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.

NY institute of Medical
Research, New York, USA.
Email:nyinstituteofmedrese
arch@verizon.net

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.
Friedens 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
Leones tuberculosis level was not only the highest in
West Africa, but filled with resistant strains of TB and
tuberculous Mycobacterium africanum that had reached

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 TBs 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 nuns mysterious, yet deadly illness.
Also, could the samples be tested for Yellow Fever? This
thermos had traveled from Zaires capital city of
Kinshasa, on a Sabena commercial flight to Belgium;
inside its deliverers 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 Piots 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 TCell 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
WHOs 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, isnt it? (Von
Bredow and Hackenbroch, 2014). Depends upon how
you look at it.
Piots specimens proved negative for Yellow Fever and

Peak J. Public Health Manag.

44

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.
Piots 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 tuberculosiss 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 Pattyns
team likewise never really considered a strain of acute
miliary TB or its viral cell-wall-deficient forms in his ruleouts 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

Broxmeyer

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 todays 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 multidrug-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 Britains
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

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 Ebolas 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 Leones 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 Organizations (WHOs)
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

Peak J. Public Health Manag.

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 pathogens 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 CrossReactivity: 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 Africas] population and
those pathogens were again; M. tuberculosis and its
related M. africanum.
Such diversion isnt 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 HIVvirus 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 protg, 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 CDCs Table 51 and not included in those
pathogens tested for cross-reacting and therefore
possibly giving false positive tests for the Ebola? Did the

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 hes 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 HIVantiretrovirals 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 Africans
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 worlds 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

Broxmeyer

47

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 likestructure; gigantic by viral standards. Its a very unusual
shape for a virus (Figure 4). To some it might be
considered worm-like, to others serpentine (Figure 5).
Originally, Piots team thought Ebola was either a
rhabdovirus or torovirus.Today its 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. WHOs 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;

Peak J. Public Health Manag.

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.
(Julin E, Roldn, 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
Mycobacterium tuberculosis.

Cell-Wall-Deficient

Forms

of

48

Broxmeyer

49

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 todays 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
HEWs attempt to vaccinate virtually the entire American
population against swine flu on the rational that the US
government didnt want another 1918 pandemic
smacked into the stone wall of the often paralyzing and
sometimes fatal Guillain-Barr 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 Finebergs The Swine Flu Affair: DecisionMaking 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

Peak J. Public Health Manag.

50

Figure 8. Map showing the true severity of the tuberculosis problem; in 20062008 - 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 years end, its Directors actions including the
assertion that Legionnaires 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 werent
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, influenzas 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.
HEWs 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 Laidlaws 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

Broxmeyer

winter following World War I.

Could then such an scenario be repeated with the
proposed Ebola vaccines? The FDAs 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 Ebolas 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 doesnt.
Then there are the guinea pigs also extremely
susceptible to TB and mycobacteria such as tuberculous
M. africanum, yet in Pattyns and Piots 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 experiments 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 mycobacterial 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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