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Vaccines as an Autism Trigger: A TB Link?

August 11, 2017

by Lawrence Broxmeyer, MD


From NEXUS Magazine, February–March 2015 (vol. 22, no. 2)
http://www.nexusmagazine.com

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

Email: nyinstituteofmedresearch@yahoo.com
Website: http://lawrencebroxmeyermd.com/

[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@ yahoo.com. For more information, visit http://lawrencebroxmeyermd.com.

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)
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Uncommon Valour
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Industry Turns a Blind Eye
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Review Article: Are the Infectious Roots of Alzheimer’s Buried Deep in the Past?

February 26, 2017

Dr. Lawrence Broxmeyer, MD

LINK-OUT TO REVIEW ARTICLE -51778-ipjpe-3-s2-2

Citation: Broxmeyer L. Are the Infectious Roots
of Alzheimer’s Buried Deep in the Past? J Mol
Path Epidemol. 2017, 3:2.

Received: January 13, 2017; Accepted: February 20, 2017; Published: February 22,
2017

© Under License of Creative Commons Attribution 3.0 License

Abstract

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

Keywords: Alzheimer’s disease, Infectious Cause of Alzheimer’s Disease, Oskar Fischer, Alois Alzheimer, Neurodegenerative Disease, Neurotuberculosis

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ALZHEIMER’S DISEASE: WHICH GERM IS IT?

October 9, 2016

NEW RELEASE………..

alzheimers-kindle-ready-front-cover-52931065_kindle-ready-front-cover-jpeg_4077485-1

grayscale

Abstract:

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

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

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

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

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

Available on Amazon: Alzheimer’s Disease – How Its Bacterial Cause Was Found And Then Discarded

Introductory YouTube Video: click here

Introductory chapter article is on: Academia.edu

 

EBOLA……….OR ACUTE, EPIDEMIC, FEBRILE, HEMORRHAGIC, VIRAL-LIKE TUBERCULOSIS?

October 8, 2014

 

Dr. Lawrence Broxmeyer, M.D.

 

The CDC recently declared:

“Diagnosing Ebola in a person who has been infected for only a few days is difficult, because the early symptoms, such as fever, are nonspecific to Ebola infection and are seen often in patients with more commonly occurring diseases, such as malaria and typhoid fever.”

Only a sin of omission. then, would explain why anyone or any group would not want to specifically mention the most commonly occurring cause of infectious death in Africa ― tuberculosis ― whose sky-high rates in West Africa make Ebola look like a dropper-full of water squeezed into the Mississippi.

If by October, 2014, Ebola had laid claim to what some say is 3,000-plus deaths since its February outbreak, certainly this ought to be weighed in the light of the approximately 600,000 Africans killed by TB in the same time-frame. Furthermore, although TB incidence is decreasing globally, incidence rates are increasing in most of West Africa (1) ― ground zero for the current Ebola outburst. Just as curiously, almost half of all TB cases in the West African Ebola zone are caused by an unusual, yet just as deadly member of tubercular family, Mycobacterium africanum ― a strain of tuberculosis exclusive to West Africa, which is fast becoming a microbe of great public ― and now possibly global concern.

Surely the CDC is aware that there is not a sign or symptom of Ebola, including its hemorrhagic tendencies that cannot be found in acute disseminated miliary (blood-bourne) tuberculosis, once called “galloping consumption” ― the single most feared form of the disease ever. And most likely it is also aware that such tuberculosis has its own viral-like forms, some of which can simulate the Ebola. Such viral TB is generally acknowledged to be TB’s preferred form ― as a survival strategy to storm any inclement conditions the microbe might find itself in. (2)

Then why did the CDC not mention TB, by name, in their short-list of possibilities that could cause Ebola-like symptoms? If such oversight stopped there it would be unremarkable, but it seems to have been carried over in the very design of the most recent diagnostic tests issued to detect Ebola.
_________________________________________________

 

In September of 1978, about 40 years ago, a team ― including a 27-year-old medical graduate, training as a clinical microbiologist at the Institute of Tropical Medicine in Antwerp, Belgium, received a blue thermos from Zaire. It was filled with the two 5ml. clotted blood specimens of an African-based Flemish nun. The Belgium doctor who sent it, Jacques Courteille, practicing in Kinshasa, included a note saying that he was at a complete loss for the nun’s mysterious, yet deadly illness. Also, could the samples be tested for Yellow Fever? This thermos had traveled from Zaire’s capital city of Kinshasa, on a Sabena commercial flight to Belgium ― inside its deliverer’s hand luggage. When the samples were received, Peter Piot, the 27-year-old medical graduate and his colleagues, among other things, placed the blood samples under an electron microscope. Piot: “We saw a gigantic worm like structure ― gigantic by viral standards. It’s a very unusual shape for a virus, only one other virus looked like that and that was the Marburg virus.”

But the new “virus” needed a name. Piot relates the interesting tale of how Ebola came to be named as Ebola:

“On that day our team sat together late into the night – we had also had a couple of drinks – discussing the question. We definitely didn’t want to name the new pathogen “Yambuku virus”, because that would have stigmatized the place forever. There was a map hanging on the wall and our American team leader suggested looking for the nearest river and giving the virus its name. It was the Ebola River. So by around three or four in the morning we had found a name. But the map was small and inexact. We only learned later that the nearest river was actually a different one. But Ebola is a nice name, isn’t it?” (3)

Depends upon how you look at it.

Piot’s specimens proved negative for Yellow Fever and he mentions that the tests for Lassa fever and typhoid were also negative. What, then, could it be? Piot: “To isolate any virus material” small amounts of the blood samples were injected into VERO cells and into mice. Several of these mice subsequently and abruptly died ― “a sign that a pathogenic virus was probably present in the blood samples that we had used to inoculate them.”

The fact that the mice died did not mean that it was at the hands of a “pathogenic virus”. Piot’s boss, Stefaan Pattyn, who Piot admitted “could be a bit of a bully”, supposedly specialized in the study of mycobacteria ― tuberculosis and leprosy, yet seemed unaware of the hemorrhagic consequences of acute TB, nor had he taken the time to use special stains and cultures to detect its viral cell-wall-deficient forms. Instead Pattyn followed his current passion. He had recently worked in Zaire for six or seven years and exotic viral illnesses were now “right up his alley”. So Pattyn’s team likewise never really considered a strain of acute miliary TB or its viral cell-wall-deficient forms in his rule-outs for an acute hemorrhagic or epidemic fever ― among them Mycobacterium tuberculosis and Mycobacterium africanum.

_______________________________________
The Ebola of its day on steroids, “galloping” acute consumptive tuberculosis could kill in days ― the mere memory of which, just a few generations ago, brought terror to the faces of those who had witnessed and were describing it. Dubos made clear that “galloping consumption” was not an isolated, but a frequent diagnosis in the 19th and early 20th centuries. (4) And despite persistent myths to the contrary, in the early phase of any new TB epidemic from a new and virulent strain, tuberculosis manifests itself as an acute disease and only much later as the chronic pulmonary tuberculosis that we know in today’s western world. An example of this can be found in the high mortality during the 1918 influenza pandemic, when African-Americans were brought to fight in France during World War I ― large numbers of them dying from a fast-tracked tubercular “galloping consumption.”

Many often underestimate the speed, contagiousness and ferocity of a TB epidemic. Khomenko’s 1993 study (5) should have cemented the notion that the explosive contagiousness of just such Ebola and influenza-like viral forms of tuberculosis are exactly the stuff that previous epidemics and pandemics could have been made of. But it didn’t.

In the US, the CDC and NIH seemed to feel differently, ignoring the historic possibility. There was much the same viral passion, at that time over “Influenza”, when in 1990, a new multi-drug-resistant (MDR) tuberculosis outbreak took place in a large Miami municipal hospital. Soon thereafter, similar outbreaks in three New York City hospitals left many sufferers dying within weeks. By 1992, approximately two years later, drug-resistant tuberculosis had spread to deadly mini-epidemics in seventeen US states, and was reported, not by the American, but the international media, as out of control. Viral forms of swine, avian and human TB can be transmitted from one species to another. So can exotic strains of tuberculosis and Mycobacterium africanum, imported into the United States through countries such as Liberia. By 1993 the World Health Organization (WHO) had proclaimed tuberculosis a global health emergency (6). That emergency has never been lifted.
________________________________________________
Anderson pointed out that such acute, untreated disseminated, “galloping”, blood-dispersed TB could kill in hours or days (7) ― its mortality, according to Saleem and Azher even today approaching 100%. (8) Ebola itself can take up to a month to kill its victims, said Ben Neuman, an expert in viruses at Britain’s Reading University ― although there are many cases that also kill in hours or days. Not only were tubercular hemorrhaging and fever both mentioned by Fox (9), but hemorrhaging of the serous cavities, the gums, and the nose, into the joints, the skin, and the bowels. Appleman (10), in the American Journal of Ophthalmology, considering massive spontaneous hemorrhages into the vitreous, mentions that Axenfeld considered acute tuberculosis an important possibility in the rule-out for bleeding into the eye. Coughing-up blood has always been a well-known scenario for TB. Hemorrhages of significance fro Read the rest of this entry »

The tuberculin skin test: how safe is safe? -the tuberculins contain unknown forms capable of reverting to cell-wall-deficient mycobacteria

May 27, 2014

Alexander P. Lysenko, Vladimir V.Vlasenko, Lawrence Broxmeyer, Artem P. Lemish, Tatiana P. Novik, Andrei N. Pritychenko

Clinical and Experimental Medical Sciences, Vol. 2, 2014, no. 2, 55 – 73.

THE TUBERCULIN SKIN TEST: HOW SAFE IS SAFE.PDF

® U.S. Library of Congress
_________________________________________________________________________

ABSTRACT

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

KEYWORDS: Tuberculin; Mycobacterium bovis; thermo stability; Cell-Wall-Deficient mycobacteria

REFERENCES:

1.WHO Report Global Tuberculosis Control 2010 World Health Organization; WHO Library Cataloguing-in- Publication Data 2010; 218pp p.16
2.Livingston V, Allen RM. Presence of consistently recurring invasive mycobacterial forms in tumor cells.Microscop Soc Bull 1948; 2: 5–18.
3.Livingston, Virginia Wuerthele-Caspe. Cancer: a new breakthrough, Los Angeles: Nash Publishing; 1972. 269pp.
4.Cantwell, A The Cancer Microbe. Los Angeles: Aries Rising Press; 1990. 283pp.
5.Guliang H, Tefu L.Mycobacterium tuberculosis L-forms. Microbial Ecology in Health and Disease 1999; 10: 129-133.
6.Song L-Y, Yan W-S, Zhao T Detection of Mycobacterium tuberculosis in lung cancer tissue by indirect in situ nested PCR; Journal of First Military Medical University; 2002:11.
7.Nalbandian A, Yan BS, Pichugin A, Bronson T, Kramnik I. Lung carcinogenesis induced by chronic tuberculosis infection: the experimental model and genetic control. Oncogen
2009 28(17): 1928-1938.
 8.Anestad G, Hoel T, Scheel O, Vainio K. Atherosclerosis and tuberculosis: are they
both chronic infectious diseases? Scand J Infect Dis 2001;33 (10):797.
9.Livingston VW, Alexander-Jackson E. Mycobacterial forms in myocardial vascular
disease. J. Amer Med Wom Assoc. 1965; 20: 449-452.
10.Broxmeyer L. Is mad cow disease caused by a bacteria? Med Hypotheses. 2004; 63 (4):731-739.
11.Cantwell AR. Variably acid-fast cell wall-deficient bacteria as a possible cause of dermatologic disease.In, Domingue GJ (Ed.) Cell Wall Deficient Bacteria.Reading: Addison-Wesley Publishing Co; 1982. pp. 321-360.
12.Cantwell AR Jr, Kelso DW. Variably acid-fast bacteria in a fatal case of Hodgkin’s
disease. Arch Dermatol 1984; 120 (3):401-402.
13.Centkowski P, Sawczuk-Chabin J, Prochorec M, Warzocha K. Hodgkin’s lymphoma and tuberculosis coexistence in cervical lymph nodes.Leuk Lymphoma; 2005: 46 (3):471-475.
14.Mattman LH Cell Wall Deficient Forms – Stealth Pathogens. CRC Press Boca Ra-
ton 3rd ed., 2001 416pp.
15.Marcova N, Slavchev G, Michailova L, Unique biological properties of Mycobacterium tuberculosis L-form variants: impact for survival under stress. Int Microbiol; 2012: 15 (2): 61-68.
16.Ghosh J, Larsson P, Singh B, Petterson BMF, Islam NM, Sarkar SN, Dasgupta S, Kirsbom LA Sporulation in mycobacteria. Proc Natl Acad Sci USA 2009, 106 (26):10781-10786.
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18.Vlasenko VV Tuberculosis in focus of problem contemporarily (in Russian) Vinnica: Nauka, 1998. 350 pp.
19.Lysenko AP, Lemish AP, Krasnikova EL Investigation of the thermal resistance of Mycobacteria tuberculosis. Probl. Tuberk Bolezn. Legk. 2007;(2):42-46.
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mycobacteria: a review. Veterinarni Medicina 2006; 51, (7): 365-389.
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Received: April 29, 2014

Heart Disease – Beyond the Stent And Bypass

April 1, 2014

 

                    Heart Disease – Beyond the Stent & Bypass

                                                                       by Dr. Lawrence Broxmeyer, MD        grayscale

[Adapted from Heart disease: the greatest ‘risk’ factor of them all. Broxmeyer L. Med Hypoth. 2004;62(5):773-9. PMID:15082105[PubMed – indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/pubmed/15082105%5D

©Copyright 2014

Summary
Once upon a time, by the turn of the last century, flying in the face of over a hundred years of research and clinical observation to the contrary, medicine abandoned the link between infection and atherosclerotic heart disease; not because it was ever proven wrong, but because it did not fit in with the trends of a medical establishment convinced that chronic disease such as heart disease must be multifactorial, degenerative and non-infectious.
Yet it was the very inability of ‘established’ risk factors such as hypercholesterolemia, hypertension and smoking to fully explain the incidence and trends in cardiovascular disease that resulted in historically repeated calls to search out an infectious cause, a search that began more than a century ago.
Today, half of US heart attack victims have acceptable cholesterol levels and 25% or more have none of the “risk factors” associated with heart disease, including smoking, high blood pressure or obesity, most of which are not inconsistent with being caused by infection. 7,56 Even the traditionalist’s 2003 assault in JAMA (Journal of the American Medical Association) to ‘debunk’ what they call the “50% risk factor myth” 20 fell woefully short under scrutiny. In one group 30% died of heart disease with a cholesterol of at least 240 mg/dl, a condition which also existed in 21% who did not die during the same period. And the overlap was obvious throughout the so-called risk categories. Under such scrutiny, lead author Greenland conceded that if obesity, inactivity and elevated cholesterol in the elderly are included, just about everyone has a risk factor and he likened the dilemma of people who do or do not wind up with heart disease akin to the susceptibility of people who are exposed and at one time contract tuberculosis, but do not presently have active disease.
In Infections and Atherosclerosis: New Clues from an old Hypothesis? Nieto stressed the need to extend the possible role of infectious agents beyond the three infections which have in recent years been the focus of research: Cytomegalovirus (CMV), Chlamydia pneumonia, and Helicobactor pylori.[39]
Mycobacterial disease shares interesting connections to heart disease. Not only is tuberculosis the only microorganism to depend on cholesterol for its pathogenesis but CDC maps for cardiovascular disease bear a striking match to those of State and regional TB case rates. Why should this be?
Ellis, Hektoen, Osler, McCallum, Swartz, Livingston and Alexander- Jackson all saw clinical and laboratory evidence of a causative relationship between the TB, its related mycobacteria and heart disease. And Xu showed that proteins of mycobacterial origin actually led to experimental atherosclerosis in laboratory animals. Furthermore present day markers suggested as indicators for heart disease susceptibility such as C-Reactive Protein (CRP), interleukin-6 and homocysteine are all similarly elevated in tuberculosis.
Although more than 120 years have passed since its discovery, Mycobacterium tuberculosis is still the leading cause of death globally due to a single infectious agent.[14] This high mortality rate exists in spite of the fact that for over 50 years tuberculosis has been a preventable, diagnosable, and treatable disease.
It therefore behooves us to explore the historical, clinical, and pathological link between heart disease, typical, and atypical tuberculosis.
Introduction
Attached at the hip, the American Heart Association (AHA), first to push towards medical heart specialization, was actually an offshoot of The National Tuberculosis Association, without whose money and help it would never have survived. In one of its first Bulletins, the AHA (American Heart Association) came up with a long list of the similarities between tuberculosis and heart disease,[2] a view supported by Ellis in The New England Journal of Medicine half a century later.[15] In a ‘name that disease’ Ellis fleshes-out a medical condition who’s mortality rate was 200 to 300 per 100,000, was widespread, and by whom many in their prime were struck down. Treatment was only partially effective. Doctors recommended diet and exercise. Special hospitals were built for it. In a tough decision, Ellis’s readers only recognized the disease as TB when he said it struck 75 years ago, the white plague of the 20th century, for the mortality rate for ischemic heart disease (IHD) at the time of Ellis’s writing was also 200 to 300 persons per 100,000.
Yet it was not until after WWII that the subject was pursued in earnest, and by two women, one of them the first female medical resident in New York. Sometime in 1965, Rutgers’ investigators Virginia Livingston, M.D. and Eleanor Alexander-Jackson PhD, fueled by Fleet and Kerr Grants, working with sterile, post catastrophic heart attack coronary artery specimens, established low-grade tubercular infection, staining ‘acid-fast’ (not decolorized with acid-alcohol) in all ischemic heart disease specimens.[32]
Even in stained slides of the heart muscle itself, Livingston documented small, acid-fast globoidal tubercular bodies which soon appeared to enter into a gradual state of digestion.[ibid]
As far back as 1896, Ludvig Hektoen, Chief Editor of The Journal of Infectious Diseases from 1904-1941, studying how tuberculosis attacked human blood vessels, saw the blood born microbes implanting themselves in vascular walls. Eventually these microbes would penetrate all layers of the arterial wall, including its muscular coat. The offshoot led, often, to the degeneration of whole arterial segments.[23] Since tubercular attack came from the inside of the vascular wall outwards, Hektoen often spotted the initial attack as involving the intimal or advantitial layers.
Even William Osler, arguably the greatest physician since Hippocrates, and to this day an icon for accurate clinical judgment, made clear that arteriosclerosis was frequently associated with tuberculosis.[42]
MacCallum[34] recognized that of all the infectious causes of heart disease, only one, tuberculosis, caused arteriosclerosis. At autopsy, he cited 101 cases of advanced tuberculosis. Of these cases, there were 49 cases in children in the first decade of life ― none of which showed arterial changes. Even in the second, third and fourth decades there were only eleven autopsies who died of TB with moderate cardiovascular sclerosis; while thirteen showed nothing. But by the fifth, sixth, seventh and eighth decades, true to current coronary timetables, there were only two autopsies with normal arteries and [26] with TB arteriosclerosis.[34]
By 1972, pathologist Phillip Schwartz, once a student of Loeffler, became aware that the ‘lardaceous’, waxy degeneration misnamed by Virchow as “amyloid” (starch was called amylum), showed that amyloid (starch-like) degeneration occurred more frequently in elderly cardiovascular systems than hardening and atheromatous lesions of their arteries. But along with this, he noticed that such amyloid degeneration, upon autopsy, usually revealed signs of lingering pulmonary and lymph node tuberculosis.[59]
Classic thought regarding atherosclerosis never was terribly convincing. It supposedly begins with the appearance of cholesterol and fat-laden macrophages (white blood cells) called “foam cells”. The fact that some of these macrophages died, just added to the debris. Macrophages died, tradition dictated, because they could not eliminate cholesterol the way they got rid of bacteria. They simply stuffed themselves compulsively with more and more cholesterol, converting into the large ‘foam cells’ that filled the plaques of advanced atherosclerosis. Macrophages, then, said orthodoxy, literally ate themselves to death at our cardiac blood vessels expense.
But there were obvious flaws to such thinking. First, unlike with other microbes, human macrophages were not that good at eliminating germs like tuberculosis, which in turn kills many of them. Second cholesterol by itself, normally the most abundant steroid in man, was on the rise in Japanese blood during the very decade (1980-1989) when the incidence of coronary heart disease was on its way down.[40] In the meantime, in the US, half the people who had a heart attack had acceptable cholesterol levels, including its HDL and LDL fractions.
Although cholesterol thus seemed an imperfect criterion for determining coronary heart disease, its intimate interaction with TB and the mycobacteria presented extremely interesting coincidental findings. Not only were virulent tuberculosis and the mycobacteria the only pathogens that actually relied upon cholesterol to enter the body’s white blood cells or macrophages,[17] but, it was the Mycobacteria that in addition were able to produce,[31] esterify,[29] take up, modify, accumulate,[4] and promote the deposition of and release[26] of cholesterol.
Orthodox thought then pronounced that smooth muscle cells of the cardiovascular system somehow responded to fat proliferation under the influence of certain platelet factors, which are otherwise supposed to function exclusively in clotting, to eventually cause inflammation. But, to many, it seemed fuzzy logic that inflammation should occur from fat proliferation to begin with. Livingston and Alexander-Jackson’s meticulous work clarified this, finding in all specimens, an infectious agent behind that inflammation and fat propagation.[32] But unfortunately, they worked as “outsiders” at a time when women doctors and scientists weren’t fully accepted.
Others Notice
A 1973 watershed study by Benditt and Benditt reported that cells found in artherogenic plague had a monoclonal origin, that is, they were derived from a single cell population.[6] Confirmatory studies[43,44] prompted the revival and legitimization of a search for an infectious cause. But by concluding that such monoclonal origins were caused by “Chemical mutagens or viruses or both” Benditt and Benditt’s agenda blindsided a third major possibility- tuberculosis and the mycobacteria, each capable of churning out its own monoclonal enzymes, once systemic.[13,45]
It was in no small part as a result of Benditt’s study, much of the world’s scientific and medical community focused on an extremely limited role for tuberculosis and the mycobacteria in heart disease, and at the same time seemed to purposefully marginalize studies that kept seeping into the Index Medicus. For example, in the same year Livingston pursued her heart work at Rutgers, the Russians, unhindered by the American brand of politicized medicine, began proving the link between tuberculosis, atherosclerosis and heart disease.[8,25,27,28]
Which Infection?
Since a 1988 report of raised antibodies against Chlamydia pneumoniae in patients with heart disease appeared, it was hoped that the microbe might be behind atherosclerosis. [21,41,50] Hurting this hypothesis was the low incidence of atherosclerosis in the tropics despite chlamydia’s high frequency there.[52]
Also Loehe and Bittman concluded that although Chlamydia, on occasions, might be present, it was not a causative factor[33] because there was no correlation between the severity or extent of atherosclerosis and the involvement of chlamydial infection at the same site. This report was in concert with Thomas[57] and Gibbs.[19] Combined, these studies seemed to ask: What if Chlamydia pneumoniae was just a passenger bacteria, a friendly bystander? And when, in 1995, MC Sutter’s editorial Lessons For Atherosclerotic Research From Tuberculosis And Peptic Ulcer, warned we might be overlooking the role of a microorganism in atherosclerosis, he did not have chlamydia specifically in mind.[53] Nevertheless, statistics showed that people who used a lot of antibiotics had less heart attacks, and so by 2000 the CDC found that 14% of the cardiologists in Alaska and West Virginia treated heart patients with antibiotics for angina, heart attacks, angioplasty or after by-pass surgery.
And certain antibiotics did seem to work, but the question was their efficacy based upon their anti-Chlamydial activity? Azithromycin, for example has a documented, if moderate activity against certain mycobacteria as well.
Something More conclusive
As the millennium approached, something much more irrefutable was happening. Xu had previously been found that injecting rabbits with normal cholesterol with protein from TB resulted in atherosclerotic changes.[61] Now George and Shoenfeld were implicating these very same proteins in not only the origin of the atherosclerosis in cardiovascular blood vessels but of fatty streak formation there as well.[18] In the meantime, Mukherjee and De Benedictis showed that an increase in antibodies against such tubercular proteins somehow already in the body was actually associated with re-stenosis or future closure of coronary vessels.[37] By 2000, it became obvious to Afek that mice injected with high doses of such tuberculoproteins developed significantly larger areas of atherosclerosis despite the fact that their diet was devoid of high fat content.1 Revisiting this subject, Xu, also using the same tubercular protein (HSP-65), proved the same thing in New Zealand white rabbits.[62] In Xu’s study, such rabbits with normal serum cholesterol injected with the TB preparation led to the formation of all the classic features of arteriosclerosis in humans – the inflammatory cell accumulation and the smooth cell proliferation (ibid) that Livingston and Alexander-Jackson had decades ago attributed to tuberculosis.
In fact, the only finding missing from Xu’s study using normal cholesterolemic animals were “foam cells”: tissue macrophages in which tuberculosis not only lived but thrived in, capable of ingesting material that dissolved during tissue preparation, especially lipids. However, this missing piece of the puzzle was soon remedied when in addition to tuberculous proteins his animals were given a cholesterol rich diet, at which point Xu saw all the lesions found in classic human heart disease, including foam cells. Obviously, tuberculoproteins were overwhelming the systems macrophages, not allowing them to get rid of ingested fat.
Man Thinks – Heaven Laughs
There was also incriminating epidemiologic evidence. The higher incidence of coronary heart disease in young males had a remarkable parallel in bacterial diseases such as TB [52]. And the association between low socioeconomic status and coronary disease found common ground with the incidence of tuberculosis.
The Centers for Disease Control and Prevention (CDC) maps for the total cardiovascular disease and death rates across the country[10] bore a conspicuous similarity to state and regional incidence for CDC TB case rates maps in the United States.9 In addition, the statins, among the most popular drugs in America (Lipitor, Lescol), though inhibitors of Coenzyme-A compound (HMG-CoA or 3-hydroxy-3-methylglutaryl CoA reductase) and as such lowered serum cholesterol levels, did much more.
Specifically, when macrophages were depleted of cholesterol by such pharmacological treatment, mycobacteria such as tuberculosis could not enter the macrophage TB liked to house in, thrive in and depend upon.[17] Furthermore, this block of macrophage uptake with cholesterol depletion was specific only for tuberculosis and the mycobacteria and no other pathogen. In other words, cholesterol played a crucial role in tuberculosis’s establishment of intracellular infection leading both to the long-term survival of the germ and the death of at least1.9 million people a year.
The large British heart protection study took many by surprise when they learned that even lowering “normal” cholesterol levels lowered heart disease risk.[12] This led again to speculation that there must be some other risk factor involved besides cholesterol itself. Lead-author Collins countered that the reason for his study’s finding was that even what we call “normal” cholesterol values are too high, but it is just as easily posited that the lower the blood cholesterol the less likely there is to be chronic mycobacterial infection which would also be of benefit derived from lower than normal cholesterol levels.
It is hardly a coincidence that studies have shown that statins, which indirectly decrease mycobacterial disease, also lower C-reactive protein (CRP). C-reactive protein is an age-old, non-specific protein, first identified in 1930, and then found in the serum of various persons with certain inflammatory and degenerative diseases.[48] Recently an elevated CRP has been touted as an excellent marker for the approximately 25 million US patients that have none of the risk factors associated with heart disease, yet are at risk for a heart attack. However CRP and elevated sedimentation rate have long been excellent markers of active tuberculosis,[22] CRP being present at all times when erythrocyte sedimentation rate (ESR) is elevated but returning to normal faster than ESR as tuberculosis, once treated, becomes inactive. Indeed CRP is a sensitive indicator of the activity of tuberculosis.[5]
Researchers have even tried to neatly tie in excessive weight and its fat cells to indirectly increasing C-reactive protein (CRP) by dumping interleukin-6 (IL-6) into the blood, which, in turn supposedly promotes an inflammatory response, key to signaling the liver, and perhaps the arterial walls themselves, to churn out more CRP. But again, and significantly, higher levels of interleukin-6 are consistently found in either the lung secretions[58] or serum[54] where TB resides. Russell noted sustained release of IL-6 repeatedly issued from human macrophages infected with TB,[49] a defense strategy the microbe uses to possibly create anergic conditions (conditions with lowered immunity) that prevent macrophages from killing them.
Others look towards elevated serum levels of homocysteine, an amino acid also linked as an index of potential heart disease, as the marker of the future even though a homocysteine marker meta-analysis appeared in JAMA, concluding that elevated homocysteine was at most a modest independent predictor of Ischemic Heart Disease (IHD) in healthy populations.[24] Nevertheless homocysteine, it is claimed by some, although not deposited in blood vessel walls like cholesterol, can damage the inside lining of these vessels and make platelets more likely to clot, the scenario which supposedly leads to stroke or heart attacks.
Homocysteine is formed from another amino acid in our diets, methionine. But methionine is also the protein that M. tuberculosis brings systemically into its host to initiate its own protein synthesis.[11] Although Homocysteine can be turned back into methionine and its level lowered in the blood, this requires two essential cofactors: vitamin B12 and “folate” or folic acid, both of which can be lowered in tubercular infection, leading to elevated homocysteine levels.[35,46]
Nieto’s extensive review concludes that the introduction of antibiotic therapies in the 1940s and 1950s could have contributed to the decline of heart disease and heart attacks in the last few decades.[39] Although the tetracyclines appeared in the 1950s it was only after the introduction of the macrolides, in particular erythromycin in the 1960s that the cardiovascular disease mortality curve began to sink. Though it was hypothesized that such decline was the effect of tetracycline and the macrolides against Chlamydia pneumonae, many of the atypical mycobacteria were also sensitive to erythromycin and the tetracycline doxycycline.[36] Also, the antibiotic time-curve Nieto cites excludes the actual introduction of anti-tubercular antibiotics.
Although erythromycin is very effective against C. pneumoniae, the microorganism may persist in the respiratory tract despite adequate blood levels of the antibiotic.[51] There can be no doubt that the availability of antibiotics lowered the morbidity and mortality of cardiovascular disease. Netter mentions that tuberculosis, once often associated with cor pulmonale was less so linked in recent years, probably because of the widespread use of antibiotics and antimicrobial agents.[38]

Conclusion – Runs Silent, Runs Deep
When Nieto stressed the need to extend the possible role of infectious agents beyond the 3 infections which have in recent years been the focus of research: namely, Cytomegalovirus (CMV) C. pneumonia and Helicobactor pylori,[39] was he picking Sir William Osler’s brain regarding that arteriosclerosis was frequently associated with tuberculosis?[42] Still many ridicule the possibility that microbes might be the agents of arteriosclerosis. These were the same minds that in another, far gone era, would have jeered the possibility that syphilis in its late stages had a special preference for the arteries and could cause devastation of major cardiovascular vessels. Eventually though, these minds were proven wrong. But the lessons of syphilis are far-gone ― or are they?
When by 1982, keynote speaker and then Harvard infectious disease guru Louis Weinstein addressed the annual session of the American College of Physicians he mentioned: “We thought initially that the disease (tuberculosis) was disappearing, but we are now seeing up to 27 different syndromes and extrapulmonary forms, etc. It is today’s great mimic, a greater mimic than syphilis ever was.”[60]
In Atherosclerosis and Tuberculosis: Are They Both Chronic Diseases?, after going over the many similarities between tuberculosis and Chlamydia pneumoniae, Anestad focuses on Norwegian 20th century statistics in which two things become obvious. First, that until 1945 tuberculosis was easily the leading cause of infectious death in Norway, surpassing cardiovascular death at the time. Second, that as the diagnosed cases of tuberculosis fell from his statistics, cardiovascular disease increased dramatically until 1975, when its stats too somewhat tapered.[3] At first glance, these statistics seem unrelated even though they are on the same bar graph. But are they? Or are we just looking at another example of Weinstein’s reference to occult TB finding an expanded niche in the cardiovascular system in one of its quests to become “a greater mimic than syphilis ever was”?
In Tuberculosis In Disguise, Rab and Rahman document cases of congestive heart failure and IHD (Ischemic Heart Disease) with chest pain, raised erythocyte sedimentation rate, leukocytosis and inverted T-waves across the chest leads otherwise indistinguishable from the real thing, which turned out to be miliary (systemic) tuberculosis.[47] Rab and Rahman again warned “confusion may occur because tuberculosis can mimic so many other conditions.”
Certainly with tuberculosis and for some time now, we have a human population affected that dwarfs syphilis in its prime. At least a staggering 1.7 million around the globe die of tuberculosis each year, while another 1.9 billion are infected with M. tuberculosis and are at risk for active disease.[14] The World Health Organization (WHO) estimates that 1/3 of the planet has contracted TB.
It would take such a disease to adequately explain the scope of cardiovascular disease, which affects about 61 million people, or almost one-forth of the population in the US alone. Almost 6 million US hospitalizations each year are due to cardiovascular disease. (www.cdc.gov/nccdphp/aag/aag_cvd.htm)
The linkage of tuberculosis to acute myocardial infarction and resulting heart attacks is nothing new; [16,30,55] yet serious clinical trials have never been undertaken. And one is left wondering whether the present flurry of trials designed to simply label the markers in the blood that TB and the mycobacteria throw our way is ever really going to quell the near epidemic cardiovascular disease that is presently in our midst.

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