Peak Journal of Public Health and Management Vol. 2(3), pp.42-52, December, 2014 http://www.peakjournals.org/sub-journals-PJPHM.html ISSN 2329-2997 ©2014 Peak Journals

Review

Is the Ebola virus real?

Lawrence Broxmeyer, M.D.

Accepted 26 November, 2014

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. Key words: Ebola virus, Mycobacterium tuberculosis, Mycobacterium africanum, hemorrhagic acute miliary tuberculosis, fever of unknown origin. Ebola vaccinations. INTRODUCTION Recently CDC director Tom Frieden, in a press conference and answering a WXIA-TV reporter, apparently lost focus for a moment ― quickly corrected himself when he said: ―Right now, there's only one patient who has ever been diagnosed with TB -- I'm sorry, with Ebola in the U.S. and that individual tragically died today.‖ Sometimes the subconscious is not far from the conscious.

Frieden‘s Centers for Disease Control and Prevention (CDC) had recently declared that ―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‖ (CDC, 2014). Only a sin of omission, then, would explain why anyone or any group would not want to specifically mention the most commonly occurring cause of infectious death in Africa;

tuberculosis (TB), whose sky-high rates in West Africa make Ebola look like a dropper-full 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 4,000 deaths since its February outbreak (WHO, 2014a), certainly this ought to be weighed in the light of the approximately 600,000 Africans slain by TB during the same window of time (Ball, 2014). Furthermore, if by October 17th, 2014 world-wide Ebola mortality stood at 4,811 then surely 81% of these deaths took place in Liberia and Sierra Leone. While Librarian health officials warned (IRIN News, 2009) 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 tuberculosis level was not only the highest in West Africa, but filled with resistant strains of TB and tuberculous Mycobacterium africanum that had ―reached

NY institute of Medical

Research, New York, USA.

Email:nyinstituteofmedrese

arch@verizon.net

Broxmeyer 43

Figure 1. Dr. Peter Piot.

an alarming level ―…..raising the question of possible consequences‖ for a future new and severe TB epidemic. (Homolka et al., 2008)

Indeed almost half of all TB cases in the West African Ebola zone are caused by such M. africanum ―an unusual, yet just as deadly member of the tubercular family, exclusive to West Africa; and fast becoming a microbe of great public, and now global concern. That tubercular M. africanum can and has already caused tuberculosis in the United States is a matter of record. (Desmond et al., 2004) Furthermore, there is a body of evidence that M. africanum requires more sustained contact, even among household members ―certainly mirrored in the current outbreak. Meanwhile, health officials continue to insist that "casual contact" cannot transmit Ebola; precisely the same claim that they have long made with TB.

Surely the CDC is aware that there is not a sign or symptom of Ebola, including its hemorrhagic tendencies that cannot be found in acute disseminated miliary (blood-borne) tuberculosis, once called ―galloping consumption‖ ― the single most feared form of the disease ever. And most likely it is also aware that such tuberculosis has its own viral-like forms, some of which, as we shall see, can simulate the Ebola. Such viral TB is generally acknowledged to be TB‘s preferred form; as a survival strategy to storm any inclement conditions the microbe might find itself in. (Mattman, 2001)

Then why did the CDC not mention TB, by name, in their short-list of possibilities that could cause Ebola-like symptoms? If such oversight stopped there, it would be unremarkable, but it seems to have been carried over in the very design of the most recent CDC-approved tests to detect Ebola. A RIVER NAMED EBOLA In September of 1978, about 40 years ago, a team; including a 27-year-old fresh out of medical school, who was training as a clinical microbiologist at the Institute of Tropical Medicine in Antwerp, Belgium, received a blue

thermos from Zaire. It was filled with the two 5 ml clotted blood specimens of an African-based Flemish nun. The Belgium doctor who sent it, Jacques Courteille, practicing in Kinshasa, included a note saying that he was at a complete loss for the nun‘s mysterious, yet deadly illness. Also, could the samples be tested for Yellow Fever? This thermos had traveled from Zaire‘s capital city of Kinshasa, on a Sabena commercial flight to Belgium; inside its deliverer‘s hand luggage. When the samples were received, Peter Piot, the 27-year-old medical graduate and his colleagues, among other things, placed the blood samples under an electron microscope. To be sure Piot‘s interest was virology and a virologist he would soon become ―best known for his work on theorizing the ‗viruses‘ behind Ebola and AIDS. To this effect, he contributed to the voluminous literature that Human T-Cell Lymphotropic Virus-1 (HTLV-1) had a role in acquired immune deficiency syndrome (AIDS), which it did not. Nevertheless Piot (Figure 1,2) would become a pioneer, and part of the group that included veterinarian Max Myron Essex in trying to define what AIDS was at WHO‘s 1985 Conference in Banqui, Africa. Piot on the Ebola: ―We saw a gigantic worm like structure; gigantic by viral standards. It is a very unusual shape for a virus, only one other virus looked like that and that was the Marburg virus‖ (Brown, 2014). But the new ―virus‖ needed a name. Piot relates the interesting tale of how Ebola came to be named as Ebola: ―On that day our team sat together late into the night; we had also had a couple of drinks, discussing the question. We definitely did not want to name the new pathogen ―Yambuku virus‖, because that would have stigmatized the place forever. There was a map hanging on the wall and our American team leader suggested looking for the nearest river and giving the virus its name. It was the Ebola River (Figure 3). So by around three or four in the morning we had found a name. But the map was small and inexact. We only learned later that the nearest river was actually a different one. But Ebola is a nice name, isn‘t it?‖ (Von Bredow and Hackenbroch, 2014). Depends upon how you look at it.

Piot‘s specimens proved negative for Yellow Fever and

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Figure 2. Piot (on the right), at the Institute of Tropical Medicine, Antwerp, in 1976.

Figure 3. The Ebola River, Circa 1976.

he mentions that the tests for Lassa fever and typhoid were also negative. What, then, could it be? Piot: ―To isolate any virus material‖ small amounts of the blood samples were injected into VERO cells and into mice. Several of these mice subsequently and abruptly expired; ―a sign that a pathogenic virus was probably present in the blood samples that we had used to inoculate them.‖ (Piot, 2014) The fact that the mice died did not mean that it was at the hands of a ―pathogenic virus.‖

Piot‘s boss, Stefaan Pattyn, whom Piot admitted ―could be a bit of a bully‖, supposedly specialized in the study of mycobacteria; tuberculosis and leprosy, yet seemed unaware of the hemorrhagic consequences of acute TB, nor had he taken the time to use special stains and cultures to detect tuberculosis‘s viral-like cell-wall-

deficient forms. Instead Pattyn followed his current passion, shared by Piot. Pattyn had recently worked in Zaire for six or seven years and exotic viral illnesses were now ―right up his alley.‖ (Piot, 2014) So Pattyn‘s team likewise never really considered a strain of acute miliary TB or its viral cell-wall-deficient forms in his rule-outs for an acute hemorrhagic or epidemic fever; among them Mycobacterium tuberculosis and M. africanum. FROM PAST TO THE PRESENT The Ebola of its day on steroids, ―galloping‖ acute consumptive tuberculosis could kill in days; the mere memory of which, just a few generations ago, brought

terror to the faces of those who had witnessed and were describing it. To Dubos and Dubos (1987), ―galloping consumption‖ was not an isolated, but a frequent diagnosis in the 19th and early 20th centuries. And despite persistent myths to the contrary, in the early phase of any new TB epidemic from a new and virulent strain, tuberculosis manifests itself as an acute disease and only much later as the chronic pulmonary tuberculosis that we know in today‘s western world. An example of this can be found in the high mortality during the 1918 influenza pandemic, when African-Americans were brought to fight in France during World War I; large numbers of them dying from a fast-tracked tubercular ―galloping consumption‖.

Many often underestimate the speed, contagiousness and ferocity of a TB epidemic. Khomenko and Muratov (1993) should have cemented the notion that the explosive contagiousness of just such Ebola and influenza-like viral forms of tuberculosis are exactly the stuff that previous epidemics and pandemics could have been made of. But it did not.

In the US, the CDC and National Institutes of Health (NIH) seemed to feel differently, ignoring the historic possibility. There was much the same viral passion, at that time over ―Influenza‖, when in 1990, a new multi-drug-resistant (MDR) tuberculosis outbreak took place in a large Miami municipal hospital. Soon thereafter, similar outbreaks in three New York City hospitals left many sufferers dying within weeks. By 1992, approximately two years later, drug-resistant tuberculosis had spread to deadly mini-epidemics in seventeen US states, and was reported, not by the American, but the international media, as out of control. Viral forms of swine, avian and human TB can be transmitted from one species to another. So can exotic strains of tuberculosis and M. africanum, imported into the United States through countries such as Liberia. By 1993, the World Health Organization (WHO) had proclaimed tuberculosis a global health emergency. (Reuters, 1993) That emergency has never been lifted.

Anderson (1877) pointed out that such acute, untreated disseminated, ―galloping‖, blood-dispersed TB could kill in hours or days; its mortality, according to Saleem and Azher (2013) ―even today ― approaching 100%. Ebola itself can take up to a month to kill its victims, said Ben Neuman, (Kelland, 2014) an expert in viruses at Britain‘s Reading University; although there are many cases that also kill in hours, weeks or days. Not only were tubercular hemorrhaging and fever both mentioned by Fox (1891), but hemorrhaging of the serous cavities, the gums, and the nose, into the joints, the skin, and the bowels. Appleman (1918), considering massive spontaneous hemorrhages into the vitreous, mentions that Axenfeld thought acute tuberculosis an important possibility in the rule-out for bleeding into the eye. Coughing-up blood has always been a well-known scenario for TB. Hemorrhages of significance from the ear secondary to tuberculous

Broxmeyer 45 otitis media are also on record. (Burnett, 1901). And the possibility of acute disseminated tuberculosis attacking the bone marrow and through fibrosis causing a partial shutdown of platelets; changing the very morphology of those platelets; as well as interfering with their function ―all combine to create a clear and present hemorrhagic danger. Even today, bone marrow biopsy is a valuable diagnostic test for tubercular involvement. In addition Extrapulmonary (outside of the lungs) tuberculosis is the most frequent cause of a prolonged Fever of Unknown Origin (FUO) and has been for a long, long time. (Kasper et al., 2004)

A fact initially carefully minimized by certain Ebola ‗authorities‘; and clarified by Feldmann (2014) is that in the current Ebola outbreak ―less than half‖ of the people infected have visible hemorrhaging. This was just enough to prompt some virologists to rethink Ebola‘s name from Ebola Hemorrhagic Fever, to the ―Ebola virus Disease‖. So much for ―hemorrhagic fever‖, yet evenin a 1978 publication of the Bulletin of the World Health Organization regarding the 1976 Ebola outbreak in Zaire it was admitted that hemorrhaging, although from ―multiple sites‖ was ―principally [from] the gastrointestinal tract‖ (Report of an International Commission, 1978). But patients with TB spread to the gastrointestinal tract can also have the same fever, abdominal pain, and gastrointestinal/rectal bleeding that patients with Ebola can have.

MORTALITY RATES OF BOTH DISEASES ABOUT THE SAME Nor do the parallels stop there. In September, as the CDC justifiably warned against nonessential travel to Sierra Leone; available data from the two Ebola facilities in that country came in with Case Fatality Rates (CFRs) for Ebola that ranged between 50 and 72%. This, although considerably higher than the 37.7% CFR that Sierra Leone‘s Ministry of Health was reporting, (Conton, 2014) averages out to an agency reported fatality rate of 61%; not much different from the approximately 67% mortality given for the untreated active tuberculosis that currently rages in West Africa and many other places around the world. (Saleem and Azher, op. cit)

Meanwhile, The World Health Organization‘s (WHO‘s) latest ―Situation Report‖ summed-up that although the rate of Ebola infections were picking up speed at an alarming rate in West Africa, the fatality rate was 53% overall, ranging from 64% in Guinea to just 39% in Sierra Leone. (Conton, op.cit) If this 53% figure was designed to make the situation more bearable, it hardly achieved its goals.

A FLAW IN DIAGNOSTIC TEST DESIGN Moreover, the design of present diagnostic tests for

Ebola, in certain respects, did not meet the sniff test. An August 6, 2014 article in the L.A.Times mentioned (Morin, 2014) that an unapproved Ebola test-tube diagnostic assay, developed by the U.S. military, was just approved for use in the US under a special emergency-use provision.

Critics claimed that the two PCR systems to be used for Ebola testing in such ―emergency situations‖ were unapproved. But there is more. While an instruction booklet issued by the Food and Drug Administration (JPM-MSC, 2014) showed impressive results for detecting and thereby being positive for known ―Ebola‖ samples; it sadly failed in its inadequate selection of those pathogen‘s that might be cross-reacting and therefore making for false positive Ebola tests.

The instruction booklet, Version 2, that accompanied the new Ebola assay mentions:―9.2.2.2 Bacterial Cross-Reactivity: Bacterial cross-reactivity of the EZ1 assay was evaluated by testing purified nucleic acid of bacteria that potentially could be infecting the majority of the population. No cross-reactivity was observed in the human DNA or any of the bacteria tested.” (Table 51 of JPM-MSC, 2014)

Yes. The only problem being that a glance at Table 51 shows practically every bacteria in existence except for the one subset of pathogens ―that potentially could be infecting the majority [of West Africa‘s] population‖ and those pathogens were again; M. tuberculosis and its related M. africanum.

Such diversion isn‘t a trivial point. As time went by, it became obvious that attempts were in the pipeline to link the pathogenesis of Ebola and AIDS, right down to their sexual transmission. By the same token, a poorly kept secret is that TB can also be sexually transmitted. (Broxmeyer, 2014) But mistakes made during the AIDS probes would have to be avoided with Ebola. For example, in the past, as the first scientist to propose HIV-virus testing, veterinarian Max Myron Essex knew that tuberculosis and its allied mycobacteria gave a false positive for the HIV virus in his tests in almost 70% of cases. Such cross-reactivity between HIV and tuberculosis was so significant, that it forced Essex and his protégé, Congo physician Oscar Kashala, to warn that both the HIV screening test, the enzyme-linked immunosorbent assay (ELISA) and western blot results ―should be interpreted with caution when screening individuals with M. tuberculosis or other mycobacterial species.‖ (Kashala et al., 1994) This, of course, automatically meant throwing away HIV serum diagnostics for, according to WHO, at least a third of the people in the known world that The World Health Organization (WHO) has proclaimed presently harbor tubercular infection.

So why then was M. tuberculosis noticeably excluded from the CDC‘s Table 51 and not included in those pathogens tested for cross-reacting and therefore possibly giving false positive tests for the Ebola? Did the

Peak J. Public Health Manag. 46 originally panel (Version 1) chosen by government scientists actually include M. tuberculosis and related microbes in its design; only to find that indeed these mycobacteria caused positive tests for Ebola as in the HIV affair? Did they feel that such results might muddy the waters, be too difficult to explain, and subsequently remove them? This is not known.

A group of researchers from Oxford University and the University of Leuven have just determined that HIV is ―almost certain‖ to have begun its spread; from Kinshasa, now the capital city of the Democratic Republic of Congo (Schlanger, 2014). Whether this research bears out or does not, Kinshasa itself has long been a hotbed for tuberculosis; and now Ebola. On top of that, a doctor in rural Liberia, swarmed with Ebola patients, says he‘s had extremely good results with HIV treatment; albeit such treatment was born out of admitted desperation (Izadi, 2014). The US NIAID, having gotten wind of this, is carefully looking into the use of some of these HIV-antiretrovirals to control Ebola. This just might work, but will it answer the reason as to why it works? The NIH, for example, has long known, though mechanisms not yet clearly worked out, that HIV treatment suppresses both the tuberculosis and the fowl tuberculosis that are currently the leading causes of infectious death in AIDS. To this effect, the NIH, decades ago recruited University laboratories to look into the reason for this (Broxmeyer, op. cit).

Therefore are the HIV drugs working against an ―Ebola‖ which is estimated to have killed well over 5,000 African‘s so far this year or the TB that killed 600,000 Africans in that same window? There still remains much work ahead to determine this. Antiretrovirals have major side effects.

The Ebola virus (also referred to as Ebola Hemorrhagic Fever) is often compared to the Marburg virus. So we have this, written in July, 2005, regarding that outbreak: ―Angola is in the grip of the world‘s worst ever outbreak of the Marburg virus. According to the World Health Organization (WHO), as of 5 April, 156 of the 181 people reported infected have died. The Ebola-like virus causes a fever that, in fatal cases, is usually accompanied by severe internal bleeding and shock. There is no vaccine or medical treatment and up to 80% of infected people die within three to seven days. Three-quarters of those affected are children under five. Diagnosing an infection with the Marburg virus can be difficult as its initial symptoms are similar to those of malaria or tuberculosis. They include diarrhea, stomach pains, nausea, and vomiting and severe chest pains‖ (Shetty, 2005).

The heavy mortality and morbidity under the age of five with Marburg brings to mind specifically a tubercular involvement, in which most children are affected also in the same age group. What has been called ‗The Golden Age of Resistance‘ against TB mortality has always been, for unknown reasons, ages six thru fifteen (Dubos and Dubos, op. cit.). In this same vein, during the Zaire Ebola

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Figure 4. The Serpentine Form of the Ebola Virus. Magnification: approximately x60,000. Micrograph from F. A. Murphy, University of Texas Medical Branch, Galveston, Texas.Courtesy: CDC Dr. Frederick A. Murphy.

outbreak of 1976, women 15-29 years of age had the highest incidence of that disease.

TB OR EBOLA?

According to Peter Piot: ―We saw a gigantic worm like-structure; gigantic by viral standards. It‘s a very unusual shape for a virus‖ (Figure 4). To some it might be considered ―worm-like‖, to others serpentine (Figure 5). Originally, Piot‘s team thought Ebola was either a rhabdovirus or torovirus.Today it‘s called a Filovirus, on the observation that it forms filamentous infectious viral particles. Filoviruses, however, are not alone. M. tuberculosis, which commonly lodges in and multiplies in the white cell defenders of our body (called macrophages)also become filamentous once inside a macrophage (Chauhan et al., 2996; Figures 6 and 7).

According to the WHO, close contact with the bodily fluids of people infected with Ebola, for example in hospitals or at burials, has in the past increased the risk of infection. Health workers have been advised to wear a mask and gloves (WHO, 2014b). Yet physicians all masked and gloved-up have contracted Ebola and Marburg. WHO‘s statement is misleading. As far back as 1995, the ability of Ebola to aerosolize or spread through airborne transmission was reported, studied and confirmed (Johnson et al., 1995; Jaax et al., 1995). Ebola, is a communicable airborne infection, just like tuberculosis.

TUBERCULAR MONKEYS, APES AND FRUIT BATS ―Ebola virus has been found in African monkeys, chimps and other nonhuman primates such as fruit bats in Africa. A milder strain of Ebola has been discovered in monkeys and pigs in the Philippines‖ (The Mayo Clinic, 2014). Interestingly, Infection by M. africanum has also been reported from chimpanzees and African green monkeys. And in 1970-71, the CDC estimated that tubercular infection in individuals in contact with these and other non-human primates was 60 to 100 times that of the population at large. Both African monkeys and great apes are susceptible to TB (Kaufmann et al., 1975). Early studies suggested that the new strain of Ebola had emerged in West Africa, but according to epidemiologist Fabian Leendertz, a disease ecologist at the Robert Koch Institute in Berlin, who led the large team of scientists to Guinea, it is likely the virus in Guinea is closely related to the one known as the Zaire Ebola Virus, identified more than 10 years ago in the Democratic Republic of the Congo (Vidal, 2014).

It is felt that the new strain probably arrived in West Africa via infected straw-colored fruit bats from another part of Africa and seems to be related to that Zaire Ebola virus identified more than 10 years ago in the Congo. These bats migrate across long distances and are commonly found in giant colonies near cities and in forests. Fruit bats are widely eaten in rural West Africa; supposedly as a delicacy.

But the same fruit bats can carry mycobacteria from the

M. tuberculosis complex (Scott, 1926; Griffith, 1928;

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Figure 5A through 5G.Which of the serpentine, worm-like forms above is the Ebola virus?The correct answer is Figure 5F. Figures 5A,5B and 5C are L-Forms (Or Cell-Wall-Deficient Forms) of TB Under theElectron Microscope. (Michailova, L et al. Morphological variability and cell wall deficiency in ‗heteroresistant‘ strains. Internat Journ of Tuberc and Lung Dis, 9:,8, Aug 2005:.907-914:,911). Figure 5D. Worm-like lethal tubercular cords from an atypical TB under the Electron Microscope. (Julián E, Roldán, M Journ. Of Bact Apr. 2010 p.1751-1760. P.1756). Such virulent cords are also represented in Figure 5E (Darzins, E. The Bacteriology of Tuberculosis Minneapolis. 1958. 488pps. p296) and Figure 5G.

Figure 6. Filamentous Cell-Wall-Deficient Forms of Mycobacterium tuberculosis.

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Figure 7. Filamentous Forms of the Ebola.Magnification: approximately x40,000. Micrograph from F. A. Murphy, University of Texas Medical Branch, Galveston, Texas.

Hamerton, 1931). Previous Ebola outbreaks saw catastrophic death rates in gorilla and chimpanzee populations, which led some scientists to think that they were the ones responsible for the disease spreading. Old World monkeys (such as African Green Monkeys) are very susceptible to human and cattle tuberculosis. Unlike humans, such monkeys have no natural resistance to the disease. When they do catch it from a human, it usually spreads fast and fatally in their bodies (as in acute miliary tuberculosis) and to areas other than their lungs. During their illness, they can spread the disease to anyone who comes in contact with them or their waste.

CONCLUSION

The current Ebola virus began in West Africa, a hotbed of tuberculosis (Figure 8). Another map recently put out by WHO lumps Ebola deaths in West Africa under the puzzling categories ―probable, confirmed, and suspected‖ (WHO, 2014c). So what is the take-home message here? At best that ―Ebola-like‖ does not always mean Ebola; at worst that Ebola does not mean Ebola.

Yet ―Ebola‖ vaccinations are well into production, the only question being what are they are actually vaccinating against? Too many have forgotten the implications of blind vaccination against ―viruses‖, whether they be Ebola or the Swine Flu. Yet the Swine Flu fiasco of 1976 offers a not unlikely possible outcome as to what happens when governments and vaccine companies push for a vaccine response for viruses such as Ebola. During that massive swine-flu vaccination

campaign, an attempt was made to vaccinate every American ― leaving 532 people partially paralyzed and 32 dead, and all for an epidemic that never happened. And although the Ebola outbreak has materialized, much of the same thinking regarding vaccinations for the ―Swine Flu‖ still exist in today‘s Ebola vaccination attempts.

By early February, 1977 — then Health Education and Welfare (HEW) Secretary Joseph Califano — in office less than two weeks, faced a vexing situation. In the fall HEW‘s attempt to vaccinate virtually the entire American population against swine flu — on the rational that the US government didn‘t want another 1918 pandemic — smacked into the stone wall of the often paralyzing and sometimes fatal Guillain-Barré Syndrome (GBS). Off balance and bedeviled, Califano commissioned Harvard sparkplugs Richard Neustadt and Harvey V. Fineberg MD to write ―as objective and clinical a report‖ regarding what had happened, and why it happened, during the 1976 Swine Flu debacle — as was possible.

Not everyone liked what they had to say.

In a 166-page smack down of health officials, big Pharma, big Government and virology in general Neustadt and Fineberg‘s The Swine Flu Affair: Decision-Making on a Slippery Disease suggested that scientists, and in particular virologists, had too much confidence in their theories about the epidemiology of influenza and indeed the biology of the virus itself, based upon far too meager evidence (Neustadt and Fineberg, 1978). The

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Figure 8. Map showing the true severity of the tuberculosis problem; in 2006-2008 - the last period before WHO's TB statistics dived as a result of including many TB cases into the wastebasket of "AIDS-defining illness". Note that the darker-colored regions are mostly in Africa. (Source: WHO).

authors bluntly stated not only that not that much was known about pandemic spread of Influenza in general — but also that aside from the three years 1918, 1957, and 1968, that had already passed — that what was being said in so far as Influenza was concerned, was mostly conjecture.

Neurstadt and Fineberg also mentioned that the recorded severity spread in those years besides the 3 mentioned varied quite enough to buttress contradictory arguments about what was being called ―influenza‖ was not ―influenza.‖ Nevertheless a hierarchy of American virologists would see to it that mass vaccination was a reality in 1976 — in the swine flu epidemic which never was.

If the CDC came into 1976 with a sterling reputation, by that year‘s end, its Director‘s actions — including the assertion that Legionnaire‘s disease, a bacteria, was also influenza — would cost the CDC its loss of ―innocence‖ — leaving a situation, mentioned Neustadt, whereby future calls for preventative medicine ―almost surely would be tagged as crying ‗wolf‘.‖

Neustadt and Fineberg implied a strong conviction that scientists, particularly government scientist health officials, seemed fueled by a variety of ―personal agendas‖. Time after time the authors/investigators hinted at disreputable motives on the part of the principal players, with Communicable Disease Center (CDC) head David Sencer squarely in their sights.

Nor was the entire concept of ―Influenza‖ itself immune from their criticism: ―…..the proportion of flu-like illness actually caused by the flu virus is unknown‖ the HEW committee said. But Neustadt and Fineberg weren‘t through: ―And all this on the words of experts,‖ they said, ―overconfident in theories validated through but two or three pandemics, without any proper review of their logic by disinterested scientists.‖ They were referencing a familiar and timelessly repeated theme, whereby ―flu experts‖ and virologists set out to squelch any and all dissent regarding Influenza by their peers. In other words: it had to be the ―flu virus‖ — simply because it was the flu virus.

To both Neustadt and Fineberg, influenza‘s very symptoms were widely misunderstood, not only by millions of Americans, but ―perhaps half the doctors in the country‖, with the word ―influenza‖ used ―for a variety of gastrointestinal troubles, ―stomach flu‖ which, according to Fineberg, had no viral flu causes and no flu vaccine prevention. ―Influenza is found in the respiratory tract and there alone‖, both HEW reviewers reminded.

HEW‘s Califano knew they had a point. Until 1933, influenza was thought to be caused by a bacteria, and before that a mycobacteria (Mycobacterium influenzae). And Laidlaw‘s study, which ―proved‖ flu to be ―viral‖ — basically because it passed through a filter, was under fire from the day it was published. Besides, the last time that a purported ―flu‖ caused widespread death was the

winter following World War I.

Could then such an scenario be repeated with the proposed ―Ebola‖ vaccines? The FDA‘s 2010 viral vaccine guidelines themselves (U.S. FDA/HHS, 2010) shed some light, especially if a vaccine maker was to overlook them.

For example: on page 11 of the 2010 FDA viral vaccination guidelines, we have: ―If the species from which your cells were derived is susceptible to infection with Mycobacterium tuberculosis, an appropriate test should be performed for this agent as well.‖ Also, on Page 18: ―If appropriate, a test for Mycobacterium tuberculosis should be performed.‖ Again on Page 15:―Under 21 CFR Part 610, you must perform tests for safety, purity, and potency of a product, as required. This includes tests for identity, bacterial and fungal sterility, the presence of mycoplasmas, Mycobacterium tuberculosis (if appropriate), and adventitious viruses (in vitro and in vivo tests). You should also consider specific tests for agents that might be present in the seed [Vero cells] due to its passage history.‖ These same Vero cells, from African Green Monkeys, are not only highly susceptible to both Mycobacterium tuberculosis and Mycobacterium africanum but were used both to ―discover‖ Ebola, and in its present day vaccination production. Could they then have influenced or led to the misinterpretation of Ebola‘s original ―discovery‖? Could there now be mycobacterial contamination in present proposed vaccination strategies?

The words ―if appropriate‖ is interpretable. To some, for example, the use of pretreated specimens with formaldehyde or formalin is thought to eradicate TB — which it doesn‘t.

Then there are the guinea pigs –also extremely susceptible to TB and mycobacteria such as tuberculous M. africanum, yet in Pattyn‘s and Piot‘s original March, 1977 Ebola papers, we see guinea pigs and susceptible suckling mice being used with no attempt whatsoever to find or test for tubercular disease in either the specimens being introduced into these animals, or the Vero cells used in the experiment‘s methodology. We also see in these original reports, a host of non-specific pathological findings which could just as well have been interpreted as being from a victim — human or animal, of acute disseminated TB. In addition filamentous forms appear, some branching — just as shown in the previous myco- bacterial literature, including cell-wall-deficient worm-like or serpentine forms subjected to cold environments. Throughout all of this, again — no concrete attempt in materials and methods to rule out tubercular disease was demonstrated in either the ―discovery‖ or present vaccination methodology. Better science is needed before submitting populations to wholesale vaccination.

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