"THE ABCs OF MMRs AND DTPs: IS THERE AN ASSOCIATION BETWEEN VACCINATION AND AUTISM?" BY ERIC LONDON:
A BIBLIOGRAPHIC ESSAY
rev. 7-21-99
http://libnt2.lib.tcu.edu/staff/lruede/autvacc.html
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.]
Commentary, "Garbage Science," Brick Walls, Crossword Puzzles, and Mercury," by Bernard Rimland, Ph.D., Autism Research Institute,
http://www.autism.com/ari/editorials/garbagescience.html
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 simplexencephalitis. …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, Clinical Research (abstracts) vol. 37, no. 2, p. 556a (1998), 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.
SIGH! It wouldnt let me post all of it! Go to the website to finish reading, is a VERY good report.
