Dr. Weeks’ Comments: We are not being told the truth.
By Bill Sardi
March 2, 2020
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.
Saying the spread of the COVID-19 coronavirus is inevitable, a CDC (Centers for Disease Control) official advised Americans “brace themselves” and prepare to shut down public schools, avoid going to church, and self-quarantine their families. These onerous measures are for a virus that has infected just 53 Americans (Feb. 25), mostly among people who traveled recently to China.
Recognizing the possibility that some officials within the CDC are potential handmaidens to the drug and vaccine industry that would benefit from such scare tactics, President Trump decided to issue all governmental statements about COVID-19 from The White House.
After all, the CDC seemed to be about ready to bring down the entire U.S. economy and shutter small businesses that would never recover from even a short quarantine.
Doomsday virus?
Irresponsible and implausible predictions that COVID-19 coronavirus could produce symptomatic viral infection in 60% of the world’s population with 45 million deaths ̶ fueled by sensationalized news reports, were purely unfounded and certainly premature. Perhaps the only thing that could be considered beneficial about these dire prognostications was when one quick-thinking woman in China used the fear of the virus in a positive way, and feigned she was infected to foil a rapist.
In the beginning of the outbreak, you could have pulled from a widely-known advertising limerick used in Las Vegas: “Whatever coronavirus starts in China, stays in China.” Now we know that this is not quite the case. Airplanes facilitate its geographical spread, but person-to-person transmission remains static. Immune status may be a controlling factor in person-to-person transmission.
Maybe just a passenger virus
But what is the sense in panicking the world over a coronavirus that is 3 times less deadly than the SARS outbreak of 2003 (9.5% vs. 3.4%). And mind you, it has still not been proved that the COVID-19 coronavirus is anything more than a non-symptomatic, non-pathogenic “passenger virus,” being picked up diagnostically but not the primary underlying cause responsible for the Pandemic/Epidemic itself.
In fact, there is direct and indirect evidence that COVID-19 is NOT from a virus at all. The SARS coronavirus, often compared with the new COVID-19 coronavirus, was present only in about half of the SARS cases and antivirals such as ribavirin and oseltamivir (Tamiflu) were not working in SARS culture plates, nor were they very effective in clinics or hospitals either. That passenger viruses do exist has been abundantly documented, as when the HTLV-1 virus (human T-cell leukemia virus Type 1) was mistakenly attributed to being causal for AIDS. And so, the question which never went away looms: are the coronaviruses merely traveler viruses from a yet to be determined primary stealth cause?
Using bacteriocidals instead of antivirals
One recent US news headline said: “Scientists claim antibiotics already on the market could treat coronavirus – despite warnings from CDC and World Health Organization that antibiotics do nothing against viruses and overusing them fuels resistant microbes.
Fact of the matter is that antiviral medicines were not found to provide benefit in either the SARS or MERS strains of coronavirus either, which broke out in 2002 and 2012, respectively. Yet this habit of administering antivirals was stubbornly clung to in the treatment of the 138 Coronavirus-infected patients hospitalized in Wuhan, China described in Wang, et al’s recently published JAMA study.
On the other hand, all of these 138 patients, and most of the 99 patients in Chen et al’s current Lancet study received at least one antibiotic, some of which have significant anti-mycobacterial as well as antibacterial activity. (Mycobacteria are small rod-shaped bacteria, some varieties which have no cell wall and are difficult to distinguish from viruses; mycobacteria cause leprosy and tuberculosis, the latter usually emanating as lower respiratory tract infection that can mimic classic pneumonia, as observed in the SARS and COVID-19 coronavirus cases.)
Antibiotics have no effect against viruses. And although it is claimed that antibiotics are and were simply being used to quell “secondary” bacterial infections in the new pandemic, the fact is that antibiotics have proved universally to be of great help worldwide to the vast majority of novel coronavirus COVID-19 victims, with or without secondary infections.
Those who cannot remember the past are condemned to repeat it
While “experts” have been telling us to wash our hands, have they really been doing the factual research needed to compare COVID-19 to say the Great Pandemic of 1918? Dr. Lawrence Broxmeyer MD, whose writings were previously published in the highly ranked The Journal of Infectious Diseases, doesn’t seem to think so. And his views, as expressed in an upcoming publication, aren’t alone.
During the SARS coronavirus outbreak, Wong et al, writing in the Journal of the Chinese Medical Association warned: “Preoccupied with the diagnosis of SARS (Severe Acute Respiratory syndrome) in a SARS outbreak, doctors tend to overlook other endemic diseases, such as tuberculosis.”
Perhaps Wong’s warning should be listened to. The present and ongoing COVID-19- pandemic, did not occur in a vacuum. By December of 2018, Liu et al., in a large multi-center study, proclaimed tuberculosis to be an epidemic throughout China, which still simmers on in a country with the second largest burden of that disease in the world ̶ a disease which also often begins with flu-like symptoms, and a disease whose bacilli are laden with RNA bacterial viruses called mycobacteriophages.
It was a non-virus in 1918 too
Demographers at UC Berkeley (Noymer and Garenne, Population Development Review 2000) claim tuberculosis was behind the many deaths in the 1918 Great Influenza Pandemic was specifically based upon the well-known concept that the secondary bacterial infections that cropped up in 1918 were common in TB-infected lungs.
And in Hiroshi Nishiura’s study (2012) not only was TB shown to be associated with influenza death, but there was no influenza death among controls without TB. Investigator Nishiura later concluded: “Should a highly fatal influenza pandemic occur in the future, testing the role of TB in characterizing the risk of death would be extremely useful in minimizing the disaster…”
But was Nishiura being listened to and learned from? Apparently not. Fast forward, Wuhan, China (2019-2020):
The chronological timetable of the present Wuhan “viral” pandemic suggests nothing “new” or “novel”. The coronavirus outbreak started in December 2019, first identified in Wuhan, after 41 people presented with pneumonia of no clear cause. The Wuhan winter is from December to February. Yang’s Wuhan study from 2004 to 2013, described the annual TB surge in Wuhan as being fueled by increased transmission in the winter, peaking in March, with a second smaller peak in September. Among the conditions Yang attributed to the increased transmission of TB in the winter was indoor crowding, subsequent vitamin D deficiency, and even air pollution.
The increasingly severe air pollution in Wuhan, powered by the influx of foreign companies and the increased use of incineration for waste disposal, resulted in a visible haze so thick that it reduced peripheral vision as far back as June of 2012 ̶a haze with inhalable particulate matter, highest in the winter, which according to Yang, was of a particulate size able to harbor Mycobacterium tuberculosis and related mycobacteria. Why is this important?
Pigs
Wuhan’s economy was on fire. With it came a greatly increased demand for poultry and swine, two staples of the Chinese diet, along with the expansion of farms to raise them and the inevitable tons of waste that this brought. Even as far back as 2015, there were five major waste incineration plants in Wuhan, with many more scheduled to be built.
That was just the beginning. By July, 2018, fourteen large pig breeding farms in Wuhan, with a combined annual pig production of 1.5 million pigs pooled investments with the intent to slaughter 2 million pigs per year. China alone accounted for more than half of the world’s pig population. That is until another purported virus (African swine fever) spread throughout China which had no cure and a near zero survival rate for infected pigs, and which, by August 2019 virtually wiped out 40% of China’s entire pig population, including those in Wuhan.
Essentially one-quarter of the world’s pigs died in one year, and just before the latest coronavirus outbreak. China then did what it had to do and began to cull thousands of pigs to control the outbreak they claimed to be caused by the African swine fever outbreak in 2018.
But how many dead animals, including those in Wuhan were buried and how many incinerated are open questions. Burning pigs and pig excrement was a sure recipe for visible haze.
The Chinese government soon came up with incentive programs for livestock farmers to sell their manure to use as fertilizer, which was only marginally successful.
During a study from 1953 to 1968 (Tubercle 1970) in the UK, an astonishing 81% of pigs were found to harbor Mycobacterium avium, or fowl tuberculosis. As reported by some workers, M. avium isolates from swine represent a major threat to human beings. The similarity pre-programmed (IS1245 RFLP) patterns of the human and porcine isolates indicates close genetic relatedness, suggesting that M. avium or fowl tuberculosis is transmitted between pigs and humans.
Fort Funston 1918, Kansas USA
Similar events occurred at Fort Funston in Kansas circa 1918, thought by many to be the birthplace of the onset of the Great Influenza Pandemic of 1918.
It was only with industrial development that the US tuberculosis epidemic traveled to the Midwest and Kansas, the very American Midwest where the 1918-flu pandemic of unknown origin hit, in rural Haskell county, Kansas, in the midst of an infectious pig slaughter of undiscovered cause, a few hundred miles from Camp Funston, today Fort Riley.
It had to be more than a coincidence that by the autumn of 1918 thousands of Midwest pigs died, seemingly from the same flu-like illness and in the same Haskell County location in which the worst human pandemic in history, which would kill between 50 and 100 million people, was about to begin.
US Inspector and veterinarian J.S. Koen, for lack of another term, and with no evidence other than a hunch, quickly called this unknown disease in pigs “swine influenza,” even as it killed pig after pig.
Pigs were dying in 1918 and in 2019-20
That thousands of pigs died in the Autumn of 1918 was problematic in that bird or fowl TB, also called Avian tuberculosis or Mycobacterium avium, routinely infects birds as well as hogs and sometimes cattle –but could, under the right conditions, also infect man. So, pigs had involuntarily become the living laboratory thru which three of the main types of tuberculosis (human, cow and fowl) could mutate through the genetic exchange by their viral mycobacteriophages, much in the same fashion as has been attributed to the influenza and coronavirus. (A bacteriophage is a virus that parasitizes a bacterium by infecting it and reproducing inside it.) But, in so far as 1918 was concerned, the stage was set for disaster.
Airborne TB
Unknown at the time, but pertinent since Kansas lies squarely in America’s “dustbowl,’’ were the results of a previous European experiment wherein guinea pigs exposed to organisms like Avian tuberculosis got little or no lung disease. However, when these mycobacteria were placed in dust aerosols with particulate matter, guinea pigs came down with progressive, fatal lung disease, not unlike what was occurring in the pandemic of 1918 as well as a prominent factor in the present Wuhan air pollution with its particulate matter haze.
Burning animal waste
Ft. Riley, Kansas was a sprawling establishment housing 26,000 men and encompassing an entire camp, Camp Funston. Within that camp, thousands of horses, hogs, mules and chickens produced in excess of a stifling nine tons of manure each month. And the accepted method for its disposal was to burn it, even against driving wind.
State Veterinarian W.J. Butler would report at the 28th Meeting of the United States Live Stock Sanitary Association: “I consider contaminated manure and stagnant water the most important factors in the spread and propagation of tuberculosis.” Wang’s recent JAMA study suggested that Coronavirus may spread fastest on cruise ships and in hospitals where workers re-use gear contaminated with feces to try to conserve supplies.
And so, on Saturday, the 9th of March, 1918, a month which just happened to coincide with the annual peak surge for tuberculosis in Wuhan, China, a threatening black sky forecast the coming of a major dust storm. When this storm combined with the ashes of over 9 tons of burning manure, a stinking, stinging yellow haze resulted.
The sun was said to have gone black in Kansas that day in 1918. Two days later, on March 11th, company cook Albert Gitchell reported to the Funston infirmary saying he had “a bad cold” with flu-like symptoms. Among his symptoms were a headache, a sore throat, muscle aches, chills and fever. He also reported cleaning pig pens on March 4th, one week before feeling sick. Gitchell would never recover from this, his last illness. And by noon of March 4th, one hundred men joined him at the Army infirmary he had walked into. Within a month one-thousand men were sick and approximately 50 dead. Camp Funston was having a deadly epidemic.
These deaths were highly unusual, but nothing like what would return in the fall, when the disease would come back with a vengeance, seeming to gain strength through human passage. Camp Funston in March, Camp Devens in September (a month that coincides with the second annual TB peak surge in Wuhan), then across the country and the world, leaving an estimated 50-100 million dead globally, at least 600,000 to a million of them American, in the span of less than a year –the most destructive plague that mankind had ever witnessed.
Implications of mistaking a mycobacterial disease for a viral disease
What are the implications of mistaking a mycobacterial disease for a viral disease? While an anxiety-filled world is losing sleep over a “coronavirus” that has resulted in the deaths of less than 2000 people, a mycobacterium called tuberculosis is encircling the planet that is killing 1.7 million people a year, and is once again, the single largest cause of infectious death on the globe. And that does not even include morbidity and mortality coming from its closely related Mycobacterium avium or fowl tuberculosis, for which, although there is treatment, we have yet to develop ideal drugs to treat.
Moreover, the preferred form of both of these pathogens, once inside the body, is their tiny, hard to diagnose viral-like cell-wall-deficient (CWD) mycobacterial forms, which require special stains and special culture media, unavailable at most diagnostic centers. This leaves a situation, in which Mycobacterium avium and its cell-wall-deficient forms, highly implicated here in the present pandemic, are being picked up, according to Mattman, only 16% of the time through traditional methods.
If we are not looking or unable to look diagnostically for the underlying Wuhan pathogen, then how can we truly treat it effectively?
In 1933 researchers claimed they had first discovered human influenza “virus.” So, what was the flu virus of 1918?
Historically, in 1892 the flu was originally named Mycobacterium influenzae because it resembled tuberculosis. In the lab, both of these pathogenic organisms stain similarly on a lab slide. Staining is one method of identifying types of bacteria. Also, it was eventually found that Mycobacterium influenzae and Mycobacterium tuberculosis have similar genetic profiles.
What about reports of re-infection from coronavirus?
Physicians on the ground in China report this COVID-19 coronavirus may produce a re-infection that is more lethal than the first. Yet tuberculosis is reported to have such a high rate of reinfection that even after triple antibiotic treatment the reinfection rate is higher than the rate of new tuberculosis.
TB: The great masquerader
“Wuhan Pneumonia.” The coronavirus outbreak started in December 2019, first identified in Wuhan after 41 people presented with pneumonia of no clear cause. Chan and colleagues have characterized the present Wuhan Coronavirus pandemic as at times progressing to an “atypical” pneumonia. Such references to atypical pneumonia were used by Rist in 1929, when he found in almost 50 per cent of 300 consecutive hospital pneumonia admissions were classified as “atypical” tubercular pneumonia.
And Farber and Clarke reported 100 cases which were admitted to a general hospital for non-tuberculous pneumonia, which were found to be of a tubercular cause.
The coronavirus kills by way of the Acute Respiratory Distress Syndrome (ARDS). With ARDS, difficulty of breathing results from inflammation with subsequent flooding of the alveolar spaces through fluids gathering at these sites in the lungs, blocking the proper exchange of oxygen. The number of TB cases in which people in the Orient die of adult respiratory distress syndrome (ARDS) has been on the rise for some time. Professor Nanshan Chen (The Lancet, Jan 2020) cautiously suggested that the percentage of blood-borne tuberculosis as a potential cause of ARDS “might not be very low.”
Roger et al, however favor suspecting tuberculosis in all cases of acute respiratory failure of unknown origin. ARDS caused by blood-borne TB is associated with just as high a fatality rate as ARDS caused by either SARS or the Wuhan coronavirus.
Young children appear to be immune
Yet perhaps one of the most puzzling features to virologists regarding the new coronavirus as with SARS and MERS (Mediterranean Respiratory Syndrome) is that compared with adults and teenagers, it seems to have a less aggressive clinical course in younger children; that is, puzzling until one reads bacteriologist René Dubos’s observation that tuberculosis is rarely severe between the ages of 5 and 12, the very age span spared by the 2019-nCOV coronavirus.
Galloping tuberculosis
As an explanation for the precipitous death in a matter of hours to a few days recorded in some with fatal coronavirus, there was the comparable acute blood-borne miliary form of virulent “galloping” tuberculosis (called “galloping consumption” during the 1890 and 1918 flu Pandemics, a disease which, according to McCall Anderson, then Professor of Clinical Medicine at the University of Glasgow, could kill within hours to a few days even without influenza. Such galloping consumption also began with high fever and pneumonia in one or both lungs.
Also, that bats came to the forefront, as a possible vehicle of the new novel coronavirus, is no surprise. Already associated with the outbreaks of the SARS and MERS coronavirus (Middle Eastern respiratory syndrome or MERS-CoV)- bats have been recognized as the natural reservoir for over 100 other viruses including MERS, Ebola virus, Marburg virus, Hendra virus, and Nipah virus, to name a few. But then again, according to three separate reports (Scott, Griffith and Hamerton), bats can also carry mycobacteria from the M. tuberculosis complex and its viral-like cell-wall-deficient forms.
Clear evidence: vitamin C
Most mammals internally secrete vitamin C from their liver and resist infection and death from TB. The mammals that don’t secrete vitamin C endogenously (humans, guinea pigs, fruit bats, primate monkeys) are vulnerable to TB and mortal pneumonia. Even Linus Pauling realized that TB was extraordinarily sensitive to killing by vitamin C. Guinea pig research led to the discovery of the tuberculosis bacterium, obviously because their liver doesn’t secrete vitamin C and makes them prone to TB infections.
If wrong diagnosis, how can it be properly treated?
If modern medicine doesn’t really know what is causing this disease, how can it effectively treat it? It has become an unspoken reality- – that sometimes the medical industry makes more money fostering a disease than curing it. Here is how modern medicine makes things worse.
A retrospective analysis of a quarantine of elderly vacationers on an ocean liner shows the isolation actually ended up causing 619 coronavirus infections rather than the projected 70 if the quarantine was not mandated. Quarantines place infected individuals indoors, away from sunshine vitamin D which can be considered an anti-viral/anti-TB supplement.
Regarding the Wuhan outbreak, Thomas M. File Jr., president of the Infectious Diseases Society of America was also concerned that the close proximity of a quarantine could expose people “to other infections that are even more easily spread than coronavirus, like tuberculosis, which is airborne, and bacterial infections that can spread among dense populations.” (New York Times, Feb 6, 2020)
Certainly Dr. File remembered that in 1990, a new antibiotic-resistant tuberculosis outbreak took place in a large Miami municipal hospital. Soon similar outbreaks broke out in three New York City hospitals from which it spread to city prisons. Like the origin of SARS, the infection spread in a nosocomial manner (hospital origin) – from patient to patient and from patient to staff.
As in Florida multi-drug-resistant strains made the New York TB cases almost impossible to treat and the majority of sufferers died, many within weeks. By 1992, resistant tuberculosis had appeared in seventeen US states, with mini-epidemics in Florida, Michigan, New York, California Texas, Massachusetts and Pennsylvania and was reported by not the American, but the international media, as out of control.
Dr. Broxmeyer often refers to this quotation by Albert Einstein: “The important thing is not to stop questioning.” With that in mind, Dr. Broxmeyer asks one final question in regard to the COVID-19 coronavirus hysteria:
“Are we to continue to let the coronavirus serve to as a tool to create political upheaval and a bonanza for drug and vaccine makers, or do we want to face reality, act in a constructive way, and have a discussion about a disease that most Chinese, including their scientists would prefer to avoid at all costs.”