Published August 13, 2016
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The New York Times reports on a new study finding that the greatest risk to infants of being infected with the bacteria that causes whooping cough, or pertussis, now comes from their older siblings. The Times explains that this is “probably a result of waning immunity among children and adolescents who had received the DTaP vaccine.”
Indeed, waning immunity is a serious problem with the DTaP combination vaccine (which contains diptheria, tetanus, and pertussis antigens). One recent study published in Pediatrics concluded, “Tdap protection wanes within 2 to 4 years. Lack of long-term protection after vaccination is likely contributing to increases in pertussis among adolescents.”
But the Times is misleading its readers by telling only one part of the story, leaving readers with the impression that simply giving more “booster” shots would solve the problem.
Waning immunity by itself doesn’t explain the trend described. As another recent study in the journal Clinical Infectious Diseases points out, “pertussis is currently the least well-controlled vaccine-preventable disease despite excellent vaccination coverage and 6 vaccines doses recommended between 2 months of age and adolescence” (emphasis added).
Undervaccination is hardly the problem.
One critical piece of information the Times doesn’t indulge its readers with is that the vaccine does not prevent transmission of the disease. Instead, vaccinated individuals may become asymptomatic carriers.
A study conducted by the FDA and published in PNAS found that vaccinated baboons “were protected from severe pertussis-associated symptoms but not from colonization, did not clear the infection faster than naive animals, and readily transmitted B. pertussis to unvaccinated contacts.”
The researchers reasoned that this was due to the differences between the kind of immunity conferred by natural infection and that conferred by the vaccine. Natural infection confers a robust cell-mediated immunity that vaccination actually preventsby favoring humoral immunity, which is to say the vaccine stimulates the production of antibodies but not the “memory” cells required for robust and long-lasting immunity.
As the FDA summarized in a press release, their findings suggested that “although individuals immunized [sic] with an acellular pertussis vaccine may be protected from disease, they may still become infected with the bacteria without always getting sick and are able to spread infection to others, including young infants.”
The director of the FDA’s Center for Biologics Evaluation and Research, where the study was conducted, described it as “critically important to understanding some of the reasons for the rising rates of pertussis”.
The New York Times, incidentally, did at the time report the findings of the FDA study that “people recently vaccinated may be continuing to spread the infection without getting sick.” It quoted the lead author of the study explaining, “When you’re newly vaccinated you are an asymptomatic carrier, which is good for you, but not for the population.”
That is the opposite of what parents are typically told about the need for vaccinations, that the “herd” needs to be vaccinated to protect those too young to receive the vaccine: infants. In fact, the logical conclusion of this finding is that parents who vaccinate a child who has an infant sibling are putting the infant at risk.
And it is infants, not older children, who are most at risk of developing serious complications from the disease.
Needless to say, that risk is not something parents are routinely informed of during visits to their pediatrician’s office (or by the media, as the Times so aptly demonstrates in this example).
But that’s not all. There is another risk of vaccination that parents are not being told.
The widespread use of the pertussis vaccine seems to have resulted in natural selection (or unnatural selection, rather) of strains of the bacteria that not only are more resistant to vaccination, but actually favors vaccinated individuals.
Just as the overuse of antibiotics has led to the alarming rise of antibiotic-resistant “superbugs”, so can vaccines put pressure on viruses and bacteria to select for resistant and potentially more virulent strains.
In the case of pertussis, the CDC has internally noted that “the recent resurgence in pertussis cases has been associated with waning immunity over time in persons who received the acellular pertussis vaccine”, but that (bold emphasis added)
a recent study suggests another explanation for decreased vaccine effectiveness: an increase in Bordetella pertussis isolates that lack pertactin (PRN)–a key antigen component of the acellular pertussis vaccine. A study that screened B. pertussis strains isolated between 1935 and 2012 for gene insertions that prevent production of PRN found significant increases in PRN-deficient isolates throughout the United States. The earliest PRN-deficient strain was isolated in 1994; by 2012, the percentage of PRN-deficient isolates was more than 50%.
CDC researchers examined data from epidemics in Washington and Vermont. Here’s what they found:
Findings indicated that 85% of the isolates were PRN-deficient and vaccinated patients had significantly higher odds than unvaccinated patients of being infected with PRN-deficient strains. Moreover, when patients with up-to-date DTaP vaccinations were compared to unvaccinated patients, the odds of being infected with PRN-deficient strains increased, suggesting that PRN- bacteria may have a selective advantage in infecting DTaP-vaccinated persons.
So, to sum up:
A) The pertussis vaccine doesn’t prevent transmission of the disease (and in fact may increase transmission since vaccinated individuals are likely to be asymptomatic and hence no precautions not to expose infants in the family will be taken).
B) Most B. pertussis strains now in circulation in the US are PRN-deficient.
C) Vaccinated individuals are at a higher risk of infection from PRN-deficient strains than unvaccinated individuals.
The corollary sees inescapable that now–ironically thanks to public vaccine policy–vaccinating children for pertussis not only places any infants in the family at risk of getting the disease, but also places at greater risk the vaccinated children themselves.
A subsequent study in Clinical Infectious Diseases looked at data from eight states and found that, overall, 85% of pertussis isolates were PRN-deficient, with a range from 67% in Colorado to 100% in New Mexico.
Moreover, vaccinated individuals were found to have “a significantly higher odds” of having PRN-deficient B. pertussis than unvaccinated individuals.
And by “significantly”, they meant that vaccinated individuals were more than twice as likely to be infected as the unvaccinated. In fact, they found that fully vaccinated case patients had “a 2- to 4-fold greater odds” of having PRN-deficient B. pertussis than the unvaccinated.
Without explicitly pinpointing public vaccine policy as the catalyst, they note the appearance of “a selective advantage to lacking the protein” for the bacteria.
Of course, one would think that such findings might call into question public vaccine policy. But an institutional myopia exists such that questioning public policy is out of the question. The FDA study finding that pertussis vaccines do not prevent transmission of the disease, for example, concluded that the solution was “the development of improved vaccines”.
The simple notion that the human body was designed naturally to have an immune system capable of fending off infectious diseases and that we ought to focus therefore on ways to build up natural immunity, such as through proper nutrition, is practically anathema to the theory underlying public vaccine policy (not to mention the mega-profits for the pharmaceutical companies who have been granted legal immunity by the federal government from damages caused by their vaccine products).
At the very least, parents ought to be properly informed by the media, public health officials, and their pediatricians. But getting even that modicum of sensibility to be widely practiced will no doubt certainly be a long, arduous road for advocates of informed consent.
Note: This article was reprinted with the author’s permission. It was originally published on Jeremy Hammond’s blog at www.jeremyrhammond.com.