History of Failure
Diphtheria is a life threatening disease which
effects the upper respiratory attacking the nose and throat, nerves and heart. The
bacterium that caused diphtheria was first described by Klebs in 1883, and cultivated by
Loeffler in 1884, who applied Koch's postulates and identified Corynebacterium diphtheriae as the agent of the disease. There
are many types of Corynebacterium diphtheriae. Most of them do not cause infections.
Most do not produce the disease causing strain. The
diphtheria bacteria lives in the mouth, nose, throat, or skin. A toxic environment
and horrible eating/drinking habits "feed" the bacterium resulting in full blown
infection. The
disease causing toxin is only produced when a specific strain of Corynebacterium is
infected with the B phage virus. Then the excessive poisoness bacteria is
carried in the blood stream. If not properly addressed, damage to the heart
muscles result putting the human body at further risk for serious cardiac issues.
The first
clinical diagnosis of diphtheria was in the 4th century B.C. References to the disease are
made in ancient Syria and Egypt. In the 17th
century, epidemics swept Europe. The
disease was known as "El garatillo" (the strangler") in Spain. The
disease became known as as "the gullet disease" in Italy and Sicily . In the 18th century, the disease
reached the American colonies where it reached epidemic proportions. In many cases whole
families died of the disease in matter of a few weeks.
Emile
Roux was a French bacteriologist who became the director of Pasteur Institute of Paris in
1904. He was considered a "diphtheria pioneer" having been involved in the
"discovery" of anthrax and rabies vaccines. 1885 Swiss bacteriologist,
Emile Yersin, collaborated with Roux in working on toxins produced by the diphtheria
bacterium. They demonstrated the presence of the toxin in the cell-free culture
fluid of C. diphtheriae which resulted in a full blown diphtheria infection when
injected in animals.
This
vaccine is made by injecting a horse with putrefied beef broth, containing the
diphtheria bacillus, until it has the symptoms of blood poisoning. The injections are
continued until the animal (if it does not die) ceases to react. It is then said to be
immune. The bleeding process then begins, usually on the third day after the last
injection. Two or three gallons of blood are drawn off over six to seven weeks until the
animal is exhausted or dies. The blood contains animal viruses and proteins foreign
to the human body. The blood coagulates, and the clear fluid that rises to the
surface is called serum. (The foreign viruses and proteins are not easily
removed). The antitoxin is removed from the serum and treated with antibiotics.
Two years later, Von
Behring and Kitasato inoculated guinea pigs with a heat-attenuated form of the toxin and
it was assumed that the sera of immunized animals contained an antitoxin able to protect
other susceptible animals against the disease. This modified toxin was then thought
suitable for inoculating animals to obtain antitoxin, only to cause severe local reactions
in humans and could not be used as a vaccine.
In U.S.
(1909), Theobald Smith made efforts to prove that the diphtheria toxin neutralized by
antitoxin (forming a Toxin-Anti-Toxin complex, TAT) gave immunity and eliminated
local reactions seen in the modified toxin. Around 1910, TAT was used for active
inoculation against diphtheria. However, it had 2 draw backs. 1- It was highly toxic, and
the amount injected could result in fatally high toxic levels of diphtheria in the blood.
2- Because the antitoxin mixture was horse serum, the components of the horse serum tended
to produce allergic reactions and make individuals hypersensitive to it. In 1919 this
experimental vaccine was manufactured by the Mulford Company in Philadelphia and approved
by the New York State Health Department as part of the ongoing experimentation. As a
result in Dallas, Texas, ten children died and sixty others seriously became ill. The Mulford Company
paid damages for every case.
In
1913, Schick designed a skin test to determine diphtheria susceptibility and or immunity
in the human body. The Diphtheria toxin will cause an inflammatory reaction when
injected directly into blood vessels or arteries. His test involved injecting a
small dose of the toxin under the skin and evaluating the injection site after 48 hours. A
positive test (inflammatory reaction) was thought to indicate susceptibility (non
immunity). A negative test (no reaction) was assumed to be proof of immunity. Possibility
that the body was able to rid itself without side effects of a full blown infection was
not considered.
In
1924, twenty-five children in Bridgewater and twenty in Concord, were stated
to having been poisoned by the TAT. Many had high fevers with their arms turning
black and swelling to two or three times their normal size. September
of 1924 of the 40 children inoculated with the TAT in a home for infants at Baden,
near Vienna, six died and others suffered from skin necroses at the
injection site.. February 1928, the Lancet mentioned "a more
recent Russian disaster " (Bull. Hygiene, August 1927, p. 667) where 14
children received toxin in place of anatoxin (i.e., toxoid); eight died within two weeks,
four of polyneuritis within a month and two recovered after symptoms of general
intoxication." In the same year there were five deaths
amongst inoculated children in China, and 37 others became very ill.
In 1928, at Bundaberg, Australia, twelve
children out of seventeen who were inoculated
with toxin-antitoxin died, five others became critically ill for quite some time. The
Public Health Department of Queensland and issued the vaccine to be safe.
In 1929, Ramon introduced
the use of formaldehyde and created the diphtheria toxoid. It's safe to assume that he
did so in hopes to reduce the fatalities after vaccination. The use of this chemical
is still used in today's diphtheria vaccines (Dt, dT, DTP and DTaP). It is used as a
germicide (germ destroying agent) to inactivate or kill the diphtheria bacteria prior to
inoculation. However, formaldehyde has been reported as a failure in doing so.
Not only does it fail as a germicide but it is also one of many carcinogenic
(cancer causing) agents used in many pharmaceutical products and to embalm dead bodies.
Failure of the formaldehyde to be a 100% effective germicide resulted in the use of
thimerosal (49.9% mercury). Mercury has also failed as a germicide for vaccines.
Yet it is still being used today because even though it does not kill 100% of
foreign microorganisms it is exposed to, it kills many. Today there are two forms of
this vaccines. The
pediatric DT form contains 3-4 times more diphtheria toxoid than the adult dT form.
Here is the confusing part. The pediatric DT form is contraindicated to be
given to children or adults over 7 years of age because of the increased risks of adverse
reactions. It is more potent with bacteria but safer for the smaller body of infants
and children under 7 years old. When adding the 4 recommended doses, infants
are getting 16 times MORE than adults. We have yet to find the scientific
data which helps makes sense of this.
| The Virus-Toxin
Law was enacted July 1, 1902 four years before the Food, Drug and cosmetic Act brought
biological products under federal regulatory control. It specifies
manufacturing, inspection, licensing, and labeling requirements. This law was the
result of an "accident" with a diphtheria antitoxin that killed several St.
Louis children earlier in the year. They died because the blood of
the horse used for the antitoxin had been contaminated with tetanus bacteria.
The law was revised in 1944 and incorporated in to the Public Health Service Act. |
The Health Director (Arlington Ailes, M.D.) for
three cities ( Lasalle, Peru and Oglesby) of Illinios (United States) reported that
amongst the 30,000 population, there were no cases of diphtheria in two and one-half
years and zero deaths from the disease in three and one-half years, with the use of
toxin-antitoxin nearly zero. However, in Chicago, where toxin-antitoxin was
aggressively used, the infection and death rates of diphtheria were high. This was in
1929.
1926 a one
year old was documented to having received the toxin-antitoxin. In 1927 she was assumed
and declared " Schick-negative" as having developed immunity to Schick's
vaccine. In 1930 she developed diphtheria and given an injection of serum on the
left side of her rear. Three days later she was injected with a second
dose on the opposite side. In three hours her backside began to swell and
became extremely tender. Eventually the whole region became black and gangrenous.
Her condition became increasingly worse, accompanied with severe pain. Twenty-seven
days into the infection she was given a blood transfusion and her skin showed black
and blue bruising, she vomited, lost consciousness and died at the age of five. The third third
and similar case was reported with a 2 year old boy. He also died.
In 1930, at
Medellin, Columbia, South America, forty-eight children were inoculated, and many were
sick during the same night, one
died the following
afternoon, fourteen others (died) within sixty hours and two more within six weeks—a total of sixteen deaths.
Vaccination
against diphtheria was introduced to Germany in 1925. In 1930 diphtheria
inoculations were mandated, and resulting in a 17% increase in the disease and over 60 deaths. After the Second World War, production of the
vaccine was halted. There was a decline in the incidence of the disease which coincided
with the fact that the vaccination was no longer being used. When the vaccine was
reintroduced the decline in the incidence of the disease slowed down.
In 1932, at
Charolles, France, 172 children were inoculated with anatoxin (toxoid). All got sick soon
afterwards, developing local abscesses that required surgery in several cases. In one case the child died. The parents of the children demanded but
received no explanation. In the province of Chiavari over 80 inoculated children
got sick, some being paralysed in arms and legs, others having their sight
injured. One child died. In Venice and Rovigo severe symptoms,
including paralysis were recorded
with ten deaths.
1937 The
British Medical Journal reported the death of a 12 year old girl and infection in 23 other
children from tuberculosis following the inoculation of Toxoid Antitoxin Floccules,
Schick's Diphtheria vaccine.
Between 1939 and
1942 it became evident that the vaccine
did not prevent contraction of the disease. Even more interesting, unvaccinated
people working in Diphtheria clinics had the organisms in their blood and never showed
symptoms of the disease. Despite this
evidence mass vaccinations of Diphtheria continued and contributed to the Diphtheria
incidence in Britain between 1940 and 1955. The largest drop in Diphtheria occurred
between 1865 and 1875, before the bacteria had even been isolated, indicating the spread
of the disease was on the way out all by itself. The antitoxin was first used
experimentally around 1900, and coincided with a large drop in recorded cases.
At the turn of the
century, diphtheria was common, occurring primarily in children, and was one of the
leading causes of death in infants and children in the United States. Data was first
collected in 1920 and show that in the United States there were approximately 150,000
cases and 13,000 deaths reported annually.
Though prevention proved
to be a failure by way of vaccination, vaccination was still being blindly pushed.
During an epidemic in Chicago in 1969, a full 25% of cases had already been injected with
diphtheria vaccine. Clearly suggesting evidence that the vaccine was worthless and
contributed to the incidence of the condition.
From 1970 to 1979, it was
reported that cases occurred only amongst populations that were not given the fully
recommended doses. In other words, if the recommendation was 2 or 3 doses and
individuals received less than that, they were put under the "non-immunized"
category. Copy cat of the polio vaccinations.
STILL FAILING
This vaccine continues to be accompanied with
reports of failure. Infections are admittedly increased in infants following the DPT
vaccinations. Dr. Henry Shinefield agrees by saying, "There are more cases now
than there were in 1945, before we had the vaccine." Dr. Robert Mendelsohn confirms with others that
"Today your child has about as
much chance of contracting diphtheria as she does of being bitten by a cobra."
Vaccinations began in 1977 in Lesotho
German. In 1989 it was admitted that vaccinations may be making the community even
more susceptible to the disease.
Between 1990-1993 an "outbreak"
in Russia was publicized. 1,211 Cases in 1991 which increased by two fold in 1992
with 3,897 cases. 90% of the diagnosed children were reported to be fully vaccinated
with 4 or more doses by the time they had started school. Showing full vaccination
coverage is 100% INeffective in disease prevention. From
1991-1997 Diphtheria was considered to be an epidemic in Australia despite coverage doses
of the DTP of up to 4 among the infected. This resulted in a presumption that
infection despite vaccination simply meant the need for another does
April-August
of 1994 there were18 cases in the Saraburi Province of Italy. Six of the children
were reported to having been given the full vaccine doses recommendation prior to
diagnosis. Once again, full coverage is shown to be a 100% failure in prevention by
those numbers. No reports of how many cases involved incomplete vaccination
"coverage" were made.
The Lancet
put out in one of their 1996 publications on the vaccination's failure in the Ukraine.
The Ukrainian Ministry of Health exposed the fact that in the first 5 months of the
year there were 1,350 cases reported with 15 deaths. Only 510 less than the same time period of
the previous year. Yet, not enough to prove that the Diphtheria vaccination campaign
resulted in a nation wide protection. This nation-wide failed effort readily
admitted by the Ukrainian Ministry of Health. Between 1997-1999 there were 1330 diphtheria cases
reported in northern India. Vaccination rates were high.
2
004 Bhubaneswar, India, 79
schoolchildren in Orissa were clinically sick, 11 of them critically, after being
vaccinated for tetanus and diphtheria as part of the state's immunization program.
2005, there were 20 cases
in Latvia. These were cases of diphtheritic polyneuropathy. In other words,
peripheral nerves were effected. 80% of the infected were considered fully
vaccinated. Again we see a 100% failure in prevention by means of compliance with
recommended doses.
Tetanus
is a problem of wound hygiene; not vaccination status. Tetanus, as a condition, is also known as
"lockjaw", and is caused by a microorganism that produces a potentially fatal
condition characterized by extreme muscular rigidity, spasms of the respiratory muscles,
asphyxia and death. The organism, which is found in soil
and the intestinal tract of some farm animals, usually enters the
body through an open wound. The incubation period for the microorganism varies from one
day to three weeks. Treatment is harsh, and involves the use of artificial airways, muscle
relaxing drugs, antibiotics and antitoxins - in short, hell on earth for whomever
contracts the condition. Since 1976 there have been less than 100 cases in the United
States, and the majority of these have been in individuals over the age of 50. Between
1982 and 1984, 9 cases occurred in children. No deaths occurred in anyone under 30 years
old. The vaccine compliance rate is about 95% with school age children. Prior to
widespread vaccines for this condition, there were about 500 cases per year. It has never
been adequately addressed to whether individuals should unequivocally receive the vaccine
without receiving an injury first.
The
tetanus vaccine is another toxoid vaccine. It elicits a reaction of swelling,
redness and abscesses in 3-13% of those receiving the injection, and allergic reactions
have been documented with repeated exposure. It is assumed that the vaccine will protect
from tetanus. This
assumption of protection came from a study conducted in 1937 where the mice used still
developed tetanus.
Long term side effects are currently unknown. Vaccination is given in a series of four
injections which appears to provide protection for 10 years. There is no known reason to
inject infants with the tetanus toxoid, especially because the infant immune and nervous
systems are not developed and the true effect on the system of the toxoid is unknown.
Children under two years old are not at risk of contracting tetanus, according to the
available research. The first injections should not be given earlier than 12 months of
age, and then every 10 years thereafter. Serious wounds might demand tetanus immune
globulin, made from human tissue sources, which contains antibodies to the tetanus
bacterium; this must be provided within 48 hours or less after any serious injury. If in
doubt, contact a qualified health professional. Tetanus toxoid or immune globulin (TIG)
can be acquired not in combination with any other vaccine, but of course you never know
what else is in the vaccine you receive.
Current ACIP
recommendations, however, oddly include both Diphtheria and Tetanus toxoid administration
in situations of wound management rather than single antigen tetanus toxoid. It is unknown
what effect both of these have together at the same time in the human body, especially in
light of the combination of chemical preservatives present in both vaccines, the
Diphtheria having its origin in animal tissue.
"Some
people having tetanus booster already have antibody levels more than 8000 (eight thousand,
just in case you thought I made a typo) times the protective level needed, suggesting
Australia's regime of a booster every 10 years is in need of a change. Community
physicians say Australia should adopt the UK regime which advises after five doses further
boosters are unnecessary". Back in 1969, tetanus boosters are advised against,
in an article of the New England Journal of Medicine, to keep down toxoid reactions.
"...This
report describes severe, generalized tetanus in a 29-year old man who had received a
primary series as a child and two booster injections. Serum obtained before administration
of tetanus immune globulin showed antibody titers to tetanus greater than 100 times the
level considered protective."
New Engl J Med, 1995, March 23, Volume 332, Number
12, Pgs 761-766: quotes: "one fifth of older children 10 - 16 years of age do not
have protective antibody levels"
- yet we do not see rampant tetanus in USA
BMJ, 13 November 1982, Volume 285 pgs 1393-94.
Tetanus after allogeneic bone-marrow
transplantation.
Scand
Journal of Infectious Diseases, 15:303-306, 1983 - "Overdose of Booster Tetanus
Toxoid Given in Error: Clinical study: repeated
exposure to an antigen, or an overdose of antigen, will not continually enhance the immune
response and may lead to
inhibition or tolerance at either T or B cell level.
Tetanus
has not been eliminated in this country and is reported to be most prevalent in nursing
homes. It is in these places that bedridden patients develop decubitus ulcers or bedsores
that are not properly cared for. The tetanus spore thrives in an open wound that has
gotten dirty and is deprived of oxygen. There is nothing about developing tetanus
and recovering that can impart immunity to this disease. If a person is careless
about wound hygiene s/he may get it again and again regardless of his/her vaccination
status.
Wound
hygiene consists of cleansing the wound properly and keeping it clean. In the case of a
deep puncture wound, be sure it bleeds and clean it with hydrogen peroxide. I always stop
the bleeding, once cleaned, with 60,000 H.U. or stronger cayenne pepper. Cayenne pepper is
a wonderful antiseptic and styptic (equalizes blood pressure and stops bleeding). If the
wound is severe and may require stitching or surgery, it is good to know about comfrey
root powder and basic natural healing principles.
Pertussis (Whooping Cough) is caused by Bordetella
pertussis and was first isolated in 1906. This infection is transmitted by route of
the respiratory by secreted droplets. Incubation period is 5-14 days.
In some cases it can go as long as 21 days.
However,
current recommendations by the Advisory Committee on Immunization Practices recommend DT
doses at 2,4,6 and 12-15 months of age, well before the immune system and neurological
myelination processes have progressed. In other words, infants are still developing their
protective coating around the nervous system called the myelin sheath.
In the 50's
and 60's there were reports of serious neurological complications and deaths following the
triple combination. In the 1990's there were 253 deaths awarded more than 61
million dollars by the US Court of Federal Claims. 224 (86%) were admitted to have
been the result of the triple combination. In 90% of these cases SIDS was the
original listed cause.
“Calculations based on
the mortality of whooping cough before 1957 predict accurately the subsequent decline and
the present low mortality. Notifications of incidence, though variable and
incomplete, follow the same pattern of steady decline in the United Kingdom and are unaffected either by small-scale vaccination beginning about
1948 or by nationwide vaccination beginning in 1957… attack-rates
may be lower and complications fewer in vaccinated children… No protection by
vaccination is demonstrable in infants…Adverse reactions and
neurotoxicity following vaccinations were studied in 160 cases. In 79, the relationship to
pertussis vaccine was strong. In 14 of these cases, reaction was transient but
characteristic of a syndrome of shock and cerebral disturbance, which, in the other 65
cases, was followed by convulsions, hyperkinesis, and severe mental defect. It
seems likely that most adverse reactions are unreported and that many are overlooked.
Precise information about the efficacy and safety of this vaccine is lacking, because
existing provisions, national and international, for epidemiological surveillance and
evaluation are inadequate. The claim by official bodies that the risks of whooping-cough
exceed those of vaccination is questionable, at least in the U.K.”
-Lancet, "Vaccination against whooping-cough.
Efficacy versus risks" 1977, G.T. Stewart (United Kingdom)
In medical
literature, the manufacturer's product label and the CDC/FDA compiled database of adverse
reactions list the following reactions: pericarditis, serum sickness, painful
neuropathies and even severe, transient parkinsonism, headace, nausea, vomiting,
arthralgias, tachycardia (racing heart), syncope (faiting), cranial verve paralysis, EEG
disturbances, seizures, encephalopathy, anaphylaxis and Gillain-Barre Syndrome.
In 1982, Dr.
William C. Torch, Director of child Neurology, University of Nevada School of Medicine
presented a study at the 24th American Academy of pediatrics (AAP) Meeting. His data
showed that the triple combination vaccine "may be a generally unrecognized major
cause of sudden infant and early childhood deaths, and that the risks of immunization may
outweigh it's potential benefits. Because his studies showed negative light to the
multi million dollar vaccination program, they were criticized as unscientific.
In 1983, a
temporal association between the vaccine and SIDS was reported in the Journal of pediatric
Infectious Disease. Of the SIDS cases reported in Los Angels county there were 145
families interviewed. The authors reported that there was a statistically
significant excess of deaths in the first day and first week after DTP. CDC further
states that any family history of convulsions or any other neuorlogical disorders should
not be considered as a risk factor with vaccinations. The lack of science in their
statement is due to the fact that only healthy children are included in prelicensure
trials. Any individuals with pre-exisiting history of convulsions or nuerological
disorders would put the studies at risk for bias conclusion.
Putting aside
apparent risks, do we know that the triple vaccine will boost the immune system and keep
infants/children from acquiring either one of the infections? Pertussis cases after
vaccination were defined and diagnosed only if coughing persists for 21 days or more.
So, children developing pertussis with coughs less than 21 days were not considered
in vaccine trials. This makes it easy for vaccine trial investigators to
"conclude" the efficacy rate of the vaccines to be as high as 95%.
However, according to CDC, "The findings of efficacy studies
have not found a direct correlation between antibody response and protection against pertussis disease."
