Vaccinating pregnant women “halves the risk of pertussis in infants’ first four months” ~ A critique by Dr Suzanne Humphries
The latest propaganda hitting the provaccine press today involves the results of a retrospective study conducted through channels at the University of Sydney, NSW Australia. Click to see the conference poster HERE .
The headlines in the press include “Whooping cough jabs for mum protect baby”, “Protecting babies against pertussis: pregnant moms and caretakers need the vaccine”, “Whooping cough vaccine advised for pregnant women”, “pertussis immunization before pregnancy halves risk.” The title of “halving risk” comes from a medical organization called the Australasian Society for Infectious Diseases. They made a statement that is not in the poster by Dr Quinn, and stated :
Importantly, 14% of case mothers and 26% of control mothers were vaccinated before delivery, most within 2 years but up to 6 years previously.
A most interesting statement given that such data is not mentioned in the cited poster, so it must be unpublished at present, and moreover that counting up to 6 years is irrational because vaccine stimulated immunity is known to wane rapidly even in children who have had 5 doses of acellular vaccine. If a child who has had numerous vaccines in succession does not have long lasting immunity, then what kind of response would a pregnant woman who has not seen a DTaP vaccine in over a decade or more, have—after six years? It is well accepted that protection against pertussis is less than optimal even with regular booster doses.
In a more precise and well-designed study reported in 2013 by Heininger et al., where cord blood antibodies were measured they found no statisticially significant correlation between antibody levels and actual protection from the disease:
Our analyses of anti-PT, anti-FHA, and anti-pertactin IgG serum antibody levels in cord blood specimens from infants who acquired pertussis in their first few months of life compared to those in control infants did not reveal statistically significant differences.
Heinenger et al. also note another limitation of even their more scientific study and that is that pertussis exposure is not controlled or known to be equal between cases and controls:
Assuming that serological correlates of protection do exist, antibody levels in some control infants may have been below that threshold and yet because of lack of exposure to B. pertussis they may not have acquired pertussis disease.
Heinenger et al. admit that little is known about what actually conveys immunity,and that it may not be relevant to antibody but cell-mediated immunity must come into play, but that measuring for it is a limited science:
Although cell-mediated immunity and non-specific mechanisms have been intensively studied in murine models of B.pertussis infections and cell-mediated responses can be elicited in young infants, the relative role of antibodies, cell-mediated immunity and innate immune mechanisms for protection or susceptibility to pertussis in humans remain unclear.
Yet their conclusion betrays the known science on pertussis vaccination:
Clinical protection against Pertussis, however, can be achieved by immunization.
Which begs the question of why so many cases are vaccinated . . .
The truth is that there is little if any scientific support for the pro-vaccine media interpretations of Quinn at al. or that vaccination has ever, or will ever, convey herd immunity or protection to infants.
The REPORT  under discussion by Quinn et al., involving 217 cases and 585 matched controls makes three points:
1) 152 of 203 (75%) case mothers and 425 of 550 (77%) control mothers reported receipt of dTpa. This is not much of a difference is it? But it is noteworthy that 14 cases and 35 controls disappeared from the analysis. The inclusion of these infants could significantly alter the results in favor of not vaccinating.
2) 47 of 193 (24%) case mothers and 189 of 507 (37%) control mothers were vaccinated at least 4 weeks before the onset of pertussis in the index infant. First off, vaccinating the mother four weeks prior to the onset of pertussis in the index infant would have no bearing on the susceptibility of the infant even if the vaccine did “work.” The vaccine takes time to effect the mother’s immune system, presumably at least 1-2 weeks and the incubation time for pertussis prior to symptoms is four weeks. Therefore the analysis, if talking about vaccinating very pregnant, near-term mothers, should have been calculated using a minimum of 6 weeks, not four weeks prior to the onset of symptoms in the infant. Second, the message in these numbers is that more of the control (uninfected infant) mothers received vaccines, 37% vs 24% of the case mothers. This is the statistic that the news broadcasts rests upon, and the one that requires much more explanation and reanalysis.
In addition the practice of vaccinating pregnant women uses an assumption of effectiveness but has never been shown to actually be of significant benefit:
. . . the concept of immunizing pregnant women against pertussis has been developed and recently recommended in the United States. This concept is based on the ASSUMPTION [emphasis mine] that transplacental antibody transfer to infants will lead to direct protection in addition to indirect protection by the so called cocoon strategy, where future close contacts of young infants are immunized before or shortly after birth of the newborns to reduce their the risk of exposure to B. pertussis. Therefore, further studies are necessary to better define whether transplacentally acquired anti pertussis antibodies do protect infants or not.
3) Households of cases were more likely to contain other children (81% vs 62%, p<0.001). The vaccine enthusiasts will use this as support for adding boosters to household contacts prior to the newborn’s arrival. But this plan, sometimes referred to as “cocooning” has failed  and will never work, no matter how many boosters are given to household contacts. That is because booster “immunity” is short-lived, and because of the issue of original antigenic sin which makes the vaccinated more susceptible to infection and longer asymptomatic carriage than the naturally immune. This is a well defined fact that is readily available in conventional medical literature.
Original Antigenic Sin
The concept of original antigenic sin was coined by Dr. Thomas Francis who became well known during the Salk vaccine era, when he oversaw and interpreted the results of the largest (and most controversial) vaccine trial in history. He explained the phenomenon of original antigenic sin using influenza as an example.
Since a vaccine creates different immunologic response pathways than natural immunity, the body will act according to how it was programmed by the vaccine. The body still sees the invader, but immunity doesn’t work against that invader the same way it would naturally, if it was first vaccinated, and that is what is meant by “original antigenic sin (OAS).”
When it comes to B. pertussis, OAS is very important and well described. B. pertussis secretes several toxins, one of which only emerges after the infection takes place. That is called adenylate cyclase toxin (ACT). Here’s how ACT works: Once whooping cough bacteria attaches to cells in the bronchi, a gene in the bacteria switches on and as a result, ACT toxin which acts like a force-field against the immune system, is produced. ACT stops the immune system from recognizing the bacteria and gives the bacteria about a two week advantage until the immune system wakes up to the fact it has been duped. In the case of natural whooping cough immunity, ACT or adenylate cyclase toxin forms the basis of the initial immune response. That front-line immune response is not only critical for eliminating the first round of pertussis bacteria, but also crucial for removing the bacteria upon later reinfection. And remember that whether or not one is vaccinated, they still become colonized when the bacteria is circulating. The difference will be that the vaccinated person will stay colonized longer and be more likely to develop some degree of cough, which is how pertussis is spread.
In natural immunity the body reacts very strongly to ACT, but because of original antigenic sin, and the absence of ACT in the vaccine, the vaccinated are not programmed to respond at all to it. Vaccines do not boost antibody to this toxin because as of yet, nobody has figured how to put that antigen into the vaccine. The naturally convalesced have over 17 times the amount of antibody to ACT than DTaP recipients have, and more than 9 times what DTP vaccinated have as measured after pertussis infection. There is only a miniscule level of ACT antibody in the vaccinated, which is the result of their immune system’s paralyzed effort to mount a response after programming by the vaccine.
When a vaccinated person contacts pertussis again, the bacteria can get a good hold, because there is little to stop it from doing so. The immune system will not respond to ACT in the future, because the program has been set by the first contact which was the needle, not the bacteria. Dr. Cherry admitted as much in his paper in 2010, when he said:
Of particular interest is the lack of a significant ACT antibody response in children for whom the DTP or DTaP vaccines failed. This induced tolerance is intriguing and may be due to the phenomenon called ‘original antigenic sin.’ 
Since then the term original antigenic sin has been abandoned. One can only surmise why. The new terminology, which points to the exact same problem, is “linked epitope suppression.”
In a previous study, it was observed that children who were DTaP vaccine failures had a blunted antibody response to the nonvaccine antigen ACT, whereas unvaccinated children with pertussis had a vigorous antibody response to this antigen . . . Linked epitope suppression applies as the immune response to the new epitopes is suppressed by the strong response to the original vaccine components. 
This was later affirmed by another doctor in the Journal of the American Medical Association.
The lesser protection provided by DTaP, both as the initial vaccine or full primary course, may be due to linked epitope suppression, when the initial exposure locks in the immune response to certain epitopes and inhibits response to other linked epitopes on subsequent exposures. 
The reason immunologists and vaccine scientists don’t talk about “original antigenic sin” is because if they had to explain to the public just what that meant in principle and in practical fact, they’d have to explain that vaccination breaches a fundamental immunological tenet. Not only would they have to admit that whooping cough vaccine immunity is vastly inferior, but that vaccine immunity has immunologic unintended consequences in the future. As an aside, OAS is also a factor in morbidity of the influenza vaccinated when H1N1 infection arrived.
The other reason ACT is important is that it is also a component to parapertussis. If you have recovered naturally from B. pertussis then you have high levels of ACT immunity that not only protect you from B. pertussis but also would be active against B. parapertussis, and of course, you won’t get that from a vaccine.
The researchers are on track with desiring immunity in mothers, but the way they are going about it is all wrong. It is true that maternal protection is important, both via transplacental and breast milk immunity. This type of immunity protects infants for up to two years, and certainly for the most vulnerable first six months of life, but not in the post vaccine era because the short lived pseudo immunity of vaccines destroyed the true herd immunity that once protected newborn infants. Mortality for pertussis was declining steadily and was nearly non-existent by the late pre- vaccine era. In the prevaccine era, mothers were immune because of their natural infection in the past and their natural boosters recieved from exposure to infected children. They were immune to ACT and PT as well as several other elements of the tricky pertussis bacterium. Today the only solution, in the age of vaccination is to vaccinate from cradle to grave. The net result of this is vaccine resistant mutant bacteria, and shift in the age of susceptibles.
According to Levine et al.:
We consider the immunologically relevant, yet epidemiologically largely neglected, possibility that a primed immune system can respond to a lower dose of antigen than a naive one. We hypothesize that during the prevaccine era teenagers’ and adults’ primed immunity was frequently boosted by reexposure, so maintaining herd immunity in the face of potentially eroding individual immunity. In contrast, low pathogen circulation in the current era, except during epidemic outbreaks, allows immunity to be lost before reexposure occurs.
The reason for the perceived need to vaccinate mothers is BECAUSE they have lost their vaccine-induced pseudoimmunity, BECAUSE they were vaccinated.
Whooping cough reports are now increasing despite very high vaccination rates. In fact the rates today are even higher than they were when vaccine uptake was much lower. Why do you suppose that is? How many whooping cough shots did children get when you were growing up? Now, we are supposed to accept the idea of “lifespan vaccination” where whooping cough vaccines are pretty much a regular event, cradle to grave, yet the incidence of clinical whooping cough today—in the most heavily-vaccinated populations, is increasing, inciting panic where the drug-sponsored media ramps up unnecessary fear, or in the case of today’s University of NSW announcement, misleading and deceptive pseudoscience.
Because of such unscientific and dangerous recommendations, meaning more vaccines for everyone, the future could bring a continuous evolution of vaccine-resistant strains, which will no doubt lead to a perceived need for newer pertussis vaccines. In fact, the development of live inhaled pertussis vaccines for newborns has already occurred. You would think that one live intra-nasal vaccine to a newborn would be enough to impart long-term immunity. But apparently it isn’t. This new vaccine is going to be added to the already dysfunctional pertussis vaccination program.
The reason that the live intra-nasal vaccines can’t be enough to provide herd immunity, even if they were competent at providing full-spectrum long-term immunity, has to do with how the rest of the population has been programmed with vaccines—committing original antigenic sin.
Given that booster shots don’t increase the bactericidal qualities in the blood, and do contribute to bacterial resistance, why even recommend them? Until those DTaP-vaccinated adolescents and adults die, they will be the main source of carriage and spread in the community, whether a safe, live, effective vaccine is put to broad use or not.
There’s still another problem with pertussis vaccines and that is that the vaccines themselves are now a source of false positive pertussis PCR tests. How do you think this complicates the doctor’s task and how is it affecting humanity overall, given the rampant and unnecessary use of potentially dangerous antibiotics to all cases that test positive?
If vitamin C in adequate doses was given to children and even newborn infants with pertussis, the reputation of B. pertussis as the devastating 100 day cough would fade into infamy. Parents would also be less likely to fall victim to pressure by the medical system’s acceptance of a vaccine that imparts only short-lived and partial protection, and has in effect made newborn infants more vulnerable. And who would benefit from that? Certainly more vaccines for everyone is much more lucrative for the influential pharmaceutical companies, who by the way could not exist without doctors and universities to conduct the research, and without governments that draft the rules on vaccination. If you think these are the words of a nutty conspiracy theorist, read THIS. 
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2. Klein NP, Bartlett J, Rowhani-Rahbar A, Fireman B, Baxter R. Waning protection after fifth dose of acellular pertussis vaccine in children. N Engl J Med. 2012;367:1012-1019.
3. Witt MA, Katz PH, Witt DJ. Unexpectedly limited durability of immunity following
acellular pertussis vaccination in preadolescents in a North American outbreak. Clin
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5. Ibid Heininger.
6. Francis T., “On the doctrine of original antigenic sin,” Proceedings of the American Philosophical Society, vol. 104, no. 6 (Dec. 15, 1960), pp.572-578.
7. Cherry JD et al., “Determination of serum antibody to Bordetella pertussis anenylate cyclase toxin in vaccinated and unvaccinated children and in children and adults with pertussis,” Clinical Infectious Diseases, February 2004, vol. 15, no. 4, pp. 502-5073.
8. Ibid., Cherry JD et al. Determination of serum antibody .
9. Cherry JD et al., “Antibody response patterns to Bordetella pertussis antigens in vaccinated (primed) and unvaccinated (unprimed) young chidren with pertussis,” Clinical and Vaccine Immunology, May 2010, vol. 17, no. 5, pp. 741-747.
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11. Rosella LC., “Assessing the impact of confounding (measured and unmeasured) in a case-control study to examine the increased risk of pandemic A/H1N1 associated with receipt of the 2008-9 seasonal influenza vaccine,” Vaccine, November 15 2011, vol. 29, no. 49, pp. 9194-9200.
12. Bodewes R et al., “Annual vaccination against influenza virus hampers development of virus-specific CD8 T cell immunity in children,” Journal of Virology, November 2011, vol. 85, no. 22, pp. 11995-12000.
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14. Octavia et al., Newly emerging clones of Bordetella pertussis carrying prn2 and ptxP3 alleles implicated in Australian pertussis epidemic in 2008-2010, Journal of Infectious Diseases, April 15 2012, vol. 205, no. 8, pp. 1220-1244.
15. Lavine JS, King AA, Bjørnstad ON. Natural immune boosting in pertussis dynamics and the potential for long-term vaccine failure.Proc Natl Acad Sci U S A. 2011 Apr 26;108(17):7259-64. Epub 2011 Mar 21.
16. Cornford-Nairns, R., “Construction and Preliminary Immunobiological Characterization of a Novel, Non-Reverting, Intranasal Live Attenuated Whooping Cough Vaccine Candidate,” Journal of Microbiology and Biotechnology, 2012, vol. 22, no. 6, pp. 856–865.
17.Hossein et al., “Aerosolized vaccine as an unexpected source of false-positive Bordetella pertussis PCR results,” Journal of Clinical Microbiology, February 2012, vol. 50, no. 2, pp. 472-474.
by Louise Kuo Habakus and Mary Holland J.D.
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