Measles overview

By 1960, for reasons that were well understood at the time, measles in Australia had become a routine childhood illness that the child’s parents nursed the child through with adequate water, protection from strong light, and adequate good food. Serious complications were rare, and deaths were almost unheard of.

In the sixth decade of an unbeaten marketing campaign for vaccines against the disease, measles has become a much-feared bogeyman that will turn your children into vegetables or worse. This previously routine illness has become a “killer disease”.

The applicability of the term “killer disease” to measles as the disease vaccination has transformed it into bears some examination.

It is true that the form of measles more common in Australia now, the vaccine strain of the disease, is not the same as the natural disease. Unlike natural measles — which offers lifelong protection against a host of ills, including measles (see Measles vaccine: effectiveness), and a warning of measles itself in the form of prodromal symptoms — the engineered measles virus offers limited protection even against infection by measles, and a “silent” form of measles infects 45% of vaccinees within four years of vaccination against the disease (see Measles vaccine: effectiveness).

It’s true too that the engineered virus does not offer the same lifelong boost to the general immune system [D] that natural measles does, drastically reducing the child’s lifetime probability of becoming asthmatic or otherwise susceptible to allergies [E]. And, admittedly, the vaccine contributes to inflammatory bowel disease and to immune overload resulting in double diabetes and other immune-mediated illnesses [F]; to genetic and chromosomal abnormalities [G]; to “immunoreactive diseases, sebaceous skin diseases, degenerative diseases of bone and cartilage, and certain tumours” [H]; and to atherosclerotic cardiovascular disease [I].

But this is not necessarily due to the engineered disease as such; it is attributable as an effect of the vaccination itself, and very likely due to its interference with natural measles. So even the engineered form of the disease does not necessarily deserve the terrible name that the medical industry has given it; and the natural form certainly does not. The natural form of measles even offers a degree of protection against atherosclerotic cardiovascular disease.

With adequate attention to nutrition (particularly vitamin A and vitamin C status) and basic nursing, measles in a society supporting good hygeine, clean water, and basic nursing care is a very low-risk illness in the infant of a year or more; with rare exception, the infant is by then capable of responding to the illness by developing lifelong immunity to it [J] and by strengthening health generally, leading to lower probability of the chronic illnesses mentioned above and lower susceptibility to measles itself in infants under one year of age [K].

The immune system of the infant less than a year old is universally recognised even by the most avid vaccinators as being incapable of responding reliably to a measles vaccination. This is so far more dependably in the infants of mothers who have themselves undergone natural measles: those mothers transmit their own antibodies to the infant at birth, protecting the infant until such time as his or her own immune system is capable of responding to wild measles virus [L].

The infant so protected from natural measles often will not undergo infection by the vaccine virus either. Vaccine advocates frequently regard such natural, passively acquired immunity as a problem, simply because they wish the infant to respond to a vaccine instead. The usual response to this conflict between profitless nature and profitable technology is not to step back and allow nature its course, as low-risk as it has been since the second half of the twentieth century in Australia; it is instead to escalate the war on maternal immune protection, seeking to undermine it with earlier and repeated infant injections [M].

FURTHER READING ON MEASLES:

Measles vaccine: effectiveness

Measles vaccine: relevance

Measles vaccine: safety

Measles vaccine: politics

 

References [D]

F.M. Burnet, “Measles as an index of immunological function”, The Lancet 1968;292(7568):610–13

References [E]

N. Kondo, O. Fukutomi, T. Ozawa, et al., “Improvement of food-sensitive atopic dermatitis accompanied by reduced lymphocyte responses to food antigen following natural measles virus infection”, Clin Exp Allergy 1993; 23: 44–50, <http://www.ncbi.nlm.nih.gov/pubmed/8439821>, <dx.doi.org/10.1111/j.1365-2222.1993.tb02483.x>

S.O. Shaheen, D.J.P. Barker, C.B. Heyes, et al., “Measles and atopy in Guinea-Bissau”, The Lancet 1996;347(9018):1792–1796, <www.sciencedirect.com/science/article/pii/S0140673696916177>

C. Bodner, W.J. Anderson, T.S. Reid, and D.J. Godden, “Childhood exposure to infection and risk of adult onset wheeze and atopy”, Thorax 2000;55:383–387, <thorax.bmj.com/content/55/5/383.long>

H. Rosenlund, A. Bergström, J.S. Alm, et al., “Allergic disease and atopic sensitization in children in relation to measles vaccination and measles infection”, Pediatrics 2009 Mar;123(3):771–778, <dx.doi.org/10.1542/peds.2008-0013>

[Reference [F]

N.P. Thompson, S.M. Montgomery, R.E. Pounder, and A.J. Wakefield, “Is measles vaccination a risk factor for inflammatory bowel disease?”, Lancet 1995 Apr 29;345(8957):1071–1074, <www.ncbi.nlm.nih.gov/pubmed/7715338>

J.B. Classen, “Review of vaccine induced immune overload and the resulting epidemics of type 1 diabetes and metabolic syndrome, emphasis on explaining the recent accelerations in the risk of prediabetes and other immune mediated diseases”, J Mol Genet Med 2014;S1:025, <dx.doi.org/10.4172/1747-0862.S1-025>

Reference [G]

G.E. Ewing, “What is regressive autism and why does it occur? Is it the consequence of multi-systemic dysfunction affecting the elimination of heavy metals and the ability to regulate neural temperature?”, N Am J Med Sci. 2009 Jul;1(2):28–47, <www.ncbi.nlm.nih.gov/pubmed/22666668>

References [H]

B. Damien, S. Huiss, F. Schneider, and C.P. Muller, “Estimated susceptibility to asymptomatic secondary immune response against measles in late convalescent and vaccinated persons”, J Med Virol. 1998 Sep;56(1):85–90, <www.ncbi.nlm.nih.gov/pubmed/9700638>

J. Mossong, D.J. Nokes, W.J. Edmunds, et al., “Modeling the impact of subclinical measles transmission in vaccinated populations with waning immunity”, Am J Epidemiol. 1999 Dec 1;150(11):1238–49, <aje.oxfordjournals.org/content/150/11/1238.long>

M. Paunio, K. Hedman, I. Davidkin, et al., “Secondary measles vaccine failures identified by measurement of IgG avidity: high occurrence among teenagers vaccinated at a young age”, Epidemiol Infect. 2000 Apr;124(2):263–71, <www.ncbi.nlm.nih.gov/pubmed/10813152>

Reference [I]

Y. Kubota, H. Iso, A. Tamakoshi, and the JACC Study Group, “Association of measles and mumps with cardiovascular disease: The Japan Collaborative Cohort (JACC) study”, Atherosclerosis 2015 Jun 18;241(2):682–686, <www.bmj.com/content/340/bmj.c1626>, <www.ncbi.nlm.nih.gov/m/pubmed/26122188>, <dx.doi.org/10.1016/j.atherosclerosis.2015.06.026>

References [J]

F.M. Burnet, “Measles as an index of immunological function”, The Lancet 1968;292(7568):610–13

W.E. Rawls, M.L. Rawls, and M.A. Chernesky, “Analysis of a measles epidemic; possible role of vaccine failures”, Can Med Assoc J. 1975 Nov 22;113(10):941–944, <www.ncbi.nlm.nih.gov/pmc/articles/PMC1956577>

Centers for Disease Control, Guidelines for Protecting the Safety and Health of Health Care Workers, Washington, DC: U.S. Department of Health and Human Services, 1988, p. 522

Masae Itoh, Yoshinobu Okuno, and Hak Hotta, “Comparative Analysis of Titers of Antibody against Measles Virus in Sera of Vaccinated and Naturally Infected Japanese Individuals of Different Age Groups”, J Clin Microbiol. 2002 May;40(5):1733–1738, <www.ncbi.nlm.nih.gov/pmc/articles/PMC130661>.

J.M. Heffernan and M.J. Keeling, “Implications of vaccination and waning immunity”, Proceedings of the Royal Society B: Biological Sciences 2009 Mar 4;276(1664):2071–2080, <http://rspb.royalsocietypublishing.org/content/276/1664/2071.long>, <http://dx.doi.org/10.1098/rspb.2009.0057>

World Health Organization, “Measles vaccines: WHO position paper”, Wkly Epidemiol Rec 2009;84:349–360, <http://www.ncbi.nlm.nih.gov/pubmed/19714924>, <http://www.who.int/wer/2009/wer8435.pdf>

“Natural infection provides lifelong immunity.” Health Victoria, Measles, <https://www2.health.vic.gov.au/public-health/infectious-diseases/disease-information-advice/measles> [accessed 16 January 2016]

References [K]

F.M. Burnet, “Measles as an index of immunological function”, The Lancet 1968;292(7568):610–13

Tove Rønne, “Measles virus infection without rash in childhood is related to disease in adult life”, The Lancet, 1985 Jan 5;325(8419):1–5, <http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(85)90961-4/abstract>, <http://dx.doi.org/10.1016/S0140-6736(85)90961-4>

P.J. Jenks, E.O. Caul, and A.P.C.H. Roome, “Maternally derived measles immunity in children of naturally infected and vaccinated mothers”, Epidem Inf (1988);101:473–476, <www.ncbi.nlm.nih.gov/pmc/articles/PMC2249400>

S.E. Robertson, L.E. Markowitz, E.F. Dini, and W.A. Orenstein, “A million dollar measles outbreak: epidemiology, risk factors, and selective revaccination strategy”, Publ Health Reports 1992 Jan–Feb;197(1):24–31, <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1403597>

N. Kondo, O. Fukutomi, T. Ozawa, et al., “Improvement of food-sensitive atopic dermatitis accompanied by reduced lymphocyte responses to food antigen following natural measles virus infection”, Clin Exp Allergy 1993; 23: 44–50, <http://www.ncbi.nlm.nih.gov/pubmed/8439821>, <http://dx.doi.org/10.1111/j.1365-2222.1993.tb02483.x>

A.J. Hall and F.T. Cutts, “Lessons from measles vaccination in developing countries”, BMJ 1993 Nov 20;307:1294–1295, <www.ncbi.nlm.nih.gov/pmc/articles/PMC1679437>

M.A. Kacica, R.A. Venezia, J. Miller, P.A. Hughes, and M.L. Lepow, “Measles antibodies in women and infants in the vaccine era”, J Med Virol 1995 Feb;45(2):227–229, <http://www.ncbi.nlm.nih.gov/pubmed/7775944>

N.P. Thompson, S.M. Montgomery, R.E. Pounder, and A.J. Wakefield, “Is measles vaccination a risk factor for inflammatory bowel disease?”, Lancet 1995 Apr 29;345(8957):1071–1074, <www.ncbi.nlm.nih.gov/pubmed/7715338>

“Contrary to current assumptions, children who survive the acute phase of measles infection have have a survival advantage compared with unimmunized, uninfected children.” P. Aaby, “Assumptions and contradictions in measles and measles immunization research: Is measles good for something?”, Social Science and Medicine 1995;41(5):673–686, <www.sciencedirect.com/science/article/pii/0277953695000389>

S.O Shaheen, D.J.P Barker, C.B Heyes, et al., “Measles and atopy in Guinea-Bissau”, The Lancet 1996 June 29;347(9018):1792–1796, <www.sciencedirect.com/science/article/pii/S0140673696916177>

R. Brugha, M. Ramsay, T. Forsey, and D. Brown, “A study of maternally derived measles antibody in infants born to naturally infected and vaccinated women”, Epidemiol Infect 1996;117:519–524, <www.ncbi.nlm.nih.gov/pmc/articles/PMC2271637>

B. Damien, S. Huiss, F. Schneider, and C.P. Muller, “Estimated susceptibility to asymptomatic secondary immune response against measles in late convalescent and vaccinated persons”, J Med Virol. 1998 Sep;56(1):85–90, <www.ncbi.nlm.nih.gov/pubmed/9700638>

M.A. Fisher, S.A. Eklund, “Hepatitis B vaccine and liver problems in U.S. children less than 6 years old, 1993 and 1994”, Epidemiology 1999 May;10(3):337–339, <http://www.ncbi.nlm.nih.gov/pubmed/10230847>

J. Mossong, D.J. Nokes, W.J. Edmunds, et al., “Modeling the impact of subclinical measles transmission in vaccinated populations with waning immunity”, Am J Epidemiol. 1999 Dec 1;150(11):1238–49, <aje.oxfordjournals.org/content/150/11/1238.long>

C. Bodner, W.J. Anderson, T.S. Reid, and D.J. Godden, “Childhood exposure to infection and risk of adult onset wheeze and atopy”, Thorax 2000;55:383–387, <thorax.bmj.com/content/55/5/383.long>

M. Paunio, K. Hedman, I. Davidkin, et al., “Secondary measles vaccine failures identified by measurement of IgG avidity: high occurrence among teenagers vaccinated at a young age”, Epidemiol Infect. 2000 Apr;124(2):263–71, <www.ncbi.nlm.nih.gov/pubmed/10813152>

U. Wahn, “What drives the allergic march?”, Allergy 2000:55:591–599, <http://www.ncbi.nlm.nih.gov/pubmed/10921457>

M.M. Braun, G.T. Mootrey, M.E. Salive, R.T. Chen, and S.S. Ellenberg, “Infant immunization with acellular pertussis vaccines in the United States: assessment of the first two years’ data from the Vaccine Adverse Event Reporting System (VAERS)”, Pediatrics 2000 Oct;106(4):E51, <http://www.ncbi.nlm.nih.gov/pubmed/11015546>

P. Aaby, F. Simondon, B. Samb, et al., “Low mortality after mild measles infection compared to uninfected children in rural West Africa”, Vaccine 2002 Nov 22;21(1–2):120–126, <http://www.ncbi.nlm.nih.gov/pubmed/12443670>

Dennis J. Cada, Terri L. Levien, and Danial E. Baker, “Formulary Drug Reviews — quadrivalent human papillomavirus (Types 6, 11, 16, 18) recombinant vaccine”, Hospital Pharmacy 12/2006;41(12):1185–1195, <http://archive.hospital-pharmacy.com/doi/abs/10.1310/hpj4112-1185>, <http://dx.doi.org/10.1310/hpj4112-1185>

E. Leuridan, “Passive transmission and persistence of naturally acquired or vaccine-induced maternal antibodies against measles in newborns”, Vaccine 2007 Aug 21;25(34):6296–6304, <http://www.sciencedirect.com/science/article/pii/S0264410X07006974>, <http://dx.doi.org/10.1016/j.vaccine.2007.06.020>

H. Rosenlund, A. Bergström, J.S. Alm, et al., “Allergic disease and atopic sensitization in children in relation to measles vaccination and measles infection”, Pediatrics 2009 Mar;123(3):771–778, <http://www.ncbi.nlm.nih.gov/pubmed/19255001>, <http://dx.doi.org/10.1542/peds.2008-0013>

J.M. Heffernan and M.J. Keeling, “Implications of vaccination and waning immunity”, Proceedings of the Royal Society B: Biological Sciences 2009 Mar 4;276(1664):2071–2080, <http://rspb.royalsocietypublishing.org/content/276/1664/2071.long>, <http://dx.doi.org/10.1098/rspb.2009.0057>

G.E. Ewing, “What is regressive autism and why does it occur? Is it the consequence of multi-systemic dysfunction affecting the elimination of heavy metals and the ability to regulate neural temperature?”, N Am J Med Sci. 2009 Jul;1(2):28–47, <www.ncbi.nlm.nih.gov/pubmed/22666668>

E. Leuridan, N. Hens, V. Hutse, et al., “Early waning of maternal measles antibodies in era of measles elimination: longitudinal study”, BMJ 2010 May 18;340:c1626, <http://www.bmj.com/content/340/bmj.c1626>, <http://dx.doi.org/10.1136/bmj.c1626>

V. Demicheli, A. Rivetti, M. Grazia Debalini, and C. Di Pietrantonj, “Vaccines for measles, mumps and rubella in children”, Cochrane Database Syst Rev 2012 Feb 15;2:CD004407, <dx.doi.org/10.1002/14651858.CD004407.pub3>

E. Leuridan, M. Sabbe, and P. van Damme, “Measles outbreak in Europe: Susceptibility of infants too young to be immunized”, Vaccine 2012;13(41):5905–5913

“However, the increasing prevalence of vaccine-derived maternal antibodies has also led to unexpected outcomes. This is most evident in the emergence of measles susceptibility in young infants living in highly vaccinated populations where the measles vaccine has been in use for decades [11–14].” Hayley A. Gans and Yvonne A. Maldonado, “Loss of passively acquired maternal antibodies in highly vaccinated populations: An emerging need to define the ontogeny of infant immune responses”, J Infect Dis 2013 Jul 1;208(1):1–3, <http://jid.oxfordjournals.org/content/early/2013/04/29/infdis.jit144.full>

Sandra Waaijenborg, Susan J. M. Hahné, Liesbeth Mollema, et al., “Waning of maternal antibodies against measles, mumps, rubella, and varicella in communities with contrasting vaccination coverage”, J Infect Dis 2013;208(1):10–16, <http://jid.oxfordjournals.org/content/208/1/10>, <http://dx.doi.org/10.1093/infdis/jit143>

J.B. Classen, “Review of vaccine induced immune overload and the resulting epidemics of type 1 diabetes and metabolic syndrome, emphasis on explaining the recent accelerations in the risk of prediabetes and other immune mediated diseases”, J Mol Genet Med 2014;S1:025, <dx.doi.org/10.4172/1747-0862.S1-025>

Y. Kubota, H. Iso, A. Tamakoshi, and the JACC Study Group, “Association of measles and mumps with cardiovascular disease: The Japan Collaborative Cohort (JACC) study, Atherosclerosis 2015 Jun 18;241(2):682–686, <www.bmj.com/content/340/bmj.c1626>, <www.ncbi.nlm.nih.gov/m/pubmed/26122188>, <dx.doi.org/10.1016/j.atherosclerosis.2015.06.026>

References [L]

M.M. Pütz, F.B. Bouche, R.L. de Swart, and C.P. Muller, “Experimental vaccines against measles in a world of changing epidemiology”, Int J Parasitol. 2003 May;33(5–6):525–545, <www.ncbi.nlm.nih.gov/pubmed/12782053>

Reference [M]

“The problem of delaying immunization until the second year may become a thing of the past in a highly vaccinated population if maternal antibody protection is lost earlier in children of vaccinated mothers. If this is the case, children will become susceptible both to natural infection and to successful vaccination earlier, and hence the age of immunization could be brought forward to the first year of life when clinic attendance is better. This would be expected to lead to a higher vaccine uptake.” P.J. Jenks, E.O. Caul, and A.P.C.H. Roome, “Maternally derived measles immunity in children of naturally infected and vaccinated mothers”, Epidem Inf (1988);101:473–476, <www.ncbi.nlm.nih.gov/pmc/articles/PMC2249400>