Posts Tagged ‘Lawrence Broxmeyer’

Vaccines as an Autism Trigger: A TB Link?

January 27, 2015


Lawrence Broxmeyer, MD

From NEXUS Magazine February–March 2015 (vol. 22,no. 2)

Vaccines as an Autism Trigger: A TB Link?
by Lawrence Broxmeyer, MD
© December 2014 – January 2015


[Sidebar Introduction]
While it can’t be said categorically that vaccines trigger autism, it can’t be denied that many vaccines still contain toxic mercury compounds as well as animal and human components which may be contaminated with tuberculosis mycobacteria, with deleterious effects.
At present, the cause of autism and its related spectrum disorders is unknown. Many hypotheses regarding what causes autism have been and will continue to be put forth, but only one will prevail: its true cause. A conversation as to whether vaccines trigger autism cannot be made in a vacuum but, rather, must be weighed against certain epidemiologic, scientific and historic considerations because its complexity is too great.

California Department of Developmental Services, Sacramento, 1999

California, in 1999, had been on high alert for some time. Level-one autism, without any of its “spectrum”, went from almost 5,000 cases in late summer 1993 to an estimated 20,377 cases by December 2002. As California’s Department of Developmental Services stood by incredulously, it witnessed a tripling of California’s autism rate and all but 15 per cent of cases were in children.

California wasn’t alone, but its autism rates had become the fastest-growing group in that state’s developmental disability system and a number of Bay Area school districts were forced to fill entire classes with youths with different forms of autism.

But even in the midst of California’s mini-epidemic, its Santa Clara County seemed particularly singled out. The California Department of Social Services’ aid, brokered by the San Andreas Regional Center, staggered to its breaking point, and its forecast for autism in Santa Clara wasn’t good.

What was behind this epidemic? A major clue, overlooked from a critical standpoint, was contained in the timeline of the department’s own 1999 autism report1 which concluded that the disease had increased dramatically between 1987 and 1998. What had happened in California in and around 1987 that could have sown the surplus of autism that California now reaped?
Division of Communicable Disease Control, Sacramento, California, 1999

While autism exploded in California, there was also, beginning in 1987, a major spike in the number of tuberculosis cases reported by the Tuberculosis Control Branch of California’s Division of Communicable Disease Control. There, division head Dr Sarah Royce proclaimed a tuberculosis (TB) epidemic in California. The epidemic peaked in 1992, had the same male preponderance as autism, and took off at precisely the same moment in time.

California’s TB epidemic was claimed to have peaked well before 1999, but this didn’t stop it from continuing to contribute the greatest number of cases to the nation’s total tuberculosis morbidity.2 But, as with autism, the problem was worldwide, and even the World Health Organization, traditionally slow to react, had declared a global tuberculosis emergency six years earlier.3

Among children, brain-seeking central nervous system tuberculosis is common in a disease that kills more children each year than any other, with the potential to cause in survivors a withdrawal from social interaction, among other things, in its devastating wake.4

It had to be more than a coincidence, therefore, that since the 1980s California experienced a dramatic increase in the number of children diagnosed with autism as well.

Santa Clara County, California, March 2006

If California was experiencing autistic tremors, then surely its Santa Clara County was at the epicentre. By 2006, Santa Clara had some of the highest rates for autism in the entire USA. Although this was for unknown reasons, again the question became: why Santa Clara? The answer pointed in a similar direction.

By 2002, it had become apparent that tuberculosis was on the rise in Santa Clara. By 2006, that county had the highest number of new TB cases in California. A news report of 2014 mentioned that Santa Clara now has “more tuberculosis cases than most US states”.5 At the same time, the immigrant share of the population in Santa Clara County, mostly from countries where TB is endemic, is at its highest point since 1870.6

Santa Clara’s Health Department sounded the alarm. Santa Clara now knew that it had two problems on its hands. Its medically trained psychiatrists, doctors, personnel and statisticians just never stopped to think that the two problems might be related.

Centers for Disease Control and Prevention, Atlanta, Georgia, September 2008

Time passed. More information came in. In September 2008, the Centers for Disease Control and Prevention (CDC) published a study7 by lead author, paediatrician and researcher Dr Laura J. Christie of the California Department of Public Health entitled “Diagnostic Challenges of Central Nervous System Tuberculosis”. Christie and colleagues identified 20 cases of unexplained encephalitis referred to the California Encephalitis Project that were indeed tubercular. The team importantly began with this significant statement: “Tuberculosis (TB) of the central nervous system (CNS)” as thought of by physicians “is classically described as meningitis. However, altered mental status, including encephalitis, is within the spectrum of [its] clinical manifestations.”

In most of the 20 cases, the California Encephalitis Project cultured out tuberculous encephalitis, the same tuberculosis considered the least likely cause for encephalitis. Yet there it was. But, as Christie pointed out, as little as 25 per cent of patients with a diagnosis of CNS TB actually cultured out TB, which was a criterion for this particular study. That means that only a quarter of possible cases were confirmed.

Subcommittee on Human Rights and Wellness, Washington, DC, September 2004

[Photo caption]
Congressman Dan Burton, Chairman of the Hearing before the Subcommittee on Human Rights and Wellness, 8 September 2004

The following excerpts are from the transcript of the “Hearing before the Subcommittee on Human Rights and Wellness of the Committee on Government Reform, House of Representatives, One Hundred Eighth Congress, Second Session, September 8, 2004”.8

[The Subcommittee’s Chairman, Congressman Dan Burton (R-Indiana), is thanking Dr Melinda Wharton, Acting Deputy Director of the National Immunization Program, Centers for Disease Control and Prevention, for her opening testimony.]

Mr Burton: Thank you for your testimony. Everybody knows the value of vaccinations. And every time you testify, you tell us how valuable they’ve been. And we already know that.

We’re not here to say that vaccinations aren’t important. They’re very important. They’ve given us the highest quality of life of any civilization in the history of mankind. That isn’t what we’re talking about. We’re talking about why they’re putting mercury in vaccinations and why it’s never been tested since 1929 when Lilly developed it.

[Congressman Burton turns his attention to Dr William Egan, the Acting Director of the Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, Food and Drug Administration (FDA).]

Mr Burton: Has thimerosal ever really been tested? Has thimerosal ever been tested by our health agencies?

Mr Egan: Only in those early tests that you know of that were done by Lilly.

Mr Burton: When was that? That was done in 1929. Let’s follow-up on that. In 1929, they tested this on 27 people that were dying of meningitis. All of those people died of meningitis, so they said there was no correlation between their death and the mercury in the vaccines. That is the only test that’s ever been done on thimerosal that I know of. Can you think of any other?

Mr Egan: No, in people, no. Except for accidental exposures over time.

Mr Burton: So we have mercury that’s being put into people’s bodies in the form of this preservative, and has been since the 1930s, and it’s never been tested by our health agencies. And yet you folks come here and you testify that there’s no conclusive evidence, and the IOM [Institute of Medicine] says, they favor, get this, they don’t say they’re sure, they say they favor rejection of a causal relationship between mercury and autism and other neurological disorders. Nobody ever gives a categorical statement, that no, mercury does not cause this, no, it doesn’t. And that’s because you can’t do it…

Mr Egan: We are diligently working, as we have testified today and previously, toward eliminating thimerosal mercury from vaccines as quickly as can be done. But there are many issues that are involved in doing this. If we were to say tomorrow that all vaccines, for example, all flu vaccines could only be administered in single dose syringes or single dose vials [thus eliminating the need for thimerosal], the capacity to fill those does not exist…

Mr Burton: OK. Now, my grandson got nine shots in one day, seven of which contained mercury. So if he got the very small amount, he’d be getting maybe nine micrograms, right?

Mr Egan: No, much less than that. Because the maximum that we calculate that a child could receive now during the first six months of life is somewhat less than three. A number of these vaccines [have] defined trace as less than one, some of them have considerably less than one.

Mr Burton: But that amount of mercury would not do any neurological damage to anybody?

Mr Egan: Not according to any guideline.

Mr Burton: No, no, no, no. I want you to say yes or no.

Mr Egan: I do not believe so.

Mr Burton: You do not believe so. I didn’t say believe. Can you say to me right now that amount of mercury being injected into a baby will not hurt it?

Mr Egan: It’s impossible to make those categorical statements with 100 percent—

Mr Burton: That’s right. So it is possible that the amount of mercury that’s being injected, even in trace amounts, could damage a child neurologically, right?

Mr Egan: I don’t think it has that capacity, no. We can argue.

Mr Burton: I know, but you don’t think it is, but you can’t say categorically, can you?

Mr Egan: Do I have evidence for every single child, for every possible dose, the answer is no…
As it turns out, the doses of thimerosal referenced in micrograms cited by Egan were small change compared to what is in certain current multidose flu shots.9 The CDC’s 2014–2015 guidelines for eligible child influenza vaccinations advise: “To protect their health, all children 6 months and older should be vaccinated against the flu each year.”10 With some multidose influenza preparations containing as high as 25 micrograms per dose of thimerosal or higher, this can add up to a lot of thimerosal. And on top of this, concurrently, the CDC still insists: “Pregnant? Get a Flu Shot!”11

Congressman Burton had established, as of 2004, that the only study ever done to conclude that thimerosal was not neurotoxic or could not precipitate the first signs and symptoms of autism was done by its manufacturer, Ely Lilly, in 1929—a study in which 22 meningitis patients (not 27, as Congressman Burton mentioned) in an Indianapolis epidemic were treated with thimerosal, all of whom died.

Lilly showcased and funded the study for one reason and one reason only: its scientist Smithburn, the study’s lead author, out of the sheer desperation of having nothing with which to cure his patients, had injected 22 of those patients dying of meningitis with large doses of thimerosal (up to 10 milligrams per kilogram intravenously) with supposedly no significantly grave consequences.12 That is, no grave consequences other than the fact that seven out of 22 of Smithburn’s patients died within one day after receiving the thimerosal. Only one patient made it to day 62 before succumbing—hardly enough of a window to investigate for chronic mercury damage from the thimerosal. Nevertheless, Lilly would next try to turn a lemon into an orange, sponsoring other scientists13 to say that the thimerosal had nothing to do with the deaths of Smithburn’s meningitis patients.

Unknown to either Burton or Egan, there was one other study testing a mercury compound on humans—a sizeable series which also appeared in the same publication, The Journal of the American Medical Association (JAMA), which had published the Lilly study. Hartz14, looking for a cure for his chronic TB patients, concluded that his trial with a mercury compound was “positively injurious and detrimental to one afflicted with tuberculosis”. Of the 14 patients to whom Hartz administered six or more injections (consisting of 1/5 gram or 13-milligram doses every second day), 12 died within from two weeks to six months after their last injection. Hartz was only using a small fraction of what Smithburn had used, yet his results for those on the receiving end of multiple injections of the mercury compound were disastrous. Hartz wrote:15

“This enormous percentage of deaths, namely, 85.7 per cent, among those [TB] patients who received six or more injections [of mercury], can be attributed only to the use of mercury, simply from the fact that the expectation of life in many of the cases chosen was very favorable indeed. In fact, on account of the age of the patients and the chronic arrested type of the disease, they were the kind of patients who live long and have a favorable prognosis.”

Also unknown to the scientists and the congressman present at the hearing was that although the 1929 Lilly investigators purportedly had an epidemic of meningococcal meningitis on their hands, as the epidemic wore on they were considering it as having originated as a mixed infection with an underlying tubercular infection—making the Hartz and Lilly publications have more in common than might at first meet the eye. It was an era when Mycobacterium tuberculosis and Neisseria meningitidis (the meningococcus) were the two most common causative organisms responsible for meningitis.16 And to this day, TB meningitis is in the differential rule-out for meningococcal meningitis.17

In back-to-back studies of the Indianapolis outbreak of 1929, Smithburn, present in the initial investigation, left the second-phase probe to Kempf, Gilman and Zerfas.18 Both publications showed how anti-meningococcal serums were of little or no use for the Indianapolis outbreak—an unexpected finding for a meningococcal meningitis epidemic.

The actual genesis of meningococcal disease was and still is not fully understood. Meningococcus colonises large numbers in the general population harmlessly, with only a very small percentage of individuals having serious illness from it—notably in the limbs and the brain. Front and centre in the follow-up study done by Smithburn’s colleagues was a mysterious “micrococcus” found in both phases of the Indianapolis outbreak. Just prior to Lilly’s publications, a similar micrococcus was uncovered by Sweany19, also published in JAMA, and subsequently by Mellon and Fisher20 in The Journal of Infectious Diseases. But both Sweany and Mellon’s micrococcus proved to be a (pleomorphic) form of cell-wall-deficient (CWD) tuberculosis (see figure 1 for an example of CWD TB). According to Kempf et al.:21

“The fact that the meningococcus could not be recovered from the blood, spinal fluid or nasopharynx does not necessarily mean that it was not there. However, it [the mysterious micrococcus] was readily recovered from the few meningococcic [meningococcal] cases that we have observed during the last few months and during the first and second years of this epidemic. One might expect to find an organism of this nature in traumatic meningitis or as a complication in tuberculosis…”

As he left the congressional hearing, very much on Congressman Dan Burton’s mind, after having grilled the FDA’s Dr William Egan, was that despite promises time and again to remove mercury from vaccines it never seemed to happen.

Figure 1: One of the stealth, viral-like forms of “cell-wall-deficient” atypical tuberculosis colonies that grew from the brain of a child who expired from the disease. Such forms of tuberculosis are extremely difficult to detect and require special stains and culture media not used routinely in today’s laboratories. (Source: Korsak, T., Acta Tuberc. Pneumol. Belg. 1975; 66[6]:445-469).

Uncommon Valour

“My name is William Thompson. I am a Senior Scientist with the Centers for Disease Control and Prevention, where I have worked since 1998. I regret that my coauthors and I omitted statistically significant information in our 2004 article published in the journal Pediatrics. The omitted data suggested that African American males who received the MMR vaccine before age 36 months were at increased risk for autism. Decisions were made regarding which findings to report after the data were collected, and I believe that the final study protocol was not followed…”22

On 27 August 2014, CDC scientist Dr William Thompson spoke out, admitting that he had co-authored a study23 which purposely cooked the data to avoid showing that African-American infants and toddlers given the MMR (measles, mumps, rubella) vaccine before 36 months of age were at a 340 per cent increased risk for coming down with autism. At the time of the study, and for a decade after, Thompson was silenced—but troubled. This was no average witness; this was a man who knew the intricacies of the study and the original data obtained like the back of his hand.

Obviously, the CDC’s doctored 2004 study was an attempt to clear the MMR vaccine of troublesome implications—an attempt to give the vaccine a clean bill of health. But if the study’s purpose was to examine honestly the possibility of a causal relationship between the MMR vaccine and autism, it failed miserably.

After Thompson came out, the CDC’s Director of Immunization Safety and Thompson’s co-author, Dr Frank DeStefano, defended the study as originally published. But Thompson was already on record. Thompson believed that the removal of some of the study’s subjects because of the lack of a Georgia birth certificate not only went against the original study protocol, but, by reducing the study size by 41 per cent, obscured the strong statistical association between the timing of the MMR vaccination and the appearance of autism in African-American male toddlers. DeStefano was lead investigator in the 2004 paper. Subsequently, DeStefano had a telephone interview with investigative reporter Sharyl Attkisson.24 Here are a few verbatim excerpts from their exchange:

Attkisson: Were you aware of any of his [whistleblower William Thompson’s] concerns of, you know, have you been aware before today of any of his concerns about this?

DeStefano: Uh, uh, yeah, I mean I’ve continued to see, uh, uh, see him for over the past ten years and we’ve interacted fairly frequently, and, uh, uh, no I wasn’t aware of this.

Attkisson: So whoever he raised his concerns to, he didn’t, he didn’t raise it to you or anybody you knew of?

DeStefano: No, I mean the last time I saw him was probably about two months ago, and he didn’t mention anything about this…

[Ms Attkisson turns up the heat, relating to lead author DeStefano, that she thought that leaving out anything in the results of the study, especially through a birth certificate criterion which went against the study’s protocol, didn’t seem appropriate. It was also hiding the true conclusion of the study, which otherwise found a 340 per cent increase in autism in black children given the MMR before 36 months.]

Attkisson: …I still think it would be pretty important to know…

[DeStefano’s reply below apparently was his way of deflecting Attkisson’s probing comment by saying that autism probably developed in the womb before 36 months anyway and that somehow this meant that an MMR vaccination given before 36 months was already too late for the vaccine to cause or precipitate the first signs of autism.]

DeStefano: No, I mean, I think, you know, the other, the other important consideration here is looking at what, what time period we’re talking about. We’re, you know, autism, as you probably are aware, is a condition that really probably has its start while the child is still in the womb. And, you know, it doesn’t, some of the behaviors and such don’t come apparent, become apparent until maybe the child is one, two, three years old. But, uh, uh, what we know about autism that, uh, the, uh, characteristics or behavioral signs do become ava–, you know, apparent by 24 months of age, so. So we had different cut-offs, before 18 months of age, there was no difference in, in any group in terms of, uh, vaccination levels, between the cases and controls. At 24 months of age, when, uh, au—you know—behaviors of autism or some features of autism become apparent, there was no difference between the, uh, cases and controls in any group, it was at 36 months where there was a slight differen—and the difference was, we’re talking about a difference between 93% versus 91%, not a, a big difference. But, so that’s at 36 months. And at 36 months, an exposure around that time period is just not biologically plausible to have a uh, uh, a causal association with autism. I mean autism would’ve already started by then…

Attkisson: Let me just, let me just interrupt, before I lose that thought. So you already made up your mind regardless of what the stats show that if it, certain things show that it didn’t make sense, you wouldn’t, you would try to find out a way to…

DeStefano: No, that’s not what we said. I’m just saying, you know, you interpret, you interpret findings, also, you know, there’s the statistics, then you have to also interpret, bring in things like biological plausibility, how do you interpret these results? So I think we had pretty strong evidence that these results at 36 months were primarily a reflection of requirements to attend early intervention special education programs for the, for the children with autism…

Attkisson: Is there any possibility that it is biologically plausible and you just haven’t, you know, that that’s, the consensus is that it’s not, among you guys, but that it is and you’re overlooking that?

DeStefano: I’m, I’m not aware of any data that would say, you know, that would s-, you know, that would say that, uh, you would have, um, onset of autism after 36 months.
Granted DeStefano’s remark that “autism, as you probably are aware, is a condition that really probably has its start while the child is still in the womb”, which many believe, what did this have to do with a vaccine like MMR exacerbating or bringing on the first signs or symptoms of an autism, perhaps from chronic infection first acquired in the womb—even if the vaccination was given just before 36 months of age? Moreover, now that the real results of the 2004 autism–vaccine study were revealed, why did they show a 340 per cent increase in young black children given the MMR before age 36 months? Autism is certainly not more prevalent in African-American children than in whites. In fact, the rates of autism in black children are considerably less.25

Sir William Osler, co-founder of Johns Hopkins Hospital and frequently described as the Father of Modern Medicine, mentioned that “a quiescent malady” such as congenital syphilis and tuberculosis “may be lighted into activity by vaccination”.26 So, perhaps the differential with the MMR might lie in the racial differential in one of the diseases which Osler mentioned. The CDC’s own statistics, for example, show that the percentage of tuberculosis in blacks is way out of proportion to their percentage in the US population, with TB rates being seven times higher in blacks than in whites.27

The MMR, then, could very well be acting adversely in the fashion described by Osler through statistical evidence alone—but there was much, much more.

Exhibit 1: Known Contents of the MMR Vaccine

Of all the issues of concern regarding a vaccination–autism link, one of the most prominent is, according to Sugarman28, the continued use of thimerosal in certain influenza shots, especially the widely used and economical multidose influenza vials through which many patients can be vaccinated using the same vial of influenza vaccine. Most of the legal battles over vaccines and autism, Sugarman mentions, have alleged that the first signs and symptoms of autism were precipitated by this mercury-containing preservative, which used to be an ingredient in many childhood vaccines and still is found in some of the multidose flu shots used by paediatricians.

Others have argued that the culprit is the measles, mumps and rubella vaccine (MMR) or perhaps MMR in combination with thimerosal. Yet in many other autistic cases, a direct causal link is not there for either. Nevertheless, the thought lingers that these agents as well as other vaccines could, in certain cases, still trigger the first signs and symptoms of autism. In the meantime, the lay term pointing to “toxins” in the vaccines is inadequate.

Whenever one deals with biologicals originating from the cow, the calf, the chicken, the chicken embryo, the swine or from another human in the form of albumen or a foetal cell line—all found in the MMR—one hits upon the potential of such biologicals used in the vaccine bearing or being contaminated by mycobacterial infection. This holds particularly true of a vaccine like MMR, whose components can potentially carry Mycobacterium tuberculosis from human fluids or tissue, Mycobacterium avium from poultry (a subspecies of which is Mycobacterium paratuberculosis) or Mycobacterium bovis from cows or the foetal tissue of cows. And in this case, we are not talking about mere environmental exposure: we are talking about direct injection through vaccination.

To say that the US Department of Health and Human Services’ Food and Drug Administration is aware of this is a stark understatement. One just need download its “Guidance for Industry”29 for viral vaccines—a 50-page paper—each page carefully framed under the heading “Contains Nonbinding Recommendations”. In such a “Guidance for Industry”, the words and warnings for human Mycobacterium tuberculosis as well as mycobacteria from animal sources are scattered throughout.

The MMR vaccine is generally administered to children around the age of one year (12 months), with a second dose before starting school (i.e., at age 4–5).
MMR is front-loaded with such entities as foetal bovine serum (FBS). Foetal bovine serum or foetal calf serum is the blood fraction remaining after the natural coagulation of blood, followed by centrifugation to remove any remaining red blood cells. FBS comes from the blood drawn from a bovine foetus via a closed system of collection at the slaughterhouse.30

This presents a problem.

Johne was the first to report a case of congenital TB in animals, his specimen consisting of the very same bovine foetus.31 Macroscopically though, he noted, the uterus and placenta of the pregnant cow were normal.

Autism has already been linked to be triggered in certain cases by an atypical tuberculosis called paratuberculosis, frequently found in cattle.32 A critical review found that this same form of tuberculosis can infect bovine cow foetuses about nine per cent of the time when the bovine mother has subclinical disease, and an average of 39 per cent of cow foetuses in cases where the expectant cow shows signs of clinical paratubercular disease.33

Industry Turns a Blind Eye

Once the most prevalent infectious disease of cattle in the US, yet today largely ignored and purportedly no longer nearly the problem it once was, bovine TB caused more losses among US farm animals in the early part of the 20th century than all other infectious diseases combined.34

By 1917, the situation had become so grave in hogs and cattle that the Cooperative State–Federal Tuberculosis Eradication Program, administered by the US Department of Agriculture (USDA) and the Animal and Plant Health Inspection Service (APHIS), had to be instituted. For in 1917, it was estimated that 25 per cent of deaths from tuberculosis in adult humans were caused by animal tuberculosis.35

Although it is claimed that in the United States TB “once was” a common disease of farm poultry flocks, cattle, swine and people, this author remains unimpressed with present governmental agency attempts to diagnose both the bacilli and, moreover, their predominant cell-wall-deficient forms.

As another strategy to hide the true incidence of TB, our domestic animals and poultry are often killed young before the onset of tubercular disease becomes obvious.36 Furthermore, most inspection is done visually.

In the meantime, the USDA continues to downplay and ignore the actual incidence of TB not only in cows and their milk (especially with regard to paratuberculosis) but in poultry and eggs. For example, when forced to address the issue of finding paratuberculosis in containers of milk, the USDA initiated a study in 1998, but first used methods like freezing and ultrasound to damage the very mycobacteria being tested for, and then ignored established techniques to isolate mycobacteria related to TB, growing samples on a culture medium which was considered inadequate—and for not nearly a long enough time.37,38 Not surprisingly, the USDA results in that study were all negative.

MMR vaccine also contains WI-38 human lung fibroblasts. A fibroblast is the most common type of cell found in our connective tissue. Although no study has addressed the possibility of mycobacteria contaminating such fibroblasts, Higuchi et al. in 2002 found that the all too common and dangerous strain of tuberculosis H37Rv can invade and grow in a WI-38 foetal cell line quite efficiently.39

Actually, WI-38 is a human cell culture line composed of fibroblasts which were derived from the lung tissue of a three-month-old white female foetus. It is commercially known as “WI-38 (ATCC® CCL-75™)”. First sequestered by Hayflick and Moorhead40 in the 1960s, WI-38 has been used ever since in the production of many of our vaccines.

Finally, in the MMR we have the chick embryo cell culture used to propagate the mumps and rubella (German measles) viruses.

Although authorities seem totally unconcerned today, Hull41, Trylich42 and Romanenko43 all certainly saw the danger of tuberculosis from tubercular hens getting into embryonated chicken eggs.

Chick embryo cell cultures also consist of hydrolysed gelatin as well as human albumen. Hydrolysed gelatin is the hydrolysed connective tissue from an animal—usually from the skin and bones of an animal, generally a pig. The process involves adding enzymes which break down the proteins. It separates the proteins along hydrogen bonds. Then the foetal calf serum from the blood drawn from a bovine foetus through a closed system at a slaughterhouse is also added.

Against all of this you have the antibiotic neomycin added to the MMR in an attempt to contend with any unknown mycobacterial content in the vaccine—which neomycin by itself is totally unequipped to do.

Almost lost in the package insert of Merck’s popular MMR II vaccine is the admission that no studies have been reported to date of the effect of the measles virus vaccine in the MMR on untreated tuberculous children: “However, individuals with active untreated tuberculosis should not be vaccinated.”44 Although infants and children are “individuals”, so difficult is it to isolate TB in them that some paediatric experts recommend a spinal tap in all children under 12 months of age.45 Yet it is specifically at 12 months of age that mandatory MMR vaccination first cuts in.

The Science of Denial

“They believe that TB is an extinct disease. I don’t know why.”46 So said Mario Raviglione, MD, infectious diseases specialist and Director of the World Health Organization’s Global Tuberculosis Programme about a disease which WHO admits infects a third of the world.

While frontal assaults on thimerosal, the MMR vaccine and the overburdened vaccine schedule have justifiably sprung up, a satisfactory and comprehensive explanation as to why and how vaccines might trigger autism has not.

In a 2013 interview, Mel Spigelman, MD, President and CEO of the TB Alliance, a nonprofit TB drug research group based in New York, said of tuberculosis: “It’s still in the US, we just don’t recognize it.”47 Perhaps this is because we just don’t want to recognise it—in ourselves, in our livestock, in the products from our livestock, and in the biologicals used in our vaccine manufacture. But it won’t let us not recognise it.

Meanwhile, we have with tuberculosis one of the few diseases that could possibly account for the soaring rate of autism—a disease which is not only the most common cause of infectious death in children48 but, according to WHO, in their child-bearing mothers aged 15–44, one million of whom die from it each year49; a disease which is extremely neurotropic (nerve-seeking) and remains, worldwide, the most common type of central nervous system infection, particularly among children50; and a disease in which 20–25 per cent of such children can manifest mental retardation as well as other anomalies often associated with neurodevelopmental disorders and the autistic spectrum.51

By 2007, Rzhetsky, in a proof-of-concept biostatistical analysis of 1.5 million patient records, had found significant genetic overlap in victims of autism and those with TB.52

No one who has done a serious study of the literature, old and new, can doubt for a second that the incidence and transfer of maternal tuberculosis, even when there are no maternal symptoms and the disease is latent, are being grossly underestimated. This has been duly noted in recent publications, but more in depth in the past writings and solid research of Charles C. Norris, Pennsylvania physician, gynaecologist, obstetrician and medical investigator. Norris wrote:53

“Pregnancy is prone to light up a latent or chronic tuberculosis, and thus produce a condition in which a bacillemia [blood-borne infection] is likely to be present. Secondary infection and metastasis [by TB] occur in the placenta in the same manner in which they affect other portions of the body.”

“Baumgarten’s theory…has done much to show that congenital tuberculosis may occur, and that tubercle bacilli may remain latent in the child for quite prolonged periods. It has been shown that the tubercle bacillus may remain latent for some time. Under such circumstances congenital tuberculosis is probably mistaken for, and classified as, a postnatal infection [of childhood].”

“Undoubtedly the strong uterine contractions incident to labor constitute a most important factor in the transmission of tubercle bacilli at the end of pregnancy. Organisms that, prior to the onset of labor, were lodged in the placenta or in the intervillous spaces, may, as the result of these contractions, be forced into the fetal circulation. Schlimpert, Schmorl and Geipel, Warthin and Cowie, Dardeleben, and others are very insistent on this point.”

Thus, throughout the first half of the 20th century, the method of choice for an expectant mother with proven TB—if it was found—was early termination of pregnancy.54

Others, like Norris, also saw the possibility of maternal– foetal transfer of even non-symptomatic TB as not uncommon.55-59 Dr Henry William Welch, often called the Dean of American Medicine and a colleague of Osler at Johns Hopkins, was already on record as saying that the mere inability to pick up TB in the foetus or newborn wasn’t an argument against frequent transmission to them.60 There were just too many factors involved, such as the hostile, low-oxygen environment of foetal blood, which could tame even the most virulent TB bacilli into dormant forms for some time, making diagnosis difficult to impossible. The history of associating what we presently call “autism” with tuberculosis is an old one, going back to John Langdon Down, a subset of whose young patients clearly were the first cases of “autism” on record. Such associations persist.61-63

While a blanket statement that vaccinations cause autism cannot be supported, the assertion that certain vaccines can aggravate and precipitate the first signs of an autism originating from chronic disease cannot be denied. A vaccine or group of vaccinations could trigger autism simply by inadvertently introducing, through their human, animal and poultry components, mycobacterial elements into the mother, foetus or young child. Mixed tubercular infection in man with human and fowl TB isn’t a new discovery: Tsukamura and Mizuno64 found it rather commonly in their 1981 study. Once introduced, one tubercular form can potentiate and make more virulent an existing tubercular infection.

Another way in which vaccine components can trigger autism was laid out by Hartz in his JAMA probe regarding how mercury compounds like thimerosal activate and make much worse an existing tubercular infection.

Finally, in vaccinations there are adjuvant oils or lipids, many of which do not have to be reported, used to increase a vaccine’s potency. Such oils or lipids are cholesterol precursors, becoming cholesterol in the body.65 Such a cholesterol surge is a big boost for any dormant systemic tuberculosis already in the body, whose very ability to maintain infection is linked to its ability to acquire and utilise cholesterol. So crucial is this unique ability of TB to use cholesterol in the body for both carbon and energy sources that if it were not for its ability to consume cholesterol, tuberculosis, unlike other pathogens, would be unable to resist eradication through cytokine attack and the attempts of certain activated white blood cells called macrophages to starve it of essential nutrients.66

In comparative and simpler terms, one might look at an injection of certain vaccine oil or lipid adjuvants, squalene among them, whether inside or outside of a vaccination, as lighting up chronic foci of tuberculosis like a Christmas tree; or, in the words of Sir William Osler, chronic tuberculosis “may be lighted into activity by vaccination”—for a few reasons, key to why vaccines, in certain cases, can trigger what a child’s parents clearly see as the first signs of autism in their toddler.

About the Author:
Pennsylvania internist and medical researcher Lawrence Broxmeyer, MD, was on the staff at NY affiliates of Downstate, Cornell and NYU for 14 years. He was the originator and lead author of a novel way to kill AIDS mycobacteria (J. Infectious Diseases 2002; 186[8]:1155-60). His ideas on phagotherapy are still in use today. He contributed a chapter to the textbook Patho-Biotechnology (Landes Bioscience, 2008). His peer-reviewed articles are on PubMed. He is the author of several books including AIDS: What the Discoverers of HIV Have Never Admitted (new edition, July 2014; see review in 20/01) and Autism: An Ancient Foe Becomes a Modern Scourge (2012). He has had several articles published in NEXUS: “Ebola…or African Strains of Tuberculosis” (22/01); “Influenza and the TB Connection” (19/01-02); and “The Untold Truth About Cancer” (17/01-02).
Dr Broxmeyer can be contacted by email at nyinstituteofmedicalresearch@ For more information, visit

Endnotes accompanying the article “Vaccines as an Autism Trigger: A TB Link?”
by Lawrence Broxmeyer, MD
Article published in NEXUS Magazine, February–March 2015 (vol. 22, no. 2)
California Department of Developmental Services, Sacramento, 1999
1. Developmental Services System. Changes in the Population of Persons with Autism and Pervasive Developmental Disorders in California’s Developmental Services System: 1987 through 1998,

Division of Communicable Disease Control, Richmond, California, 1999
2. Ussery, X.T., Valway, S.E., McKenna, M., et al. Epidemiology of Tuberculosis among Children in the United States. Pediatric Infectious Disease Journal 1996; 15:697-704
3. Dolin, P.J., Raviglione, M.C., Kochi, A. Global Tuberculosis Incidence and Mortality during 1990–2000. Bull. of the World Health Organization 1994; 72:213-20
4. Subramanian, P. Extrapulmonary Tuberculosis. In Walsh & Hoyt’s Clinical Neuro-Opthalmology, Vol. 3. Edited by Neil R. Miller, MD and Nancy Newman, MD. Philadelphia: Lippincott, Williams & Wilkins, 2005, p. 2690

Santa Clara County, California, March 2006
5. Bay City News Service. Santa Clara County has more tuberculosis cases than most U.S. states,
6. Center for Immigration Integration. University of Southern California,

Centers for Disease Control and Prevention, Atlanta, Georgia, September 2008
7. Christie, L. J., Loeffler, A. M., Honamand, S., Flood, J. M., Baxter, R., Jacobson, S., Alexander, R., Glaser, C.A. Diagnostic Challenges of Central Nervous System Tuberculosis. Emerg. Infec. Dis. 2008 Sep; 14(9):1473-75

Subcommittee on Human Rights and Wellness, Washington, DC, September 2004
8. Hearing before the Subcommittee on Human Rights and Wellness of the Committee on Government Reform, House of Representatives. One Hundred Eighth Congress. Second session. September 8, 2004. Serial No. 108-262. U.S. Government Printing Office. Washington, DC, 2005,; video of Hearing available at
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14. Hartz, H. J. Ultimate Results in the Treatment of Pulmonary Tuberculosis with Mercury Succinimid. JAMA 1910 Sep; 55(11):915-18
15. Hartz, ibid., p. 917
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17. Ramachandran, T.S. Tuberculous Meningitis Differential Diagnoses. Medscape,
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19. Sweany, H.C. Mutation forms of the tubercle bacillus. JAMA 1926; 87(15):1206-1211
20. Mellon, R.R., Fisher, L.W. New studies on the filterability of pure cultures of the tubercle group of microorganisms. J. Infect. Dis. 1932; 51:117-128
21. Kempf, op. cit., p. 450

Uncommon Valour
22. Statement of William W. Thompson, PhD, regarding the 2004 article examining the possibility of a relationship between MMR vaccine and autism,
23. DeStefano, F.I., Bhasin, T.K., Thompson, W.W., Yeargin-Allsopp, M., Boyle, C. Age at first measles-mumps-rubella vaccination in children with autism and school-matched control subjects: a population-based study in metropolitan Atlanta. Pediatrics 2004 Feb; 113(2):259-66
24. Audio of Sharyl Attkisson telephone interview with CDC’s Dr. Frank DeStefano about his questioned MMR-autism study, August 26, 2014,
25. Child Trends DataBank. Figure 2. Percentage of Children Ages 3-17 with Autism Spectrum Disorders (ASD), by Race/Hispanic Origin, 2007 and 2011/12,
26. Duke, W.D. Multiple Infections – A study of the relation of one infection to another. JAMA 1918 Nov 23; 71(21):1703-1706
27. CDC Factsheet. Tuberculosis In Blacks,

Exhibit 1: Known Contents of the MMR Vaccine
28. Sugarman, S.D. Cases in vaccine court—legal battles over vaccines and autism. N. Engl. J. Med. 2007; 357(13):1275-77
29. U.S. Department of Health and Human Services Food and Drug Administration (FDA). Guidance for Industry. Characterization and Qualification of Cell Substrates and Other Biological Materials Used in the Production of Viral Vaccines for Infectious Disease Indications. Center for Biologics Evaluation and Research. Rockville, MD, February 2010 (50 pp.),
30. Jochems, C. et al. The Use of Fetal Bovine Serum: Ethical or Scientific Problem?. Altern. Lab Anim. 2002 Mar-Apr; 30(2):219-227
31. Norris, Charles C. Gynecological and Obstetrical Tuberculosis, New York & London: D. Appleton & Co., 1923, p. 58: Johne, H.A. Deutsche Zeitschr. f. Thiermed. (Leipzig) 23:207; also Forts. d. Med. 1885; 3:108
32. Dow, C.T. Mycobacterium paratuberculosis and autism: is this a trigger?. Med. Hypotheses 2011 Dec; 77(6):977-81. Epub 2011 Sep 7
33. Whittington, R.J., Windsor, P.A. In utero infection of cattle with Mycobacterium avium subsp. paratuberculosis: a critical review and meta-analysis. Vet J. 2009 Jan; 179(1):60-9. Epub 2007 Oct 24

Industry Turns a Blind Eye
34. USDA Factsheet: Bovine Tuberculosis. Animal and Plant Health Inspection Service, Maryland, August 2002
35. Youmans, G.P. Tuberculosis. Philadelphia: W.B. Saunders Co., 1979
36. Mutalib, A.A., Riddell, C. Epizootiology and Pathology of Avian Tuberculosis in Chickens in Saskachewan. Can. Vet. J. 1988 Oct; 29(10):840-842
37. Stabel, J.R., Steadham, E.M., Boilin, C.A. Heat Inactivation of Mycobacterium paratuberculosis in Raw Milk: Are Current Pasteurization Conditions Effective?. Applied and Environmental Microbiology 1997; 63:4975-77
38. Greger, M. Paratuberculosis and Crohn’s Disease: Got Milk? USDA Farce? section. January 2001,
39. Higuchi, K., Harada, N., Yamada, H., Kobayashi, K., Takeda, M. The invasion of Mycobacterium tuberculosis into non-phagocytic cells. Kekkaku 2000 Nov; 75(11):649-59
40. Hayflick, L., Moorhead, P.S. The serial cultivation of human diploid cell strains. Exp. Cell Res. 1962; 25:585-621
41. Hull, T.G. Diseases Transmitted from Animals to Man. Springfield, Illinois: Charles G. Thomas Publisher, 1947, 3rd ed.
42. Trylich, C. Some Thoughts on Tuberculosis of Domestic Animals Particularly as Relating to Meat Inspection. Canadian Journal of Comparative Medicine 1957 Apr; 21(4):121-133
43. Romanenko, V.F., Diachenko, A.M., Kravchenko, N.A., Mikitin, O.O. Experimental findings on the role of chicken eggs in the epidemiology of tuberculosis. Probl. Tuberk. 2001; 6:40-1
44. Package Insert. M-M-R® II (Measles, Mumps, and Rubella Virus Vaccine Live). Merck & Co., Inc., Whitehouse Station, NJ 08889. Revised June 2014,
45. Rock, R.B., Olin, M., Baker, C.A., Moliter, T.W., Peterson, P.K. Central Nervous System Tuberculosis: Pathogenesis and Clinical Aspects. Clinical Microbiology Reviews 2008 Apr; 21(2):243-261

The Science of Denial
46. Abrams, L. This is the infectious disease you should be worried about. October 24, 2014,
47. Reuters. Los Angeles health officials concerned about TB outbreak on skid row. February 22, 2013,
48. Walia, R., Hoskyns, W. Tuberculous meningitis in children: problem to be addressed effectively with thorough contact tracing. Eur. J. Pediatr. 2000 Jul; 159(7):535-38
49. WHO. TB Is Single Biggest Killer Of Young Women. Press Release, Geneva, Switzerland. WHO/40, 26 May 1998
50. Waecker, N.J. Jr, Connor, J.D. Central nervous system tuberculosis in children: a review of 30 cases. Pediatr. Infect. Dis. J. 1990; 9:539-543
51. Garg, P.K. Tuberculosis of the central nervous system. Postgraduate Med. J. 1999; 75:133-40
52. Rzhetsky, A., Wajngurt, D., Park, N., Zheng, T. Probing Genetic Overlap among Complex Human Phenotypes. Proceedings of the National Academy of Sciences 2007 Jul 10; 104(28):11694-99
53. Norris, Charles C., Gynecological and Obstetrical Tuberculosis, New York & London: D. Appleton & Co., 1923, pp. 46, 56, 54
54. Kobrinsky, S. Pregnancy and Tuberculosis. Canad. M.A.J. 1948 Nov; 59:462-64
55. Warthin, A.S., Cowie, D.M. A Contribution in the Causuitry of Placental and Congenital Tuberculosis. J. Infectious Diseases 1904; 1:140-169
56. Weber, F.P. Congenital tuberculosis. Br. J. Children’s Dis. 1916; 13:321,359
57. Dorozhkova, I.R., Deshkekina, M.F., Ereneeva, A.S., Zemskova, Z.S., Ilyiash, N.I, Zhukova, E.K. Congenital Tuberculosis. Probl. Tuberk. 1972; 50(10):80-83
58. Insanov, A.B., Gadzhiev, F.S. Comparative Analysis of the Results of Spinal Fluid Microbiological Study in Children and Adults Who Suffered from Tuberculous Meningitis. Probl. Tuberk. 1996; 5:25-28
59. Adhikari, M., Pillay, T., Pillay, D.G. Tuberculosis in the Newborn: An Emerging Problem. Pediatr. Infect. Dis. 1997; 16:1108–12
60. Welch, W.H. Papers and Addresses, Vol. 2: Bacteriology. Baltimore: Johns Hopkins University Press, 1920
61. Schoeman, C.J., Herbst, I., Nienkemper, D.C. The Effect of Tuberculous Meningitis on the Cognitive and Motor Development of Children. South African Medical Journal 1997 Jan; 87(1):70-72
62. Gourion, D., Pélissolo, A., Orain-Pélissolo, S., Lepine, J.P. Neonatal Tuberculous Meningitis in a Patient with Asperger’s Syndrome. Journal of Autism and Developmental Disorders 2003 Oct; 33(5):559-60
63. Broxmeyer, L. Autism: An Ancient Foe Becomes a Modern Scourge – The Return of a Stealth Pathogen. North Charleston, SC: CreateSpace, 2012 (159 pp.)
64. Tsukamura M., Mizuno, S. Occurrence of Mycobacterium tuberculosis and strains of the Mycobacterium avium–M. intracellulare complex together in the sputum of patients with pulmonary tuberculosis. Tubercle 1981; 62:43-46
65. Carlson, B.C., Jansson, A.M., Larsson, A. The Endogenous Adjuvant Squalene Can Induce a Chronic T-Cell-Mediated Arthritis in Rats. American Journal of Pathology 2000 Jun; 156(6):2057-65
66. Pandey, A.K., Sassetti, CM. Mycobacterial Persistence Requires the Utilization of Host Cholesterol. PNAS 2008 Mar 18; 105(11):4376-80

AIDS and the “HIV” Hypothesis

October 11, 2012


by Lawrence Broxmeyer, MD

© 2012 All Rights Reserved ; Registered: US Library of Congress

Lawrence Broxmeyer, MD, is a Pennsylvania internist and medical researcher. He was on staff at New York affiliate hospitals of SUNY Downstate, Cornell University, and New York University for approximately fourteen years. In conjunction with colleagues in San Francisco and at the University of Nebraska, he first pursued, as lead author and originator, a novel technique to kill AIDS mycobacteria and tuberculosis, producing outstanding results [see Journal of Infectious Diseases 186, no. 8 [October 15, 2002]: 1155–60]. Recently he contributed a chapter regarding these findings to Sleator and Hill’s textbook Patho-biotechnology, published by Landes Bioscience. In addition, Broxmeyer has written many peer-reviewed articles, available on PubMed of the US Library of Medicine, National Institutes of Health, at: Broxmeyer’s research covers the most challenging medical problems of our times, including AIDS, Alzheimer’s disease, Diabetes, Parkinson’s and cardiovascular disease. Among the books that Dr. Broxmeyer has published is AIDS: What the Discoverers of HIV Never Admitted ISBN-10: 1890035297 ISBN-13: 978-1890035297   : 81 pages  Publisher: New Century Press; 3rd edition (February 18, 2003).


The manuscript below AIDS and the “HIV” Hypothesis, is an adaptation of this AIDS book as well as peer-reviewed articles done by Dr. Broxmeyer. Excerpts from reviews regarding Broxmeyer’s AIDS book are below:


“I am of the opinion that this book may offer a solution to the mystery surrounding the AIDS pandemic with regards to a possible vaccine or cure for AIDS in the near future.

Finally the author should be congratulated for “daring where Angels feared to tread.”

                                                                         -PROFESSOR P S IGBIGBI


“I have never learned so much in such a short time – your book, “AIDS : What the Discoverers of HIV Never Admitted”, is absolutely the most revealing and clearly documented work I’ve ever read! Talk about a superb journalistic documentary –amazing.”



“ I think you are a PIONEER…………..YOU have to make the discoveries because apparently no one has gone there before you!! Sometimes the best beginning discoveries are the people who ask the controversial QUESTIONS that cast doubt on the status quo. Like WHAT IF?????”










Once upon a time, a small group of politically powerful scientists rammed a flawed theory on the origin and cause of AIDS down America’s and then the  world’s throat.

Yet  we  are  still  led  to  believe that we  are  fortunate, even ‘lucky’ that retroviruses, only discovered in the 1970s, were uncovered just in time to label them the culprit in a killer AIDS epidemic. And ‘lucky’ that two ‘HIVs’ were discovered in rapid succession and the technology and theory to  link AIDS to the ‘HIV’ retrovirus were fully in place, for the first  time in  history, only  a  few  years prior  to the recognition of the AIDS epidemic.

Lucky? Even as of the 20th anniversary of the first reported AIDS cases passed, AIDS had infected nearly 60 million people of which almost 22 million, including nearly half a million Americans died, and 8,500 AIDS deaths occurred daily. Yet the  prospects for a cure  or vaccine are as remote as they were three decades ago.

And according to one website, almost 3,000 scientists, doctors and educators have expressed doubts, on the makeshift, contrived evidence to this point provided that “HIV” causes AIDS.


Nevertheless, the mantra that “HIV is the sole cause of AIDS” is so well-known and accepted universally that any suggestion to the contrary is usually met with disdain by the AIDS establishment. One notable example of this disdain was provided by Taiwanese-born TIME magazine’s Man of the Year in 1996, AIDS researcher David Da-i Ho MD[1], who famously and absurdly declared: “It’s the virus, stupid!”

Despite such blather, it is important to realize that the statement “HIV is the sole cause of AIDS” is just a hypothesis. There are unanswered questions and controversy concerning the role of HIV “as the sole cause of AIDS.” And until they are resolved, a cure is not possible.

First, let me say that having practiced treating AIDS patients and done AIDS-based research during and after the deadly US AIDS coastal epidemic, with peer-reviewed studies to that effect, including one which landed in the Journal of Infectious Diseases — it is inconceivable to me that anyone can address the question of AIDS origin without seeing that it began as a highly transmittable infectious disease which could be sexually transmitted.

Let me assure you, to think differently is merely to box oneself into a scientifically untenable position. The case of Gaëtan Dugas alone, the French-Canadian Air Canada flight attendant who single-handedly infected either by himself, or through his sexual contacts, 40 new cases AIDS, speaks differently — much differently.

On the other hand the growing number of scientists that doubt that the HIV retrovirus or any other retrovirus could not be behind the AIDS epidemic, stand on firm ground.

So reasonable is the latter assumption, in fact, that eventually Dr. Luc Montagnier himself, HIV’s primary discoverer, came out with his ‘cofactor’ theory, which basically admitted that HIV in and of itself could not even approach the destruction rendered in AIDS patient.


AIDS picture: dying man


So the emphasis here, and I might add, the only correct emphasis to pursue, will not be whether AIDS can be caused by an infectious factor, but whether the so-called “HIV virus” is really a virus or retrovirus to begin with.

AIDS One HIV regimine, supposedly ‘antiretroviral’, like the pills in this patient’s hand, seemingly keep AIDS at bay, but can take a harsh physical toll.


One argument often used by HIV pharmaceutical-sponsored devotees is to show how their antiretrovirals increase life spans of AIDS victims. But does antiretroviral therapy [HAART] really prolong lives? Depends upon how you look at it. To some orthodox believers, yes, by an average of 13-15 years. To others, this is absurd —citing that the rate of death among “HIV/AIDS” was just being increasingly redefined by the HIV powers that be to include illnesses less life-threatening than that behind the original AIDS epidemic.

Yet, though HAART might or might not greatly prolong life on the average, there is at least some reliable testimony that individuals have experienced clinical improvement on it, often dramatic and immediate. However logic insists that such immediate benefit cannot be the result of any antiretroviral action, whose supposed benefits [decrease in ‘viral load’, rise in CD4] come slowly. Rather such testimony likely reflects an antibiotic or anti-inflammatory effect.

If such antiretrovirals are indeed exerting an antibiotic affect, the question then becomes :which microorganism [and not virus] are the they hitting? Kirk et al reported that antiretrovirals cause a marked decrease in the incidence of TB and to an even larger extent the fowl tuberculosis (Mycobacterium avium), which many experts consider inevitable with AIDS. [2] And unlike what the manufacturers of such antiretrovirals would like to hear, Kirk was hard pressed to explain the significantly lower risk of fowl tuberculosis in AIDS to merely an increased CD4 immune cell count. Rather such a dramatic drop in tubercular mycobacterial avium suggested to him a direct affect on the part of “antiretrovirals” against AIDS-borne fowl tuberculosis.

This opens up the interesting question as to whether “antiretorvirals” aren’t acting more like poorly designed, super-expensive, anti-tubercular agents and increasing CD4 counts merely by suppressing typical and atypical forms of TB. It has always been terribly important to pharmaceutical interests to give the impression to both lay and scientific community alike that their antiretrovirals, and only their “antiretrovirals”, could increase a CD4 immune count in AIDS patients. Yet we know that one of the most dramatic restorations of CD4 count on record occurred in  patients with “HIV” and TB when only anti-TB treatment was used — in  John’s  study where a CD4  count of 89/ll climbed to 760/ll. [3] This of course doesn’t fit into Big Pharm’s agenda, as all anti-tb antibiotics are now off patent and cannot generate nearly the profit of their antiretrovirals.

Just as disconcerting to American pharmaceutical interests was the unexpected find in early AIDS autopsies of the surprisingly high proportion of difficult to diagnose fowl tuberculosis or Mycobacterium avium-intracellulare, [4] in up to 55% of American cases in early studies. [5] In all likelihood this American percentage was much higher as statistics used did not include respiratory and gastrointestinal colonization without clinically evident infection. According to the National Institute of Allergy and Infectious Diseases, TB is still the major attributable cause of death in AIDS patients.

Pharmaceutical interests could not just ignore this, so they began publishing studies which showed, how with antiretrovirals, tubercular infection dramatically [6] declined. [See Figue 1]


Figure 1. Incidence of Disseminated Fowl tuberculosis [Mycobacterium avium Complex] Infections in US AIDS. The HIV Outpatient Study 1994-2007.
Figure is based on data from Buchacz K, Baker RK, Palella FJ Jr, et al. AIDS-defining opportunistic illnesses in US patients, 1994-2007: a cohort study. AIDS. 2010;24:1549-59.

The purposeful loosening of criteria by HIV scientists to include tuberculosis —which infects, according to the CDC, a third of the world —  as well as fowl tuberculosis as “AIDS-defining” illnesses was simply a survival strategy to keep the HIV hypothesis viable. HIV diehards early realized that up to 70% of people with TB were “HIV-positive”.  And although there were other “AIDS-defining” illnesses postulated, none came close to the number of people infected by TB. Besides, early HIV investigators knew very well that not only were tubercular mycobacterial infections the main cause of bacterial infection during AIDS; but that they often preceded other infections in AIDS by 1–10  months. [7]

So above all, tuberculosis had to be made an “AIDS-defining” illness. In fact the definition of HIV now, thanks to their active efforts, became so loosely constructed that even patients with verifiable tuberculosis and no HIV, but who nonetheless reacted positively for  HIV, could be incorporated under the umbrella of having AIDS despite the fact they didn’t have HIV.

No more was the hypersensitivity, and evasive tactics of “HIV experts” on display towards tuberculosis and its related mycobacteria than in the 2005 book entitled Retroviral Testing and Quality Assurance Essentials for Laboratory Diagnosis [8]. Here forgetful “HIV experts” left out on page 24 TB and its related mycobacteria from their list of “medical conditions” suspected or known to produce false-positive screening and Western blot tests in AIDS. Included among these “experts” were those from the University of Maryland’s Viral Diagnostics, The Institute of Human Virology, The FDA, the Director of the National Serology Reference laboratory in Australia, the World Health Organizations [WHO] and the Centre on HIV/AIDS [also in Australia].

And the fact that this entire group studiously ignored what is hands down the biggest cause of such AIDS false-positive screening tests and “indeterminate” Western Blots didn’t even seem to faze them. Moreover, that this was oversight on the part of these “HIV experts” is extremely doubtful if one knows the history involved.


Veterinarian Max Myron Essex, a key figure in early “HIV” research.


Well-known since the first scientist to propose HIV testing — Veterinarian Max Myron Essex — tuberculosis gives a false positive for “HIV” in almost 70% of cases. In fact such cross reactivity between “HIV” and tubercular pathogens was so significant that it forced Essex and his colleague Kashala to warn that both the HIV screening test [ELISA] and Western Blot results “should be interpreted with caution when screening individuals  with M. tuberculosis or other mycobacterial species.” [9] This of course automatically meant throwing away HIV serum diagnostics for at least 1/3 of the people in the known world — and that fraction doesn’t even include M. avium, the fowl tuberculosis also so common in AIDS.


ELISA HIV AIDS Test Screening



AIDS Western Blot Test to confirm the person is HIV positive.


But there were other problems in the proclamation that AIDS antiretrovirals extended lives an average of 15 years. And they soon became apparent. While the original AIDS patients were desperately ill, many of them showing fowl tuberculosis early in their disease, presumably through rectal transmission……….as time went on not all cases of “AIDS-defining”  TB were ill, many of them being dormant or asymptomatic.  Such AIDS individuals would survive longer.  In the meantime, with all the literature touting that antiretrovirals increase the life of AIDS patient, with or without such drugs, the greatest risk of death [median age] from “HIV” disease remains 35-45 years-old, much as when AIDS began.

And then there was the terrible toxicities of these antiretrovirals. The fact that certain studies claim that antiretrovirals extend the life of an AIDS patient does not mean that they are benign in the least. As just one example, and putting aside the black box warnings regarding liver failure, kidney failure and severe neuropathy — many cardiac complications of HIV are not affected by antiretroviral cocktails [HAART] and such heart problems continue to develop in AIDS either with antiretroviral treatment, or because of antiretroviral treatment. This is because viral treatment itself can cause a metabolic syndrome, characterized by altered body-fat distribution and an insulin resistance. This together with other factors that such retroviral cocktails create are associated with increased atherosclerosis and subsequent risk of peripheral artery and coronary artery diseases such as heart attacks. [10]

Also in the HIV Positive population of patients receiving highly active antiretroviral therapy (HAART), there has also been an increase in the incidence of severe facial lipoatrophy [facial wasting], at times quite grotesque.


AIDS Facial lipoatrophy from antiretrovirals.


In 2000, French retrovirologist Luc Montagnier, at least the co-discoverer, and in the eyes of  many, the discoverer of HIV — who seldom saw a retrovirus that he didn’t feel was either infective or lethal to humans — said:

“it is tuberculosis that constitutes the greatest public health problem today: 1.7 billion people have latent infections of Mycobacterium tuberculosis [the bacillus that causes tuberculosis], while eight million are actively infected.” [11] Actually in 1990, tuberculosis killed more people than any other single disease – almost 3 million.

Perhaps, it might have been better, therefore had Montagnier redirected his thoughts into his hypothesized retroviral cause of AIDS. For example:

The  first reports of fowl tuberculosis in US AIDS appeared in 1982, the year previous to Montagnier and Barré-Sinoussi’s, original Pasteur report on their mysterious retrovirus. At UCLA Zakowski [12] found that “all of the homosexual patients that have died of acquired immunodeficiency at the UCLA Medical Center for the Health Sciences have had disseminated MAC [fowl tuberculosis] infection.” Furthermore, the team mentions: “Because of this preliminary observation, we now vigorously seek evidence of mycobacteria [tubercular] infection in homosexuals with unexplained lymphadenopathy [a disease, disorder or enlargement of the lymph nodes].” Zakowski, in fact mentions that he did not feel it unreasonable to treat AIDS patients empirically for fowl tuberculosis”, pending the results of mycobacterial cultures, even if acid-fast [tubercular] bacilli are not identified on smears or tissue sections.” In fact, in the eyes of Zakowski and his colleagues, such anti-tubercular treatment could very well be life-saving.



Mycobacterium avium in lymph node tissue of
an AIDS victim. Ziehl-Neelsen stain. Histopath-
ology of lymph node shows tremendous numbers of acid-fast tubercular bacilli within plump histiocytes. CDC/Dr. Edwin P. Ewing, Jr.



Tuberculosis of a lymph node (lymphadenopathy) in the neck.


Microscopic picture of TB of the lymph node. In the right upper corner insert are classical red (acid-fast) tubercular bacilli.



Therefore one can only wonder why Luc Mantagnier not only ignored but didn’t even consider this disease before sending Françoise Barré-Sinoussi in with his human HIV-reverse-transcriptase Geiger counter to look exclusively for a “retrovirus” in the white blood cells called lymphocytes taken from the enlarged lymph nodes of their first case of “HIV” — a young gay man sick with AIDS. After all, these first French AIDS specimens, taken in 1983 had a medically indicated differential diagnosis protocol to follow. In fact, soon thereafter McCabe appeared [13] in The Journal of the American Medical Association [JAMA], offering that not only did TB clearly preponderate as the cause of enlarged lymph nodes in adults, but that atypical TB, such as Mycobacterium avium [fowl TB] was hands down the number one cause of infectious lymph node involvement in children. Shouldn’t this have given Montagnier and Françoise Barré-Sinoussi pause to test for such pathogens before attributing these first French AIDS lymph nodes specimens exclusively to a “retrovirus”?  Apparently not, as not even the mention or afterthought of tuberculosis or fowl tuberculosis [M. avium] was in their report.

And yet despite this, TB and Fowl TB were the two leading causes of infectious death in AIDS, both having bacillary [or a bacillus form] as well as viral forms — every bit as capable of throwing off signals for the reverse transcriptase registering on Montagnier and Françoise Barré-Sinoussi’s  equipment as retroviruses were.



AIDS Virologist Françoise Barré-Sinoussi


From its first publication, “HIV” was questionable. Biochemist Kary Mullis, who in 1993 was ironically awarded his Nobel Prize for his work with the Polymerase Chain Reaction [PCR] used in HIV detection said:“If there is evidence that HIV causes AIDS, there should be scientific documents which either singly or collectively demonstrate that fact, at least with a high probability. There is no such document.”

And to Dr. Heinz Ludwig Sanger, Emeritus Professor of Molecular Biology and Virology, Max-Planck-Institutes for Biochemistry, Munchen said that it had become obvious that: “Up to today there is actually no single scientifically really convincing evidence for the existence of HIV. Not even once such a retrovirus has been isolated and purified by the methods of classical virology.”


The meticulous research of the Perth Group best summed things up:

“What we are doing and have been doing from the very beginning is to question the accepted cause of AIDS and to put forward an alternative theory for the cause of AIDS which has a number of well-defined predictions, most of which have been satisfied.”[14]

“Since in our view at present no evidence exists that AIDS is caused by a retrovirus, we see no reason for AIDS patients to be treated with antiretroviral drugs. We did write a critical analysis on the use of AZT as an antiretroviral agent when we showed that, given its pharmacological properties, it is not possible for it to have an antiretroviral effect. We have also presented evidence that AZT and nevirapine do not prevent mother-to-child transmission. However, we never advised that antiretroviral drugs should never be prescribed since up till now the possibility had not been excluded that they may have clinical benefits acting by means other than as antiretroviral agents. However, given the latest publication on HAART, this may not be the case.”

The thesis of this paper is that what is called “HIV” is in reality viral forms of cell-wall-deficient atypical tuberculosis complicating a picture of earlier exposure and acquisition of a tubercular infection, active or latent. Such previous infection could have occurred at any time in the life of an individual, and most often does so in the formative years. But when existing tubercular infection is then coupled with extremely virulent atypical tubercular forms [such as M. avium] commonly found in US AIDS, this deadly one-two punch of immunosuppression sets the stage for the real so-called “opportunistic” infections that also jump on board in AIDS. Furthermore, if the antiretrovirals have any benefit towards the extension of the life of an AIDS patient, which some reports claim is an average of 15 years, this has little to do with their action against “HIV” and a lot to do with the fact that such antiretrovirals, though mechanisms still being worked out, serve to suppress the two leading causes of infectious death in AIDS: Mycobacterium tuberculosis and Mycobacterium avium.  It will also be shown that even the use of these antiretrovirals still apparently is not enough to prevent tubercular pathogens from being the leading cause of death, even in societies with free access to such HIV antiretrovirals. [15]


  1. Ho DD, Neumann AU, Perelson AS, Chen W, Leonard JM, Markowitz M: Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection. Nature 1995, 373:123-126.
  2. Kirk O et al  Infections with Mycobacterium tuberculosis and Mycobacterium avium among HIV-infected Patients after the Introduction of Highly Active Antiretroviral Therapy American Journal of Respiratory and Critical Care Medicine 2000Vol. 162: 865-872.
  3. John  J. J., Kaur  A. Tuberculosis and HIV infection. Lancet 1993; 342(2): 676.
  4. Welch K., Finkbeiner W. Autopsy findings in the  acquired immune deficiency syndrome. JAMA 1984; 252:1152–1159.
  5. Kiehn T. E., Edwards F. F. Infections caused by Mycobacterium avium complex in immunocompromised patients: diagnosis by  blood culture and fecal  examination, antimicrobial susceptibility tests, and morphological and seroagglutination characteristics. J Clin  Microbiol 1985; 21:168–173.
  6. Buchacz K, Baker RK, Palella FJ Jr, et al. AIDS-defining opportunistic illnesses in US patients, 1994-2007: a cohort study. AIDS. 2010;24:1549-59.
  7. Bisburg E. Central nervous system tuberculosis with  the acquired immunodeficiency syndrome and its related complex. Ann Intern Med 1986; 105: 210–213.
  8. Constantine NT, Callahan JD, Watts DM. Retroviral testing: essentials for quality control and laboratory diagnosis. Boca Raton, Florida: CRC Press, 1992:117-118.
  9. Kashala O, Marlink R, Ilunga M, et al. Infection with human immunodeficiency virus type 1 (HIV-1) and human T cell lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 cross-reactivity and antibodies to lipoarabinomannan. J Infect Dis 1994; 169:296-304
  10. Barbaro G, HIV infection, highly active antiretroviral therapy and the cardiovascular system  Cardiovascular Research 60 [2003] 87-95
  11. Montagnier L Virus  New York  WW Norton & Company, Inc, 2000.
  12. Zakowski P., Fligiel S. Disseminated Mycobacterium avium- intracellulare infection in homosexual men dying of acquired immunodeficiency. JAMA 1982; 248: 2980–2982.
  13. Lai KK, Stottmeier KD, Sherman IH, McCabe WR. Mycobacterial cervical lymphadenopathy: Relation of etilogic agents to age. JAMA 1984; 251:1286-1288.
  14. Papadopulous-Eleapulos E, Turner VF  The Perth Group Challenges John Moore.  Rethinking AIDS Sept 23, 2006
  15. Saraceni V et al.  Tuberculosis as primary cause of death among AIDS cases in Rio de Janeiro, Brazil. Int. J. Tuberc Lung Dis. 2008, 12(7):769-772.





Manhattan, 1979


By 1979, doctors in Manhattan began to notice a strange new disease killing what had been up to then healthy gay men. As reports mounted, the Centers for Disease Control (CDC) was forced to circulate similar notices of homosexual men in New York and Los Angeles with a weakened immune system dying from heretofore rare causes. [1]


The first AIDS cases were uncovered in Manhattan in 1979.


From  its conception AIDS was a  nightmare of  anguished  victims, washed with wave after wave of terrible disease, whose physicians, like so many medical priests, helplessly watched them die. U.S. Coastal hospitals in San Francisco, New York and Los Angeles soon turned into  war  zones.

The strange disease lurked among the gay habitual visitors of bathhouses.  Men began dying of pneumonia and other respiratory illnesses, but only after drastically losing weight and developing horrific skin lesions on their faces, necks, backs, and chests.  This disease became known in the gay community as “gay cancer”.  It was particularly volatile, and it progressed rapidly.

As more cases of the mysterious killer emerged, the name was changed from “gay cancer” to “gay-related immune deficiency” (GRID).  This, at least, was an open recognition that whatever was causing the disease was compromising a body’s immune system.  It didn’t explain, however, the rather esoteric choice of gay men, [and soon discovered] IV drug users as victims.  Gay men realized the danger.  Many made the intuitive leap early that perhaps certain activities, such as anal intercourse, might be transmitting the causative agent.

Rare  diseases like Pneumocystis carinii,  a tiny one-celled protozoa, filled gay lungs to the  point of suffocation and requests for pentamidine aerosols to combat Pneumocystis trickled, and then poured into the CDC. Another uncommon killer, Kaposi’s Sarcoma [KS)of the skin, became the  most common form  of this gay-related immune deficiency.


Kaposi’s Sarcoma. Black arrows point to rounded tubercular microbes shaped as cocci and granules in the tissue.


That AIDS could be sexually transmitted was incontrovertible, through the gay sexual activities of Gaëtan Dugas alone. Dugas, a French-Canadian male air stewardess, was responsible for infecting at least 40 different men either by himself or through other men that had had contact with him. And of the 248 cases known before the detection of the virus, in excess of 40 of these AIDS victims had direct or indirect contact with Gaëtan Dugas.

Dugas, who was on a collision course with history, only became sexually active in 1972. Born February 20, 1953, he would soon acquire the infamous name of Patient Zero.

Gaëtan Dugas: at one point said to be patient zero of the North American AIDS Pandemic.


On October 31, 1980 – ominously enough, Halloween night – the gay male airline steward Gaëtan Dugas visited a gay bathhouse for the first time on a layover in New York City. There it is speculated that Dugas caught the disease first. Sometime later, after having casual sex in a darkened room, a male interviewee later reported that when he had turned on a light in the room where Dugas lay, he spotted the lesions (Kaposi’s sarcoma) that were the classic earmarks of “gay cancer” on Dugas’ chest.  When he remarked about it, Dugas replied sardonically, “It’s gay cancer.  Maybe you’ll get it.” And so Gaëtan Dugas, the narcissistic and embittered flight attendant, was given the code name “Patient Zero”, though he was indeed not the first to contract AIDS.  AIDS now had a face.


Kaposi’s Sarcoma- Papular type.


Nor  was  it  only   gays   at  risk.   Drug   addicts sharing needles and hemophiliacs, given pooled clotting factor VIII from  blood so they would not  bleed to death, soon became  prey, again developing Kaposi’s sarcoma and pneumocystis pneumonia. America’s entire blood supply was in jeopardy, for by the early 1980s, gay and bisexual men  accounted  for  1 of 4 American blood donors.

AIDS throttled the immune system, in some cases shutting it down, and the  primary site of attack always seemed traceable to the body’s T-cells: white blood cell lymphocytes  which held the  body’s invaders at bay.

By 1977 much evidence indicated that the  basis   of cellular immunity was  tied  in with  T-cells  lymphocytes — colorless, motile, cellular elements of lymph. Chief in importance among these was the T-helper or CD4 lymphocyte, which fought infection. It soon became apparent  that in AIDS CD4  cells  were either severely depleted or they fell off the  blood map altogether.

Panic stricken virologists and other epidemiologists worked feverishly to isolate the source of this sexually transmitted disease whose first endemic wave washed upon American homosexual men’s shores. Without delay, these  same virologists, who  for decades had failed miserably to  find   a  retroviral  cause for  cancer, pounced on  AIDS, dismissing any  possibility other than a virus or a retrovirus: ignoring that it could just  as easily  be either one or a combination of older microbes presenting in an all-new way. Among them – Robert Gallo and Luc Montagnier.

Virologists initially told physicians to pass on the word that it was the Cytomegalovirus [Ibid] that caused AIDS.  Doctors dutifully obeyed, not  fully realizing that all people, with time, are infected with  Cytomegalovirus.

Epidemiologist/retrovirologist Donald Francis, who would direct laboratory efforts for AIDS at the  CDC, and was also assistant director of the  CDC’s Division of Viral Diseases — had his  own  peculiar theory. Oddly enough, it was one also shared with epidemiologist James  Curran, eventual director of AIDS research at CDC. It went like this: combine hepatitis with  feline leukemia in cats—a retrovirus on which Francis wrote his doctorate — and you had Kaposi’s Sarcoma and the opportunistic infections seen in AIDS. Or maybe, just  maybe, it was a retrovirus similar to the cat retrovirus — which in and of itself, alone, was solely responsible. Curran and Francis had worked together years ago developing the  Hepatitis B vaccine. They had all the connections in the scientific world that they needed.


Donald P. Francis, M.D., D.Sc.


Francis, one of  the few  at  CDC  who had  actively wiped out  smallpox worldwide, was  considered an  expert  on both epidemics — and the cat  leukemic virus. He would now  combine his fields of ‘expertise’, quickly concluding that AIDS was cat leukemia in people. It was an impulsive long  shot, and by most treated as such — at least initially.





  1. MMWR,  Morb  Mortal Weekly Rep 30:250–2. 1981.







America, Turn of the century.


Indeed, the history of retroviruses mirrored cancer research.


In1904, Ellermann and Bang, searching for an infectious  bacterial  cause  for chicken leukemia [4], succeeded in transferring it from one fowl to  another by  injecting cell-free tissue infiltrates. They sought a bacteria, but simply because it  passed through a filter, the  responsible agent was assumed to be a virus.

That same year, the first  lentivirus, later claimed to be related to HIV, was isolated as a filterable equine infectious agent in horses by Valle and Carre at the Pasteur Institute. [16] Yet Roux, an authority on  ‘invisible  microbes’  at that time, shrugged off Valle and Carre’s finding as no more than ‘small bacteria’. [14]

Most authorities now realize that there are  some viruses almost as  large as bacteria and some bacteria as small as viruses, forms of which can  easily  pass  through filters. This  realization was quickly disputed by HIV enthusiasts Francis et al. [5], when they falsely mentioned ‘since the  infectious agent had obviously passed through  a filter, it had to be  a virus.’

It did not.

Peyton Rous was credited with the discovery and isolation of the first retrovirus. By 1911, Rous wanted to know why if one chicken got cancer, others followed. [13] Rous, who  reproduced the tumor at will in Plymouth Rock fowls, favored a bacterial cause over a filterable virus. However, it was a question that he never definitely answered.

Dr. Francis Peyton Rous (1879-1970),


By 1933 Shope reported a viral tumor in cottontail rabbits, and Bittner reported  on a  milk-born mouse breast cancer attributed to still another virus. [1]

In fact by the1950s, and with the advent of the electron microscope, particles later questionably ascribed to retroviruses were readily being detected. As a result, and at a time when established medicine had about-faced and was now firmly set against an infectious cause for cancer, two controversial minority camps splintered from mainstream, each diametrically opposed.

There were the virologists, who claimed that cancer was viral or retroviral. And another group whose careful, peer-reviewed research, demonstrated that the retroviruses in Rous, Bittner and Shope tumors were actually filterable forms of mycobacteria. [10] Tuberculosis-like, these ‘viruses’ stained with acid-fast dyes; readily passed through a filter, but actually were  a class of bacteria having many of the characteristics of mycobacteria such as tuberculosis.

This work, spearheaded by physician-researcher Virginia Livingston of Rutgers [9], validated earlier work on Rous as a  bacteria. [3,6]  But soon others would join [2,7,15]. Livingston’s network, questioning the very existence of retroviruses, and the retrovirologists did not like it. A scientific life-and-death cancer struggle ensued.

By 1960, biologist turned retrovirologist Howard Temin sought to contrive an explanation for his observation as to why retroviruses, composed of RNA, Rous among them, were inhibited by Actinomycin D — an  antibiotic and known bacterial DNA inhibitor. Based  on  this finding, Temin elaborately hypothesized the concept of reverse transcription with its “reverse transcriptase”. But, in truth, since antibiotics did not affect viruses, Temin’s observation regarding Actinomycin D’s inhibition of Rous still made more sense if the Rous retrovirus was  bacterial to begin with. It was later shown that Temin’s reverse transcriptase was also utilized by other microbes, including Mycobacterium tuberculosis.


Howard M. Temin, PhD


Nevertheless, quickly capitalizing on the flawed logic of Temin, cancer viral investigators of the 1960s and 1970s reacted by conveniently misinterpreting his non-specific enzyme discovery [reverse transcriptase], which in fact arose primarily as either a function of normal cellular healing, or could be found in other pathogens — as a primary indicator for the newly scrutinized retroviruses. It was as a direct result of Temin’s enzyme, that ‘oncoviruses’, purported to cause cancer, suddenly became known as ‘retroviruses’.

It was to Rutger’s researcher Virginia Livingston’s solid disadvantage that when Richard Nixon signed his National Cancer Act on December 23, 1971, he unwittingly placed virologist Frank J. Rauscher Jr. as  director of  the just established  National Cancer Program (NCP).


Dr. Frank J. Rauscher Jr.


With Rauscher at the controls it was only a matter of time before cancer virologists, retrovirologists and immunologists were pushed to the vanguard of ‘America’s War on Cancer’. Once entrenched, they would remain at  the helm even as, incredibly, their  failed cancer attempts now morphed towards finding the retroviral cause for AIDS.


Bacterial L-forms, the connecting link between viruses and bacteria, were  first  described by Emy Klieneberger at England’s Lister Institute, for which she named them “L-forms”. Such bacteria were ‘cell-wall-deficient’ (CWD) because they either had a disruption or lack of a rigid bacterial cell wall. This lack of rigidity allowed them the plasticity to assume many forms (pleomorphic), some of them viral-like but all of them different from their classical parent. Such forms were also poorly demonstrated by ordinary staining, [8] and many of them, just like viruses, easily passed the finest of filters.  Of all the bacteria, it is tubercular L-forms that predominate and are crucial to the survival of tuberculosis and the mycobacteria. It is mostly in its cell-wall-deficient (CWD) forms, that TB can escape destruction by the body’s immune system. And at the same time CWD forms of the  tuberculosis-like mycobacteria react in Elisa blood tests [11], similar to the ‘HIV retrovirus’, which they can simulate in every way.

Some years later, when HIV discoverer Luc Montagnier was interviewed for  a  French AIDS documentary, film-maker Djamel Tabi asked how he had isolated HIV. Incredibly, Montagnier’s  reply  was  that he did not isolate HIV, he  just  found something that looked like  a retrovirus. [12]


Klieneberger, as well as Livingston, also saw parallels between the filterable forms of tuberculosis and ‘mycoplasmic-like forms’ because without intact cell walls the mycobacteria were often mistaken for the virus-like bacteria mycoplasma, which has no cell wall. [8] The differentiation between mycoplasma and cell-wall-deficient bacteria, reported Mattman, was difficult at best. [11]


1. Bittner J. J. Some possible effects of nursing on the mammary gland tumor incidence of mice. Science 1936; 84: 162.

2. Diller  I. Donnelly experiments with  mammalian tumor isolates. Ann N Y Acad Sci 1970; 174(2): 655–674.

3.  Duran-Reynals F. Neoplastic infection and cancer. Am J Med 1950; 8(4): 440–511.

4. Ellermann V., Bang O. Experimentelle Leukamie bei Huhnern. Zbt Bakt  1908; 46:  595–609.

5. Francis D. P., Curran J. W. Essex M  Epidemic acquired immune deficiency syndrome: epidemilogic evidence for a transmissible agent. J Natl Cancer Inst 1983; 71:  1–4.

6. Glover T., Scott  M. A. Study of the Rous Chicken Sarcoma No.1. Canada Lancet  and Practicioner 1926; 66(2):49–62.

7. Alexander-Jackson E. A specific type  of microorganism isolated from  animal and human cancer: bacteriology of the organism. Growth 1954; 18:  37–51.

8. Klieneberger-Nobel E. Origin, development and signifincance of L-forms  in bacterial cultures. J Gen Microbiol 1949; 3: 434–442.

9. Livingston V. A. Specific type of organism cultured from malignancy: bacteriology and proposed classification. Ann N Y Acad  Sci 1970; 174: 636–654.

10. Livingston V. Cancer: A New Breakthrough. Los Angeles: Nash Publishing, 1972.

11. Mattman L. Cell Wall Deficient Forms – Stealth Pathogens. Boca Raton: CRC Press, 1993.

12. Null G. AIDS: A second opinion. Townsend Letter  for Doctors and Patients, June  2000.

13. Rous P.A. Sarcoma of the Fowl transmissible by an agent separable from  the  tumor cells. J Exp Med 1911; 13: 397–411.

14.  Roux  E. Sur les microbes dits  inviibles. Bull Inst Pasteur 1903; 1: 7–12,  49–56.

15. Seibert F. B., Feldman R. L. Morphological, biological, and immunological studies on  isolates from  tumors and leukemic bloods. N Y Acad  Sci 1970; 174(2):690–728.

16. Vallee H., Carre H. Nature infectieuse de l’anemie du chevale. CR Acad Sci Paris 1904; 139: 331–333.







Armed  Forces Institute of Pathology, Washington, 1989


Dr. Shyh-Ching Lo, MD was a senior scientist at the  prestigious, world-renowned Armed Forces  Institute of Pathology in  Washington. As he watched events unfold, and it became obvious that it was  going to  be dictum that HIV caused AIDS, he just  had one  problem: whenever  he  examined someone who  had died  of AIDS, he could never find  HIV, not even a trace of HIV-infected tissue damage. So Lo began his own search for an AIDS cause which led him to a ‘virus-like infectious agent’. [8] Knowing he was onto something, Shyh-Ching Lo followed his conscience, against the  grain of  most other scientists, and finally isolated not a virus but a mycoplasma. And in one study of 24 people with AIDS, he found antibody titers to it in practically everyone. [9]  Shyh-Ching Lo would  co-published again, with Saillard. [13]


Shyh-Ching Lo, MD, about to give a presentation regarding Recent Studies of Epidemiology of MLV-related Human Retroviruses.


That same year Livingston died and a year later Luc Montagnier, the discoverer of HIV, almost got booed off a 1991 San Francisco podium by HIV activists at the Sixth International AIDS conference — for endorsing Lo’s mycoplasma as a necessary co-factor for the AIDS virus to become fatal. [10]

Montagnier and Lemaitre had done a hornet’s nest of an experiment which put HIV activists on the  edge of their chairs. In 1990 the two scientists published that cells  cultured with ‘HIV’, which normally died, grew well in the presence of two antibiotics, minocycline and doxycycline. [5] Antibiotics do not  affect  retroviruses, so they were not  working against HIV – it was a bacteria. Montagnier decided that that bacteria was probably Lo’s  mycoplasma. He  had done so, unaware of the fact that the  two  particular antibiotics he  was  using also  had activity also against Livingston’s atypical tuberculosis. [3,12,14,15] In the meantime Mattman made her claim that, even under the best of circumstances, it was difficult to differentiate certain mycoplasmas from cell-wall-deficient tuberculosis.




Rutgers-Presbyterian Hospital Laboratory for the Study of Proliferative Diseases,  Bureau of Biological  Research, Rutgers  University, New Jersey, 1950


Livingston associate and prominent Cornell microbiologist Eleanor Alexander-Jackson [1], a lifelong colleague, had a problem. As long  as  Alexander-Jackson held her reputation as one of the leading tuberculosis experts in the  world, American medicine embraced her, but when she tried to attribute cancer to Livingston’s tuberculosis-like germ, it would move to crush her.

Alexander-Jackson, whose advanced mycobacterial staining and culture techniques appeared in a 1944 issue of Science, carefully set  a trap  insured to  ensnare virologists. Rous, as a retrovirus, was supposed to be an RNA virus. So Alexander-Jackson knew that  finding DNA  in  it would automatically mean that it  was  bacterial. It was understood that Retroviral DNA should be  present only in human or animal cells and nowhere else. But Alexander-Jackson’s paper on the ‘Ultraviolet Spectrogramic Microscope Studies of Rous Sarcoma Virus  Cultured in Cell Free Medium’ demonstrated that there was DNA present in this Rous, characteristic of  bacteria. [2]  Why  was  it still being called a retrovirus?

When Livingston confronted Rous that his ‘retrovirus’ could be dried, shelved, stored and mixed months later in saline only to grow out on  bacterial culture plates, he reminded her that he had never said  it was a  virus, carefully using ‘tumor agent’.

Dr. Virginia Livingston, MD.


To be certain, the Livingston network concluded that oncogenic, supposedly cancer-causing viruses, were in fact L-forms of tuberculosis-like mycobacteria and related organisms. And Livingston was coming much too close to proving her point to suit American retrovirologists.

Dr. Robert Gallo


Threatened by Livingston and Alexander Jackson’s findings, HIV co-discoverer Robert Gallo huffed:

‘What is going on in this country? This is insanity! She can have her  theories and what can I say?  I don’t  know of anything to  support it. I can’t see any basis and I don’t know what to say or what analogy to give  you’. [11]

But Livingston’s findings, with worldwide stature, were not about theories of retroviruses yet  to  be  isolated. She had, in fact,  come much closer than any  of the retrovirologists in  proving a direct causation between her organism and cancer by showing that her germ  manufactured human growth hormone (HCG), long  associated with  malignancy. [7]

Before her death, Livingston would give one  more clue towards unraveling what had become AIDS. There were ‘less known’ and ‘little  publicized’ microorganisms that were transmitted sexually. Through bacteriological studies she had confirmed that the very same L-forms of tubercular mycobacteria she found in Rous, by some called mycoplasma, could be  found in the  semen of man. [6]


1.Alexander-Jackson E. A. Specific  type  of microorganism isolated from  animal and human cancer: bacteriology of the organism. Growth 1954; 18:  37–51.

2.Alexander-Jackson E. Ultraviolet spectrogramic microscope studies of Rous  Sarcoma. Ann N Y Acad  Sci 1970; 174(2):765.

3.Burns D. N., Rohatgi P. K. Disseminated Mycobacterium fortuitum successfully treated with  combination therapy including ciprofloxin. Am Rev Respir  Dis 1990; 142(2): 468–470.

4.Gupta I., Kocher J. Mycobacterium haemophilum osteomyelitis in an AIDS patient. N J Med 1992; 89(3):  201–202.

5.Lemaitre M., Guetard D. Protective activity of tetracycline analogs against the  cytopathic effect  of the  human immunodeficiency viruses in CEM cells.  Res Virol 1990;141(1): 5–16.

6. Livingston V. Cancer: A New Breakthrough. Los Angeles: Nash Publishing, 1972.

7.Livingston V., Wuerthele-Caspe, Livingston A. F. Some cultural, immunological and biochemical properties of progenitor cryptocides. Trans N Y Acad  Sci Ser II 1974;36(6):  569–582.

8. Lo S. C. Isolation and identification of a novel virus  from patients with  AIDS. Am J Trop  Med Hyg 1986; 35(4),  675–6.

9. Lo S. C., Dawson M. S. Identification of Mycoplasma incognitos infection in patients with AIDS; an immunohistochemical, in situ  hybridization and ultrastructural study. Am J Trop  Med Hyg 1989; 41(5): 601–616.

10.Ostrom N. Co-discoverer of AIDS virus  says  it may  have microbial accomplice. New  York Native 1991; October 21.

11. Parachini A. New  ‘cure’  for cancer stirs  controversy. Los Angeles Times 1984; April 6.

12. Roussel G., Igual J. Clarithromycin with minocycline and clofazimne for Mycobacterium avium intracellulare complex lung disease in patients without the  acquired immune deficiency syndrome. GETIM. Groups d’Etude et de Traitement des  Infections a Mycobceries. Int  J Tuberc  Lung Dis 1998; 2(6): 462–470.

13.Saillard C., Carle  P. Genetic and serologic relatedness between Mycoplasma fermentans strains and a mycoplasma recently identified in tissures of AIDS and non-AIDS patients. Res Virol 1990; 141(3): 385–395.

14.Tasaka S., Urano T. A case  of Mycobacterium fortuitum pulmonary disease in a healthy young woman successfully treated with  ciprofloxacin and doxycycline. Kekkaku 1995; 70(1):  31–35.

15.Tsukamura,M. Chemotherapy of lung disease due to Mycobacterium avium–Mycobacterium intracellulare complex by  a combination of sulfadimethoxine, minocycline and Kitasamycin. Kekkaku 1984; 59(1): 33–37.









Although tuberculosis was and still is, in scientific off-the-record fashion rarely spoken of as a sexually transmitted disease, the potential for this has always existed. In the presence of prostatitis, it may be transmitted through the semen. [20]


As long as the mysterious killer behind AIDS remained comfortably within the gay community not much was done to truly investigate it. As soon as AIDS found its way into the heterosexual population, though, suddenly America’s interest in ferreting out the cause of AIDS became paramount.


Anyone who watched AIDS evolve in not only gay America but heterosexually in Africa and Asia could not help but be struck by its travel and spread along the epidemiologic highways of sex,  drugs, migrants, prostitutes, bath houses and venereal disease clinics. Yet the realization that sexual transmission of  AIDS could occur between a man with  risk  factors and a woman came late. [3] Soon thereafter, female to male transmission,  originally thought unlikely, was  also found to occur. [29]  By 1984, the pivotal importance female prostitutes played in the  propagation of AIDS in equatorial Africa had become evident. [33]


But despite the magnifying forces of high tech tests such as the Polymerase Chain  Reactors [PCRs], protein broths which make multiple copies of hard to find pathogens, its use in AIDS was never clear. Critics contested PCR vastly exaggerates “HIV” by making numerous copies of fragments of nucleic acid which might or might not even be HIV to begin with. And HIV itself could only  be detected in  a distinct minority of semen samples: one  in 25.  [34]


On the other hand, ignored and unnoticed, the very real possibility of the genital transmission of M. tuberculosis, a disease affecting almost 2 billion people, intimately linked with and considered a reliable sign of AIDS. [4,5] and frequently found in the   genitourinary tract. [38]




The Research Center for Genitourinary Tuberculosis, Kingsbridge Veterans Hospital, Bronx  New York,  1954


For 25 years, Dr. John K Lattimer, MD was a professor and chairman of the urology department at the College of Physicians and Surgeons of Columbia University.


By 1954, a pattern had emerged at Dr. John Lattimer’s Center for Genitourinary Tuberculosis. Men who developed tuberculosis epididymitis [inflammation of the testicles] were usually found to have an active focus of tubercular  infection in  their  prostate  and  cultures of their semen were  frequently positive for tubercle bacilli. [20]

But while documenting sexual transmission, what puzzled John Lattimer most was why more husbands with prostatic TB were not infecting their wives. Two possibilities came to mind. First, the resistance of the thick stratified vaginal epithelium to tubercular infection; second, the scorched earth policy of prostatic tuberculosis, whereby it sought to destroy glandular elements of  the prostate [Ibid], severely decreasing semen volume. Many of his male patients, in fact, complained that orgasm produced only slight moisture at the tip of their penis with over half of his experimental group having a semen volume of less than 0.5cc — too  scanty to  infect the  vaginal or vulvar epithelium, if it  reached them at all. As almost a testament to this finding — of 40 men with tuberculous genital  infections,  only  one  produced  a child. [Ibid]

Nevertheless, seeing sexual spread in a disease with staggering numbers right in front of him, he gave notice to the scientific world. [20] But few listened and adequate descriptions of tuberculosis as a sexually transmitted disease never really reached medical texts. Despite this tuberculosis is often unofficially listed among or with the sexually transmitted diseases.


Niagara Penisula Sanatorium, St. Catharine’s, Ont., Canada, December  1954


Dr. Edgar T. Peer was more than a bit  skeptical as he reviewed Lattimer’s  study regarding the  seminal transmission of tuberculosis.

He  himself had recovered tubercle bacilli  from  a patient’s semen in1952, but dismissed it as lab error. He would later write that like most dismissals of the tubercle bacilli on similar grounds, it  would come back to haunt him.


Dr. Edgar T. Peer


By 1954, Peer’s cases  of sexually transmitted tuberculosis were mounting and struck by similarities beyond coincidence, he  saw  an  ‘extremely  probable source’  of tuberculosis coming from  the  male genital tract.

Peer published, warning that if physicians did not wake up to the  possibility of sexually transmitted genital tuberculosis, its  diagnosis would continue to  be  unsuspected and underestimated, [28] which one day could lead to potentially catastrophic consequences.

Nor were Peer and Lattimer alone. Netter mentioned that the spread of the tubercle bacilli through the female genital tract of the tubercle bacilli by coitus with a tuberculous male could not be denied. [26]  In fact,  wherever culture of the seminal fluid  showed Mycobacterium tuberculosis, there was  a  possibility of  transmission  of genital tuberculosis from male to female via the semen through sexual intercourse. [6] While Lattimer [21]and Peer [28] showed that the development of tuberculous ulcers in the  vagina or vulva resulting in swollen lymph nodes in the  groin was  due to semen positive males harboring M. tuberculosis — Hellerstrom clocked the actual incubation period from the date of coitus during which the wife was exposed — to the development of a vaginal or vulvar ulcer and enlargement of inguinal lymph nodes — to approximately three to four weeks. [14]


Tuberculosis of the vulva


Heins then offered a better idea of the potential potency of sexually transmitted mycobacteria such as tuberculosis, demonstrating that  even the tame Mycobacteria smegmatis, found  in  the smegma of the  genital  secretions of every man and woman alive — when introduced into the vaginas of female mice — resulted in the  immediate death of over half of an experimental group of fourteen.  [13]

Lattimer’s  cases were  compiled from  European and American literature. The ulcer and enlarged nodes in the female, often misdiagnosed, closely resembled lymphogranuloma inguinale, syphilis or chancroids [Ibid] — all diseases that could coexist with  tubercular sexually transmitted disease. [20]

And, just as men could transmit mycobacterial tubercular disease to women, so too  could women infect men. [21] By1870 Soloweitschnick had documented the first  observation of a tuberculous ulceration of the  penis. [2]

Lewis  cites 110  cases of  tuberculosis of  the  penis written up  before 1946. Twenty-nine additional  cases were  subsequently reported by  Lal. [19]  In his  series of primary cases, Lewis  pointed to 14 of venereal origin —12 penile ulcerations being definitely the  result of coitus and two as a result of oral  sex.  [21]

Penile ulcer from tuberculosis


Penile ulcers, newly attributed to primary HIV, [15] were already well documented in TB literature [16,17,21,37]. And the ‘giant  cells’  claimed to  originate from  HIV [22,30] were  decades ago seen at the base of these ulcers. [21] Long a hallmark of tuberculosis, multinucleated giant cells form in the tissues and engulf the tubercle bacilli  in an attempt to kill them. [23]

Lewis mentions that of all the ways in  which the penis  could  be   infected  with tubercle bacilli, direct contact was by far the most common. Although he documented transmission mostly through vaginal sex and occasionally oral  sex,  rectal transmission was  not explored. [21]

To explain  cases claimed  not  to  arise from direct vaginal inoculation,  woman to man, Lewis borrowed from Verneuil’s  hypothesis, somehow overlooked by later writers. In 1883,  Verneuil, in “Hypothesis On the Origin of Genital Tuberculosis In The Two Sexes”, proposed a mechanism whereby men with infected urine or semen first inoculated the  vaginal vault of their partners, and then, through subsequent sex became themselves re-inoculated at the corona or frenulum of their own penises [35]. Years passed. But voices  of warning persisted.

By 1972, five years before gays started dying in the U.S., Rolland wrote “Genital  Tuberculosis, a Forgotten Disease?”. [31] And ironically, in 1979, on the eve of AIDS recognition, Gondzik and Jasiewicz showed that even in the laboratory, genitally infected tubercular male guinea pigs could infect healthy females through their semen by an  HIV-compatible ratio  of 1 in 6 or 17%, prompting him to warn his patients that not only was tuberculosis probably a sexually transmitted disease, but also the necessity of  the application of  suitable contraceptives such as condoms to avoid it. [12]

Gondzik’s solution and pre-AIDS date of publication are chilling; his findings — too significant to ignore. Even in syphilis at its most infectious stage, successful transmission in humans was possible only in 30%  of contacts. [32]

Two years later, investigators in South Africa, itself perched on the precipice of its own devastating sexually transmitted AIDS epidemic, issued a report of 91 cases of tuberculosis of the  penis. [25,36] This  was  followed by documentation in which ‘HIV’ in young African females came only  after  first  contracting genital TB. [11]

Moreover, the fact that Mycobacterium avium-intracellulare — also known as fowl or swine  tuberculosis, and considered an ‘atypical’  tuberculosis — could  also act like a  sexually  transmitted disease, set  up  an explosive scenario. [8–10]

Avium had, in the short space of 30 years, gone from relative obscurity to the leading infectious disease in U.S. AIDS. And despite the fact that DePaepe’s group used only conventional Ziehl-Neelsen tubercular stain without culture of either testicular tissue or  semen, they still found M. avium in these specimens in 32% of AIDS patients with systemic M. avium — the  same M. avium that would eventually kill most U.S. AIDS patients that did  not die from other AIDS-related disease. [27]



Queens Hospital Center, Long Island Jewish-Hillside Medical Center, Jamaica, New York,  1984


Dr. Pascal De Caprariis saw a dying 30-year-old Haitian man with AIDS before him. A biopsy of the lymph node in the  patient’s groin showed Mycobacterium avium-intracellulare [fowl tuberculosis] seemingly gone systemic — spreading to the liver. Despite using different combinations totaling seven different anti-tubercular drugs, the patient died. If ever there was a harbinger of things to come, this was it.

Then, just before the patient’s death an ulcerative lesion of the corona of the penis formed. Tests for herpes were negative. Upon culture, and only upon culture, Mycobacterium avium was  isolated from  the penile crater, and De Caprariis started speculating that with this and the his patient’s right groin lymphatic swelling, sexual transmission of Avium [fowl tuberculosis] seemed neither far-fetched nor  improbable. [9]


Mycobacterium avium in lymph node tissue of an AIDS victim. Ziehl-Neelsen stain. Histopathology of lymph node shows tremendous numbers of acid-fast tubercular bacilli within plump histiocytes. CDC/Dr. Edwin P. Ewing, Jr.



Department of  Microbiology, Mount  Sinai  Hospital, New York, 1985


Mount Sinai Hospital in New York, NY.


AIDS is what defined the decade of the 1980s, a decade that lived in fear beneath the partial shadow of a certain and tortuous death from a highly communicable pathogen.

But no one came closer to unlocking its true cause and mystery than American microbiologist Beca Damsker,MD. Damsker found overwhelming fowl tuberculosis infections of the colon and rectal tissues in U.S. gay AIDS time and time again — and knew that an anorectal portal of transmission had to be considered important in its transmission. Damsker was also picking up fowl tuberculosis in the buffy coat of the blood of recently acquired AIDS victims — that fraction of an anticoagulated blood sample that contains most of the white blood cells and platelets following centrifugation

Gay men had instinctively realized the implications of Damsker’s colon and rectal studies. Many had already made the intuitive leap that perhaps certain activities, such as anal intercourse, might be transmitting the causative agent. It was just that no one knew the specific agent being transmitted. Beca Damsker had just found that agent in fowl tuberculosis [Mycobacterium avium, or simply M. avium], but had no way of knowing how universal the process she was examining really was. But the regularity with which Damsker found Avium, also known as swine tuberculosis, in gay stool and lower intestinal biopsy specimens, stunned even herself. [8] Indeed, what she saw before her was a microcosm of the killer AIDS epidemic just outside her Mount Sinai research facility. Beca Damsker’s study was published in The Journal of Infectious Diseases in 1985.

Avium, or fowl tuberculosis, is a ubiquitous germ, found in animal reservoirs such as pigs, among others. [7] As to how AIDS originated in man, Damsker was not unaware of the possibility that a small subset of homosexuals had a proclivity for bestiality — sexual activities with animals — a  potential vector for their transmission to man, which when combined with the fragility of the rectal mucosa to local trauma or intercourse and antigenic challenge, [24] could have led to calamitous unchecked multiplication of M. avium in gay AIDS, possibly of animal origin, in the intestinal mucosa and nearby lymph nodes. This then would set the stage for AIDS spread into the blood, with consequent targeting of other systems. [8] Damsker already had all the evidence she needed.

Tuberculosis in swine is almost always caused by M. avium [18] and such avian tuberculosis leads to some of the highest financial losses in the swine and poultry farm industry. [1]

Although fowl tuberculosis was thought of as an ‘opportunistic’ infection which occurred only late in the immunosuppression of AIDS, Damsker encouraged a closer look regarding the temporal relationship between fowl tuberculosis infection and the inception of American AIDS. In foreseeing this, Becca Damsker’s assessment of what doctors were picking up —as nothing other than a stepwise advance and increment of its causal germ — was squarely on target. From a rectal portal of entry, the germ merely progressed in ferocity and immunosuppression as the disease advanced and lowered CD4 counts. [8] Indeed, Becca Damsker, in speculating this, presented the single most plausible cause for American AIDS written to that point.


1. Berthelsen J. D. Economics of the  avian TB problem in swine. J Am Vet Med Assoc 1974; 164: 307–308.

2. Brunati J. Tuberculosis of the  penis; surgical form-case. Rev Chir  Paris 1937; 75:  213–233.

3. Centers for Disease Control (CDC) Immunodeficiency among female sexual partners of males with  acquired immune deficiency syndrom (AIDS) – New  York.  Morb Mortal Weekly Rep 1983; 31:  700–1.

4. CDC  Tuberculosis – United States, 1985 – and the  possible impact of human T-lymphotropic virus  type  III/ lymphadenopathy associated virus  infection. Morb  Mortal Weekly Rep 1986; 35:  74–6.

5. CDC Diagnosis and management of mycobacterial infection and disease of persons with  human immunodeficiency virus infection. Ann Int  Med 1987; 106: 254–6.

6. Chakravarty S. C., Sircar D. K. Genital tuberculosis in males. Seminal fluid culture and vaso-seminal vesiculography studies. J Indian Med Assoc 1968; 51(6): 283–286.

7. Chapman J. S. The Atypical Mycobacteria and Human Mycobacteriosis. New  York:  Plenum Press, 1977.

8. Damsker B., Bottone E. J. Mycobacterium avium- Mycobacterium intracellulare from  the intestinal tracts of patients with  the  acquired immunodeficiency syndrome: concepts regarding acquisition and pathogenesis. J Infect Dis 1985; 151(1): 179–181.

9. De Caprariis P. J., Giron J. A. Mycobacterium avium- intracellulare infection and possible venereal transmission. Ann  Intern Med 1984; 101(5): 721.

10. De Paepe M. E., Guerrieri C., Waxman M. Opportunistic infections of the  testes in the  acquired immunodeficiency syndrome. Mt Sinai J Med 1990; 57(1):  25–29.

11. Giannacopoulos K. C., Hatzidaki E. G. Genital tuberculosis in a HIV infected woman. Eur  J Obstet  Gynecol  Reprod  Biol 1998; 80(2):  227–229.

12. Gondzik M., Jasiewicz J. Experimental study on the possibility of tuberculosis transmission by  coitus. Z Urol Nphrol 1979; 72(12): 911–914.

13.  Heins  H. C., Jr, Dennis E. J. The  possible role  of smegma in carcinoma of the  cervix. Am J Obstet  Gynecol  1958; 76: 726–735.

14.  Hellerstrom S. Acta Dermato-Venereol 1937; 18(4):  465.

15.  Hirschel B. In:   Polsky, Clumeck (eds).  HIV and AIDS. London: Mosby-Wolfe, 1999.

16. Jaisankar T. J., Bhagath R. G. Penile Lupus  vulgaris. Int  J Dermatol 1994; 33(4):  272–274.

17. Jeyakumar W., Ganesh R. Papulonecrotic tuberculids of the glans penis: case  report. Genitourin Med 1988; 64: 130–132.

18.  Karlson A. G. The incidence of tuberculosis in animals in the USA. Bull Int Union Against Tuberc  1968; 40:  61–63.

19.  Lal D. N., Sekhon G. S. Tuberculosis of the  penis. J Indian Med Assoc 1971; 56:  316–318.

20. Lattimer J. K., Colmore H. P. Transmission of genital tuberculosis from  husband to wife via the  semen. Am Rev Tuberc  1954; 69(4):  618–624.

21. Lewis E. L. Tuberculosis of the  penis. Report of 5 new  cases and complete review of the  literature. J Urol 1946; 56:  737.

22. Lifson  J. D., Reyes  G. R. AIDS retrovirus induced cytopathology; giant cell formation and involvement of CD4 antigen. Science 1986; 232(4754): 1123–1127.

23. Livingston V. Cancer: A New Breakthrough. Los Angeles: Nash Publishing, 1972.

24. Mavligit G. M., Talpaz M. Chronic immune stimulation by sperm alloantigens. Support for the  hypothesis that spermatozoa induce immune dysregulation in homosexual males. JAMA 1984; 251(2): 237–245.

25. Morrison J. G. L., Fourie E. D. The  papulonecrotic tuberculide: from  Arthus reaction to Lupus  vulgaris. Br J Dermatol 1974; 91:  263–270.

26. Netter FH. Reproductive system. The Ciba  Collection of Medical Illustrations. New  Jersey:  West  Caldwell, 1987; 2: 188.

27. Nightingale S. D., Byrd L. T. Mycobacterium avium– intracellulare complex bacteremia in human immunodeficiency virus  positive patients. J Infect Dis 1992; 165: 1082–1085.

28. Peer  E. T. Genitourinary transmission of tuberculosis. Am Rev Tuberc  1957; 75:  153.

29. Piot P., Quinn T. C. Acquired immunodeficiency syndrome in a heterosexual population in Zaire.  Lancet  1984; 2: 65–69.

30. Popovic M. Detection, isolation and continuous production of cytopathic retroviruses (HTLV-III) from  patients with AIDS and pre-AIDS.  Science 1984; 224(4648):497–500.

31. Rolland R., Schellekens L. Genital tuberculosis, a forgotten disease. Ned  Tijdschr Geneeskd 1972; 116(52): 2377–2378.

32. Smith L. H., Wyngaarden J. B. Cecil Textbook  of Medicine. Philadelphia: W.B. Saunders, 1988.

33. Van de Perre  P., Clumeck N. Female prostitutes: a risk group for infection with  human T-cell lymphotropic virus  type  III. Lancet  1985; 2: 524–526.

34. Van Voorhis B. J., Martinez A. Detection of human immunodeficiency virus type 1 in semen from seropositive men using culture and polymerase chain reaction deoxyribonucleic acid  amplification techniques. Fertil  Steril 1991; 55:  588–594.

35. Verneuil A. Hypothesis on the origin of genital tuberculosis in the  two  sexes. Gaz  Hebt d Med 1883; 25:  225.

36. Wilson-Jones E., Winkelmann R. K. Papulonecrotic tuberculosis; a neglected disease in Western countries. J Am Acad  Dermatol 1986; 14:  815–826.

37.  Wood B. An unusual cause of penile ulceration. South African Med J 1991; 79(1):  284.

38. Wyngaarden J. B., 19th ed   Cecil Textbook  of Medicine; vol. 2. Philadelphia: W.B. Saunders, 1992: 1740.









Pasteur Institute, Paris, January, 1983


The Pasteur Institute squeezed head of cancer virology, Luc Montagnier, into the  pressure cooker of finding an AIDS retrovirus when its production of Hepatitis B vaccine, accounting for a significant part of its income, and in part processed from pooled American homosexual blood, came under fire. And frankly, they didn’t care how he “proved” it.


Dr. Luc Montagnier


Montagnier, who for his part was exclusively looking for a retrovirus related to Gallo’s failed HTLV-1, instead came upon the retrovirus “LAV” which, in wastebasket category fashion, stood for “Lymphadenopathy Associated  Virus”. How did he know it existed? Because his assistant  Françoise Barré-Sinoussi said that she found it……….or at least she found something that looked like it.

LAV was so named because the French homosexual fashion designer it was first isolated from had enlarged, inflamed neck nodes [lymphadenopathy], a common early AIDS feature. Thirty-three and promiscuous, he had also  visited New York City  in 1979, and had a 50-gay-partner-a-year history.

Betting the obvious — that the agent responsible for AIDS could be more readily detected in these swollen lymph nodes, Barré, in January, 1983, packed a small piece of the homosexual’s just  biopsied lymph node en Toto in ice at Paris’s Pitie-Salpetriere Hospital and delivered it to Montagnier at Pasteur. This patient did not yet have full-blown AIDS, but his  history and symptoms were strongly suggestive. [1] He would die 5 years later of the disease.


Montagnier and Barré-Sinoussi


At Pasteur, Montagnier put the tissue into cell cultures of T-lymphocytes. Immediately questions arose as to the procedure. Looking only  for a retrovirus, the  team cultured whole tissue lymph node lysates. The ‘virus’ was  never isolated in its pure form. It would be the beginning of a long, long  line  of research work  based on indirect evidence.

Later, looking at Montagnier’s tissue cultures microscopically there were many granules, some of which were felt to look like retroviruses. But they were inside cells and tissues – not whole viral  particles — and had different shapes and sizes.  No two were alike.  They seemed to  show all  forms of  ‘viral   maturation’, but were they viral?

As early as 1928, Eleanor Alexander-Jackson began discovering unusual,  and to  that  point, unrecognized forms of the TB bacillus. Jackson  marveled  at  the many  forms of  tuberculosis,  including the tiny granules  which the German Hans Much saw in 1908, that soon became known as  Much’s granules. [4] In 1910 Fontes proved that Much’s granules, as a sub-classification of Kleinberger’s  L-forms,  were  filterable and therefore also  often mistaken for viruses. In fact, in certain circles the variable acid-fast granules were  called ‘the  TB virus’.  [2]

But even  prior  to  Livingston [1970], Mellon and  Fisher had warned that filterable forms of M. Avium andtuberculosis could  easily be mistaken for the virus Montagnier and Barré thought they had [3] and might explain ‘the common finding by French workers of tubercular acid-fast bacilli in the glands of guinea-pigs into which viral-like [cell free] filtrates of tuberculosis material had been injected.’ [Ibid]


1. Barré-Sinoussi F., Chermann J. C. Isolation of a T-lymphotropic retrovirus from  a patient at risk  for acquired immune deficiency syndrome (AIDS). Science 1983; 220: 868–871.

2. Fontes A. Bemerkungen uber die  Tuberkulose Infektion und ihr  virus. Mem Inst Oswaldo Cruz  1910; 2: 141–146.

3. Mellon, Fisher  New studies on the filterability of pure cultures of the tubercle group of microorganisms. J Infect Dis 1932;51:  117–128.

4. Much H. Die Variation des  tuberkelbacillus in form and wirkung. Beitr Klim Tuberk 1931; 77:  60–71.








Pasteur Institute, Paris, 1983


Institut Pasteur, Paris


Gallo’s leukemic retrovirus (HTLV), which Barré and Montagnier thought they had isolated, should have led to the wild proliferation of lymphocytes. But all that Françoise Barré-Sinoussi found in subsequent trips  to the  lab  was how well it was slaughtering them. This deeply disturbed her, as retroviruses typically didn’t kill cells. How could she explain this?

By January 25th, 1983, Barré-Sinoussi’s reverse transcriptase radioactivity counter was clicking-away with increased activity, which to her, as a  retrovirologist, meant that her lymph node ‘retrovirus’ LAV must be  multiplying.

But reverse transcriptase was nonspecific and was also found elevated in  events leading to the death of CD4 lymphocytes by tuberculosis [16], as well as in M. avium [fowl tuberculosis] infection of neck lymph nodes [2], probably the very event  Françoise Barré-Sinoussi was watching. Again, why had she not considered these as a possible AIDS causes?

In actuality, previously having been retroviral cancer researchers, Barré-Sinoussi and Montagnier where solely attuned, intellectually and technologically to detecting “retroviruses”. Barré had been trained in mouse retroviral techniques requiring the measurement of reverse transcriptase in Robert Bassin’s National Cancer Institute (NCI) lab. Her  procedures were  not  designed to  explore for some unknown pathogen. In effect, Françoise Barré-Sinoussi and Luc Montagnier found a retrovirus because that was all that they were looking for.

Within weeks Montagnier called a staff meeting. The new ‘retrovirus’  wasn’t Gallo’s discredited  HTLV-1, so everyone could breathe a sigh of relief. He also wasn’t asserting that his retrovirus HAV actually caused AIDS……..but it was possible. In the future he would send samples of the tissue culture to Gallo who headed AIDS research at NCI to stimulate further research.

Approximately one year later, after receiving French samples from Montagnier, retrovirologist Gallo isolated and announced that he felt that his newly isolated HTLV-3 retrovirus must cause AIDS — a retrovirus, which proved to a carbon copy of Montagnier’s LAV retrovirus………which he said was a productive Lentivirus infection with all forms of  viral maturation.


A colleague had suggested that Montagnier characterize his virus as  a Lentivirus [‘Lenti’ means slow] on a hunch. Lentiviruses were  large viruses which, after  entering cells, did  not  leap  into activity at once, but later shot into action. But so-called “slow viruses” had been implicated, but never proven, in diseases such as Creutzfeldt-Jakob, and Alzheimer’s as well. Prominent American retrovirologist Peter Duesberg, who  did  much of the pioneer work on retroviral ultrastructure, knew that as direct pathogens the retroviruses were not ‘slow’ viruses. They were not even lentiviruses like Visna, with which HIV was often compared. Visna never acted like that. Rather, if Visna reached high enough blood concentration, Duesberg related, it was rapidly pathogenic. [10]  HIV [Gallo’s HTLV-3 or Montagnier’s HAV] however, was not to  be found in  such high amounts in the blood. Perplexed, Duesberg concluded that there was no such thing as a slow  virus, ‘only  slow  virologists’. [7] On the basis of his experience with retroviruses, Duesberg has challenged the virus‐AIDS hypothesis in the pages of such journals as Cancer Research, Lancet, Proceedings of the National Academy of Sciences, and The New England Journal of Medicine.


Peter H. Duesberg Ph.D.


The discovery of LAV (HIV) allowed virologists to worm their way into taking the high ground in American medicine. No longer would practicing physicians like Livingston, who  had seen disease face to face, assume leadership on policy issues. The new medical shamans would be  laboratory gene splicers, molecular biologists, virologists and immunol- ogists, who told doctors what to think about conditions they never had ever clinically treated. A dangerous precedent was  being set.



Cambridge University Clinical School, Cambridge, England, September, 1983


Former viral cancer researcher Abraham Karpas, worked out of the  Department of Hematological Medicine at Cambridge. By September, 1983 he had identified a ‘transmissible agent’ through electron micrographs of the  blood of a gay AIDS patient. [8]

Dr. Abraham Karpas


Karpas was having a problem with Gallo’s HTLV1 and was unable to confirm previous reports of this purported AIDS retrovirus in Africans. Many blood tests finding HTLV1 positive by previous investigators were found negative when retested in Karpas’s lab. [9]

Karpas, probably the second man in the  world to see the AIDS agent, fired  off a quick report on his transmissible agent complete with a microphotograph, but was having difficulty getting the paper published. He had the honesty to admit that he wasn’t certain that the 55 nm particles with their 10 nm electrodense cores were viruses at all, and  began  his  paper  with the phrase ‘assuming it is a virus’, though, whatever it was, he later found it identical to Montagnier’s “HIV”.

Experts in the field sided with Karpas’s restraint. Not only were retroviral particles ‘no proof that a virus was involved’, but such particles were ubiquitous – a  statement supported by O’Hara’s Harvard study which found ‘viral particles, morphologically indistinguishable’ in 90% of the enlarged lymph nodes in  both AIDS and non-AIDS patients. [13] O’Hara’s study stood out as the one study to date which used suitable controls, finding ‘viral  particles’ indistinguishable from HIV in a variety of swollen lymph nodes without HIV.

Similarly, African studies of the lymph nodes of patients with HIV also showed them indistinguishable from those with just tuberculosis and without AIDS. [12,15] O’Hara concluded ‘The presence of such particles  do not, by themselves, indicate infection with HIV’. Yet it was photomicrographs of the same particles which first  informed the  world that there was  an  HIV.

In Reproduction of RNA Tumor Viruses,  Badar  warned that in vitro cultures, even virus free, ‘can be induced to produce particles which resemble RNA tumor viruses in every physical and chemical respect’ [3], an event many saw  applicable to the rigors and harsh processes Montagnier and Gallo  put their AIDS tissues thru.

Oddly, it would not be until 1997 that two independent groups would examine these HIV particles in  accordance with   accepted  international  procedure.  [6,4] Both  teams saw an excess of fluid  filled,  many formed [pleomorphic] ‘contaminating’  vesicles, ranging in  size from 50 to 500 nm  as opposed to a minor population of particles of about 100 nm.

The latter were assumed to be viral,  but proved, according to critics, to be  too large, of the wrong shape and containing too much material to be retroviruses. In fact, both the  particles and vesicles of Bess and Gluschankof share common antigenic determinants with and could easily have been the variably-acid-fast tubercular mycobacterial L-forms microphotographed by Seibert [14], Alexander-Jackson [1], Livingston [11] and Cantwell [5]. Livingston showed a protoplast of tuberculosis with L-form inclusions budding out vesicles from its surface not unlike the vesicles in the 1997 AIDS verification studies, while Seibert and Cantwell showed particles similar to those attributed to HIV. And the ‘substantial  amount’  of  both RNA and DNA  found by in “HIV” vesicles, Bess found, points more toward a bacterial or mycobacterial origin.

Suddenly, it seemed as if the world had been sold a bill of sale on a non-existent retrovirus.



1. Alexander-Jackson A. Specific type of microorganism isolated from  animal and human cancer: bacteriology of the organism. Growth 1954; 18:  37–51.

2. April M. M., Garelick J. M. Reverse transcriptase in situ polymerase chain readtion in atypical mycobacterial adenitis. Arch Otolaryngol Head Neck Surg 1996; 122(11):1214–1218.

3. Bader  J. P. Reproduction of RNA humor viruses. Comprehensive Virol 1975; 4: 253.

4. Bess J. W. Microvesicles are  a source of contaminating cellular proteins found in purified HIV-preparations. Virology  1997; 230(1): 134–144.

5. Cantwell A. R. Histologic observation of variably acid-fast coccoid forms suggestive of cell wall deficient bacteria in Hodgkin’s disease. A report of four  cases. Growth 1981; 45:168–187.

6.Gluschankof P., Mondor I. Cell membrane vesicles are  a major contaminant of gradient enriched human immunodeficiency virus  Type-1 preparations.  Virology1997; 230(1): 125–133.

7. Health Education AIDS Liaison (HEAL), HIV 101: 10 Scientific Reasons  Why HIV Cannot Cause  Aids. Toronto, 2001.

8. Karpas A. Unusual virus  produced by  cultured cells  from  a patient with  AIDS. Letter  to Editor. Mol Biol Med 1983; 1:457–459.

9. Karpas A., Maayan S. Lack of antibodies to adult T cell leukemia virus  and to AIDS virus  in Israeli  Falashas. Nature1986; 319: 794.

10. Lairmore M. D., Rosadio R. H. Ovine lentivirus lymphoid interstitial pneumonia. Rapid  induction in neonatal lambs. Am J Pathol 1986; 125: 173–181.

11. Livingston V. Cancer: A New Breakthrough. Los Angeles: Nash Publishing, 1972.

12. Nambuya A., Sewankambo N. Tuberculosis lymphadenitis associated with  human immunodeficiency virus  (HIV) in Uganda. J Clin  Pathol 1988; 41:  93–96.

13.O’Hara C.J., Groopman J.E. The ultrastructural and immunohistochemical demonstration of viral  particles in lymph nodes from  human immunodeficiencyvirus-related and non-human immunodeficiency virus-related lymphadenopathy syndromes. Hum  Pathol 1988; 19(5):545–549.

14.Seibert F. B., Feldmann F. M. Morphological, biological, and immunological studies on  isolates from  tumors and leukemic blood. Ann  N Y Acad  Sci 1970; 174(3): 690–728.

15. Voetberg A., Lucas  S. B. Tuberculosis or persistent generalized lymphadenopathy in HIV disease. Lancet  1991; 337: 56–57.

16. Watson E., Hill L. L. Apoptosis in Mycobacterium tuberculosis infection in mice  exhibiting varied immunopathology. J Pathol 2000; 190(2): 211–2203.







Like chameleons, HIV scientists continued to scurry about, changing their scientific hypotheses to  blend  into  whatever  new  facts came along, much of it interpreted through the lens of earlier research done on TB and the mycobacteria. And since the doctors and scientists who bought into the  HIV theory were now in the clear majority, and that majority ruled, their funding and literature mushroomed into a  self-fulfilling archive such as previously had occurred with their failed HTLV-1 AIDS virus —  while those that did  not  agree found themselves labeled “denialists”, or lost their tenure or research funding, and even their jobs.

By 1983, the certain knowledge that AIDS had begun its wholesale slaughter of Africans, mainly through heterosexual sex, sent shudders down the  back of a world in which, not since the last great sexual pandemic of syphilis five centuries before, had there been the specter of anything comparable. Men and woman were transmitting AIDS back and forth sexually in heretofore unheralded numbers.


A map of TB prevalence by country. Notice its distribution in Africa and compare to map below.
of HIV/AIDS in Africa.


“AIDS” in Africa, with roughly the same distribution as the TB map above.


Wave after wave of epidemic tuberculosis had hit the world. It was a disease of big numbers. In the 100 years from 1850 to 1950, it was estimated that 1 billion persons died  from tuberculosis. [3] Even today, according to the World Health Organization, TB infects over one-third of the world’s inhabitants. And at least one person is infected with it per second — someone dying from TB every ten seconds. Tuberculosis, indeed kills two to three million people each year, more than any other infectious disease in the world today. It did not need to be defined by any harmless retrovirus……….it did its own defining.



From England tuberculosis spread to the shores of Western and then Eastern Europe — and by 1900, North and South American waves began to peak. But in the developing countries of Asia and Africa, where the AIDS epidemic was still new in 1983, epidemic waves of  tuberculosis had not yet reached their zenith. [10] As this TB epidemic continued to seethe, it was these very continents that would show the highest TB mortality and morbidity, even before AIDS came into the picture [7] — and would prove to be the future epicenters for AIDS.


Foreigners called the all-too-common wasting syndrome of African AIDS ‘slim disease’; Africans themselves just called it ‘slim’. Serwadda wrote about it in Slim Disease: a New Disease in Uganda  [9] but of 82 patients diagnosed with this wasting syndrome, he found 44% to have disseminated tuberculosis — earlier called ‘consumption’, because, like ‘slim disease’, TB seemed to consume the flesh off of a person’s skeletal structure .


“Slim’ disease”, the term used in Uganda to describe “HIV” wasting.


Tubercular “consumption”.


And so, referring to what he felt to be the tip of an iceberg, Serwadda suggested that a substantial proportion, if not all, so called “Slim Disease” in AIDS was actually due to disseminated tuberculosis. [2] In addition, disseminated M. Avium or fowl tuberculosis too was believed to be a major cause of wasting syndrome in patients with AIDS with approximately 40% of M. avium victims having the same nausea or diarrhea so frequently attributed to ‘HIV’. [6,8]

True, tuberculosis and diarrhea, prominent in African AIDS, had been killing Africans for some time, but suddenly they had become untreatable. Drug-resistant forms were then not so much in the public and scientific cross-hairs. So a new name was needed for an old affliction. And that name, AIDS, was supplied, hurriedly, perhaps too  hurriedly.

It was in Africa that those who  hailed HIV as the cause of AIDS faced their first and most serious challenge over extremely suspicious circumstances. Not only were over 65% of African AIDS patients not  HIV-positive [Lancet, Oct. 17, 1992], but, of  those that tested positive, data suggested that the antigens in HIV-1 Elisa and Western Blots, originally claimed to  belong solely to  HIV,  were cross-reacting with TB and the mycobacteria.  [5]

Nor was it just one, but a series of “HIV” proteins that cross-reacted with tubercular proteins. Tubercular cell wall components, phenolic glycolipid [PGL] and lipoarabinomannan [LAM] were noted not only to strongly cross-react with p24, the sacred cow of ‘HIV isolation’, but p31,  also  favored in the  detection of HIV in the  blood. [5] Even the most prominent and persistently detected antigen in AIDS tests [11], p41, could be  found in  bacteria  such as tuberculosis.

Defensively, HIV diehards shot back that tuberculosis in AIDS was merely an  ‘opportunistic infection’, a label that  most North American AIDS experts were originally extremely reluctant  to  assign. For example, to John and Kaur, in Lancet,  the term ‘opportunistic’ seemed inappropriate for TB. Only infections due to normally non-disease-causing microbes should be called “opportunistic”. [4] Mycobacterium tuberculosis, the only infectious pathogen ever  to  force  the  UN to  issue a [1993]  global emergency, could hardly be termed non-disease causing, and therefore should never be labeled as “opportunistic”.

Many physicians were also quite wary of the contrived terms used to describe HIV. Yet they still remained silent. Makeshift expressions, like ARC (Aids-Related-Complex), PGL (Persistent Generalized Lymphadenopathy) and ‘pre-AIDS’ were scrutinized in disbelief. There were  similar forms of latent TB, yet  none were  ready to  call  them pre-tuberculosis  or Tuberculosis-Related-Complex (TRC).

By 1986 Montagnier’s group, puzzled, found a patient in  West  Africa  with  AIDS but no  HIV antibodies in  the blood. Rather than rethink their whole hypothesis, the  discoverer of HIV proceeded to simply say that it was another retrovirus at work: HIV-2, said to be responsible for a large West African epidemic, mainly transmitted through heterosexual intercourse. [1]


Lacor hospital Gulu. Uganda.


Lacor Hospital in Gulu, Uganda, was in effect  a TB sanitarium, but  roughly half of the patients who remained there for two months or more came down with AIDS. And so Africans died, with the bleeding gums and anemia claimed at  different times to  come from both HIV and TB, but their blood was HIV-negative. In a word, they died  of wasting, —or consumption.




1. Clavel F., Guetard D. Isolation of a new  human retrovirus from  West  African  patients with  AIDS. Science 1986; 233:343–346.

2. DeCock K. M. Tuberculosis and HIV infection in sub-Saharan Africa.  JAMA 1992; 268: 12.

3. Iseman M. D. Evolution of drug resistant tuberculosis: a tale of two species. Proc Natl  Acad Sci USA 1994; 91: 2428–2429.

4. John J. J., Kaur A. Tuberculosis and HIV infection. Lancet1993; 342(2): 676.

5. Kashala O. Infection with  human immunodeficiency virus type  1 (HIV-1) and human T-cell lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 cross-reactivity and antibodies to lipoarabinomannan. J Infect Dis 1994; 169(2): 296–304.

6. Kemper C. A., Meng T. C. Treatment of Mycobacterium avium complex bacteremia in AIDS with  a four-drug oral regimine: rifampin, ethambutol, clofazimine and ciprofloxacin. Ann  Intern Med 1992; 116: 466–472.

7. Lowell AM. Tuberculosis in the World.  DHEW  Publication No. CDC  76-8317. Washington, DC: US Government Printing Office,  1976: 3–27.

8.Modilevsky T., Sattler F. R. Mycobacterial disease in patients with human immunodeficiency virus  infection. Arch Intern Med 1989; 149: 2201–2205.

9. Serwadda D. Slim disease: a new  disease in Uganda and its association with  HTLV-III infection. Lancet  1985; 2(8460): 849–852.

10. Stead  W. W., Asim  K. D. Epidemiologic and host factors in Tuberculosis. In: Praeger Monographs in Infectious Disease; vol.  2. New  York:  Praeger, 1983.

11. Veronese F. M. Characterization of gp41 as the transmembrane protein coded by  the  HTLV-III/LAV envelope gene. Science 1985; 229: 1402.









The scientific vagueness and deception to bolster the HIV theory continued. Important to the basic mechanism of AIDS is the destruction of CD4 (T-cells) lymphocytes, key to  the body’s  resistance  against  infection. As  this  CD4  cell count falls in the blood of an AIDS patient, many treacherous infections are able to jump on  board.


HIV was early-on claimed to destroy these CD4 white blood cells, yet the exact mechanism for this was never made clear. [17] Papadopulos-Eleopulos points out that retroviruses were never known to kill cells.  This was the one thing retrovirologists always knew and agreed upon. Therefore, she asked, how could the HIV retrovirus kill CD4 cells? Instead, it seemed to Papadopulos that CD4 T Lymphocyte death might be due to  the  many non-HIV factors present in HIV inoculate,  including other infectious agents. [28]


And  although attempt after attempt has been made to say that low  CD4  is synonymous with HIV, the  fact  is  that  known  AIDS-risk groups may have low  CD4, even in  the face of  persistently negative HIV antibody tests. [7,9,26]


That HIV is not the cause of apoptosis [a sort of remote-control immune cell  destruction] of CD4+ cells is more than amply shown in chronically infected retroviral cell lines, where although what is claimed to be “HIV” is produced, apoptosis is not detected. [28] Even HIV discoverer Luc Montagnier [as well as others] has confirmed that HIV does not kill T-cells like  CD4+ directly. [11,20]


On the other hand, virulent TB can and ferociously does depress the CD4 count [34], and kills T-cells like CD4+ as well as macrophages directly, through nitric oxide secretion. [32]


In 1978, the first European measurement of a low CD4 in AIDS was on a patient with disseminated atypical tuberculosis [Mycobacteria fortuitum], [5] closely related to  Mycobacterium tuberculosis.


As early as 1987, Canadian researchers realized that  mycobacteria such as tuberculosis alone could be responsible for  direct CD4 killing and much of the immunosuppression found in AIDS. Furthermore, such a tubercular immune system throttle could persist for life, even when the  disease wasn’t progressive. [19]


In the same vein, Mudaki, in Zaire, showed how fast a CD4 count could shrink below 200/ul just by tuberculosis, without HIV being present. [25] Moreover, TB often presented before the development of immune dysfunction, either with  or without HIV. [30]


In  fact of all  the infections involved in AIDS, none were associated with as low CD4  cell counts as were tubercular infections. [27] And  those patients with either M. Avium or M. tuberculosis in their blood had significantly lower  CD4  counts. [14]


Yet there had to be more – a missing link. It has long been known that a low CD4 count in and of itself did not automatically lead to the severe  immunodepression found in AIDS. [18]




Case  Western  Reserve University, Ohio, July, 1998



Case Western Reserve University. Cleveland Ohio.

Although previously demonstrated [19,8], the actual ferociousness of CD4 tubercular attack was amply shown in papers such as Hirsh’s 1999 Ohio study, which showed that not only were 30% of CD4 but also non-CD4 slaughtered within 98 hours of co-culture with  TB, a  20-fold  increase. [15] Hirsch’s electric expose was published by the Journal of Infectious Diseases. But it didn’t stop there. The immune systems B cells,  [6,22] and macrophages [12,24] were also decimated by tuberculosis.

As if this wasn’t enough, the fact that both TB specific and non-specific T cells were equally affected in any tubercular attack accounted for tuberculosis’s silent role in the depressed responsiveness towards such diseases as Candidal thrush, Pnuemocystis, and other AIDS opportunistic organisms. After all, normally, it was just such non-specific, non-CD4 lymphocytes that normally protected against these other diseases.

In a follow-up study, Hirsch found that destruction through apoptosis of immune cells was increased at the site of active MTB infection in patients with pleural TB, regardless of whether the patient had “HIV” or did not have “HIV”. [35] This included macrophages.

And it was the annihilation of just such infection swallowing macrophages, critical to reticuloendothelial ultrastructure, that M. Tuberculosis, M. avium (4), or more almost certainly both working in concert, furnished the key to AIDS comprehensive devastation to the human immune system.



California Pacific Medical Center Research Institute, San Francisco,

California, 1999


Part of the Pacific Campus of the California Pacific Medical Center.


Conveniently, a stagnant HIV hypothesis, much in need of rejuvenation, was  expanded to include infection of macrophages, long the home base of tuberculosis and now claimed to be the most important reservoir of the AIDS ‘virus’ from which a sustained, long term attack on the body’s lymphocytes was staged. [16] Although Duesberg and Levy saw HIV infection of macrophages as possible, neither saw their subsequent killing by HIV as a possibility.  [10,21]

Indeed, key to the wanton destruction of immunity in AIDS was an attack on the  macrophage. It had long been known that certain white blood cells called macrophages ate [phagocytosed] bacteria, a good thing for health and well-being. And how tuberculosis and the mycobacteria became the  greatest assassins ever, had a lot to do with how they not only resisted lysosomal degradation once inside the macrophage, but multiplied there [1], and ate it up, from the inside out. [13]  Inside every human macrophage swim two thin-membraned vacuoles: one, the  phagosome, containing ingested bacteria; the other the lysosome containing lysozyme, a destructive enzyme tailored to  kill bacteria. Usually, with  infection, the two fuse or join, the acidic and enzymatic content of the lysosome then killing bacterial elements harbored in the phagosome. It is how the macrophage defends the body. But after eons of evolution virulent tubercular mycobacteria have developed a survival strategy which includes coating the phagosomes they find themselves in with proteins to prevent their enzymatic destruction [29], punching holes into the phagosomal membrane for nutrition and the release of toxic  products [33], evading enzymatic destruction even with vacular fusion [2], and learning to escape from such fused vacuoles [23], only  to  eventually kill the macrophage — as the hunter becomes the hunted. Thus TB and the  mycobacteria enjoy and thrive in a macrophagal lifestyle deadly to most other pathogens. [31]

At California Pacific Research Institute, for example, Bermudez, Parker and Petrofsky watched ferocious AIDS Mycobacterium avium fowl tuberculosis destroy 28–46% more macrophages than uninfected cultures. [4] And although it was known that both Avium  and tuberculosis could escape dying macrophages only to kill and infect others, in the case  of AIDS Avium, Bermudez saw a particularly menacing event in front of him: macrophage kill only made Avium more virulent and hungrier than ever [3], as it sought out its next macrophage victim.

If ever therefore, an atypical virulent tuberculosis such as Fowl TB could join in a previous and commonly acquired latent tuberculosis with its own immune devastation — that combination would be all that was needed to create a perilous human Acquired Immune Deficiency. And that is exactly what the world had decided to call “AIDS”.



1.Armstrong J.A., Hart P.D. A Response of cultured macrophages to Mycobacterium tuberculosis, with observations on fusion of lysosomes and phagosomes. J Exp Med 1971; 134: 713–740.

2. Armstong J. A., Hart  P. D. Phagosome–lysosome interactions in cultured macrophages infected with  virulent tubercle bacilli. Reversal of the  usual nonfusion pattern and observations on  bacterial survival. J Exp Med 1975; 142: 1–16.

3. Bermudez L. E., Parker A. Growth within macrophages increases the  efficiency of Mycobacterium avium to invade other macrophages by  complement receptor independent pathway. Infect Immun 1997; 65:  1916–1925.

4. Bermudez L. E., Parker A. Apoptosis of Mycobacterium avium-infected macrophages is mediated by  both tumour necrosis factor TNF and Fas, and involves the  activation of caspases. Clin  Exp Immunol 1999; 116: 94–99.

5. Bultmann B. D., Flad  H. D. Disseminatred mycobacterial histiocytosis due to M. fortuitum associated with  helper T-lymphocyte immune deficiency. Virchow’s Arch 1982; 395: 217–225.

6. Chaouchi N., Arvanitakis L. Characterization  of transforming growth factor-B1 induced apoptosis in normal human B cells  and lymphoma B cell lines.  Oncogene 1995;11:  1615–1622.

7. Detels R., English P. A. Patterns of CD4+  cell changes after HIV-1 infection indicate the  existence of a codeterminant of AIDS. J Acquir  Immune Defic Syndr  1988; 1: 390–395.

8. Dlugovitzky D., Luchesi S. Circulating immune complexes in patients with  advanced tuberculosis and their association with  autoantibodies and reduced CD4+  lymphocytes. Braz J Med Biol Res 1995; 28(3):  331–335.

9. Donahoe R. M., Bueso-Ramos C. Mechanistic implications of the  findings that opiates and other drugs of abuse moderate T-cell surface receptors and antigenic markers. Ann N Y Acad  Sci 1987; 496: 711–721.

10. Duesberg P. H. Aids epidemiology: inconsistencies with human immunodeficiency virus  and with  infectious disease. Proc  Natl  Acad  Sci 1991; 88:  1575–1579.

11. Duesberg P. H. AIDS acquired by  drug consumption and other noncontiguous risk factors. Pharmacol Ther 1992; 55: 201–277.

12. Fratazzi C., Arbeit  R. D. Macrophage apoptosis in mycobacterial infections. J Leukoc  Biol 1999; 66(5):  763–764.

13. Gangadharam P. R., Pratt P. F. In vitro  response of murine alveolar and peritoneal macrophages to Mycobacterium intracellulare. Am Rev Respir Dis 1983; 128(6):1044–1047.

14. Gilks C. F., Richard J. B. Disseminated Mycobacterium avium infection among HIV infected patients in Kenya. J Acquir Immune Defic Syndr  Hum  Retroviral 1995; 8(2): 195–198.

15.Hirsch C. S., Toossi Z. Apoptosis and T cell hyporesponsiveness in pulmonary tuberculosis. J Infect Dis1999; 179: 945–953.

16. Ho D. D., Rota T. R. Infection of monocyte-macrophages by human T-lymphotropic virus  type  III. J Clin Invest 1986; 77:1712–1715.

17. Jaworowski A., Crowe S. M. Does  HIV cause depletion of CD4+ T cells in vivo by the  induction of apoptosis? Immunol Cell Biol 1999; 77(1):  90–98.

18.  John  J. J., Kaur  A. Tuberculosis and HIV infection. Lancet 1993; 342(2): 676.

19.  Lamoureux G., Davignon L. Is prior  mycobacterial infection a common predisposing factor to AIDS in Haitians and Africans? Ann Inst Pasteur Immunol 1987; 138(4): 521–529.

20. Lemaitre M., Guetard D. Protective activity of tetracycline analogs against the  cytopathic effect  of the  human immunodeficiency viruses in CEM cells.  Res Virol 1990;141(1): 5–16.

21. Levy J. Mysteries of HIV-challenges for therapy and prevention. Nature 1988; 333: 519–522.

22.McDonald I., Wang H. Transforming growth factor B1 cooperates with anti-immunoglobulin for the  induction of aptosis in group I (biopsy-like) Burkitt lymphoma cell lines. Blood 1996; 87:  1147–1154.

23. McDonough K. A., Kress  Y. Pathogenesis of tuberculosis: interaction of Mycobacterium tuberculosis with macrophages (published erratum appears) in  Infect  Immun1993 Sep.;  61(9):  4021–4) Infect  Immun 1993; 61(7): 2763–2773.

24. Molloy A., Laochumroonvorapong P. Apoptosis, but not necrosis, of infected monocytes is coupled with  killing of intracellular bacillus Calmette-Guerin. J Exp Med 1994; 180: 1499–1509.

25. Mudaki Y., Perriens J. H. Spectrum of immunodeficiency in HIV-1-infected patients with  pulmonary tuberculosis in Zaire.  Lancet  1993; 342(8864): 143–146.

26. Novick D. M., Brown  D. J. C. Influence of sexual preference and chronic hepatitis B virus  infection on T lymphocyte subsets, natural killer activity, and suppressor. Hepatol 1986; 3: 363–370.

27. Ohtomo K., Wang S. Secondary infections of AIDS autopsy cases  in Japan  with  special emphasis on  Mycobacterium avium-intracellulare complex infection. Tohoku J Exp Med 2000; 192(2): 99–109.

28. Papadopulos-Eleopulos E., Turner V. E. A critical analysis of the HIV-T4-Cell AIDS hypothesis. Genetica 1995; 95:  5–24.

29. Pieters J. Entry  and survival of pathogenic mycobacteria in macrophages. Microbes  Infect 2001; 3(3): 249–255.

30.  Reeve  P. A. Tuberculosis & HIV infection. Lancet  1993; 342(2): 676.

31. Rhoades E. R., Ullrich H. J. How  to establish a lasting relationship with  your host: lessons learned from Mycobacterium spp.  Immunol Cell Biol 2000; 78(4): 301–310.

32. Rojas M., Olivier M. TNF-alpha and IL-10 modulate the induction of apoptosis by virulent Mycobacterium tuberculosis in murine macrophages. J Immunol 1999;162(10): 6122–6131.

33. Teitelbaum R., Cammer M. Mycobacterial infection of macrophages results in membrane-permeable phagosomes. Proc  Natl  Acad  Sci 1999; 96(26): 15190–15195.

34.  WHO:  Statement of AIDS and Tuberculosis. Geneva: WHO, 1989.

35. Hirsch CS, Toossi Z, Johnson, JL et al  Augmentation of Apoptosis and Interferon-y Production at Sites of Active Mycobacterium tuberculosis Infection in Human Tuberculosis.  The Journal of Infectious Diseases 2001, March 1st); 183: 779-88.








Dr. David Da-i Ho


By 1995 David Da-i Ho, of “It’s the virus, stupid!” fame and then head of New York’s Aaron  Diamond AIDS Research Center, assumed the mantel of titular head of the U.S. AIDS establishment; he and his colleagues proclaiming a new proactive stance, asserting that HIV was  never inactive and multiplied astronomically in the body each day, killing CD4  cells. Ho was a Taiwanese American who pioneered the use of protease inhibitors for treating ‘HIV-infected patients’.

But there was  still  no hard physical evidence, only theory, as to how the retrovirus called  “HIV” killed. Ho speculated that the  carnage took place  in the  lymph nodes, so that there were few signs of infected CD4 in the blood. Then, the HIV not involved in this hypothesized slaughter shot out into the blood stream, creating a ‘viral load’. To eradicate viral load, Ho was suggesting early and aggressive anti-viral drugs taken in potent ‘cocktails’, with serious side-effects, and probably for the life of the patient. The problem was, as Robert Gallo later noted, that just about everyone he knew realized from  the  start that Ho’s theory was absolutely wrong.

Nevertheless, soon HIV  scientists were  proclaiming that the  amount of virus  in the  blood, the so-called “viral load” was  the  most important determinant in AIDS prognosis. [9] But the fact is that HIV is so sparse in the blood as to require Polymerase Chain Reactors (PCR),a nucleic acid  broth which makes copious copies of hard-to-find pathogens, to even detect it.

PCR inventor Kary Mullis would not support the use of his  test  to  amplify and exaggerate what is being perceived as  HIV  in  measuring ‘the  viral  load’,  as  is  currently being done. To many, the massive amounts  of RNA  supposedly representing “HIV” in the circulation were suspect. Furthermore, others wanted to know if you made a thousand copies of a dollar bill,  how many real dollar bills did  you still really have to begin wiith?

The ‘viral load test’, presently in use makes only copies of fragments of nucleic acids  attributed to HIV[6]– and does not  count HIV itself.  Since it does not count HIV itself and other infections, in particular the  mycobacteria such as tuberculosis, can also yield  similar nucleic acid fragments, a positive viral load  test cannot be regarded as signaling “HIV” itself. Meanwhile, nobody ever questioned the validity of using a non-quantitative PCR in the  detection of another hard to find  pathogen…… tuberculosis, not even Mullis.

By 1994, British  researcher John  Kay walked up  to  a New  Hampshire podium before the  Proteolytic Enzyme Conference and announced that Hoffman-LaRoche’s protease inhibitor RO31-8959, called saquinavir or Inverase, hadn’t worked out clinically in  an  18-month trial with 400 AIDS patients. [3] The reason given was that after an initial improvement in symptoms, HIV developed resistance to the  agent and that for the  time being Roche was  imposing a blackout on the disappointing trial.  Biochemist David Rasnick, an expert on the proteases, saw things differently. The inhibitors were  performing their job as designed, and that was to block HIV production. It wasn’t mutation or resistance that were the  problems, it was that HIV did not  cause AIDS (Ibid).


Dr. David Rasnick


By 1984, Rasnick was in a pivotal position to capitalize on protease momentum but quickly decided that to kill a harmless retrovirus was an exercise in futility; often at the risk of severe and yet-as-unknown side-effects, some fatal  in animals.

Although it was generally acknowledged by the HIV establishment that by the 1990s Highly Active Antiretroviral Therapy (HAART) made headway in braking the steep rise in  both AIDS and AIDS-related deaths in the U.S., no randomized study to that point had ever  been done comparing those on these drugs to those that are  not. [10] Furthermore, the precipitous drop  in  AIDS  deaths  in 1995 predated the  introduction of  the  protease inhibitors,  which first  came onto the  market in late 1996, by one  year. This seems much akin to tuberculosis, which began to decrease long before any  specific measures or drugs were  used against it. [4]

HAART, to be sure, from its onset was palliative. Specifically, with HAART,  in many cases, the CD4+ count is partially restored and supposedly therefore the necessity for  continuing  drugs  specifically against M. Avium in certain cases stopped. But M. avium infection rebounds when these anti-HIV drugs are stopped or fail. [8]Furthermore, the antiretrovirals in HAART were  not the  only  agents which could restore a CD4  count. This restoration also  occurred in  patients with HIV and TB when anti-TB  treatment alone was used, as in  John’s  study where a CD4  count of 89/ll climbed to 760/ll. [5]

In truth, the  entire story has  not  been nearly unraveled   regarding  America’s  potent  anti-retroviral drugs. Regush mentions that the  types of antiviral drugs used in ‘cocktails’  ‘have antimicrobial properties that could, to  varying degrees, target other infections that are common to AIDS’. (10) Regush was correct and today we know tht the antiretrovirals have suppressive affects on both TB and fowl tuberculosis.

FDA approval for any of these antiretroviral agents did not require information as  to  whether they were  bactericidal. Therefore, studies which show that widespread HAART reduces the  risk  for  TB or  may  bring about the further decline of TB among persons infected with  HIV [7] can never answer with  certainty that the  reason for this  is not some heretofore unknown direct antitubercular activity on the  part of HAART.

For example, in 1999 Bermudez et al. (1) documented that the  intense macrophage and lymphocyte killing by American AIDS M. avium fowl tuberculosis was significantly reduced by protease inhibitors called caspases.

These investigators, in effect, established that certain protease inhibitors, a first  line  of defense against ‘HIV’ found  in   HAART,  were able to  curtail  Mycobacteria avium’s virulence,  thus   pinpointing  a much more specific and satisfying reason as to  why, all of  a sudden, MAI  prophylaxis was not necessary and symptomatic improvement noted then that HAART was ‘bolstering the immune system’. But the questions remained: At what price in toxicity, and for how much gain in years — a problem almost unascertainable in the face of changing definitions as to what constitutes AIDS by HIV/AIDS gurus — among which was the inclusion of tuberculosis as an ‘AIDS Defining’ illness.



1. Bermudez L. E., Parker A. Apoptosis of Mycobacterium Avium infected macrophages is mediated by  both tumor necrosis factor (TNF) and Fas and involves the  activation of caspases. Clin  Exp Immunol 1999; 116: 94–99.

2. Centers for Disease Control. Weekly surveillance report. October 20,  1986.

3. Conlan MG. Interview with  David Rasnick Ph.D.: On Columbia’s AIDS Conference and the  Nature of Science. Zenger’s News  Magazine San Diego; 1998 Jan.

4. Dubos R., Dubos J. The White  Plaugue. New  Brunswick: Rutgers University Press, 1952.

5.  John  J. J., Kaur  A. Tuberculosis and HIV infection. Lancet 1993; 342(2): 676.

6. Johnson C. The  PCR to prove HIV infection. Viral load  and why  they can’t be  used. Continuum (London) 1996; 4: 33–37.

7. Jones J.L., Hanson D.L. HIV-associated tuberculosis in the era of highly active antiretroviral therapy. The  adult/ asolescent sprectrum of HIV disease group. Int J Tuberc Lung Dis 2000; 4(11):  1026–1031.

8.  Kaplan J. E., Hanson M. S. Epidemiology of human immunodeficiency virus-associated opportunistic infections in the  United States in the era of highly active anti-retroviral therapy. Clin  Infect Dis 2000; 30(Suppl 1): S5–S14.

9. Lyles R. H., Tang  A. M. Virologic, immunologic, and immune activation markers as predictors of HIV-associated weight loss  prior  to AIDS. Multicenter AIDS Cohort study. J Acquir  Immune Defic Syndr  1999; 22(4): 386–394.

10.  Regush N. The Virus  Within. New York: Plume Press, 2001.








Once upon a time, a small group of politically powerful scientists rammed a flawed theory on the origin and cause of AIDS down America’s and then the  world’s throat.

Yet  we  are  still  led  to  believe that we  are  fortunate that retroviruses, only discovered in  the 1970s, were uncovered just in time to label them the culprit in a killer AIDS epidemic. And lucky that two ‘HIVs’ were discovered in rapid succession and the technology and theory to  link AIDS to  the HIV retrovirus were fully in place, for the first  time in  history, only  a  few  years prior  to the recognition of the AIDS epidemic.

Lucky? As of the 20th anniversary of the first  reported AIDS case, AIDS had already infected nearly 60 million people of which almost 22 million, including nearly half a million Americans died, and 8,500 AIDS deaths occurred daily. Yet the  prospects for a cure  or vaccine are as remote as they were three decades ago.

Historically, not that long ago,  and at the  end of the 19th century, after 150  years of denial, the medical establishment recognized that there were bacteria, and suddenly every disease seemed to be caused by a bacteria. But with the advent of the  electron microscope, unknown disease  was more and more attributed to a virus or a retrovirus, often to no avail.  Thus it was that scientists were certain that a virus was behind Lyme’s disease, Mycoplasma pneumonia, and Legionnaires’ disease before their respective bacteria were  found.


Vladimir Zworykin (seated) and James Hillier demonstrate an early electron microscope.


By 1931, Rudenberg, hoping to visualize the polio virus, filed a patent for his electron microscope and during WWII investigators never gave up on an electron search for a cancer retrovirus, despite one dismal failure after another.

Then an AIDS ‘virus’ was  found, primarily because it was looked for;  and not because it  caused  AIDS — and was soon bolstered by half-truths, flawed theory and downright hocus-pocus.

HIV scientists cited that ‘unassailable epidemiological evidence’ [2] has  established HIV or a virus as the cause of AIDS, including those epidemiological studies carried out by the CDC on filtered factor VIII blood transfusions for hemophiliacs. Blattner cites Peterman in his  article as saying ‘it is also  noteworthy that HIV infection, and not infection with any other  infectious agent,  is linked to blood transfusion-associated AIDS.’ [35] But blood transfusions do not distinguish between HIV and other  filterable infectious agents especially, as in the case of tubercular mycobacteria, if these other infectious agents are not screened for. Yet, one  of the  original factor VIII transfusion cases happened in Canton, Ohio,yielding a diagnosis of oral thrush and disseminated  Mycobacterium avium. [8]

John Lattimer could not foresee the unusual situation which, decades later, might be  involved with  the direct insemination of particularly virulent  tubercular mycobacteria rectally onto the vulnerable one layered epithelium of the prostate during gay sex. Nor could Lattimer forecast the hyper-virulent strains of AIDS Mycobacterium tuberculosis and Mycobacterium avium that would one day, decades later, be  shared in much greater numbers, heterosexually, and in a world-wide epidemic called AIDS. But who could have? Nor  could Gondzik realize the  profound significance of warning his patients, on the eve of the AIDS epidemic in 1979, to wear condoms lest they acquire sexually transmitted tuberculosis. [14]

Mycobacterial infections are the main cause of bacterial infection during AIDS [34]; and often precede other infections by 1–10  months. [1] The fact that three decades after AIDS started killing people, tubercular mycobacteria, despite their prevalence in AIDS, are not considered its cause, is in no  small  part  due to  the  lack  of  scientists and the lay public to understand the  ability of mycobacterial and tubercular infection, once contracted, to lie seemingly dormant for extended lengths of time in humans [49], and at the same time begin to melt the  immune system away. [27]



Tissue section of lung in a fatal case of AIDS. Arrows point to round tubercular forms. These forms proved to culture out from broncoscopic washings as Mycobacterium avium or fowl tuberculosis.
(below), Acid-fast stain, x1000, in oil.



Laboratory culture of Fowl tuberculosis [Mycobacterium avium] cultured from the patient above. The culture is pleomorphic [has many forms], in that it contains acid-fast rod forms and non-acid-fast round coccal forms, as indicated by arrows. These vary in size. Acidfast stain, x1000, in oil.


Nor was it emphasized that both tuberculosis, whose chronic lymphadenitis is its most common extra-pulmonary manifestation [22],  and M. avium, the most common cause of lymphadenitis in children [18], can attack lymph nodes [41] and the entire body additively and simultaneously. [42]

AIDS is a mycobacterial disease and patients with advanced TB or Avium are  indistinguishable from  those with ‘HIV’. Even in  the  earliest AIDS cases on record, dating back to 1959, tuberculosis [47] and the atypical mycobacteria [40] [17] were clinically and bacteriologically  diagnosed.

Perhaps one of the most convincing arguments for the intimate causal link between tubercular infection and AIDS comes from the widespread geographical overlap of the two. Worldwide, by the most conservative estimates, around one in three people is infected with Mycobacteria tuberculosis alone, or 1.8  billion people [48] and the very  cities, in  which up  to  80%  have tuberculosis,  are the  epicenters of AIDS. The  last world AIDS conference that was held in Barcelona admitted that 1/3 of all AIDS deaths were from diagnosed tuberculosis. [30]

Almost a million new  cases  of AIDS were  estimated to be  attributable to  tuberculosis in 1995, and by  the  year 2000 there were  probably 8  million co-infected people worldwide. [36]  Figures such as  these make it unconvincing that  AIDS  ever surpassed tuberculosis as  the leading cause of death in the  world, especially in lieu  of cross-reacting sera  that opens up the question as to just how  many cases  attributed to  HIV are  in  fact  from  tuberculosis or its allied  mycobacteria.


Gottlieb’s One-Two Punch


Dr. Michael Gottlieb: immunologist and AssocIate Clinical Professor of Medicine at the David Geffen School of Medicine at UCLA in Los Angeles.


When the AIDS epidemic officially began in June,1981, allergist- immunologist Michael Gottlieb of UCLA, after  first  implicating cytomegalovirus (CMV), headlined that the: “Ongoing AIDS Epidemic Could  Be Product of Dual Pathogen  Infection”, concluding that AIDS resulted from  not one but two microbial infections. [15] Unexpected in early AIDS autopsies was the surprisingly high proportion of difficult to diagnose fowl tuberculosis or  Mycobacterium avium-intracellulare, [46] in up to 55% [24] of American cases. But  in  Haitian and African AIDS patients, undoubtedly just  as exposed to Avium,  death by Mycobacterium tuberculosis predominated. Gottlieb had himself referred several AIDS patients with fowl tuberculosis or Mycobacterium avium to  Zakowski for further study at the UCLA Medical Center.


Indeed, most convincing evidence points to Gottlieb’s hypothetical duel pathogens as being atypical mycobacteria such as Avium in somehow getting into a human blood pool already harboring latent or active Mycobacterium tuberculosis. The ‘acquired’ in Acquired Immune Deficiency Syndrome is Mycobacteria avium or a similar non-tuberculous mycobacteria; ‘immune deficiency’ but the result of  a  savage double  attack on  the   immune system by an atypical mycobacterium [such as M. avium] and M. tuberculosis. Avium alone has, in the  short space of 30 years, gone from  relative obscurity to  the leading infectious disease in U.S. and European AIDS, And there is no dearth in the literature to explain just how this could have happened — ranging from human sexual transmission [5,6], to bestiality [5,23], to certain Voodoo practices such as African  ritualistic drinking of animal blood (37), to the medical or addict’s use of shared needles. (38) Thus was the groundwork laid for tubercular and mycobacterial mayhem — the introduction and spread of virulent mycobacteria into the  human blood pool, whether in Africa, the  U.S., Europe or the  rest  of the  world.


From the onset, lymph nodes were recognized to be important in AIDS. And if in the late 1960s, lymph nodes from 368 swine from Transvaal and Natal South Africa were examined and found to mostly contain Mycobacteria avium complex (MAC) [25] — these very same tubercular strains reappeared —as smoking guns — in the lymph nodes of African AIDS victims in the early 1970s. [26]


Only  a few strains of MAC [Mycobacterium avium complex] are  found in human AIDS. [24]  Notably these are  also  found in  the simian AIDS in monkeys. [19] Weiszfeiler and Karczag [45] succeeded in isolating 50 strains of Mycobacteria, including MAC from [33] monkeys — significant in that millions of pre-AIDS Africans were  vaccinated with an  early  polio vaccine attenuated in living monkey kidney tissue. Some saw a correlation between where the  bulk of polio vaccine was administered and the  epicenters of AIDS. [20] The Simian-Avium (SAV) group of mycobacteria share characteristics of both Mycobacterium avium and Mycobacterium simiae,  which by itself is entirely capable of causing a lethal AIDS infection. [29] Also soil-borne MAC is found in cats, swine, and primates, all significant in early retroviral theories regarding AIDS.

The fertile soil upon which Mycobacterium avium and similar ‘atypical’  mycobacteria plants AIDS is pre-existing TB, often latent, always immunosuppressive. Despite WHO estimates, Fox maintained that nearly half the world has TB, [10] — but others feel that number to be even greater.

Cantwell, who  repeatedly found tubercular acid-fast forms in AIDS, felt  it  reasonable to assume that the initial immunosuppression in that disease must also  be present in many ‘healthy’ people as studies indicate that some promiscuous but otherwise ‘healthy’ gays were actually immunosuppressed to begin with. [4] Mycobacteria tuberculosis, both in its  vast  reservoir of seemingly well and its human immune-killing potential, certainly fulfills this criterion. Papadopulos-Eleopulos [33] mentions that in African  AIDS, ‘HIV’ infection usually follows  TB.

The first case of human disease due to Mycobacterium avium-intracellulare (MAC) was  reported in a middle-aged Mesabi Range iron  miner in 1943. His  symptoms were  pulmonary [9], and until the emergence of AIDS, lung infection alone typified Avium, though differentiation between fowl or Avium tuberculosis and tuberculosis itself was at times nearly impossible. [32]  The first reports of MAC in AIDS appeared in 1982 were Zakowski found that  “all of the homosexual patients that have died of acquired immunodeficiency at the UCLA Medical Center for the Health Sciences have had disseminated MAC infection.”[50] Furthermore, the team mentions “Because of this preliminary observation, we now vigorously seek evidence of mycobacterial infection in homosexuals with unexplained lymphadenopathy”

Soon  the  devastatingly  immunosuppressive potential of co-infection with  M. tuberculosis and  M.  avium was shown. [42] As already mentioned, this ability of mycobacteria to attack simultaneously is a recurrent theme in the literature, occurring over  and over  again. But in AIDS, it would bring on a combined immunosuppression the likes of which man had never had to deal  with. The documented ability for AIDS and TB to potentiate one another [13] is a result of such double-pronged mycobacterial attack between ‘AIDS’, the atypical tubercular mycobacterial infection — and tuberculosis.

In such a scenario HIV is simply one of the L-forms of an atypical tuberculosis,  in particular M. avium and until it is recognized as such no  ‘retroviral’  vaccine or cure  will be  possible.

In the U.S., on the surface, AIDS is characterized by the severe immunosuppression of Mycobacteria avium [MAC] and opportunistic infections like Kaposi’s Sarcoma and Pneumocystis Carinii. In Africa it is a wasting disease characteristically ending with death by Mycobacteria tuberculosis. “HIV” should cause the same disease where it from the same cause.

In disseminated  Mycobacterium  avium  Infection Among HIV Infected  Patients in Kenya,  Gilks approaches this most perplexing AIDS enigma in terms of the mycobacteria, addressing the apparent relative rarity of disseminated MAC in AIDS in Africa and the  developing countries. [12] That MAC exists in the  African  as well as the  American environment [43]  cannot be  denied. Nor can the fact that African skin tests prove antibodies to MAC already in African  blood. [44]  Gilks acknowledges that AIDS patients in developing countries are probably dying of more virulent tubercular infections before they become immunosuppressed enough to show Avium.  Inderlied [21] and O’Keefe  [31] agree.

Gilks mentions that AIDS patients in Africa, already infected with latent tuberculosis, are more likely to reactivate this mycobacteria with  catastrophic results before  reaching the  low  CD4  level  associated with  clinical MAC.  This however, does not preclude the fact  that Avium or a similar non-tubercular mycobacteria, as causative, plants AIDS in the soil of previous tubercular infection, whether in Africa or elsewhere.

The full extent of drug-resistant TB in African countries is unknown but at least  as prevalent as it is in New York, Haiti or the Ivory Coast. [28] Frieden found 30%  of resistant strains of tuberculosis in  New York [11] AIDS patients, but Shafer assured that with or without  HIV, drug resistant tuberculosis was comparable. [39] How much of multi-drug resistant (MDR) TB is in fact a fusion with the atypical mycobacteria like MAC or SAV is an open question. Meanwhile, there hasn’t been a new TB drug in 37 years. [30]  And for its part Avium (swine, or fowl tuberculosis) and the ‘atypical’ mycobacteriain man has never had a truly satisfactory treatment. [16]  Whether this situation will  change with novel strategies now in the  pipeline [3] remains to be  seen.

It is only fitting that a bizarre tale — the history and promoting of “HIV” and its drug cocktails — end in a bizarre way: that drugs called antiretrovirals only real benefit is to toxically try to contain tubercular infections, which they were not designed  to do in the first place.

Yet until some honest reassessment of the situation occurs among the reactionary forces that have handed us this, millions will be the slaves to substandard toxic treatment using antiretrovirals for a disease that is of mycobacterial origin and causation to begin with.



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