIV is the sole cause of AIDS" is just a hypothesis. There are unanswered questions and controversy concerning the role of HIV "as the sole cause of AIDS." And until they are resolved, a cure is not possible. This paper explores the possible role of acid-fast tuberculous mycobacteria as "primary agents" in AIDS.

At present, the cause of autism and its related spectrum disorders is unknown. Many hypotheses regarding what causes autism have been and will continue to be put forth, but only one will prevail: its true cause. A conversation as to whether certain vaccines trigger autism cannot be made in a vacuum but, rather, must be weighed against epidemiologic, scientific and historic considerations because its complexity is too great.

Today, the Ebola, and for that matter the Marburg virus have assumed general acceptance. Yet according to David Rasnick, a previous member to the Presidential AIDS Advisory Panel of South Africa, there is no convincing evidence, and “certainly no confirmatory evidence of human isolation”, in either case. This is, to be certain, not only a direct challenge that the “Ebola virus” is behind the current Ebola outbreak; but that this “virus” is pathogenic at all. Nor is Rasnick alone. To date, there has been at least one Freedom of Information Act request to the Centers for Disease Control and Prevention (CDC) that this author is aware of mentioning, among other things: “This is a request for published records, data, studies, electron microscope photographs, work notes, and internal correspondence relating to and describing, in detail, the direct isolation of the Ebola virus from human beings.”This request has, to the present, gone unaddressed and unanswered. If the virus called Ebola is not causing the current epidemic, then what is? Historically, surrounding most outbreaks or epidemics there has been a call for vaccination, and Ebola is no different. The transient question is just what are we vaccinating for? The Swine Flu fiasco of 1976 reminds us of possible outcomes to what governments and vaccine companies are now pushing for with regard to Ebola. During that swine-flu vaccination, an attempt was made to vaccinate every American. 532 people were partially paralyzed and 32 died, and all for an epidemic that never materialized.

The US Centers for Disease Control and Prevention (CDC) recently declared: "Diagnosing Ebola in a person who has been infected for only a few days is difficult, because the early
symptoms, such as fever, are nonspecific to Ebola infection and are seen often in patients with more commonly occurring diseases, such as malaria and typhoid fever."

Only a sin of omission, then, would explain why anyone or any group would not want to mention specifically the most commonly occurring cause of infectious death in Africa—tuberculosis (TB)—whose sky-high rates in West Africa make Ebola look like a dropperful of water squeezed into the Mississippi.
If by October 2014 Ebola had laid claim to what the World Health Organization (WHO) claimed was well over 3,338 deaths since its March outbreak, certainly this ought to be weighed in the light of the approximately 600,000 Africans slain by TB during the same time window. Furthermore, by 20 October 2014, worldwide Ebola mortality stood at 4,868, with just over 81 per cent of these deaths recorded in Liberia and Sierra Leone. While Liberian health officials warned as early as 2009 that TB was skyrocketing out of control, a mixed scientific coalition from Sierra Leone and Germany cautioned that Sierra Leone's own tuberculosis level was not only the highest
in West Africa but was filled with resistant strains of TB and tuberculous Mycobacterium africanum which had "reached an alarming level…raising the question of possible consequences" for a future new TB epidemic.

Tuberculin is made from proteins derived from tubercle bacilli that have been “killed” by heating. Yet in both Zwadyk’s 1994 study and Bemer-Melchior’s 1999 investigations ‘heat-killed’ tuberculosis and its related mycobacteria, whether in tuberculin, vaccination or otherwise, have dormant, practically indestructible cell-wall-deficient forms which can revert back to virulent TB bacilli “killed” ― by neither heat nor sterilization. The ability and actual preference of mycobacteria such as Mycobacterium tuberculosis and Mycobacterium bovis to form filterable, multi-shaped cell-wall-deficient (CWD) forms and spores in order to survive unfavorable conditions has in fact been known for some time. But the possibility of PPD tuberculins
for human use containing such potentially virulent CWD forms, even after autoclaving, sterilizing and ultrafiltration, has not. Autoclaved ultra-filtrates of the various mycobacteria
used to produce tuberculin skin tests, consisting of M. Tuberculosis, M. bovis, and M. avium were investigated. All samples were mixed with growth stimulant, incubated, and placed on a special nutrient medium with a 1% agar base. Within 2-10 days after incubation colonies of a variety of non-acid-fast forms were noted, yet all of these proved, through PCR real time with FAM probe to still have antigens in common with their classic tubercular parent-form,
from which they originated. Moreover, in true cell-wall-deficient fashion, the isolates, upon guinea pig inoculation, did not immediately produce visible lesions, but nevertheless persisted.
However, tissue homogenates of the infected animals, once placed on a growth-enhancing medium showed cell-wall-deficient mycobacterial forms interspersed with classical acid-fast rods. And a repeated passage of such tissue homogenates back into non-infected guinea pigs,
not only induced small mycobacterial granulomas in their livers, but a distinct increase in acid-fast rods. Moreover, similar cell-wall-deficient mycobacterial forms with acid-fast rods occurred when embryonated chicken eggs were inoculated with PPD tuberculins as well. The autoclaved and supposedly “sterilized” purified protein derivative [PPD] used in tuberculin skin tests contain cell-wall-deficient forms capable of eventually reverting back to virulent acid-fast tuberculosis, both typical and atypical.

Summary By the turn of the last century, flying in the face of over a hundred years of research and clinical observation to the contrary, medicine abandoned the link between infection and atherogenesis; not because it was ever proven wrong, but because it did not fit in with the trends of a medical establishment convinced that chronic disease such as heart disease must be multifactorial, degenerative and non-infectious.
Yet it was the very inability of ‘established’ risk factors such as hypercholesterolemia, hypertension and smoking to
completely explain the incidence and trends in cardiovascular disease that resulted in historically repeated calls to search out an infectious cause, a search that began more than a century ago.
Today, half of US heart attack victims have acceptable cholesterol levels and 25% or more have none of the “risk
factors” associated with heart disease, including smoking, high blood pressure or obesity, most of which are not
inconsistent with being caused by infection.
Even the case of the traditionalist’s latest 2003 JAMA assault to ‘debunk’ what they call the “50% risk factor myth”
falls woefully short under scrutiny. In one group 30% died of heart disease with a cholesterol of at least 240 mg/dl,
a condition which also existed in 21% who did not die during the same period. And the overlap was obvious throughout
the so-called risk categories. Under such scrutiny, lead author Greenland conceded that if obesity, inactivity and
elevated cholesteriol in the elderly are included, just about everyone has a risk factor and he likened the dilemma of
people who do or do not wind up with heart disease akin to the susceptibility of people who are exposed to tuberculosis
but do not get the disease.
In Infections and Atherosclerosis: New Clues from an old Hypothesis? Nieto stressed the need to extend the possible
role of infectious agents beyond the three infections which have in recent years been the focus of research:
Cytomegalovirus (CMV) Chlamydia pneumoniae and Helicobactor pylori [39].
Mycobacterial disease shares interesting connections to heart disease. Not only is tuberculosis the only
microorganism to depend on cholesterol for its pathogenesis but CDC maps for cardiovascular disease bear a striking
similiarity to those of State and regional TB case rates.
Ellis, Hektoen, Osler, McCallum, Swartz, Livingston and Alexander-Jackson all saw clinical and laboratory evidence
of a causative relationship between the mycobacteria and heart disease. And Xu showed that proteins of mycobacterial
origin actually led to experimental atherosclerosis in laboratory animals [61,62].
Furthermore present day markers suggested as indicators for heart disease susceptibility such as C-Reactive Protein
(CRP), interleukin-6 and homocysteine are all similarly elevated in tuberculosis.
It therefore behooves us to explore the link between heart disease and typical and atypical tuberculosis.

The word "cancer" is of Latin derivation and means "crab". Today, cancer "cure" is a vast industry. But by the turn of the 20th century, the medical profession had come to the conclusion that it was not a matter of whether infectious disease caused cancer, but of which one.
For over 200 years, a cancer germ had been discovered and rediscovered, named and renamed, each scientist adding to the knowledge but to no avail. Then, in 1910, certain American medical powers did a 180-degree rotation, deciding that cancer was not caused by a microbe and that anyone who thought otherwise was a heretic, a charlatan or a quack.
Dr Virginia Wuerthele-Caspe Livingston and her network were none of the above, their meticulous peer-reviewed research and publications produced at the height of US post–World War II technology. Dr Dean Burk, who cofounded the US National Cancer Institute and headed its cell chemistry department for 34 years, went so far as to say that Livingston's cancer germ
was as real and certain as anything known about cancer. Researcher Dr Alan Cantwell, Jr, grew up thinking that all germs responsible for the important diseases were supposed to have been discovered already. But much to his dismay, he found one that had been left out: the cancer germ. Cantwell
knew that Livingston had already been branded by the medical orthodoxy for finding this cancer germ—thus, what he thought to be perhaps the major discovery of the 20th century was left largely discredited.

The Politics of Cancer:

It was public knowledge in early 1951 that the Black–Stevenson Cancer Foundation intended to award two huge grants of $750,000 towards cancer research, and that the first would go to Dr Virginia Livingston's group at the Presbyterian Hospital in Newark, New Jersey, with an equivalent amount to go to New York's Memorial Hospital for Cancer (from 1960, the Memorial Sloan–Kettering Cancer Center) which Cornelius Rhoads headed. The trustees having already decided this, the actual allocation was left in the hands of Newark lawyer Charles R. Hardin, but fate intervened. According to Livingston: Hardin, the lawyer in charge of allocation, soon would lie dying of cancer at Memorial and while still alive was prevailed upon by design of Rhoads to sign a paper giving Rhoads power over how Presbyterian's grant was to be spent. And that wasn't going to include further research towards an infectious cause for cancer.

Still, Rhoads was not finished with her...

The word ‘cancer’ is of Latin derivation and means crab. By the turn of the 20th Century organized medicine had come to the conclusion that it was not a matter of whether infectious disease caused cancer, but which one. For over two hundred years a cancer germ had been discovered and rediscovered, named and renamed, each scientist adding to the knowledge, but to no avail. Then, in 1910, certain American medical powers did a 180-degree rotation, deciding that cancer was not caused by a microbe, and that anyone who thought otherwise was a heretic, a
charlatan or a quack. But Dr. Virginia Livingston and her network were none of the above, their meticulous peer reviewed research and publications, done at the height of US post World War II technology. And Dean Burk, Head of Cell Chemistry at the NCI went so far as to say that Livingston’s cancer germ was as real and certain as anything known about cancer. Researcher, MD Alan Cantwell Jr. grew up thinking that all germs responsible for the important diseases were supposed to have already been discovered. But much to his dismay, he found one that was left out: the cancer germ. Cantwell already knew that for finding this, Livingston had already been branded by traditional medicine, leaving what he thought to be perhaps the major discovery of the 20th century largely discredited. The striking analogy
between cancer and tuberculosis was noticed long before the tubercle bacillus was discovered. In 1877, Sir John Simon clearly pointed out the similarity and in fact argued very strongly in favor of a microbial origin for cancer. But Simon’s vindication would have to wait for Livingston’s germ, which although tuberculosis-like, was not tuberculosis but an atypical form of this mycobacterium, melded from the mycobacterium and other related Actinomycetales. Had medical science and the powers that be spent as much time in investigating and destroying Livingston’s germ as they did in attacking her and those around her, cancer might be curable today.

Several Medline studies have shown that inoculating with influenza vaccine is also protective against tuberculosis. New evidence and older historical findings which explain this phenomenon bring up the possibility that influenza doesn't originate from a virus.

As the greatest influenza pandemic of all time continued to rage, other doctors were speaking out. In 1920, with the killing fields of 1918–19 laid out before him, British physician Marcus Paterson took yet another jab at the "flu" epidemic. He wrote: "During the time I was Resident Medical Officer at Brompton, it was usual to classify a rise of temperature in an ordinary case of 'chronic' pulmonary tuberculosis as influenza, even when there was no epidemic."

Summary Influenza is Italian for ‘‘influence’’, Latin: influentia. It used to be thought that the disease was caused by
a bad influence from the heavens. Influenza was called a virus long, long before it was proven to be one. In 2005, an
article in the New England Journal of Medicine estimated that a recurrence of the 1918 influenza epidemic could kill
between 180 million and 360 million people worldwide.
A large part of the current bird-flu hysteria is fostered by a distrust among the lay and scientific community regarding
the actual state of our knowledge regarding the bird flu or H5N1 and the killer ‘‘Influenza’’ Pandemic of 1918 that it is
compared to. And this distrust is not completely unfounded. Traditionally, ‘‘flu’’ does not kill. Experts, including Peter
Palese of the Mount School of Medicine in Manhattan, remind us that even in 1992, millions in China already had
antibodies to H5N1, meaning that they had contracted it and that their immune system had little trouble fending it off.
Dr. Andrew Noymer and Michel Garenne, UC Berkely demographers, reported in 2000 convincing statistics showing that undetected tuberculosis may have been the real killer in the 1918 flu epidemic. Aware of recent attempts to isolate the ‘‘Influenza virus’’ on human cadavers and their specimens, Noymer and Garenne summed that: ‘‘Frustratingly, these findings have not answered the question why the 1918 virus was so virulent, nor do they offer an explanation for the unusual age profile of deaths’’. Bird flu would certainly be diagnosed in the hospital today as Acute Respiratory Distress Syndrome (ARDS). Roger and others favor suspecting tuberculosis in all cases of acute respiratory failure of unknown origin.
By 1918, it could be said, in so far as tuberculosis was concerned, that the world was a supersaturated sponge ready to ignite and that among its most vulnerable parts was the very Midwest where the 1918 unknown pandemic began. It is theorized that the lethal pig epidemic that began in Kansas just prior to the first human outbreaks was a disease of avian and human tuberculosis genetically combined through mycobacteriophage interchange, with the pig, susceptible to both, as its involuntary living culture medium. What are the implications of mistaking a virus such as Influenza A for what mycobacterial disease is actually causing? They would be disastrous, with useless treatment and preventative stockpiles. The obvious need for further investigation is presently imminent and pressing.