In another forum, I shared the following. I’m publishing it here to have a shareable source. For the short and sweet version, check here.
Weekly Topic 03: Meningococcal Vaccine (Meningitis)
What are the “meningitis vaccines”?
There are two basic types of meningitis: viral and bacterial. There are no vaccines targeting viral meningitis. There are three vaccines targeting causes of bacterial meningitis: HiB, pneumococcal, and meningococcal. Meningococcal will be discussed here and the others in future Weekly Topics. According to the CDC Vaccination Schedule (2015), the meningococcal vaccine is given at 11-12 years and again at 16-18 years . In Canada, depending on province/territory, meningococcal vaccines may be given in infancy, in grade school, and/or in high school .
What is meningococcus?
Neisseria meningitidis, the meningococcal bacteria, is passed by coughing or contact with saliva and is normally present in the respiratory tracts of healthy people without causing disease [3, 4, 5]. In fact, probably no one escapes infection. Symptomatic disease is quite rare for N. meningitidis. As such, 100% of the population, vaccinated or not, are asymptomatic carriers at some point in their lives. In fact, at any time, 5-35% of the population is silently carrying the bacteria, though the numbers often rise to nearly 100% in close quarters, such as military barracks and college campuses . (However, despite the widespread rate of infection on college campuses, the CDC states, “Overall incidence [of meningococcal disease] among college students usually is similar to or somewhat lower than that observed among persons in the general population of similar age.”  On the other hand, the rate among college students is 3.2/100,000 for those living in dormitories versus 1.0/100,000 for those living off-campus .) Asymptomatic carriers carry the bacteria for many months at a time, sometimes for years, and are contagious [4, 5].
There are two basic types of N. meningitidis, capsular bacteria (which have serogroups and are considered pathogenic, meaning they can cause disease) and noncapsular bacteria (which do not have serogroups and are considered nonpathogenic, meaning they cannot cause disease). About one third of carriers are infected with a type that is considered nonpathogenic . The most common serogroups today are B (targeted by one vaccine) and A, C, Y, and W-135 (targeted by another vaccine). Serogroup B is now responsible for 60% of U.S. cases of meningococcal disease . Natural infection with one serogroup confers immunity against all serogroups [4, 5]. Though it’s not fully understood why at this time, natural infection with another similar nonpathogenic species, N. lactamica, also confers immunity to all serogroups of N. meningitidis [8, 9]. It’s quite rare for an unvaccinated individual to be infected with one serogroup and then later become infected with a different serogroup .
According to the CDC (2013), “For unknown reasons, incidence has declined since the peak of disease in the late 1990s, and approximately 800–1,200 cases are reported annually in the United States. This decline began before implementation of routine use of meningococcal vaccines in adolescents and have occurred in all serogroups.”  However, their estimated number of cases is not supported by their own more recent data, which found 386 (2014), 556 (2013), 551 (2012), 759 (2011), and 980 (2010) cases for a 5-year average of 646 cases per year . In the U.S. last year (2014), there were a total of 386 meningococcal disease cases and estimated 39-58 deaths (given the CDC’s estimated case fatality rate of 10-15%) [10, 11].
Meningococcal disease occurs more frequently in the winter and studies have found that the sickest children with meningococcal meningitis are those with extremely low vitamin C levels. This gives us a hint as to why some children are completely unaffected by the bacteria, which live harmlessly in their noses and throats, while others are susceptible to meningitis—namely, that their immune systems are better equipped to fight the bacteria. Factors which make a child or adult susceptible to meningococcal meningitis may include: tonsillectomies (tonsils are immune system glands in the throat), antibiotic use, poor diet, low vitamin C, smoking, recent viral infection, immune depression (such as by over-vaccination, use of acetaminophen/paracetamol, antihistamines, and antibiotics), and lack of exercise. [3, 5, 12] Natural techniques for prevention and healing include adequate rest, good nutrition, fresh air, not sharing anything that might be tainted with saliva (e.g., food, drinks, eating utensils, towels, lipstick, etc.), frequent hand-washing, gargling or washing the nasal passages with colloidal silver or with a Lugol’s solution and a netty pot, increased vitamin C intake (3-6 G/day for an adolescent/adult), and increased vitamin D intake. In the case of a known exposure, antibiotics (along with a probiotic) may be prudent .
How does meningococcus evolve in response to vaccination?
The most common serogroups were once A, C, Y, and W-135, and the first vaccines targeted all four of these serogroups or C alone. However, serogroup B then became the most common serogroup, and so a new vaccine specifically targeting serogroup B was added. Given the microevolutionary history of other vaccine-targeted species, it would not come as a surprise to find a new serogroup not targeted by the vaccine appear in the near future.
Unfortunately, what we find with most vaccines is that the strains not covered by the vaccine are the more dangerous strains, and they become more common when the covered strains are selectively reduced. If there is no vaccine, children are typically infected by the most common strains, which are generally less dangerous and therefore give them immunity against all strains with lower associated risk.  (Examples: pneumococcus and HiB, which will be covered in future Weekly Topics.) However, when the more dangerous strain becomes the most common, cases in both vaccinated and unvaccinated are more likely (but in the vaccinated, most likely) to be caused by the dangerous strains not covered by the vaccine.
Dr. Tenpenny also addresses this issue. She explains that the vaccine doesn’t just increase other more dangerous strains that were kept in control by a high quantity of the less dangerous strains, but that some vaccines increase other species by eliminating ones that kept them in control. She explains that was the case with HiB, where the vaccine resulted in an increase in pneumococcal bacteria, hence a pneumococcal vaccine, which resulted in an increase in meningococcal bacteria, hence a meningococcal vaccine.  Time will tell what species comes next.
How effective are the vaccines at preventing asymptomatic carriage?
One study suggested that vaccination against serogroups A, C, Y, and W-135 may reduce the length of (but not eliminate) asymptomatic carriage . However, the vaccine against serogroup B does not prevent asymptomatic carriage [3, 14]. Thus, the vaccines should not be relied upon for herd immunity.
How effective are the vaccines at preventing disease?
As discussed above, natural infection with one serogroup or with a similar species confers immunity against all serogroups; however, vaccination only provides potential protection against the serogroups included in the vaccine [4, 5]. It’s said to be 85% effective against the serogroup(s) included in the vaccine . However, whether the vaccine actually protects against the serogroup(s) in question has not yet been proven. In fact, the first vaccine against serogroup B, Bexsero, was rejected by the U.K. because the efficacy studies demonstrated only that children developed quickly waning antibodies, not that it protected against disease, and, though accepted by the U.K. government, the same issue existed with the serogroup C vaccine [7, 16]. In fact, one country’s post-vaccine review found an increased risk of meningococcal disease following vaccination .
How does this happen? The term “original antigenic sin” describes a phenomenon wherein vaccination against one strain or serogroup trains the body to respond only to the antigens in the vaccine strain/serogroup, thereby handicapping the body’s immune response to different but related strains or species, which have some familiar and some unfamiliar antigens . This may be why the vaccine may increase rather than decrease the risk of meningococcal disease , as mentioned above, and why there are VAERS reports of college students developing bacterial meningitis within weeks of getting the vaccine .
Furthermore, as discussed above, it’s quite rare for an unvaccinated individual to be infected with one serogroup and then later become infected with a different serogroup . However, in the presence of vaccination, N. meningitidis can and does first infect the vaccinated individual and then change its own serogroup within a few days to one against which the vaccine offered no protection and thereby cause disease in and even kill the vaccinated individual . This possibility was highlighted in a case report published in the New England Journal of Medicine, in which they concluded, “The rapidity of the serogroup switching arouses concern about the induction of herd immunity against single serogroups by vaccination programs in which capsular antigens (e.g., serogroup C polysaccharides) are used. Without lowering the incidence of meningococcal disease in the long run, such programs may rapidly increase the incidence of serogroup B meningococcal disease, for which no vaccine is available.”  Although a serogroup B vaccine is now available, the same rule would apply to any other or any new serogroups in the future—namely, that the bacteria can and will simply change serogroup after infecting the vaccinated individual to one against which the vaccinated individual has no protection, making vaccination essentially of no effect.
So if there’s no proof that the vaccine actually prevents disease, does it at least result in an antibody response?
Many, perhaps a majority, of those vaccinated don’t develop an appropriate antibody response to the vaccine. In one study of infants given four doses of the vaccine at 6 wks, 3 mo, 5 mo, and 10 mo, about half did not develop an appropriate antibody response following the third dose, while 87% did not respond following the fourth dose . In fact, the New Zealand Ministry of Health found that children had an **increased** risk of meningococcal disease following the third dose and responded by adding a fourth dose, ostensibly hoping this would reduce the risk but with no evidence to that effect .
Furthermore, the antibodies produced in response to meningococcal vaccination wane very quickly. According to the lead author of the MenZB (New Zealand’s serogroup B vaccine) studies, it resulted in less than 7 months of “protection” as determined by antibody levels .
New Zealand utilized fearmongering to introduce meningococcal vaccination, where the “informed consent” for the “MenZB” meningococcal vaccine included a photo of a dying child.  However, following the four-year vaccination campaign, the New Zealand Herald reported that there were 109 cases of the vaccine-covered strain of meningococcal bacteria in vaccinated people, with 60 partially and 49 fully vaccinated. The consent failed to mention that the immunity fell below protective levels within months, as discussed above, and “officials were determined to conceal anything that might cause unease.” For 2006, 2007, and 2008, there were 12 meningococcal deaths, and all were in vaccinated children. There were no meningococcal deaths in unvaccinated children. Furthermore, the total meningococcal death rate was steadily declining prior to the introduction of the vaccine, but shot upward during the vaccination campaign. [14, 20] Yet in spite of this, health officials claimed they were scrapping the vaccination campaign because the vaccine had successfully ended the epidemic .
Is the vaccine safe?
The short version is a resounding no. The group at highest risk of developing meningococcal disease is infants, due to immature immune systems, followed by college students, due to crowded housing . However, the number of expected deaths from meningococcal disease in all age groups per year in the U.S. is significantly outnumbered by the expected number of deaths due to meningococcal vaccination of U.S. college students, assuming an 85% efficacy rate (and, as mentioned above, there’s no evidence to support an alleged 85% efficacy rate).
As mentioned above, there were a total of 386 meningococcal disease cases in all age groups last year (2014) for the entire U.S. and estimated 39-58 deaths (given the CDC’s estimated case fatality rate of 10-15%) [10, 11]. If both a vaccine for A, C, Y, and W-135 and a vaccine for B is administered to every Colorado college student, judging by the package inserts’ estimated serious adverse event rate of 1% (A, C, Y, and W-135) and 2% (B), and the CDC Pink Book’s estimated rate of death secondary to serious adverse events from meningococcal vaccination of 0.3%, we can anticipate 12,000 serious adverse events and 36 deaths due to the vaccines among the approximately 400,000 college students in Colorado alone [11, 15]. In fall of 2015, the anticipated college enrollment for the entire U.S. is 20.2 million students . That correlates to an estimation of 202,000 serious adverse events and 606 deaths from A, C, Y, and W-135 vaccination and 404,000 serious adverse events and 1,212 deaths from B vaccination, for a total of 606,000 serious adverse events and 1,818 deaths from meningococcal vaccination of all U.S. college students as compared to 386 meningococcal cases and an estimated 39-58 deaths of all U.S. residents in all age groups. That’s assuming each student has only one of each vaccine per year, although it properly involves a 2- to 4-dose priming series  and, given the short duration (less than 7 months) of presumed “protective” antibody levels after vaccination, as discussed above, should actually involve biannual boosters.
So if there’s no evidence of efficacy or safety, why was meningococcal vaccination pushed? And why does the U.S. recommend it for adolescents rather than for the highest risk category, infants?
A meningococcal vaccine targeting A, C, Y, and W-135 serogroups was first introduced in the U.S. in 1981, but wasn’t considered for government coverage until 2004. (The U.S. government buys and distributes over half of all vaccines in the U.S., so government coverage is critical for widespread use of a vaccine.) At that time, it was known not to be cost effective due to the extremely rare incidence of meningococcal meningitis and high cost of the vaccine, to say nothing of its effectiveness or safety. However, teens were rarely vaccinated with the recommended adolescent vaccines, so it was suggested that parents might be more willing to get their teens vaccinated in general if they could be frightened into accepting the meningococcal vaccine: “Frightening parents about the consequences of failing to vaccinate their children will most likely be part of the campaign. For that task, meningococcal meningitis is ideal.” 
In New Zealand, it was pushed for manifold corrupt reasons, as uncovered by a pair of investigative journalists .
Are the meningococcal vaccines linked to autoimmune diseases?
Meningococcal serogroup C or A, C, Y, and W-135 vaccines have been linked to two autoimmune diseases, Henoch-Schönlein purpura and bullous phemigoid, and tentatively linked to a third autoimmune disease, Guillain-Barré Syndrome .
The serogroup B antigens are “autoantigens,” meaning they are very similar to structures on human cells. Although natural infection with meningococcal serogroup B does not result in autoimmunity, meaning that the body does not react to the autoantigens on the bacteria but rather reacts only to the bacterium-specific antigens, vaccine adjuvants force the immune system to react to the antigens included in the vaccine. For this reason, the human body may mistake “self” structures for autoantigens included in the vaccine and begin attacking itself. This is the basis of autoimmune diseases and one reason why vaccines cause autoimmune diseases, though it may take anywhere from days to years for the self-inflicted damage to become so severe that symptoms develop. Aware of this issue, serogroup B vaccine theorists and developers have discussed the risk of MenB vaccines causing autoimmune diseases, specifically autoimmune diseases of the central nervous system (brain and spinal cord) because sugar sequences on the surface of the bacterial capsule are very similar to sugar sequences on human brain and nerve cells. For this reason, current MenB vaccines generally use subcapsular antigens (i.e., antigens that appear inside the capsule rather than on its surface). However, MenB vaccines are too new and relatively untested (having been fast-tracked through the FDA approval process and similar approval processes in other countries) for us to know at this time whether it is associated with the development of autoimmune diseases [7, 8, 9, 26].
What vaccines are offered against meningococcus?
(NOTE: These ingredients lists are not complete; they only list the most alarming ingredients.)
In the U.S., the A/C/Y/W-135 meningococcal vaccines are
- Menomune by Sanofi (contains antigens from serogroups A, C, Y, and W-135; casein [a milk protein]; lactose; and 25 mcg thimerosal [27, 28])
- Menactra by Sanofi (contains antigens from serogroups A, C, Y, and W-135; diphtheria toxoid; casein; 2.66 mcg formaldehyde; and ammonium sulfate )
- Menveo by Novartis (contains antigens from serogroups A, C, Y, and W-135; diphtheria toxoid; 0.3 mcg formaldehyde; amino acids; and yeast )
In the U.S., the B serogroup meningococcal vaccines are
- Bexsero by Novartis (contains antigens from serogroup B; 1.5 mg aluminum hydroxide; histidine; sucrose; 0.01 mcg kanamycin; and E. coli )
- Trumenba by Pfizer (contains antigens from serogroup B; 0.25 mg aluminum phosphate; 0.018 mg polysorbate 80; histidine; and E. coli )
So what’s the bottom line?
The bottom line is that meningococcal bacteria infect probably 100% of the population and exceptionally rarely cause disease. Natural infection with one serogroup confers immunity against all serogroups whereas vaccination provides immunity only against the serogroups targeted by the vaccine and increase one’s risk to serogroups not included in the vaccine. After infecting a vaccinated person, the bacteria can change their serogroup to one against which the vaccinated individual has no protection. Furthermore, in some populations, vaccination was demonstrated to increase the risk of meningococcal disease and death. The risk of death from the vaccine far outweighs the risk of death from the disease. The vaccine does not prevent asymptomatic carriage, so the vaccine offers no herd immunity effect.
A NOTE ON SOURCES: There are two sources below (5 and 19) that are paywalled, meaning you have to pay to read them. Free full-text versions were available on www.whale.to, and so those are the links I provided; however, this site is not considered a credible source, so I advise against using it in any debates or essays.
 https://www.youtube.com/watch?v=SFQQOv-Oi6U (0:18:20-0:22:40)
 For Barbara Sumner Burstyn and Ron Law’s investigative journalism story of how the vaccine was adopted in New Zealand in spite of evidence of inefficacy, illegality, and more (http://www.scoop.co.nz/stories/HL0502/S00064.htm); and the government’s response to the published investigation (http://www.scoop.co.nz/stories/HL0505/S00352.htm). Following three years of Burstyn and Law’s investigative reporting, the Norwegian Minister of Health was forced to apologize for the damage caused by the vaccine (http://www.scoop.co.nz/stories/GE0710/S00127.htm).
 Shoenfeld, Y., Agmon-Levin, N., & Tomljenovic, L. (2015). Vaccines and Autoimmunity (pp. 185-190). Hoboke, NJ: Wiley Blackwell.