VRAN Newsletter – Fall, 1999
By Edda West
Following the deaths of two teens and another 22 confirmed cases of invasive meningococcal disease (IMD) in the Edmonton area in recent months, health officials launched a massive vaccine campaign aimed at 70,000 teens between the ages of 15-19. As the campaign got under way, a heightened fear of the disease took hold, and the public demanded an expansion of the meningitis campaign to include all children from the age of 2 onward. One concerned parent who called VRAN to inquire about vaccine side effects said that numerous adverse reactions to the vaccine like nausea and vomiting had also been reported. Edmonton health officials identified the reported cases as group C of neisseria meningitis.
Meningococcal disease is primarily relegated to the late winter months and often seems to hit teen populations. Health Canada’s web site indicates that 200-300 cases of meningococcal disease occur each year. Mortality can range from 5% to 15% of cases.
Meningitis is the term used to describe infections of the central nervous system and “can be caused by almost any infectious agent, including bacteria, mycobacteria, fungi, spirochetes, protozoa, helminths, and viruses. Certain symptoms and signs are common to all types of central nervous system infection: headache, fever, sensorial disturbances, neck and back stiffness, positive Kernig and Brudzinski signs, and cerebrospinal fluid abnormalities. Central nervous system infection constitutes a medical emergency.” (1)
A few years ago, Kitchener/Waterloo area was host to the neisseria meningitidis pathogen, which claimed the lives of several young people. One teenage girl developed meningitis and died a week after getting the vaccine which health officials explained away as not enough time to develop immunity, which takes about 10-14 days. Pathogens commonly linked to meningitis are haemophilus Influenza B, pneumococcal organisms, and the numerous sub groups of neisseria meningitidis.
Menomune, produced by Aventis Pasteur (previously known as Connaught), is the quadrivalent vaccine used in Canada during outbreaks to ‘protect’ from 4 groups of neisseria mengitis – A,C, Y & W135. Product information indicates that 20% of reported cases of meningococcal disease occurs in infants and about one quarter of resulting deaths are in infants. Thimerosal, a mercury derivative is added to the vaccine as a preservative. How long ‘protection’ lasts is not indicated in the product information sheet.
A frightening possibility is that the vaccine might actually fuel the outbreak of serogroups not covered. Smith Kline’s statement about it’s meningitis vaccine Mencevax reflects this concern. “The use of Mencevax ACWY may increase the meningococcal carriage rates, especially for meningococcal groups not included in the vaccine.”
The most commonly occurring groups that appear in Canada are C and B. However, the vaccine does not ‘protect’ from sub-group B. The age distribution of group B and group C varies greatly. Infants with meningococcal disease were significantly more likely to be infected with group B disease than group C, and children below the age of one year have the greatest age specific incidence of the disease. The graph posted below is from Health Canada’s web site and indicates the percentage of reported cases according to serogroups, in 1995 and 1996. Clearly, group B is quite dominant as it comprises 48% and 46% respectively in these years. (2) Undoubtedly, this is why health officials are often seemingly reluctant to do sweeping vaccination campaigns because group B meningitis antigen is not included in the vaccine. And they know that statistically nearly half the cases that are likely to occur may be ‘unprotectable’ by the vaccine.
In addition, there is a growing awareness in the research community that use of the vaccine may actually precipitate the switching of group C to group B. In a letter to the editor of the New England Journal of Medicine, January 20, 2000, German researchers had this to say. “In view of the fact that an outbreak of meningococcal disease follows transmission of the meningococcus within only a few days, our report illustrates the extraordinary speed with which meningococci switch capsular serogroups. In the case we describe, the serogroup changed as a result of the transfer of serogroup-specific genes during the short period of transmission of the disease isolate. 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.”(13)
Another abstract from the Journal of Infectious Diseases (June, 1998) emphasized a similar concern. “The appearance of serogroup B:ET15 was related temporally and geographically to mass immunization campaigns designed to control serogroup C meningococcal disease in Canada. Since there is no vaccine available to control serogroup B meningococcal disease, the appearance of this variant may have public-health significance if it demonstrates the same epidemic potential as its serogroup C counterpart.” (14)
Nature has provided strong and effective protection to babies from meningitis through breastfeeding. Researchers at Howard University College of Medicine in Washington DC found that breast-milk samples studied contained “significant titres of specific IgG and IgA to four organisms; Bordetella pertussis, Haemophilus influenzae type B, Streptococcus pneumoniae and Neisseria meningitidis……, and that the antibody levels to the four organisms were higher in breast-milk than in both maternal and infant sera……. the significant concentrations of specific IgG and IgA antibodies in milk samples may indicate a protective role for breast-milk against the four infections in early childhood”. (3)
In the U.S. where college students are urged to get the meningitis vaccine, it is estimated that college students are at increased risk of developing meningitis. Some observers are linking their susceptibility to meningitis to stress, overcrowded dormitories, cigarette smoke, alcohol consumption, late nights, inadequate sleep and poor nutrition.(4) Although Canadian high school students don’t live dormitory life styles, they are also subjected to high stress levels just by virtue of the fact that teen years are a very difficult time of life. Coupled with peer pressures, school pressures, and nutritional status that is often suboptimal – all are contributing factors to lowered immunity and lowered resistance to disease.
Dr. Cheraskin’s research in the mid 1970’s demonstrated that refined sugar lowers the white blood cell count dramatically. He sampled people’s blood before and after sugar intake, and found that eating a few teaspoons of sugar lowers the white blood cell count up to 50% or more, within an hour, and that it takes 5-6 hours for blood chemistry to normalize. Sugar can drastically impair white blood cell activity, sending the immune system into a tailspin. Teens need real health education that teaches them nutritional ways to protect their immune systems. And they need to understand the role of junk foods, fast foods, highly sugared foods and drinks in lowering their bodies’ resistance to pathogens.(12)
Canadian health officials have in recent years targeted teen populations with diphtheria/tetanus & polio vaccine ‘catch-up’ campaigns. Consider this. “When we know that vaccine antigens are nearly all a neurocerebral tropism* the question that arises when a child presents with meningitis is: Has the child had a vaccination of some sort? In nature dangerous meningococci do not wander about haphazardly. Vaccinations predispose to more aggressive bacterial strains, which will soon have nothing to fear from all our antibiotics.” (*Turning of (part of) particular organism in a particular direction in response to external provocation.) (5, 13)
The provocation effect caused by vaccines in precipitating meningitis is well documented. The Urabe strain of mumps vaccine has been linked to meningitis, as was an outbreak of asceptic meningitis in Brazil that started in August, 1997, 3 weeks after the highly publicized “national vaccination day” when an intensive mass vaccination campaign against MMR (measles, mumps and rubella) was launched. In a survey of 87 children hospitalized in one area of the country (ages 1-11), it was determined that 86 % had been vaccinated with MMR. According to a Reuters news report, on March 3, “The researchers “conservatively estimated” that the risk of aseptic meningitis is about 1 in 14,000 MMR vaccine doses.” (6)
Commenting on asceptic viral meningitis, Dr. Viera Scheibner Ph.D. recounts a brief history of the redefinition of polio. “When the first injectable polio vaccine was trialed on 1.8 million of American children in 1954, within 9 days there was a huge outbreak of paralytic polio in the just vaccinated and some of their parents and other contacts. The U.S. Surgeon General discontinued this trail for 2 weeks. The vaccinators put their heads together and came back with a new definition of poliomyelitis. The classical definition of polio: a disease with residual paralysis which resolves within 60 days changed into a disease with the residual paralysis which persists for more than 60 days. This nifty administrative move “eradicated” some 99% of cases of polio. When a vaccinated child gets polio, it will be diagnosed as viral or aseptic meningitis. According to one of the 1997 issues of the MMWR, there are between 30,000 to 50,000 cases of viral meningitis in the U.S. each year. That’s where all those cases of polio now are: hidden under a new name.” (7)
An article in Lifeforce magazine (summer/99) presented an overview of a meningitis outbreak in Niger, Africa in 1997: Dr Marc Vercoutere having studied the official figures had this to say. “You will note the appreciable and constant increase in the epidemic, particularly at the end of March, when the vaccination campaign had virtually ended and protection was supposed to be effective after 8 days. Despite massive vaccination which, in principle, should have given protection for about 3 years, we counted, in March 1996 after a new epidemic, 341 deaths in 2945 cases. On 8 October 1997, after yet another epidemic (within the supposed period of vaccine protection), they announced 504 deaths from 4925 cases.” Dr Vercoutere noted a slight increase in the deaths-to-cases ratio, which would suggest increasing resistance to the antibiotic treatment, in addition to the inefficacy of the vaccinations. A review of the 1996 epidemic in Nigeria, which killed 8000, provided similar results.” (5, 13)
And then there is the fluoride question. Edmonton drinking water has been fluoridated for many years. Fluoride suppresses the thyroid gland, which in itself leads to a huge assortment of health problems. In Europe fluorides were used for many years as effective anti-thyroid agents, even at doses below the level deemed “optimal” for water fluoridation. Its use was abandoned due to its high toxicity and accumulative nature. Product information for current anti-thyroid agents state that when patients are on anti-thyroid drugs vaccinations should not be administered because anti-thyroids may lower the body’s resistance and chances are high that one might get the infection the immunization is meant to prevent. (9)
Fluoride manipulates and interferes with a myriad of biochemical functions. It acts as an adjuvant, intensifying the activity of pathogenic organisms. Department of Microbiology, University of Iowa, showed how fluoride proved to be a most potent adjuvant when given intragastrically to rats. The authors warned that the supplemental fluoride prescribed for infants and especially that which is inadvertently ingested by children and adults given fluoride gels, is within the concentration range of that which produced the effects observed in rats in their studies, concluding that the fluoride adjuvant effect described should have relevance for fluoride therapy worldwide.(8) In other words, fluoride increases the risk of susceptibility to infectious organisms.
Other studies have documented the fact that fluorides enhanced mating activity of certain organisms which cause meningitis and that mating activity was dependent on body temperature. The lower the body temperature the higher the mating activity. Again, low body temperature is a sure-tell sign of an underfunctioning thyroid gland. (10) Maharajan et al (1978) investigated 20 patients suffering from meningococcal meningitis and other acute febrile illnesses and found that in all patients thyroid function was significantly low. (11)
- Current Medical Diagnosis & Treatment, edited by Lawrence M. Tierney Jr, S.J. McPhee & Maxine A. Papadakis – 34th edition, 1995.
- Health Canada website:
- Ann..Trop Paediatrics 1989;4:226-232 (also quoted in Hilary Butler’s position paper on The Role of Vaccines In SIDS at the Sixth SIDS International Conference, Auckland University, New Zealand, Feb. 11/2000)
- The Unknown Killer: What is Meningitis & Who is at Risk – from ABCNEWS.com
- Vaccination Information (UK) & Lifeforce magazine
- Reuters Health Report(Mar 3/00) – quotes from Am J Epidemiology 2000;151:524-530. Forwarded to VRAN by Raymond Gallup
- Viera Scheibener – Statement to U.S. House of Representatives – Hearings on safety of hepatitis B vaccine.
- Butler et al [Butler JE; Satam M; Ekstrand J – “Fluoride: an adjuvant for mucosal and systemic immunity.” Immunol Lett26(3):217-20 (1990) Department of Microbiology, University of Iowa.
- With many thanks to Andreas Schuld – Parents of Fluoride Poisoned Children, for providing fluoride related resources for this article.
- (->hypothyroidism.) (Dong et al, 1998) [Dong H, Courchesne W – “A novel quantitative mating assay for the fungal pathogen Cryptococcus neoformans provides insight into signalling pathways responding to nutrients and temperature.” Microbiology144 ( Pt 6):1691-7 (1998)]
- [Maharajan G, Etta KM, Singh A, Ahuja IS, Ahuja GK – “Thyroxine, triiodothyronine and thyrotrophin levels in meningococcal meningitis, typhoid fever and other febrile conditions.” Clin Endocrinol (Oxf) 9(5):401-6(1978)
- W.M. Ringsdorf, JR., D.M.D., M.S., E. Cheraskin, M.D., D.M.D., and R.R. Ramsay, JR., D.M.D., “Sucrose, Neutrophilic Phagocytosis and Resistance to Disease,” Dental Survey 52 no. 12 (December 1976): 46-48.
- The New England Journal of Medicine — January 20, 2000 — Vol. 342, No. 3 .
- Journal of Infectious Diseases, 1998 Jun;177(6):1754-7 (PUBMED abstract)
J Infect Dis 1998 Jun;177(6):1754-7
Serogroup B, electrophoretic type 15 Neisseria meningitidis in Canada.
Kertesz DA, Coulthart MB, Ryan JA, Johnson WM, Ashton FE
Bureau of Infectious Diseases, Laboratory Centre for Disease Control, Health Canada, Ottawa.
Invasive meningococcal disease is nationally reportable in Canada. In recent years, a serogroup C genotype, designated electrophoretic type 15 (ET15), has been the most frequently isolated meningococcal genotype in Canada and has caused epidemics across the country. Between August 1993 and September 1995, there were 9 cases of invasive meningococcal disease caused by a variant of this genotype, expressing group B capsular polysaccharide. The appearance of serogroup B:ET15 was related temporally and geographically to mass immunization campaigns designed to control serogroup C meningococcal disease in Canada. Since there is no vaccine available to control serogroup B meningococcal disease, the appearance of this variant may have public-health significance if it demonstrates the same epidemic potential as its serogroup C counterpart.
New England Journal of Medicine January 20, 2000
Vol. 342, No. 3
Rapid Serogroup Switching in Neisseria meningitidis
To the Editor:
In Neisseria meningitidis, the horizontal transfer of siaD genes encoding polysialyltransferases has been shown to result in capsular serogroup switching in vitro. (1) The presence of closely related clones with different serogroups suggests that serogroup switching also occurs in vivo. (2, 3) However, the time course of the transfer of siaD genes in humans is unknown.
We describe a case of unexpectedly rapid serogroup switching in virulent meningococci. A 16-year-old girl died of fulminant serogroup B meningococcal septicemia. Examination of nasopharyngeal swabs from close contacts revealed massive colonization with serogroup C meningococci in the girl’s boyfriend. Isolates from the girl and her boyfriend were identical with respect to the typing of porin antigens (15:P1.16) and the sequence type (ST 32). (4) We used pulsed-field gel electrophoresis and the restriction endonuclease SpeI to demonstrate the direct clonal descendence of the strains. (5) The two strains yielded almost identical restriction fragments. However, the serogroup C strain had one unique band of approximately 210 kb, which hybridized to a probe specific to the serogroup C siaD gene. In the serogroup B strain, this fragment was cleaved into two fragments of approximately 160 kb and 50 kb, which hybridized to a serogroup B siaD probe. To show that these differences were due to siaD exchange, the siaD genes of both strains were amplified by the polymerase chain reaction (PCR) and digested with SpeI. As with the result obtained by pulsed-field gel electrophoresis, the PCR product of the siaD gene in the serogroup B strain was cleaved by SpeI, whereas the PCR product of the siaD gene in the serogroup C strain was not (Figure 1).
In view of the fact that an outbreak of meningococcal disease follows transmission of the meningococcus within only a few days, our report illustrates the extraordinary speed with which meningococci switch capsular serogroups. In the case we describe, the serogroup changed as a result of the transfer of serogroup-specific genes during the short period of transmission of the disease isolate. 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.
Ulrich Vogel, M.D.
Heike Claus, B.Sc.
Matthias Frosch, M.D.
97080 Wurzburg, Germany
- Frosch M, Meyer TF. Transformation-mediated exchange of virulence determinants by co-cultivation of pathogenic Neisseriae. FEMS Microbiol Lett 1992;79:345-9.
- Swartley JS, Marfin AA, Edupuganti S, et al. Capsule switching of Neisseria meningitidis. Proc Natl Acad Sci U S A 1997;94:271-6.
- Kertesz DA, Coulthart MB, Ryan JA, Johnson WM, Ashton FE. Serogroup B, electrophoretic type 15 Neisseria meningitidis in Canada. J Infect Dis 1998;177:1754-7.
- Maiden MC, Bygraves JA, Feil E, et al. Multilocus sequence typing: a portable approach to the identification of clones within populations of pathogenic microorganisms. Proc Natl Acad SCI U S A 1998;95:3140-5.
- Vogel U, Morelli G, Zurth K, et al. Necessity of molecular techniques to distinguish between Neisseria meningitidis strains isolated from patients with meningococcal disease and from their healthy contacts. J Clin Microbiol 1998;36:2465-70. [Erratum, J Clin Microbiol 1999;37:882.]