http://libnt2.lib.tcu.edu/staff/lruede/autvacc.html
"THE ABCs OF MMRs AND DTPs: IS THERE AN
ASSOCIATION BETWEEN VACCINATION AND AUTISM?" BY ERIC LONDON:
A BIBLIOGRAPHIC ESSAY
rev. 7-21-99
Laura J. Ruede, MLS
Prologue
The February 28, 1998 issue of the prestigious medical journal The
Lancet contained a preliminary report on a study which occasioned much
discussion and controversy: "Ileal-lymphoid-nodular hyperplasia,
non-specific colitis, and pervasive developmental disorder in children,"
by Andrew Wakefield and a team of British scientists.1 The British
group investigated, initially, a group of twelve children; by January 1998
Wakefield’s team totaled fifty-one investigations of children with regressive
autistic spectrum disorders and inflammatory bowel disease and, as of July
1998, had at least one year’s worth of additional examinations scheduled as
parents of similarly autistic children ‘queued up.' Intriguingly, the
scientists found measles virus proteins in the germinal centers of the
children’s intestinal lymphatic tissues, along with indications of classic
inflammatory bowel disease. The children had previously been vaccinated with
the MMR/MR vaccines or had experienced wild measles.
In a recent issue of NAARRATIVE, newsletter of the National
Alliance for Autism Research, issue number 3 from fall 1998, appears an article
entitled, "The ABCs of MMRs and DTPs: Is There an Association
Between Vaccination and Autism?" According to the organization’s web
site description, NAAR is a national nonprofit, tax-exempt organization begun
by parents in 1994, dedicated to finding the causes, effective preventive
strategies, effective treatment and, ultimately, the cure for the autism
spectrum disorders (www.naar.org). As a member of NAAR’s
Scientific Advisory Board, Joseph T. Coyle, MD, commented, "the
pervasive developmental disorders have been neglected unduly but are now
approachable by serious research efforts given the rapid advances in
neuroscience (www.naar.org :
Mission)." NAAR’s stated mission is to fund, promote and support
biomedical research on autism. "NAAR aims," the site states, "to
have an aggressive and far-reaching research program developed with the expert
guidance of its prestigious Scientific Advisory Board."
Unfortunately, the "ABCs" article in NAARRATIVE
newsletter treats pivotal issues using narrowly-selected details from an
equally narrow range of resources, and which contains vague allusions,
unfounded or false statements, and injudicious speculation. The issues raised
in Dr. London’s article are significant and should be considered at length by
autistic persons (where possible) and their families, as well as the
professionals, the pharmaceutical industry, and the units of government whose
work and decisions profoundly effect them. This paper is a work-in-progress
which is offered in the spirit of scholarly inquiry and critical thought, to
assist those attempting to make decisions regarding the vaccination/autism
issue. This paper or parts thereof may be reproduced for purposes of study or
reference. Concerning endnotes, several reference numbers will appear out of
sequence; initially, a traditional reference sequence was adopted--1, 2, etc.,
appearing consecutively; later in this paper's evolution, a random numbering
approach was adopted. Endnote numbers should lead readers to the correct
citations, regardless.
[Link to Eric London’s article on NAAR’s website (NAARRATIVE no. 3,
Summer/Fall 1998) at http://babydoc.home.pipeline.com/naar/naar.htm,
or www.naar.org : NAARRATIVE.]
Contents
Fundamental issues
Cause(s)
of autism
The attenuated
virus: infectious or not?
The Wakefield
study—and others
Vaccine necessity:
manufactured epidemics
The ‘Thalidomide
Connection’
Popular statistics
(Vaccine safety, efficacy and other figures)
Factoid Fallacies
Autism
and schizophrenia
Brain autopsies and
imaging
Scientific evidence
"Vaccinations
Save Lives"
The myth of disease
eradication
"Vaccines are
safe and effective"
The danger of
vaccine-preventable diseases
The autoimmune
theory of autism
The purpose of
vaccination
Measles vaccine
fears
Should you
vaccinate your children?
Caveats
Consider
the source
Conflicts of
interest
Scientific
propaganda
Parents vs.
professionals?
The psychology of
causal attribution
Autism research
overdue
NAAR representation
and support
Fundamental issues
The cause(s)
of autism
In "The ABCs…" London
asserts that autism has been proven to be a simple (single-faceted) genetic
disorder which begins before birth, and thus is not related in any way to
vaccination, but cites only a few selected studies in supporting this idea. In
formulating his argument he casts doubt on the validity of the memories and
reasoning of parents who observe a period of initial normality in their
children, before vaccination. The first major failure of reporting in this
article lies in the lack of differentiation between typical, or
"Kanner’s," autism and atypical or regressive autism, and childhood
disintegrative disorder—or any of the other pervasive developmental disorders.
The next lies in London’s argument that autism is either solely genetic, or a
result of genetic traits combined with prenatal environmental influences, as
opposed to immunological insults after birth. In fact, the only proven genetic
causes of autism to date are well-defined syndromes like the Fragile X
chromosome anomaly—which do not explain the autism of any of the children
"ABCs" concerns. London’s thesis is contradicted in important works
from the autism literature, and even in some of the works he cites:
Diagnostic
and Statistical Manual of Mental Disorders: DSM-IV (fourth edition), 1994, pages 66 and 69. DSM-IV specifies that "Autistic
Disorder (defined as "early infantile autism…or Kanner’s autism")
must be differentiated from other Pervasive Developmental Disorders…
Autistic disorder differs from Childhood Disintegrative Disorder,
which has a distinctive pattern of developmental regression following at least 2 years of normal development.
In Autistic Disorder, developmental abnormalities are usually noted within the
first year of life," pages 66 and 69 [emphases mine]. [It is important to
note that DSM-IV’s definition of autistic disorder differs markedly from
earlier definitions, and that autistic spectrum subtypes are still very much in
the definition stage.]
Cohen and Volkmar, eds., Handbook of Autism
and the Pervasive Developmental Disorders, 2nd edition, 1997:
Chapter 18, MEDICAL CONDITIONS[:] Infections…Immunological Association[:]
The claim has been made that a small but significant proportion of children
develop autism as a result of pre-or post-natal infections—for example, with rubella, cytomegalovirus, herpes
simplex, HIV, and so on…Interest in the immune system and autism arises from
the various case reports in which infections (and possibly altered immune
response) are associated with the development of autism or autistic
features" (p. 398).
Margaret L. Bauman
and Thomas Kemper’s The Neurobiology of Autism (Johns Hopkins Press),
1994, is listed among London’s references at the conclusion of "ABCs;"
the work of Bauman and Anthony Bailey are also used by London as supports for
the idea that autism results from a genetic, prenatal maldevelopment of the
brain—yet the Introduction to Neurobiology, written by Isabelle Rapin,
clearly states, "missing from this book, because of the dearth
of prospective information, is a focus on the many potential nongenetic
etiologies of the autistic spectrum… Another topic of interest,
because of its potential therapeutic implications, that is not considered as
such in this book is autistic regression. At least 40 percent of
parents report that their infant or toddler, whose development may or may not
have been entirely normal up to then, experienced a regression, usually
insidious but occasionally abrupt,
in language, sociability, and play… Development resumes after a plateau…but, in
most cases, never returns to its previous level… Many speculations have
been offered…to explain autistic regression: slow viral infection, autoimmune
phenomenon, lack or insufficiency of a growth factor at a particular
time in development... Data need to be collected to investigate these
speculations" (pages 13-14).
Bauman and Kemper resume, in chapter 2, "The Genetics of Autism,"
with the following passages occurring on pages 30 to 31 of Neurobiology:
Environmental
Factors[:] In examining the
importance of genetic factors in the etiology of autism, evidence for
environmental factors should be reviewed as well. Unfavorable pre-, peri-, and
neonatal factors have been shown to occur more commonly in autistic individuals
than normal controls….. Modes of Inheritance[:] Although the importance
of hereditary factors in the etiology of idiopathic autism is well established,
particularly genetic mechanisms have not yet been identified…it is almost
certain that autism is an etiologically heterogeneous [multi-causal]
disorder. It is known, for example, that autism can develop in
association with etiologies as diverse as congenital rubella, tuberous
sclerosis, and the fragile X anomaly, as well
as in the absence of any identifiable, co-occurring, etiologically defined
condition [emphases mine]. Among autistic individuals without identifiable,
associated etiologic conditions, several points suggest that there may also be
genetic heterogeneity. [See also the discussion of T. C. Binstock's research
paper, "Changing the autism paradigm: a critique of Kemper &
Bauman's speculations regarding in-utero timing," in Factoid fallacies, below.]
Journal
of Autism and Developmental Disorders, vol. 28, no. 5. 1998 (entirely devoted to the genetics of autism; preface
by Eric Fombonne): as one would surmise, the general tone of the separate
contributions indicate the strong possibility of a genetic component in autism
(though the writers rarely differentiate between subtypes), but this research
is far from finished, and does not exclude other factors, as London implies. In
P. Szatmari, et al., "Genetics of Autism: Overview and New Directions,"
the authors observe that the genetics of autism in its various manifestations
is likely to involve the complex interaction of multiple genes, but even in
this event "it is too early to say what type of complex genetic disease
autism/PDD represents." A variety of factors may interact to produce these
conditions (pages 355; 365)—possibly different mechanisms for each ‘type’ of
autism (page 365). The authors venture so far as to say that "certain
severe insults" during pregnancy and birth might "play a causative
role in the development of PDD: "For some children, genetic
vulnerability may interact with insults on the developing nervous system to
lead to autism." Such insults might
lead to PDD even in the absence of genetic factors—for instance, thalidomide
exposure or congenital rubella (page 364). The authors do not examine the
period of development after birth, but it is likely that the same reasoning
could apply to the developing nervous system during the first three years of life—or
even later.
Marian Sigman and
Lisa Capps’ Children With Autism: a Developmental Perspective (Harvard
University Press), 1997 asks, in Chapter 8, In Search of Core Deficits and
Causes: "What Are the Causes of Autism?" "Autism
is not a unitary disease with a single etiology," the authors state.
"It is a heterogeneous behavioral syndrome found in association with
many etiologies…Complications in any part of… development…could cause damage
that leads to autism. Infections affecting the central nervous system in
early life could also have this effect (pp. 171-2). Evidence for genetic
factors is mounting, they note, but "it is not clear, however, whether
all forms of autism are genetically transmitted in the same way (pp.
172-3)." Syndromes like the fragile X-chromosome anomaly and tuberous
sclerosis are distinct from other pervasive developmental disorders.
"Autism accompanied by mental retardation is inherited differently than
when not…" Evidence suggests that multiple genes are involved (pp.
173-4).
C. Gillberg and M.
Coleman, The Biology of the Autistic Syndromes—2nd edition, 1992.
Chapter 8, GENETIC FACTORS[:] "It is currently believed that a genetic
disease underlies 10 to 20 percent of all autism cases…" (page 96);
"There is another autism subgroup in which the autistic symptomatology is
linked to disease processes currently thought to be, in many instances, of a
non-genetic (or at least ‘non-inherited’) character" (page 103). Chapter
18, INFECTIOUS DISEASES[:] Postnatal infections[:] …Can an infection
after birth cause an autistic syndrome? "…In summary…infectious
agents in the prenatal or postnatal period may be a factor in the development
of autism. The most common mechanism appears to be a direct toxic effect on
brain cells from the infection (encephalitis)… It is of interest that, in
reports concerning both rubella and HSV infections, cases with late onset are
found. An infectious aetiology is a strong contender in the
differential diagnosis of autistic symptoms…"
(pages 222-4).
Schopler and Mesibov,
eds., Diagnosis and Assessment in Autism (1988). Chapter authors
Schopler and Michael Rutter note on page 28, "[Considering] the very
fact that the clinical picture of autism can arise from diseases as diverse as
congenital rubella, tuberous sclerosis, encephalopathy…cerebral lipoidosis, and
neurofibromatosis…it remains quite uncertain whether the…cases with a known
pathologic cause represent phenocopies of some other unitary disorder with
(an as yet undiscovered) single etiology…." Page 86 quotes
Volkmar and Cohen, "…it is clear that the preponderance of available
evidence suggests the importance of multiple biologic factors acting through
one or more mechanisms to produce the autistic syndrome." On pages
295-6, chapter authors Watson and Marcus note the importance of a medical
assessment paralleling psychological and other testing: "it is
important to recognize the possible medical factors associated with autism. A
variety of biologic conditions have been documented including…certain viral
infections, abnormalities in purine metabolism and intestinal absorption…" The authors refer readers to Coleman and
Gillberg, quoted above, for comprehensive information on the medical aspects of
autism.
Shirley Cohen, Targeting
Autism, 1998, pages 139 and 140: "There is increasing evidence of
immune system abnormalities in autism. A substantial number of reports of
research on this subject have appeared in medical journals since the 1980s, and
most of these articles present data that appear to support the theory of a
connection between immune system dysfunction and some cases of autism…study
of immune system abnormalities in autism has attained the status of mainstream
medical research."
The Centers for
Disease Control, [1998],
"Vaccines and Autism: Is There a Relationship?" (http://www.cdc.gov/nip/vacsafe/vac_autism.htm):
Notoriously pro-vaccine, the CDC nevertheless says, of autism, "Some
prenatal factors included intrauterine rubella; tuberous sclerosis;
chromosomal abnormalities, such as Down’s Syndrome, as well as brain
abnormalities, like hydrocephalus. …postnatal conditions associated with
autism are untreated phenylketonuria, infantile spasms, and herpes
simplex encephalitis. …Evidence that genetics is an important,
but not exclusive, cause of autism includes a three to eight
percent risk of recurrence in families with one affected child. …An
issue unresolved [by a working group convened by the National
Institutes of Health in 1995] was
the role of immune factors in autism spectrum disorders; it was suggested that
studies to clarify the situation are needed."
Uta Frith,
Autism: Explaining the Enigma, 1989/1994, p. 79, "The theory
that psychotic illness can be due to immune dysfunction and/or viral infection
has particular justification in the area of Autism. It has been shown …that a
virus infection in a young child preceded the onset of typical symptoms of
Autism, before which there was a period of apparently normal development…If the
central nervous system becomes infected at a critical time, either before or
after birth, Autism may result…Of special
interest are certain types of virus called retrovirus, which totally integrate
themselves in genetic material in the body cells…These can remain dormant for
years but from time to time can be reactivated."
Van Gent, et al. present a review of the
literature in the emerging field of "psychoneuroimmunology" through
1997 in "Autism and the Immune System," Journal of Child Psychology
and Psychiatry, vol. 38 no. 3, March 1997, pp. 337-349. "Over the last
30 years increasing evidence has been found for the existence of complex links
between the immune system, the central nervous system and the endocrine system
on the one hand, and psychological phenomena…on the other…: prenatal and early
childhood experiences could have prominent effects on the development of the
responsiveness of the immune system, with far-reaching and long-lasting
consequences for the immune capacity at a later age. Conversely, early
derailments in the normal development of immune function, as, for instance, in
the induction of autoimmunity in an early phase of the immunological
developmental traject, could have important effects on the development of the
nervous and endocrine systems… [Regarding autism,] two etiologically relevant
immune hypotheses in particular have emerged: a viral and an autoimmune
hypothesis, which are interrelated (p.345). The basic neuroimmunologic premise of these hypotheses
is that autoimmune and/or viral processes in some way affect the nervous system
and alter central nervous system activity" (pages 337-8).
William Shaw, Biological
Treatments for Autism and PDD, 1998. Shaw reports finding in children with
autism and PDD none of the signs characteristic of known, inborn (genetic)
conditions causing metabolic disorders (pages 31; 35-37; 68-9; 129). On pages
103-4, "Role of immunizations in causing immune deficiencies[:]
"In several cases, electron microscopy has revealed live measles virus in
the intestinal lining of children with autism,
raising the possibility that the MMR may actually be responsible for some of
the gastrointestinal abnormalities common in children with autism." Shaw
also notes "some interesting parallels between autism and tetanus," citing Ellen Bolte’s paper, "Autism and
Clostridium Tetani: An Hypothesis" [Medical Hypotheses, vol.
51, 1998, pages 133-144] (Shaw page 22).
H. H. Fudenberg,
NeuroImmuno Therapeutics Research Foundation, "Classic Infantile
Onset Autism is an Autoimmune Disease,"
http://members.aol.com/nitrf/autism1.htm,
accessed May 20, 1998:2 In the process of describing transfer factor
therapy studied in 40 autistic patients, Fudenberg notes, "The gene for
classic autism has been localized to human chromosome-6, the site of human
immune response genes and [is] linked to haplotypes containing the C4 null
allele."
"Role of
Immunogenetics in the Diagnosis of Postvaccinal CNS Pathology,"
Massimo Montinari, et al., Department of Pediatric Surgery, University of Bari,
Italy, presented May 9, 1996 (text available http://www.healthy.net/library/articles/coulter/biochem.htm):
after thirty children were found to have signs of central nervous system and
genetic damage following vaccination, the authors remark, "A
study of the disease associated with genes of the HLA system has shown that
this genetic complex can be responsible for a particular genetic
susceptibility, predisposing to various diseases characterized predominantly by
immune-system pathogenesis… results indicate
that autoimmune pathology is more frequent in countries where vaccination is
more widespread….." [A fuller description of this study will be found in
"The attenuated virus--infectious or not?" below.]
T. Binstock,
Researcher in Developmental & Behavioral Neuroanatomy, Denver, Colorado,
"Familial does not mandate genetic[:]…Four categories of familial
illness or disorder." "Only one of [the first] three categories
is purely genetic [--category A:]" A) familial occurrences indicating an
actual gene-mutation that is hereditary; B) familial occurrences reflecting a
genetically encoded susceptibility factor; C) familial illness via
environmental factors. D) familial clustering of increased small intestinal
permeability in families with Crohn's Disease. In category B, "the mutated
gene is not the primary cause but is merely an inborn way that a person
is more statistically likely, over time, to experience the primary cause. Genetically
encoded immunodeficiencies are an example of 'susceptibility factor.' [With
autism,] the most common genetic susceptibility factor is having a null allele
of complement 4b" (referenced communication
to Autism listserv originating at St. Johns, University, New York
[autism@maelstrom.stjohns.edu], September 16, 1997, 08:39:13 -0700).
G. Trottier et al.,
"Etiology of infantile autism: a review of recent advances in genetic
and neurobiological research" (Journal of Psychiatry and
Neuroscience, vol. 24, no. 2, March 1999, pp. 103-15): "The etiology
of autism is complex, and in most cases the underlying pathologic mechanisms
are unknown… Recent research has investigated…immunological factors. On the basis of family and twin studies, there
appears to be a genetic basis for a wide 'autistic syndrome.' …Autoimmunity
also may play a role; antibodies against myelin basic protein are often found
in children with autism, who also have increased eosinophil and basophil
response to IgE-mediated reactions. In summary, the prevailing view is
that autism is caused by a pathophysiologic process arising from the
interaction of an early environmental insult and a genetic predisposition."
A. M. Comi, et al.,
"Familial clustering of autoimmune disorders and evaluation of medical
risk factors in autism" (Journal of Child Neurology, vol. 14,
no. 6, June 1999, pp. 388-94): "Autism is an age-dependent neurologic
disorder that is often associated with autoimmune disorders in the patients’
relatives… The most common autoimmune disorders…[are] type 1 diabetes, adult
rheumatoid arthritis, hypothyroidism, and systemic lupus erythematosus… An
increased number of autoimmune disorders [in patients’ families] suggests that
in some families with autism, immune dysfunction could interact with various
environmental factors to play a role in autism pathogenesis."
Barak, Y., et al.,
"Autistic subjects with comorbid epilepsy: a possible association with
viral infections" (Child Psychiatry and Human Development, vol.
29, no. 3, Spring 1998, pp. 245-51): "This study evaluates the comorbidity
of epilepsy as a variable supporting a viral hypothesis in Autism. Data
covering a thirty-year period (1960-1989)…were collected… The annual birth
pattern of subjects with comorbid epilepsy fit the seasonality of viral
meningitis. These findings support the role of viral C.N.S. infections in the
causality of this disorder."
"Serological
Association of Measles Virus and Human Herpesvirus-6 With Brain Autoantibodies
in Autism" (Clinical Immunology and Immunopathology vol. 89,
number 1, October 1998, pp. 105-8): this study is the first to report an
association between virus serology and brain autoantibody in autism; it
supports the hypothesis that a virus-induced autoimmune response may play a
causal role in autism.
The pattern of normality
followed by regression, loss of development, or halted development and
appearance of odd behavioral features was not fabricated by parents, as London
implies; it is well represented in the autism literature. Probing the issue of
genetics in autism, an important possibility goes unmentioned in London’s
"ABCs:" the genetic factor in regressive autisms and PDDs
could well be a particular configuration of immune system components—in
essence, vulnerabilities in the immune system such that affected children
cannot adequately deal with the challenges posed by the current, frequently
trivalent live-virus vaccines. Like Fudenberg, Van Gent, et al. observe that
"the immune response is regulated by genetic material located mainly on
the sixth chromosome." Failure or lack of crucial components within
this system can lead to disruption of normal cell-mediated immune responses.
Virus infections may induce autoimmunity, and autoimmunity may result in
increased susceptibility to infections and subsequent damage to the CNS.
Besides viral infections as a cause, it is possible that "a genetic predisposition to
a relative deficiency of specific immune cells may be involved" (pp.
344-5).
The
attenuated virus: infectious or not?
Oddly, rubella and other
viral infections have been considered causal for autism if they occur before
birth, or after birth if they occur ‘naturally,’ as in measles encephalitis,
but not if they occur after vaccination. On page 16 of the NAARRATIVE issue in
question, London claims that the viruses in vaccines are either dead or
attenuated, and thus "can no longer cause disease." That live,
attenuated viruses cannot cause disease is an astounding assertion given that,
first, many polio cases have been caused by the oral polio vaccine—sometimes in
persons caring for the vaccinee.3 Jonas Salk, its inventor, once
commented that the polio vaccine is the leading cause of polio today. An issue
of Pediatrics (vol. 84, no. 5, November 1989, pp. 851-5) studies "Anemia
of a mild viral infection: [using] the measles vaccine as a model."
In this study, live attenuated measles virus was given to 93 infants in order
to induce mild viral infections, in order to study hematologic changes
(hemoglobin was shown to drop significantly in these infants). According to Molecular
Virology, 1994, Chapter 3, Vaccines and Immunotherapy, "all
live viruses are subject to a range of concerns… (p. 76)." Page 78
charts advantages and disadvantages of the different types of vaccines: live
attenuated vaccine viruses can not only revert to virulence, but "may cause
[a] mild form of disease;" or, due to the presence of viral genomes,
"may be[come] pathogenic or oncogenic (cancer causing) in some [people’s]
systems."4 Aside from these forms of infection, persistent
(also called chronic, or ‘slow’) or latent infections may be engendered by
viruses (MV, pp. 39-41). Viral "replication strategies may enable
them to remain intracellular, either as latent or as persistent infections.
Their replication, or their mere presence in the cell, may interfere with
differentiated cell functions…Viruses have the potential to cause a number
of pathological changes, which may have profound and long-lasting clinical
effects even after the virus has been eliminated from the body" (Van
Gent, pages 340-341). In Van Gent, p. 341, the authors warn that the immune
system is particularly susceptible to tolerance induction when the cells of the
immune system have not yet reached maturity. The condition of viral ‘tolerance’
is explained in Molecular Virology (David R. Harper, Bios Scientific
Publishers, 1994), pages 39-40, and in The Immunology of the Immune System
(Oxford University Press, 1977), pages 77-78.
Chronic viral infections can reactivate,
moreover—sometimes years after initial infection. In Subacute Sclerosing
Panencephalitis (SSPE), "virus replicates at low levels without producing
infectious virus with altered production of viral proteins and an atypical
immune response" (MV, p.39). But there is still another means by which a
live virus vaccine can cause disease: since vaccine viruses are grown in animal
or human cells, contaminating or endogenous (‘produced from within’) animal
viruses can inhabit the vaccine and infect a vaccinated individual. Early
batches of killed polio vaccine, for instance, were found to be contaminated with
Simian Virus 40 (Molecular Virology, pp. 39-43; 75-6; 78-9), which has
been linked with cancer years after infection. Other animal viruses—and viral
proteins—have been known to contaminate vaccines, due to the use of particular
animal cells or tissues in vaccine-making. Dr. John W. Martin has done
extensive work in detecting such "stealth viruses" in the systems of
vaccinees (texts of numerous papers and conference presentations are available
at http://www.ccid.org ). Contamination can
also occur in a more limited setting, as with bacterial contamination during
the manufacturing process. Accidents of other kinds can occur with vaccine
manufacture, as with incomplete or incorrect inactivation or attenuation.
Viral infection--whether by vaccine viruses
or those contacted in the environment--can cause or precipitate chronic disease
in astonishing variety. Determined and skillful survivors, viruses can change
form when "eradicated" by vaccines and reappear as new diseases,
which seemingly unrelated to the original infection (at least, until viral
proteins or other indications are discovered in researching these diseases).
Live viruses from vaccines can bring about the death of vaccinees--either
immediately after vaccination or years afterward--and can interact dangerously
with antibodies already present in "second-generation" vaccinees
(e.g., vaccinated children of fully-vaccinated parents). Due to their nature
and methods of survival, in addition, vaccine viruses can change the very
nature of their human hosts by altering genetic coding.
SELECTED STUDIES AND ARTICLES CONCERNING
VACCINE VIRUSES
Acute reactions to vaccines
"Febrile
seizures in the developing brain result in persistent modification of neuronal
excitability in limbic circuits," (Nature Medicine, vol. 5, no. 8,
August 1999, pp. 888-894):
Acute infection by
vaccine viruses
"Mumps
meningitis following measles, mumps, and rubella immunisation
[letter]" (The Lancet, vol. 2, July 8, 1989, p. 98; comments in
vol. 2, August 12, 1989, pp. 394-5; vol. 2, September 16, 1989, p. 677): in the
primary letter, mumps meningitis was reported in a three-year-old girl
twenty-one days after measles, mumps, and rubella (MMR) immunization. The child
exhibited lethargy, vomiting, headache, dry cough, fever, irritability, and
meningeal irritation. There was no known exposure to the measles, mumps or
rubella natural infections. No bacterial or other infections were found. In the
August 12 issue of Lancet, a West German physician reported, also in a
letter, a two-year-old boy with mumps meningitis twenty-one days following a
different manufacturer's MMR vaccine. There was no exposure to natural mumps
virus. The author of August 12 concludes, "The incubation time for
mumps is about 21 days. In some patients, time-lag between immunisation and
manifestation of meningitis was very close to 3 weeks, without known previous
mumps contacts. These facts strongly suggest that some patients may have had
vaccine mumps meningitis, and not wild mumps infection." In the
September 16 issue of Lancet, two British physicians report two
16-month-old boys with mumps meningitis admitted to the hospital 18 and 19 days
following MMR immunization. Mumps virus was isolated from cerebrospinal fluid
of both boys. One boy did not exhibit a rise in mumps antibodies in spite of
vaccination and post-vaccinal meningitis. [Other vaccinal mumps meningitis
citations: "Mumps meningitis, possibly vaccine related," Canada
Disease Weekly Report, vol. 14-40, 1988, pp. 209-11; "A case of mumps
meningitis: a post-immunization complication?" Canada Disease Weekly
Report, vol. 13-35, 1987, pp. 155-6; "A case of mumps meningitis: a
complication of vaccination?" Canadian Medical Association Journal,
vol. 138, 1988, p. 135; "Vaccine-induced mumps-like disease," Development
of Biological Standards, vol. 43, 1978, pp. 269-72; "Aseptic
meningitis after vaccination against measles and mumps," Paediatric
Infectious Diseases, vol. 8, 1989, pp. 302-8.]
"Epidemics
of aseptic meningitis due to enteroviruses following national immunization days
in Bahrain" (Annals of Tropical Paediatrics, vol. 18, no. 2,
June 1998, pp. 101-9): Two successive epidemics of aseptic meningitis due to
enteroviruses were observed after national immunization days against polio,
comprising 286 and 169 cases, respectively, from July 1995-September 1996.
Another report, "Update of enterovirus infection in infants and
children" states, in a section titled "Viral meningitis,"
that natural polioviruses were an important cause of viral meningitis before
vaccination (cases were called "nonparalytic poliomyelitis"). Now,
"rare" cases of viral meningitis are attributed to the attenuated
polioviruses in vaccines, in both vaccine recipients and their contacts (Pediatric
Bulletin, http://home.coqui.net/myrna/virus.htm).
"Disease
caused by Haemophilus influenzae type b in the immediate period after
homologous immunization: immunologic investigation" (Pediatrics,
vol. 85, number 4 part 2, April 1990, pp. 698-704): "One concern with the
use of [current HIB vaccines] was the suggestion that the incidence of invasive
disease caused by H influenzae type b in the immediate period after
immunization might be increased; this idea was supported by evidence from
several sources." In one case-controlled study, 4 children were
hospitalized for invasive disease within 1 week of immunization; the rate of
invasive disease was 6.4 times greater than the background rate in unvaccinated
children.
"Neurologic
complications associated with oral poliovirus vaccine and genomic variability
of the vaccine strains after multiplication in humans," Acta
Virologica, vol. 42, number 3, June 1998, pp. 187-94: The oral poliovirus
vaccine (OPV) sometimes occasions paralytic poliomyelitis in vaccine recipients
and their susceptible contacts. Molecular biology studies of polioviruses from these
patients demonstrate genomic modifications known or suspected to increase
neurovirulence. The same genomic modifications have been identified in strains
isolated from non-symptomatic vaccinees. Other neurologic complications such as
meningitis, encephalitis, convulsions, transverse myelitis and Guillain-Barre
Syndrome have also been associated with this vaccine.
"Paralytic
poliomyelitis in a rural area of north India" (National Medical
Journal of India, vol. 10, no. 1, January-February 1997, pages 8-10): In a
house-to-house survey conducted between 1990 and 1991, several cases of
paralytic poliomyelitis were identified, 60 percent of which had had
intramuscular injections preceeding paralysis, in treatment of minor fevers.
"Poliomyelitis
trends in Pondicherry, south India, 1989-91" (Journal of
Epidemiology and Community Health [London], vol. 51, no. 4, August 1997,
pages 443-48): About 54 percent of children lamed as a result of poliomyelitis
had received three doses of oral polio vaccine before the onset of paralysis.
"Paralytic
Poliomyelitis -- United States, 1980-1984" (Morbidity Mortality
Weekly Report, vo. 46, no. 4, January 31, 1997, pp. 79-83): The Advisory
Committee on Immunization Practices (ACIP) observes that vaccine-associated
paralytic poliomyelitis (VAPP) continues to occur; the risk of VAPP has not
decreased. Of 125 cases associated with the vaccine, 46 cases occurred among contacts
of vaccine recipients.
"Comparative
evaluation of immunization with live attenuated and inactivated polio vaccines"
(Annals of the New York Academy of Science, vol. 754, May 31, 1995, pp.
97-107): With both oral attenuated polio vaccine (OPV) and the enhanced potency
inactivated polio vaccine (EP-IPV), revertant or non-revertant viral shedding
occurred in body wastes for up to 60 days following vaccination. The authors
concede, after saying the combined polio vaccines should be effective in
establishing immunity in recipients, and should lower the rate of
vaccine-associated paralytic poliomyelitis (VAPP) in recipients, that VAPP is
expected to continue effecting susceptible contacts.
"Poliomyelitis
associated with type-2 poliovirus vaccine strain. Possible transmission from an
immunised child to a non-immunised child" (The Lancet, vol. 1,
March 30, 1968, pp. 661-3): a sixteen-month-old boy hospitalized for high fever
and paralysis had never received any poliovirus vaccine. From playing and
sharing a bed with a cousin, he apparently had contracted paralytic
poliomyelitis from the cousin, who had received type-2 oral poliovirus vaccine
thirty-three days before. Virological and serological investigation revealed a
vaccine-like strain of type-2 poliovirus. The patient's history revealed no
particular susceptibility to infections.
L. J. Morse, et
al., Journal of the American Medical Association, vol. 197, 1966, p.
1034: A case of paralytic poliomyelitis in an unvaccinated mother was reported,
apparently acquired after exposure to her infant, who had received trivalent
live, oral polio vaccine twenty-two days earlier.
"Transmission
of vaccine strain varicella-zoster virus from a healthy adult with
vaccine-associated rash to susceptible household contacts" (Journal
of Infectious Disease, vol. 176, no. 4, October 1997, pp. 1072-5): Twelve
days after receiving an investigational Oka strain live attenuated varicella
vaccine, a 38-year-old healthy woman developed a rash consisting of 30
scattered lesions. Sixteen days later, her two children also developed a rash.
Varicella-zoster DNA obtained from the skin lesions was determined to be the vaccine
type. "This case documents transmission of varicella vaccine type virus
from a healthy vaccinee to susceptible household contacts…ongoing studies will
define the frequency of this transmission."
"Live Virus
Vaccines, High-Dose Steroids Don't Mix" (Pediatric News, cited
November 28, 1998, via@access1.net, 10:49
a.m.): Dr. Larry K. Pickering, a member of the American Academy of Pediatrics'
"Red Book Committee," was quoted following a meeting at the
University of South Dakota, saying children receiving more than 2 mg/kg per day
of systemic glucocorticoids should not be given live virus vaccines, due to the
risk of disseminated infection from the vaccines. Killed virus vaccines do not
present the same risk. [Note: steroids such as prednisone partially suppress
the immune system.]
"Acute
encephalopathy followed by permanent brain injury or death associated with
further attenuated measles vaccines: a review of claims submitted to the
National Vaccine Injury Compensation Program," Pediatrics, vol.
101, no. 3, Part 1, March 1998; pages 383-387: This study details cases wherein
48 children, ages 10 to 49 months, who had been so affected. Eight children
died, and the remainder had mental regression and retardation, chronic
seizures, motor and sensory deficits, and movement disorders. "CONCLUSIONS: This
clustering suggests that a causal relationship between measles vaccine and
encephalopathy may exist as a rare complication of measles immunization."
[Note regarding rarity: A huge number of vaccine reactions are never
reported, and most of the thousands of vaccine injuries which are reported do
not meet the current, very narrow VAERS/FDA criteria (a very few specific
symptoms must occur within a very short timespan, in order for symtoms to be
considered vaccine-related), and thus are not reported as vaccine-injury cases
by government tabulators. Serious vaccine complications thus are said to be
"rare" in quoted statistics. If independent research proves that the
measles vaccine and PDD/autism are causally related, this kind of vaccine
damage will inflate by thousands the cases of vaccine damage now on record.
This tally, then, may be inflated further by the number of ADD/ADHD-diagnosed
children with inflammatory bowel disorders, per the Georgetown University study
cited in "Wakefield," below.]
"Measles-Mumps-Rubella
(MMR) Vaccine as a Potential Cause of Encephalitis (Brain Inflammation) in
Children," Harold E. Buttram, MD, Townsend Letters, December 1997
(available at http://www.mercola.com/issue5.htm).
Childhood autism is the result of encephalitis affecting primarily the limbic
system of the brain, located below the cerebral cortex. A relatively few number
of cases are due to genetic causes, but officially the great majority are of
unknown causes. It is now generally thought that the process of encephalitis,
whether from wild viruses of live-virus vaccines, is associated with an
interference with the myelination process brought about by the development of
antibodies against myelin basic protein, a constituent of the myelin sheaths.
Chronic infection by
vaccine viruses
"Effect
of subclinical infection on maintaining immunity against measles in vaccinated
children in West Africa" (The Lancet, vol. 353, January 9,
1999, pp. 98-102): Exposure to natural measles in 87 vaccinated children
yielded 39 subclinical cases of measles. Antibody concentrations increased
45-fold and remained raised for at least six months [note: in such a recent
study, opportunity has not yet presented itself to ascertain antibody levels
one or two years after vaccination, etc.].
E. R. Bolte, "Autism
and clostridium tetani" (Medical Hypotheses vol. 51, 1998, pp.
133-144): "This paper outlines the possibility of a subacute, chronic
tetanus infection of the intestinal tract as the underlying cause for symptoms
of autism observed in some individuals. A significant percentage of individuals
with autism have a history of extensive antibiotic use. Oral antibiotics
significantly disrupt protective intestinal microbiota, creating a favorable
environment for colonization by opportunistic pathogens. Clostridium tetani is
an ubiquitous anaerobic bacillus that produces a potent neurotoxin. Intestinal
colonization by C. tetani, and subsequent neurotoxin release, have been
demonstrated in laboratory animals… The vagus nerve is capable of transporting
tetanus neurotoxin (TeNT) and provides a route of ascent form the intestinal
tract to the CNS…once in the brain, TeNT disrupts the release of
neurotransmitters by the proteolytic cleavage of ynaptobrevin… Lab animals
injected in the brain with TeNT have exhibited many of these behaviors. Some
children with autism have also shown a significant reduction in stereotyped behaviors
when treated with antimicrobials effective against intestinal clostridia… A
review of atypical tetanus cases, and strategies to test the validity of this
paper's hypothesis, are included."
T. Zecca, D.
Grafino, et al., University of Medicine and Dentistry, New Jersey and
Children's Hospital of New Jersey, Newark, "Elevated rubeola [measles]
titers in autistic children linked to MMR vaccine" (abstract
submitted to the National Institutes of Health, 1997-8; text available at http://webpages.netlink.co.nz/~ias/mmraut1.htm):
Rubeola (measles) titers were compared in autistic and normal children.
Children diagnosed with autism revealed "a three fold increase" in
their rubeola titers over expected normal range. "A Wilcoxon Kruskal
Wallas test comparing 13 rubeola titers from normal children reveals a
statistically significant P-value of 0.0050." The authors note that
neurological sequelae following MMR are widely reported: "MMR therefore
may play a role in the pathogenesis of Autism. The elevated titers of
anti-measles antibodies in Autistic children may signify a chronic activation
of the immune system against this neurotropic virus."
H. Trier and T.
Ronne, "Duration of immunity and occurrence of secondary vaccine
failure following vaccination against measles, mumps and rubella" (Ugeskr
Laeger, vo. 154, no. 29, July 13, 1992, pp. 2008-13): While discussing loss
of immunity after vaccination, the authors observe, "Subclinical infection
is not uncommon after all three vaccines."
"Characterisation
of poxviruses from sporadic human infections" (South African
Medical Journal, vol. 72, no. 12, December 19, 1987, pp. 846-8): An
orthopoxvirus was isolated from…a man in Natal who died in coma… Analysis of
the viral DNA showed that it was a vaccinia virus, more closely related to the
virus of South African smallpox vaccine than to other [natural] vaccinia
viruses. DNA analysis also showed that an orthopoxvirus isolated from a
sporadic case of severe pustular rash in Nigeria was a vaccinia virus closely
related to the smallpox vaccine virus used there… [It was] suggested that some
natural transmission of the virus had occurred…originat[ing] from the use of
smallpox vaccine. No similar cases have been detected since smallpox
vaccination was discontinued."
"Vaccinia
virus persistence in a child against the background of immune deficiency"
(J. Hyg. Epidemiol. Microbiol. Immunol., vol. 30, no. 2, 1986, pp.
177-83): " A young girl, vaccinated against smallpox 6 years before[,]
suffered from a persistent vaccinia virus infection and a congenital skin
disesase, i.e. epidermolysis bullosa. The virus was isolated from skin lesions
at the vaccination site and remote sites and repeatedly from the blood…
Examination of the child did not show any quantitative immune deficiency… The
possible genesis of the virus persistence and the role of the virus in the
clinical course of the disease are discussed." (A selected Medline [National
Library of Medicine] "MESH" subject tracing for this report is
"Smallpox Vaccine--adverse effects.")
O. Laitinen and A.
Vaheri, University Central Hospital and Department of Virology, University of
Helsinki, Finland, "Very high measles and rubella virus antibody titres
associated with hepatitis, systemic lupus erythematosus, and infectious
mononucleosis" (The Lancet, vol. 1, February 9, 1974, pp.
194-7): When patients with typical acute measles or rubella infections and
their complications were excluded, certain groups of patients with very high
antibody levels to measles and/or rubella viruses remained and were studied.
These "patients showed very high measles or rubella antibodies although
there had been no recent typical rubella or measles infection… Our data suggest
that atypical viral infection plays an active role in the pathogenesis of at
least some of the abovementioned conditions… these viruses may cause chronic
infections with raised antibody levels…moreover, sera from some patients with
other diseases…show very high levels of antibody against these two viruses… In
multiple sclerosis raised levels of measles antibodies have been previously
reported." Antibodies to many other viruses and to Mycoplasma and
Toxoplasma were normal. The authors acknowledged the possibility that an
abnormal immunological defense mechanism had lead to an abnormal virus
infection—"e.g., carrier infection, reinfection, or incomplete measles or
rubella virus infection—in some susceptible individuals…[;] however[,]…no 4-fold
or greater changes occurred in virus antibody levels in any patient with
systemic lupus erythematosus, chronic active hepatitis, or infectious
mononucleosis [as happens with autism, in
which titers are often four to seven times that of normal]…" Evidence did not exclude chronic virus
infection as an important factor in these diseases.
Reactivation of vaccine
viruses "after the fact"
"Measles, Mumps, Rubella Vaccine
Induced Subacute Sclerosing Panencephalitis," Journal of the Indian
Medical Association, November 1997, vol. 95 no. 11, page 594: a particular
case of SSPE is described in a thirteen-year-old girl who had been
immunized against all childhood diseases; receiving the MMR vaccine at the age
of nine months. The girl’s intellectual functioning until development of
illness had been very good. After illness developed, the child verbalized
little and was socially inappropriate; her memory and thinking abilities were
impaired. She grew progressively worse, and added myoclonic jerks of the upper
limbs, with depressed deep tendon reflexes. The authors concluded that
Subacute, Sclerosing Panencephalitis was engendered as a delayed adverse effect
of measles vaccine. The authors note other cases of SSPE induced by the
attenuated measles vaccine.
"Measles Encephalomyelitis
in a Patient With a History of Vaccination," Acta Paediatrica
Japonica, vol. 37, number 3, June 1995, pp. 374-376: A twelve-year-old girl
vaccinated with a live attenuated measles vaccine developed an
encephalomyelitis ten years post-vaccine. "The patient’s definite history
of measles vaccination, high titers of HI and IgG antibodies…indicated that
this patient has an encephalomyelitis due to Secondary Vaccine Failure of
measles. It is suggested that measles virus can be a pathogen of encephalitis
without symptoms indicative of ordinary measles in individuals who received
live attenuated measles vaccines."
"Polymerase
chain reaction detection of the hemagglutinin gene from an attenuated measles
vaccine strain in the peripheral mononuclear cells of children with autoimmune
hepatitis," Archives of Virology volume 141, 1996, pages
877-884: "The measles virus is known to be persistent in patients with
subacute sclerosing panencephalitis (SSPE) and measles inclusion body
encephalitis (MIBE). Since the introduction of measles vaccines,
vaccine-associated SSPE has increased in the USA. Therefore, we should
pay attention to SSPE after inoculation with measles vaccine, despite the
decrease in the incidence of [wild] measles."
Infection by vaccine
contaminants
"Children
exposed to CJD infecton risk from vaccines" (Antony Barnett, Public
Affairs Editor, The Guardian/The Observer [Guardian Media Group],
Sunday May 30, 1999; text available http://www.guardianunlimited.co.uk/Archiv…le/0,4273,3870082,00.html?cantsetcookie=0): from 1989 to 1993 thousands of human vaccines for
such diseases as tetanus and pertussis were knowingly approved for use by the
Department of Health (UK), which may have been based on matter derived from BSE
("mad cow disease")-infected cattle. Before "mad cow
disease" became a concern in 1988, vaccines were made with bovine serum
without awareness of the possibility of contamination. Sir Richard Southwood,
Professor of Zoology at Oxford University, stated that injection posed a far
greater risk of CJD than eating foods made from infected cattle. When BSE is
contracted by humans, it becomes Creutzfeld-Jacob Disorder, or CJD.
"[Infectious
diseases of animals and their prevention]" (Bratisl. Lek. Listy.,
vol. 99, nos. 8-9, August-September 1998, pp. 465-73): "Infectious
diseases of animals are the subject of continuous concern… Undoubtedly,
microbes and parasites take part also in the development of malignant
transformation of cells. The question of possible transfer of animal oncogenic
[cancer-causing] microorganisms (retroviruses in particular) to humans remains
open. The study points to the changes in the incidence of orthopoxviruses which
occurred after 'eradication' [quote marks added] of human variola [smallpox]
and the increasing importance of bartonelloses… We enter a period in which the
resistance of animal organism begins to affect the transfer of genes encoding
non-specific and specific protective [immunological] mechanisms of
organisms."
"The
African polio vaccine-acquired immune deficiency syndrome connection"
(Medical Hypotheses, vol. 48, no. 5, May 1997, pp. 367-74):
"Seroepidemiological, clinical and molecular findings suggest that the
acquired immune deficiency syndrome virus Human Immunodeficiency Virus-1*
was introduced into the human species at the the (late 1950s) and in the
geographic area (Zaire) in which millions of Africans were vaccinated with
attenuated poliomyelitis virus strains that were produced in kidney tissue
obtained from monkeys. …it is reasonable to suspect that a then non-detectable
monkey virus with human-1-like properties was unknowingly cocultured with the
attenuated poliovirus and subsequently administered to the vaccinees. The
possibility of such a polio vaccine-acquired immune deficiency syndrome
connection is a reminder of the unpredictable danger of artifically crossing
natural species-barriers in biomedical laboratories" [*bold
text capitals added].
"The origin
of HIV-1, the AIDS virus" (Medical Hypotheses, vol. 41, no. 4,
October 1993, pp. 289-99): "a substantial case is presented that HIV-1 is
a natural recombinant of Bovine Leukemia Virus (BLV) and Visna Virus. This
natural recombinant may have been inadvertently transferred to humans through
the Intensified Smallpox Eradication Program conducted in sub-Saharan Africa in
the late 1960s and most of the 1970s."
"Simian
cytomegalovirus-related stealth virus isolated from the cerebrospinal fluid of
a patient with bipolar psychosis and acute encephalopathy" (Pathobiology
, vo. 64, no. 2, 1996, pp. 64-6): a cytopathic 'stealth' virus was cultured
from the cerebrospinal fluid of this patient, who developed a severe
encephalopathy leading to a vegetative state. DNA sequencing of a polymerase
chain reaction-amplified product from infected cultures revealed kinship to the
African green monkey simian cytomegalovirus.
Immunosuppression and
opportunistic infection
Abstract: also relevant to the London
article, occasioned by concern over the MMR vaccine, the measles virus is noted
for its ability to suppress the immune system, particularly cellular immunity.
A person sustaining a chronic measles infection may therefore be increasingly
subject to numerous other infections, whether viral, bacterial, or fungal [such
abnormalities are well documented in autism].5 Measles and rubella
virus themselves, in addition, are associated with distinct central nervous
system pathologies.6
"Epidemiology
of encephalitis in children. A prospective multicentre study," European
Journal of Pediatrics, vol. 156, number 7, July 1997, pp. 541-5:
Investigators found 175 cases with acute encephalitis in children aged 1 month
to 15 years during a two-year surveillance period in 1993-1994. Varicella
zoster, respiratory and enteroviruses, Epstein-Barr virus, herpes simplex and
rota viruses, and the new infections chlamydia pneumoniae and HHV-6 were found.
While mumps, measles, and rubella virus associated encephalitis had been almost
eliminated due to vaccination programs, these other viruses had increased in
frequency and occurred in younger age groups. "Conclusions:
The spectrum of encephalitis in children has changed due to vaccination
programs. The incidence, however, appears to be about the same due to
increasing frequency of other associated old and new microbes"—i.e., the
number of cases of MMR-encephalitis eliminated have been replaced by an equal
number of encephalitis cases from other microbes, previously not seen.
[Note: the
following report does not address the cause of the systemic viral infection
detailed; Epstein Barr is, however, capable of arising opportunistically when
immune system responses are inhibited, as occurs in measles immunosuppression.
Temporary or permanent neurological damage, or chronic disease, can result from
such unhindered viral activity.] Ito, H., et al., "Antineuronal
antibodies in acute cerebellar ataxia following Epstein-Barr virus infection,"
(Neurology, vol. 44, no. 8, August 1994, pp. 1506-7): A 29-year-old man
developed acute cerebellar ataxia following Epstein-Barr infection. The ataxia
gradually improved. The authors concluded that their findings in this case
suggested a role for autoimmune mechanisms in the pathogenesis of acute
cerebellar ataxia.
Pathogenesis:
proliferation of disease
Persons—especially children—with Crohns
disease, asthma, diabetes, ear infections and disorders; immunosuppression and
secondary viral infections (EBV, CMV) have been found to harbor organisms,
often those associated with vaccine-preventable diseases. Addressing bacterial
infections, G. J. Domingue and H. B. Woody of Tulane University School of
Medicine state, "A considerable body of experimental and clinical evidence
supports the concept that difficult-to-culture and dormant bacteria are
involved in latency of infection and that these persistent bacteria may be pathogenic…
A series of experimental studies involving host-bacterium interactions
illustrates the probability that most bacteria exposed to a deleterious host
environment can assume a form quite different from that of a free-living
bacterium… These organisms can survive and persist in a latent state within the
host, and they can cause pathologic responses compatible with disease. A series
of cases illustrating idiopathic conditions in which cryptic bacteria have been
implicated…include nephritis, rheumatic fever, aphthous stomatitis, idiopathic
hematuria, Crohn's disease, and mycobacterial infections…[;] nonculturable
bacilli have been identified in patients with Whipple's disease and bacillary
angiomatosis" ("Bacterial persistence and expression of disease,"
Clinical Microbiology Review, vol. 10, no. 2, April 1997, pp. 320-44).
"Polymerase
chain reaction detection of the hemagglutinin gene from an attenuated measles
vaccine strain in the peripheral mononuclear cells of children with autoimmune
hepatitis," Archives of Virology, volume 141, 1996, pages
877-884: the authors observe, "Apparently, the attenuated vaccine is also
capable of persisting, like sporadic wild strains, in certain immune
diseases."
H. C. Huber, "The
pathogenesis of postvaccinal complications" (Fortschr. Med.,
vol. 99, no. 11, March 19, 1981, pp. 380-1): "Paraspecific reactions to
vaccines are--induction of autoimmune mechanisms, --immunosuppression,--
induction of inflammation (e.g. "reactogenicity"). These undesirable
side effects of vaccination are important factors in pathogenesis of
postvaccinal complications."
Myocarditis
Diabetes
"Hemophilus
vaccine and increased IDDM, causal relationship likely" (British
Medical Journal, vol. 318, May 7, 1999); this letter conveys a re-interpretation
by J. Bart Classen of data reported in "Association between type 1
diabetes and Haemophilus influenzae type b vaccination: birth cohort study"
(British Medical Journal, vol. 318, May 1, 1999, pp. 1169-1172), which
Classen Immunotherapies initiated and funded. "…the potential risk of the
vaccine [in fact] exceeds the potential benefit." Classen discusses this
data in the context of compensation for vaccine-damaged children with diabetes.
Coulter, Harris,
Ph.D., Center for Empirical Medicine, Washington, D.C., "Childhood
vaccinations and juvenile-onset (type-1) diabetes: testimony before the
Congress of the United States, House of Representatives…April 16, 1997"
(Committee on Appropriations, subcommittee on Labor, Health and Human Services,
Education, and Related Agencies; text available at http://909shot.com/hcdiabetes.htm):
the incidence of diabetes in the U. S. had increased 20 times since 1947.
Healthcare costs are significant, both from the primary disease and from its
complications such as cardiovascular disease, stroke, gangrene of the
extremities, kidney failure, and blindness. A shortened lifespan is to be
expected. Diabetes appears to be influenced by a genetic susceptibility, but
environmental factors tend to lead to onset. Both pertussis toxin and rubella
virus, ingredients of two mandated childhood vaccines, are capable of acting on
the insulin-producing portions of the pancreas. "There is copious
evidence[, also,] of a causal relationship between clinical mumps and
subsequent development of diabetes [through pancreatitis]…many reports in the
literature of Type-1 diabetes [report the condition] emerging after mumps
vaccination." "There is no reason to make a distinction between…the
disease process and…a vaccination… In both cases immune complexes are formed
and persist in the host organism for lengthy periods. Immune complexes from a
vaccination can attack the pancreas just as easily as if they were from
contenital rubella syndrome. The actual mechanism of such an attack[, however,]
is probably multifactorial[, …the most probable one being] the generation of an
autoimmune state….." References are given to medical case reports
describing the emergence of type-1 diabetes following vaccination.
Adverse Events
Associated with Childhood Vaccines: Evidence Bearing on Causality (Washington, D.C.: National Academy of Sciences,
Institute of Medicine, 1994): About the issue of vaccination and type-1
diabetes, the IOM Committee stated that "biologic plausibility data
implicating the mumps virus in the pathogenesis of Type-1 diabetes include: 1)
the association between viral infections, including mumps, and Type-1 diabetes
in humans; 2) the detection of circulating autoantibodies against pancreatic
antigens, particularly islet cells, during convalescence from mumps infection
as well as early in the course of Type-1 diabetes; and 3) in vitro studies
demonstrating that the wild-type mumps virus can infect human pancreatic beta
cells" (p. 159).
Asthma
"Measles
virus infection synergizes with IL-4 in IgE class switching" (Journal
of Immunology, vol. 162, no. 3, February 1, 1999, pp. 1597-1602):
"Increasing evidence suggests that viral infections are associated with
the induction and exacerbation of asthma… These data provide the first
indication of a potential mechanism for M[easles] V[irus] induced IgE
up-regulation and suggest a model for a viral-induced exacerbation of
IgE-mediated disorders such as asthma.
"Is infant
immunization a risk factor for childhood asthma or allergy?" (Epidemiology,
vol. 8, no. 6, November 1997): "Results of the Christchurch Health and
Development Study, conducted by a team of New Zealand researchers, found a
greater rate of asthma and allergy episodes among immunized children… The
comparison produced similar results at ages five and 16, and the discrepancy
does not appear to result from use of health services, ethnicity, socioeconomic
status, or parental atopy or smoking."
"Risk
factors for invasive Haemophilus influenzae disease among children 2-16 years
of age in the vaccine era, Switzerland, 1991-1993" (International
Journal of Epidemiology, vol. 25, no. 6, December 1996, pp. 1280-5):
"Continued surveillance, and detailed investigation of direct and indirect
effects of conjugated vaccines and risk factors…are important." 143 cases
with invasive disease were selected, and vaccination status ascertained.
"Cases more often than controls reported suffering from asthma and
allergies… The observed association between asthma and epiglottitis is novel
and deserves further investigation."
"Very high
measles and rubella virus antibody titres associated with hepatitis, systemic
lupus erythematosus, and infectious mononucleosis" (The Lancet,
vol. 1, February 9, 1974, pp. 194-7). The authors note the existence of high
viral titers in several diseases, including asthma: "[in] the other
patients in whom only very high antibody levels to rubella…could be
measured…bronchial asthma [was the only disease which was not rare, and for which]
a possible viral role in their pathogenesis cannot be excluded."
Disorders of the ear
Blood disorders
"Thrombocytopenic
purpura as adverse reaction to recombinant hepatitis B vaccine" (Archives
of Disease in Childhood, vol. 78, no. 3, March 1998, pp. 273-4): Three
cases of [auto]immune thrombocytopenic purpura after the first dose of
recombinant hepatitis B vaccine occurred in infants under six months of age.
There were no other possible causes; defect in platelet production was excluded
in two children. Antiplatelet antibodies were present. The babies were treated
with corticosteroids.
Hepatitis
"Polymerase
chain reaction detection of the hemagglutinin gene from an attenuated measles
vaccine strain in the peripheral mononuclear cells of children with autoimmune
hepatitis," Archives of Virology volume 141, 1996, pages
877-884: Four pediatric and two adults patients with autoimmune hepatitis were
tested and followed in this study. Twelve healthy children served as controls,
who had either been infected with measles or vaccinated with an attenuated
measles vaccine in the past. All controls were negative for measles virus
except a recent (two week) vaccinee. Of the hepatitis patients, all were
positive for measles virus—the children with vaccine-strain measles
virus, and the adults with different strains. Conclusion: "our results
demonstrated that children with autoimmune hepatitis can have persistence of
the vaccine strain in vivo for many years after vaccination [abstract, page
877]." The authors state that the persistence of the measles virus might
play some role in the pathology of autoimmune hepatitis, but further studies
are needed to prove this hypothesis (page 883).
Also in "Polymerase,"
the authors observe that high levels of serum antibodies to measles virus have
been reported in patients with autoimmune hepatitis (p. 877). References add
systemic lupus erythematosus and infectious mononucleosis to the tally of
autoimmune diseases with connections to measles (pages 883-4). [Note: high
antibody titers of measles and rubella are also associated with autism.]
Some provocative quotes, page 882: "Apparently, the attenuated vaccine is
also capable of persisting, like sporadic wild strains, in certain immune
diseases. The measles virus is known to be persistent in patients with subacute
sclerosing panencephalitis (SSPE) and measles inclusion body encephalitis
(MIBE). Since the introduction of measles vaccines,
vaccine-associated SSPE has increased in the USA. Therefore, we should
pay attention to SSPE after inoculation with measles vaccine, despite the
decrease in the incidence of [wild] measles."
[Note: the
following study did not broach the subject of vaccine involvement in diseases;
rather it serves to point out the relationship of viral presences to disease.]
…Department of Virology, University of Helsinki, Finland, "Very high
measles and rubella virus antibody titres associated with hepatitis, systemic
lupus erythematosus, and infectious mononucleosis" (The Lancet,
vol. 1, February 9, 1974, pp. 194-7): In patients without preceding rubella or
measles infection, "raised levels of viral antibodies were a constant
finding in two repeated analyses" of hepatitis patients. The authors felt
that "it is conceivable that rubella and/or measles infections or
reinfections may cause acute hepatitis and persist in some individuals…such
aberrant virus infection might be responsible for some clinical manifestations….."
Chronic virus infection could not be excluded as an important factor in these
diseases.
Inflammatory and autoimmune bowel disease
"Paramyxovirus
infections in childhood and subsequent inflammatory bowel disease" (Gastroenterology,
vol. 116, no. 4, April 1999, pp. 796-803): "Measles virus has been
implicated in the etiology of both inflammatory bowel diseases (IBDs), Crohn's
disease and ulcerative colitis… Mumps infection before age 2 years was a risk
for ulcerative colitis… Measles and mumps infections in the same year of life
were significantly associated with ulcerative colitis and Crohn's disease…but
not with IDDM… Atypical paramyxovirus infections in childhood may be risk
factors for later I[nflammatory] B[owel] D[isease.]" [Notes: measles-mumps-rubella vaccine is usually given
around the age of 16 months. When vaccine viruses induce infection, the
resulting illness is often atypical in character. A Reuter's Medical news
release pertaining to this study, found at http://www.reutershealth.com/frame_about.html,
cited mumps infection in the same year as monovalent measles vaccination
appeared to increase the risk of later Crohn's disease.]
Lupus, multiple sclerosis and rheumatoid arthritis
Abstract: autoimmune diseases
are becoming increasingly common. The majority seem to have viral associations.
"Vaccine-induced autoimmunity"
(Journal of Autoimmunity, vol. 9, no. 6, December 1996, pp. 699-703):
the authors summarize of case reports attributing autoimmune diseases and
autoimmune phenomena to vaccines, and suggest possible mechanisms by which the
two could be related. "The subject is complicated," they say,
"by the fact that one vaccine may cause more than one autoimmune phenomenon,
and a particular immune process may be caused by more than one vaccine.
Furthermore, vaccines differ in their pathogenic influence on the immune
system... The subject of the vaccine-autoimmunity relationship is still
obscure; reports have been rare, [and] no laboratory experimentation on this
topic has been undertaken....." (Oddly, the authors state that the
benefits of vaccination outweigh the risks of disease, but given the authors'
contentions that vaccines can cause one or more types of autoimmune disease,
that reports are few and research non-existent, this statement is unsupported.
Further, they conclude that "laborious clinical and laboratory studies
should be initiated in order to evaluate the ...subject.")
C. M. Poser, Harvard Medical School, "The
pathogenesis of multiple sclerosis. Additional considerations" (Journal
of Neurological Science, vol. 115, April 1993, Supplement pp. S3-15):
"Multiple sclerosis is acquired as a systemic "trait" by
individuals who are genetically susceptible…It develops as the result of an
antigenic challenge by a viral protein, either from a viral infection or a
vaccination."
"Multiple sclerosis and infectious
childhood diseases" (Neuroepidemiology, vol. 17, no. 3, 1998,
pp. 154-60): multiple sclerosis patients studied had had measles, mumps, and
varicella (chicken pox) infections at a later age than healthy controls.
"These results are compatible with the hypothesis that the risk of
developing multiple sclerosis may be associated with acquiring certain infectious
childhood diseases at a later state in comparison to normal controls."
[Early vaccination for these diseases, therefore, may predispose vaccinees to
MS, as immunity from vaccinations frequently wanes in the years following early
childhood vaccination (unlike immunity to natural infection). In the event of
such a vaccine failure, natural infection may occur at a later age.]
"Chronic arthritis after rubella
vaccination" (Clin. Infectious Disease, vol. 15, no. 2, August
1992, pp. 307-312. After reviewing a wide range of information sources, The
Institute of Medicine, Washington, DC, found a causal relationship between
rubella vaccination and chronic arthritis in adult women.
--for lupus, see <<cognitive disorders
in systemic diseases,>> below--
Parasthesias/paralytic
and muscular diseases
"Drug Points:
Transverse Myelitis After Measles, Mumps, and Rubella Vaccine," BMJ
[British Medical Journal], vol. 311 (7002), August 12, 1995, p. 422: a
twenty-year-old man was vaccinated against rubella with the MMR vaccine. Five
days later he developed fever, malaise, sore throat, and a transient,
upper-body rash. Within the next two weeks, he developed an ascending
paraesthesia. He was hospitalized on developing a rapidly progressive flaccid
paraplegia. Serological tests showed a significant rise in rubella antibodies.
Postvaccination transverse myelitis was diagnosed.
"Poliovirus vaccine options" (American
Family Physician, vol. 59, no. 1, January 1, 1999, pp. 113-8, 125-6):
"Of 142 confirmed cases of paralytic poliomyelitis reported in the United
States from 1980-1996, 134 were classified as vaccine-associated paralytic
poliomyelitis (VAPP). Persons with VAPP have a disabling illness….."
"Demonstration of specific antineuronal
nuclear antibodies in sera of patients with myasthenia gravis" (Neurology,
vol. 24, no. 7, July 1974, pp. 680-3).
Other disorders of
the brain and nervous system
Vijendra K. Singh and others have found a significant association between
autoimmune processes in autistic patients and viral presences--in particular,
anti-myelin basic protein (anti-brain) antibodies, often in association with
high antibody titers against specific microbes. In this regard, see also "Demonstration
of specific antineuronal nuclear antibodies," above, and the
description of T. Zecca's report, "Elevated rubeola [measles] titers
in autistic children linked to MMR vaccine," above. Study of other
cognitive, behavioral, and movement disorders has revealed immune system
involvement.
<<seizure
disorders>>
"Autistic subjects with comorbid
epilepsy: a possible association with viral infections" (Child
Psychiatry and Human Development, vo. 29, no. 3, Spring 1998, pp. 245-51):
Data covering a 30-year period was examined in Israel. The annual birth pattern
of 290 autistic subjects with comorbid epilepsy fit the seasonality of viral
meningitis. "These findings support the role of viral C[entral] N[ervous]
S[ystem] infections in the causality of this disorder."
"Neurologic complications after
vaccination against diphtheria, tetanus and whooping cough (Cesk.
Pediatr., vol. 47, no. 2, February 1992, pp. 122-4): Both in children free
from neurological disease and in children with neurological disease the most
frequent type of complications from DTP vaccination were "encephalopathies
and febrile attacks as a consequence of metabolic and toxic changes following
vaccination." Persisting neurological disorders were, in the majority,
epileptic in character.
"Vaccination against whooping-cough.
Efficacy versus risks," The Lancet, vol. 1, January 29, 1977,
pp. 234-7: "Adverse reactions and neurotoxicity following
vaccination was strongly related to pertussis vaccine in 79 of 160 cases
studied. A shock reaction and cerebral disturbance was seen, in
most of these cases followed by convulsions, hyperkinesis, and severe mental
defect. The authors conclude, "It seems likely that most adverse
reactions are unreported and that many are overlooked…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."
O. Tonz and S. Bajc, "Convulsions after
whooping-cough vaccination" (Schweiz. Med. Wochenschr., vol.
110, no. 51, December 20, 1980, pp. 1965-71): Convulsions or status epilepticus
in 11 infants after pertussis vaccination are reported. In three of 11 cases,
grand mal epilepsy persisted and two children developed infantile epileptic
encephalopathy (Lennox Syndrome). "The following conclusions are drawn
from these observations: 1) In view of the usually benign course of whooping
cough today, current vaccination is hardly satisfactory. Improvement of the available
vaccines is an urgent necessity… 2) Parents whould be better informed about the
risks involved in pertussis vaccination. 3) Booster inoculations should be
abandoned. 4) Health authorities should decide whether the current pertussis
vaccination program should be abandoned. 5) Complications following vaccination
should be registered….."
<<behavior
and movement disorders >>
"A controlled study of serum anti-locus
ceruleus antibodies in REM sleep behavior disorder" (Sleep,
vol. 20, no. 5, May 1997, pp. 349-51): "The newly identified association
of human nonnarcoleptic rapid eye movement (REM) sleep behavior disorder (RBD)
with human leukocyte antigen (HLA) DQwl class II genes raises the possibility
that RBD may arise from autoimmune mechanisms."
[The following reports are not
vaccine-specific; rather they serve to underline one of the possible conditions
resulting from altered permeability of, or damage to the intestine, as occurs
in association with measles and other viruses. Note: strep-type bacteria are
among those which can translocate from the gut; strep bacteria have been
implicated in cases of Obsessive-Compulsive Disorder and Tourette Syndrome.]
"Bacterial translocation from the gastrointestinal tract" (Trends
in Microbiology, vol. 3, no. 4, April 1995, pp. 149-54): Viable indigenous
bacteria from the gastrointestinal tract can migrate to other sites within the
body, such as the mesenteric-lymph-node complex, liver, spleen, and
bloodstream. Three mechanisms support bacterial translocation: intestinal
bacterial overgrowth, deficiencies in host immune defenses and increased
permeability or damage to the intestinal mucosal barrier.
"Case study: a new
infection-triggered, autoimmune subtype of pediatric OCD and Tourette's
syndrome" (Journal of the American Academy of Child and Adolescent
Psychiatry, vol. 34, no. 3, March 1995, pp. 307-11): the authors
hypothesize that infections with group A beta-hemolytic streptococci, among
other bacterial agents, may trigger autoimmune responses that cause or exacerbate
some cases of childhood-onset obsessive-compulsive disorder (OCD) or tic
disorders including Tourette's Syndrome. In this study, four boys aged 10 to 14
years presented with OCD or Tourette's Syndrome in the moderate to very severe
range. Two had evidence of recent group A beta-hemolytic streptococci
infections, and the others had histories of recent viral illnesses.
"Speculations on antineuronal
antibody-mediated neuropsychiatric disorders of childhood" (Pediatrics,
vol. 93, no. 2, February 1994, pp. 323-6): "Several converging lines of
evidence suggest that some behavioral and neurological abnormalities of
childhood may be mediated through antineuronal antibodies. These antineuronal
antibodies appear to arise in response to group A [beta]-hemolytic
streptococcal (GABHS) infections and to cross-react with cells within the
central nervous system (CNS). Based on clinical observations of children with
Sydenham's chorea, Tourette's syndrome (TS), and/or obsessive-compulsive
disorder (OCD), we hypothesize that neuroimmunological dysfunction secondary to
antineuronal antibodies may result in behavioral disturbances, such as anxiety,
emotional lability, obsessive compulsive symptoms, hyperactivity, and sleep
disturbances, and neurological abnormalities, such as motor and phonic tics,
ballismus, chorea, and choreiform movements."
"Antineuronal antibodies: tics and
obsessive-compulsive symptoms" (Journal of Developmental and
Behavioral Pediatrics, vol. 15, no. 6, December 1994, pp. 421-5): 19 or 38
cases from an ongoing study of childhood neurodevelopmental disorders had
existing or previously documented OCS [OCD] and attention-deficit hyperactivity
disorder (ADHD), with or without concomitant tics. 19 controls had ADHD, but no
tics or OCS. Evidence was found of basal ganglia involvement in OCS, and a
generalized central nervous system response [to infection] was suggested.
"Bipolar disorders, dystonia, and
compulsion after dysfunction of the cerebellum, dentatorubrothalamic tract, and
substantia nigra" (Biological Psychiatry, vol. 40, no. 8,
October 1996, pp. 726-30): the mechanism of the legions was not abstracted in
this report; however, after focal cerebellar circuit lesions, these disorders
presented in three of fifteen subjects.
"Antineuronal antibodies in movement
disorders" (Pediatrics, vol. 92, no. 1, July 1993, pp. 39-43):
24 children with recent-onset movement disorders (Tourette Syndrome, motor
and/or vocal tics, chorea, and choreiform movements) as well as ADHD, behavior
disorders, or learning disabilities were studied. The authors concluded that
their data strongly suggests an association between antecedent group A
beta-streptococcal infection and serum antineuronal antibodies, which may, in
turn, be linked to childhood movement disorders.
"Antibodies to human caudate nucleus
neurons in Huntington's chorea" (Journal of Clinical Investigation,
vol. 59, no. 5, May 1977, pp. 922-32): IgG antibodies against nervous system
components were detected in patients afflicted with Huntington's and
Parkinson's Diseases, as well as in asymptomatic spouses of patients.
"These data may support an environmental or infectious factor somehow
involved in the ultimate expression of HD."
[The following report is not
vaccine-specific, but underlines a radical shift in thinking about cerebral
palsy, and a variety of other neurological impairments, toward an infectious
etiology.]
"Infections may underlie cerebral palsy"
(Science News, vol. 154, no. 16, October 17, 1998, p. 244; available at http://www.sciencenews.org/sn_arc98/10_17_98/fob1.htm): "Most doctors have believed that cerebral
palsy--a form of brain damage that impairs movements--results from a difficult
birth… While asphyxia may indeed be a cause of cerbral palsy, a new study
provides evidence that the brain damage might often arise from some
other…assault on an unborn child. Molecular clues now lead to inflammatory
infection as a possible culprit, says Karein B. Nelson, a pediatric neurologist
at the National Institute of Neurological Disorders and Stroke in Bethesday,
MD." A study was performed by Nelson and colleagues which compared blood
from normal and CP infants: the team found that all the stricken children
harbored greater concentrations of substances indicating immune activation. In
some of the children, indications of autoimmunity were seen as well. (Study
citation: "Neonatal cytokines and coagulation factors in children with
cerebral palsy," Annals of Neurology, vol. 44, October 1998, p.
665.)
"Increased
prevalence of antibrain antibodies in the sera from schizophrenic patients"
(Schizophrenia Research, vol. 14, no. 1, December 1994, pp. 15-22);
"Antibodies to brain tissue in sera of schizophrenic
patients-preliminary findings" (European Archives of Psychiatry and
Clinical Neuroscience, vol. 242, no. 5, 1993, pp. 314-7): Antibrain
antibodies have been found in the sera of schizophrenic patients, but not in
normal controls. These seem to be directed against brain centers affected in
schizophrenia. (More notes on schizophrenia are available under "Factoid Fallacies," below.)
<<cognitive disorders in systemic diseases>>
"Characteristics
of antineuronal antibodies in systemic lupus erythematosus patients with and
without central nervous system involvement: the role of mycobacterial
cross-reacting antigens" (Israeli Journal of Medical Science,
vol. 26, no. 7, July 1990, pp. 367-73): indirect immunofluorescence of human
brain tissue sections revealed, in thirteen of sixteen patients, high
antineuronal antibody titers. Competition assays showed that the binding of the
antineuronal antibodies was blocked by mycobacterial glycolipids and bovine
brain extracts. "This finding suggests an additional link between
mycobacterial infection and SLE."
<<cognitive
disorders of the aged>>
"Neuroautoimmunity:
pathogenic implications for Alzheimer’s disease" (Gerontology,
vol. 43, no.s 1-2, 1997, pp. 79-94): "Immune factors such as cellular
immunity, autoimmunity, and inflammation may play a pathogenic role in
Alzheimer’s disease… Antibrain antibodies may contribute through a
cell-specific autoimmune assault leading to neurodegeneration of the
A[lzheimer’s ] D[isease] type."
"Immunoblot
detection of antibodies to myelin basic protein in Alzheimer’s disease patients"
(Neuroscience Letters, vol. 147, no. 1, November 23, 1992, pp. 25-8): 16
of 18 Alzheimer’s disease patients, as opposed to 7 of 90 controls (healthy
adults and elderlies, and adult and child patients with other diseases or disorders
such as Parkinson’s disease and Down syndrome proved positive for anti-MBP
antibodies.
"An
immunological approach to dementia in the elderly" (Age and Ageing,
vol. 5, no. 3, August 1976, pp. 164-70): Immunofluorescence studies showed
"an excess of antineuronal reactivity and a fall in antinuclear antibody
in females with senile dementia."
<<cognitive
developmental disorders>>
"Serum
autoantibodies to brain in Landau-Kleffner variant, autism, and other
neurologic disorders" (Journal of Pediatrics, vol. 134, no. 5,
May 1999, pp. 607-613): "Etiologically unexplained disorders of language
and social development have often been reported to improve in patients treated
with immune-modulating regimens. Here we determined…children with L[andau]
K[leffner] S[ydrome] V[ariant] and A[utistic] S[pectrum] D[isorder] have a
greater frequency of serum antibodies to brain endothelial cells and to nuclei
than children with non-neurologic illnesses or healthy children. The presence
of these antibodies raises the possibility that autoimmunity plays a role in
the pathogenesis of language and social developmental abnormalities in a subset
of children with these disorders.
"Serological
Association of Measles Virus and Human Herpesvirus-6 With Brain Autoantibodies
in Autism." Clinical Immunology and Immunopathology, vol. 89,
number 1, October 1998, pp. 105-8. This study is the first to report an
association between virus serology and brain autoantibody in autism; it
supports the hypothesis that a virus-induced autoimmune response may play a
causal role in autism.
"Positive
Titers of Measles and Measles-Mumps-Rubella Antibody Are Related to Myelin
Basic Protein Autoantibody in Autism." Abstract of study prepared for
the annual meeting of the American Association of Immunologists (AAI) /
Federation of American Societies for Experimental Biology (FASEB), San
Francisco, April 1998. A significant number of autistic children exhibit
positive titers of measles and MMR [measles-mumps-rubella] antibody, which in a
vast majority of cases is associated with the presence of MBP [myelin basic
protein, or brain] autoantibody. A measles- and/or MMR-triggered autoimmune
response to myelin may play a pathogenesis role in autism.
"Association
of Anti-MBP and Anti-NAFP Antibodies With HHV-6 Antibodies in a Child With
Autistic Regression." Journal of Allergy and Clinical Immunology,
vol. 101.1, S122, January 1998, part 2 (in section entitled, "Program
and Abstracts of Papers to Be Presented During Scientific Sessions [at the] 54th
Annual Meeting, March 13-18, 1998").
"Circulating
Autoantibodies to Neuronal and Glial Filament Proteins in Autism." Pediatric
Neurology, vol. 17, number 1, July 1997, pp. 88-90. A significant increase
in incidence of anti-NAFP [neuron-axon-filament-protein] and anti-GFAP was seen
in autistic subjects, but not in mentally retarded subjects. Clinically, these
autoantibodies may be related to autoimmune pathology in autism.
"Hyperserotoninemia
and Serotonin Receptor Antibodies in Children With Autism but Not Mental Retardation."
Biological Psychiatry, vol. 41, number 6, March 15, 1997, pp. 753-5.
"Elevated
Serotonin Levels in Autism: Association With the Major Histocompatibility
Complex." Neuropsychobiology, vol. 34, number 2, 1996, pp.
72-5. Two of the most consistently observed biological findings in autism are
increased serotonin levels in the blood and immunological abnormalities
(including autoreactivity with tissues of the central nervous system). The
major histocompatibiligy complex (MHC) regulates the immune system, and is
associated with autoimmune disorders. In this study, a positive relationship
was observed between elevated serotonin levels and the MHC types previously
associated with autism.
"Plasma
Increase of Interleukin-12 and Interferon-gamma. Pathological Significance in
Autism." Journal of Neuroimmunology, vol. 66, numbers 1-2, May
1996, pp. 143-5. Immune factors such as autoimmunity have been implicated in
the genesis of autism, a neurodevelopmental disorder. Since autoimmune response
involves immune activation, the plasma levels of interferon-alpha (IFN-alpha),
IFN-gamma, interleukin-12 (IL-12), and IL-6 were measured, along with tumor
necrosis factor (TNF-alpha) and soluble intercellular adhesion molecule-1
(sICAM-1). The levels of IL-12 and IFN-gamma were significantly higher in
autistic patients than in controls (the remaining measures were not
significantly different). It is suggested that IL-12 and IFN-gamma increases
may indicate antigenic stimulation of Th-1 cells pathogenetically linked to autoimmunity
in autism.
"Immunogenetic
Studies in Autism and Related Disorders." Molecular Chemistry and
Neuropathology, vol. 28, numbers 1-3, May-August 1996, pp. 77-81. The major
histocompatibiligy complex comprises a number of genes that control the function
and regulation of the immune system. One of these, the C4B gene, encodes a
product that is involved in eliminating pathogens such as viruses and bacteria
from the body. A deficient form of the C4B gene, termed the C4B null allele (no
C4B protein produced) was previously seen to have an increased frequency in
autism. In this study, this finding was confirmed, and this same condition was
detected in related [neurodevelopmental] disorders as well. In addition, two
alleles of the DR beta 1 gene also had significantly increased representation
in autistic subjects.
"Antibodies
to Myelin Basic Protein in Children With Autistic Behavior." Brain,
Behavior and Immunity, vol. 7, number 1, March 1993, pp. 97-103.
Approximately 58% of the sera of autistic children were found to be positive
for anti-MBP [anti-brain antibodies]. This result was significantly different
from that of the controls, among whom were children with normal health, idiopathic
mental retardation, and Down syndrome. It is possible that anti-MBP antibodies
are associated with the development of autistic behavior.
"Possible
Association of the Extended MHC Haplotype B44-SC30-DR4 With Autism." Immunogenetics,
vol. 36, number 4, 1992, pp. 203-7. The complement C4B null allele appears to
be associated with infantile autism. In this study, the incidence of
B44-SC30-DR4 was increased by almost six-fold in the autistic subjects as
compared with healthy controls. Moreover, the total number of extended
haplotypes expressed on chromosomes of autistic subjects was significantly
increased as compared with those expressed on chromosomes of healthy subjects.
Conclusion: a gene related to, or included in, the extended major
histocompatibility complex may be associated with autism.
"Increased
Frequency of the Null Allele at the Complement C4b Locus in Autism." Clinical
Experiments in Immunology, vol. 83, number 3, March 1991, pp. 438-40.
Associations between C4 deficiency and autoimmune disorders have been found
over the past several years. In this study, autistic subjects and their mothers
had significantly increased phenotypic frequencies of the C4B null allele,
compared with controls. The siblings of the autistic subjects also had an increased
frequency of the C4B null allele, but this was not significant. The fathers did
not display this allele. All family members had normal frequencies of the C4A
null allele, all normal C4A and C4B alleles and all BF and C2 alleles.
"Changes of
Soluble Interleukin-2, Interleukin-2 Receptor, T8 Antigen, and Interleukin-1 in
the Serum of Autistic Children." Clinical Immunology and
Immunopathology, vol. 61, number 3, December 1991, pp. 448-455. Findings
indirectly indicated that the activation of a subpopulation of T cells occurs
in some children with autism, as opposed to healthy children or children with
mental retardation (non-Down's syndrome).
"Deficiency
of Suppressor-inducer (CD4+CD45RA+) T Cells in Autism." Immunological
Investigations, vol. 19, number 3, June 1990, pp. 245-51. Autistic subjects
as compared to a group of 35 healthy age-matched subjects had a significantly
reduced number of lymphocytes, a decreased number of CD2+ T cells and reduced
numbers of CD4+ and CD4+CD45RA+ lymphocytes. Results suggest that an alteration
in the suppressor-inducer T-cell subset is associated with autism.
"CD4+
Helper T Cell Depression in Autism." Immunology Letters, vol.
25, number 4, September 1990, pp. 341-5. Autistic subjects had a significantly
lower percentage and number of CD4+ cells, a lower number of T cells (CD2+
cells) and B cells (CD20+ cells), and a lower percentage and number of total
lymphocytes than siblings and normal subjects. The level of blood values for
female subjects appeared lower than those for males as compared to normal
subjects of the same sex. Results suggest that a decrease in CD4+ cells is
associated with autism.
--for
cognitive disorders see also "Vaccination against whooping-cough.
Efficacy versus risks," The Lancet, vol. 1, January 29, 1977,
pp. 234-7, above, in <<seizure
disorders>>.
"Survival of the
fittest"—‘morphing’ of eradicated viral diseases into new diseases
Dr. Bruce P. Squires remarked, "it is
ironic that as smallpox was finally being eradicated in the late 1970s, another
virus [HIV] was being transmitted to unsuspecting hosts" (Canadian
Medical Association Journal, vol. 149, 1993, p. 919). Dr. James H.
Battershill comments on this in the January 15, 1994 issue of the Journal
(vol. 150, no. 2, p. 128): "…I have often wondered whether there was a
relation between the cessation of small-pox vaccination and the appearance of
AIDS. A shared antigen, perhaps?" Whatever the case, viruses are extremely
clever survivors, able to mutate into new disease forms when their original
presentations are defeated by vaccines. In Factoid Fallacies, below, the
section on "Disease eradication" deals with this theme in part.
"Is
RA27/3 rubella immunization a cause of chronic fatigue?" (Medical
Hypotheses, vol. 27, no. 3, November 1988, pp. 217-20): "Patients with
chronic fatigue syndromes (primary fibrositis syndrome, major affective
disorder, etc.) have elevated IgG serum antibodies to multiple common viruses.
Only IgG rubella antibodies are positively correlated with the intensity of
symptoms and have a height that is clearly significant compared to healthy
controls…A new more potent strain of live rubella vaccine (strain RA27/3) was
introduced in 1979. Within three years reports of patients with chronic fatigue
began surfacing in the literature. Considering all this, the possible role of
rubella immunization in the etiology of chronic fatigue syndromes deserves
further study."
"Second generation" --
layered -- antibodies
A problem unforeseen in the development of vaccines for common diseases is the advent of high antibody counts in fully-vaccinated parents who, in time, have children who are also vaccinated. Similarly, the effects of repeated vaccination or vaccination of persons with high antibody levels warrants careful observation and study. In "Combination vaccines for childhood immunization: Recommendations" (American Academy of Pediatrics/American Academy of Family Physicians), the safety and efficacy of administering combination (multivalent) vaccines to patients who already have immunity to one or more vaccine component (natural or via monovalent vaccine) is listed as a future research priority, indicating that the safety of this practice has not been proven. Even for persons not already immune to vaccine components, "the effects on immunogenicity and safety of simultaneous or repeated exposures to the same proteins used as antigens…and/or as carrier components" is at issue (pp. 10-12, Morbidity and Mortality Weekly Report, vol. 48, RR05, May 14, 1999, pp. 1-15; text available http://www.cdc.gov/epo/mmwr/p