Introduction: Measles Vaccinations
Measles vaccinations in the United States and many other countries began in the early 1960s, at a time when measles incidence was declining due to natural causes and approaching an 18-year low. This is why, at first glance, it may seem that vaccinations have reduced the incidence of disease. However, this was only a coincidence with the natural dynamics of measles.
The measles example is just one of many examples of all the childhood infectious diseases for which vaccines have been developed. Whenever any vaccine against measles appeared and its use became widespread, reports of outbreaks and epidemics of measles, even with one hundred percent coverage of the population with this vaccine, began to fill the pages of medical journals.
Reports of serious reactions, including death, are also occurring with increasing frequency. This is a topic for a separate article.
Price and reviews
The cost of live measles vaccine sold through the pharmacy chain ranges from 425 to 587 rubles. In Moscow, you will have to pay 1,515 rubles for vaccination with the Russian gastrointestinal virus in the clinic (taking into account the cost of a preventive appointment with a pediatrician and drawing up a report).
Experts express confidence that professional vaccination, competent preparation for vaccination and a properly organized post-vaccination period allow one to avoid significant side effects and complications.
Atypical measles is a new phenomenon that occurs only in vaccinated people
Little is known to the general public that vaccinated children have begun to develop a particularly dangerous form of measles, which is associated with an altered host immune response caused by the harmful effects of the measles vaccine. This form resists all conventional treatments and results in high mortality.
It became known as atypical measles (AK).
Rauch and Schmidt (1965) described nine cases of AK that occurred during the 1963 measles epidemic in Cincinnati. The authors followed 386 children who received three doses of the measles virus-killed vaccine in 1961. Of these 386 children, 125 contracted measles, and 54 of them developed the disease.
New, atypical measles occurring in vaccinated individuals is characterized by high fever, unusual rash, and pneumonia, and there is often a history of inoculation with killed measles vaccine.
Rauch and Schmidt (1965) concluded: “It appears that three injections of killed vaccine did not protect against measles in a large percentage of children exposed to it within two and a half years of immunization.”
Fulginiti (1967) also described the occurrence of atypical measles in ten children who had received inactivated (killed) measles virus vaccine five to six years previously.
Nichols (1979) wrote that atypical measles is generally considered to be a hypersensitivity reaction to natural measles infection in individuals who have previously received killed measles vaccine, although some investigators have reported AK-like illness in children vaccinated only with live measles vaccine.
He wrote that during the 1974–1975 measles epidemic in Northern California, many physicians reported laboratory-confirmed measles in patients with signs and symptoms consistent with AK.
We developed diagnostic criteria based on serology, rash distribution, and morphology. In typical measles, a maculopapular rash appears first at the hairline, progresses caudally, is concentrated on the face and trunk, and is often accompanied by Koplik spots. In AK, the rash morphologically consists of a mixture of maculopapular, petechial, vesicular and urticarial components. It usually begins on the extremities and is mainly concentrated on them, progresses in a cranial direction and is not accompanied by Koplik spots. Cases were classified as AK if the patient had: 1) a rash with a distribution and morphology characteristic of AK, and 2) a fourfold or greater increase in the titer of complement-bound measles antibodies or an increase to 256 in the titer in a convalescent.
Contraindications for vaccination
Among the contraindications for vaccination in adults are acute respiratory viral infections or chronic diseases that have worsened at the time of the proposed vaccination. With these symptoms, doctors postpone vaccination for an average of a month.
Adults also have absolute contraindications for vaccination, among which doctors cite allergies to bird eggs, allergic reactions to antibiotics, previous vaccinations, pregnancy and breastfeeding.
In children, contraindications for injections against viral infections are:
- any disease in the acute stage;
- primary immunodeficiency;
- AIDS;
- use of blood products and immunoglobulin the day before;
- complications associated with previous vaccination;
- intolerance to aminoglycosides, protein;
- oncology.
Unfounded optimism about eliminating measles in the United States by October 1, 1982
Despite the apparent lack of success with measles vaccinations, in October 1978, Department of Health Secretary Joseph A. Califano Jr. announced: “We are engaged in an effort to achieve a measles-free United States by October 1, 1982.”
As expected, this unrealistic plan failed: after 1982, the United States experienced repeated large and even more persistent measles epidemics, mostly among fully vaccinated populations. Blame was placed primarily on "the ineffective formalin-inactivated ('killed') measles vaccine administered to hundreds of thousands of children between 1963 and 1967." However, measles outbreaks and epidemics continue to occur even if this first vaccine has been replaced by a two-dose live measles virus vaccine and the age of vaccination has been changed.
The warnings were not heeded. As Swiss doctors wrote (Albonico et al., 1990), “we have lost the common sense and wisdom that usually prevailed in the approach to childhood illnesses. Too often, instead of strengthening the body's defenses, fever and symptoms are mercilessly suppressed. This is not always without consequences.”
Is a vaccinated person contagious to an unvaccinated person?
A weakened measles pathogen is practically non-viable; its isolation in the post-vaccination period from the body of a vaccinated person, even with discharge due to respiratory symptoms, is not capable of infecting others.
For unvaccinated individuals, including children and immunocompromised adults (pregnant women, cancer patients, patients undergoing immunosuppressant therapy), a vaccinated person is not contagious.
Destruction of immunity transmitted through the placenta by vaccinations
Immediately after the introduction of measles vaccinations in the United States, many researchers warned that generations of children born to mothers who were vaccinated as children would be born with poor immunity or no immunity at all, and children would develop measles and other diseases too early. diseases.
Lennon and Black (1986) showed that “haemagglutination inhibitory antibody titers and neutralizing antibody titers are lower in fairly young women who have received vaccinations compared with older women.” (Hemagglutination is the adhesion and precipitation of red blood cells. Since the measles virus has the ability to agglutinate red blood cells, which is inhibited [inhibited] or neutralized by antibodies, this property is used to determine the quantitative activity of the virus. - Approx. transl.
) The same goes for whooping cough. This explains why a large number of children at pre-vaccination age develop these diseases, among which whooping cough is especially talked about.
Composition and mechanism of action
Half a milliliter of measles vaccine (vaccination dose) consists of:
- the main active component is low-active viral fractions of the Leningrad-16 strain, cultured on quail embryos;
- auxiliary ingredients: antibacterial substances of the aminoglycoside series, drug stabilizer.
The introduction of cultured LCV, as it were, trains the body’s defense system: it triggers the same processes that occur during infection with the wild measles virus, only in a weakened version. Having detected the damaging agents, the immune system gradually produces liquidators of this infection over several days.
After their extermination, the bulk of the defenders disappear, leaving their residents in the lymph nodes, ready to quickly activate the production of the required number of liquidators when they meet the agents again. As a result, the disease either does not occur at all, or proceeds easily, without significant clinical manifestations or complications.
Impaired cholesterol metabolism due to measles vaccinations
Soon after measles vaccinations became widespread, the medical press began to fill with reports expressing concern about elevated cholesterol levels and abnormal high-density lipid ratios in young children.
Vicari et al. (1979, "Effect of measles and measles vaccine on serum cholesterol", Lancet
10:326) quote Drs Matthews and Phiri (1978) who
reported that immunization with influenza vaccine is likely accompanied by a subsequent increase in serum total cholesterol and a decrease in HDL levels. They suggested that immunization with viral antigens or natural viral infection may contribute to changes in lipid levels.
And further:
We measured total serum cholesterol levels in 97 children (mean age 2 years) before and 6 weeks after measles vaccination (Rimevax, RIT, Belgium) and in serial serum samples from 27 measles patients (mean age 4 years). The children received good nutrition. Antibody titers were analyzed by hemagglutination inhibition, and serum cholesterol was measured using the Leppilnen method. Samples taken from the same child were measured in the same series. Five children showed an exceptionally high relative increase (equal to 40% or higher) in serum cholesterol after vaccination, although the absolute values remained within the normal range. There was no significant correlation between initial cholesterol values or changes in cholesterol values and measles antibody responses. After 8 and 10 months, a relative increase in serum cholesterol was still observed in two children. Following natural measles infection, mean cholesterol levels were low in samples collected 1 to 7 days after symptom onset...
Vicari et al. (1979) concluded:
Our data show that natural measles in the acute phase of the disease reduces serum cholesterol levels. This is consistent with the observations of Lees et al., who showed that experimental mosquito virus infection reduced serum cholesterol levels for at least 10 days. Whether the same reduction in cholesterol levels occurs after vaccination against measles and, possibly, after vaccination with other viruses needs to be clarified. Our observations support the view expressed by Matthews and Phiri (1978) that natural viral infection or immunization with viral antigens causes changes in serum lipid levels in humans.
Bell et al. (2012) wrote:
In a large population-based sample of Australian schoolchildren, we found a higher incidence of abnormal lipid profiles compared with American data. In addition, many children have levels outside the normal range for healthy Australian children. Research is needed to follow the lipid profile of Australian children into adulthood to understand the association of these levels with future cardiovascular risk.
In her 72-page doctoral dissertation, Louise Strandberg (2009) took an exhaustive, in-depth look at the relationships between diet, obesity and the immune system.
It is important to note that she writes the following:
In the 1950s, it was first recognized that dietary fat may contribute to cardiovascular disease in the Western world. However, the Greenland Eskimos are known to eat large amounts of fat, but they still have a very low incidence of cardiovascular disease. In the 1970s, Bang and Dyerberg found that Eskimos had low levels of cholesterol and lipoproteins other than high-density lipoprotein, which [sic] is now known as "good cholesterol" ... the quality of dietary fat, not the quantity, is important for the development of heart disease. vascular diseases.
This was a generation of unvaccinated Eskimos.
Based on medical research, it is logical to conclude that an important underlying cause of observed abnormal cholesterol and triglyceride levels in children may be invasive medical intervention in the form of vaccinations.
LITERATURE
Rauh LW, and Schmidt R. 1965. Measles immunization with killed virus vaccine. Am J Dis Child
109:232–237.
Fulginiti VA, Eller JJ, Downie AW, and Kempe CH. 1967. Altered reactivity to meats virus. Atypical measles in children previously inoculated with killed-virus vaccines. JAMA
202(12):1075–1080.
Scott TF, and Bonanno DE 1967. Reactions to live-measles-virus vaccine in children previously inoculated with killed-virus vaccine. NEJM
277(5):248–251.
Barratta RO, Ginter MC, Price MA, Walker JW, Skinner RG. et al. 1970. Measles (Rubeola) in previously immunized children. Pediatrics
46(3):397–402.
Conrad JL, Wallace R, and Witte JJ. 1971. The epidemiologic rationale for the failure to eradicate measles in the United States. Am J Publ Health
61(11):2304–2310.
Linnemann CC, Hegg ME Rotte TC et al. 1973. Measles MgE response during re-infection of previously vaccinated children. J Pediatrics
82:798–801.
Gustafson TL, Lievens AW, Brunell PA, Moellenberg RG, Christopher BS et al. 1987. Measles outbreak in a fully immunized secondary-school population. NEJM
316(13):771–774.
Black EI, Berman LL, Reichelt CA, de Pinheiro P et al. 1984. Inadequate immunity to meats in children vaccinated at an early age: effect of revacination. BULL WHO
62(92):315–319.
Robertson SE, Markowitz LE, Dini EF, and Orenstein WA. 1992. A million dollar outbreak: epidemiology, risk factors, and selective revaccination strategy. Publ Health Reports
197(1):24–31.
Sutter RW, Markowitz LE, Bennetch JM, Morris W, Zell ER and Preblud WSR. 1991. Measles among the Amish: a comparative study of meats severity in primary and secondary cases in households. J Infect Dis
163:12–16.
Hedrich AW. 1933. Monthly estimates of the child population “susceptible” to meats, 1900–1931, Baltimore, MD. Am J Hygiene
613–635.
Lennon and Black 1986. Maternally derived meats immunity in the era of vaccine-protected mothers. J Pediatr
108(1):671–676.
Matthews and Feery 1978, Lancet
ii: 1212–1213.
Bell et al. (2012). Lipids in Australian children: cause for concern? 2005—2007 Busselton Health Study. J Paediatr & Child Health
Oct 2012: 863–953.
How can you get infected?
Measles infection occurs through airborne droplets. The contagiousness index is 95%, that is, it is a highly contagious disease. To transmit the infection, direct contact with the patient is necessary; transmission of the virus practically does not occur through common things and third parties.
Cases of the disease are recorded all year round, but more often during the cold season. Children aged 4 and 5 years are most often affected. Babies under one year old who have received antibodies against the virus from their mother are immune in the first 4 months of life. In the future, the immune system weakens, and the child may become infected upon contact with a sick person. The patient remains infectious until the fifth day from the onset of the rash, and with complications until the tenth day.
The only bright spot in all this is the very powerful lifelong immunity after illness.
