





News and commentary on the autism epidemic and my beautiful boy who is living with autism.
Autism: Bridging the Gap Between Knowledge and Practice for Clinicians
Rationale:
Autism, including its possible causes and treatments, is a highly-charged, polarizing subject within the medical, public health, and even the autism community. Maine CDC/DHHS is hosting a medical conference to provide an update on the latest science on possible causes, diagnostic tools, and treatment of autism. The conference will feature several national researchers, Maine treating physicians and an interactive format, allowing the Maine clinical community an opportunity to ask questions and discuss issues with presenters. Some areas that will be covered include some of the murky areas in causes and treatment of autism, particularly those treatments that parents embark on with or without the knowledge, guidance or approval of the child’s physician. Examples include DAN, special diets, and avoiding vaccines. By addressing these more controversial areas, we hope to address one of the overall goals of helping to break down the barriers between physicians and parents in order to ultimately provide more comprehensive and collaborative care for children with autism
Primary Audience
Pediatricians and other primary care clinicians who care for children Objectives
By the end of the conference, participants will be able to:
- Describe the trends of autism (Autism Spectrum Disorders = ASD).
- Identify the first signs and symptoms of Autism.
- Explain when and how to refer for specialized diagnostics.
- Apply universal autism screening with recommended tools.
- Describe the use of the AAP Autism Toolkit.
- Describe what is available for diagnostic and therapeutic services in Maine.
- Define co-morbidities to autism and ways to effectively identify and treat them.
- Identify effective strategies to address some of the challenges parents and children with autism face in clinical settings.
- Discuss the newest research on the causes of autism, including genetic and environmental theories.
- Discuss the newest research on the treatments of autism, including those that are commonly used by families, but not necessarily widely accepted by the medical community.
Conference Agenda
8:00 Registration, Networking, Coffee 8:30 Introduction and Overview of Autism in Maine
Dora Anne Mills, MD, MPH9:00 Autism 101
Carol Hubbard, MD
Victoria Dalzell, MD
Mary Ellen Gellerstedt, MD
Don Burgess, MD
First signs and symptoms, Maine’s new screening tool, how and when to refer for specialized diagnostics, how a diagnosis is made, AAP Autism Toolkit, diagnostic and therapeutic services in Maine.11:00 Keynote by Tim Buie, MD
Gastrointestinal and Nutritional
Co-Morbidities in Autism, followed by Q&A12:30 Lunch – Voices of Autism 1:30 Keynote by Martha Herbert, MD, PhD
Genes and Environment, Developmental and Chronic: An Inclusive Approach to Autism Science, followed by Q&A3:00 Keynote by Jon Poling, MD, PhD
Looking Forward Beyond Vaccines: How Do We Know What Autism IS NOT if We Do Not Know What Autism IS? Followed by Q&A with other conference speakers.Speakers
Timothy Buie, MD
Pediatric Gastroenterologist
Massachusetts General Hospital
Harvard Medical School
Don Burgess, MD, Pediatrician
Past President of the Maine AAP
Southern Maine Medical Center
Victoria Dalzell, MD
Developmental-Behavioral Pediatrician
Maine Medical Center
Mary Ellen Gellerstedt, MD
Developmental-Behavioral Pediatrician
Eastern Maine Medical Center
Martha Herbert, MD, PhD
Pediatric Neurologist
Massachusetts General Hospital
Harvard Medical School
Carol Hubbard, MD
Developmental-Behavioral Pediatrician
Maine Medical Center
Dora Anne Mills, MD, MPH
Director, Maine Center for Disease Control and Prevention
State Health Officer
Jon Poling, MD, PhD
Neurologist, Clinical Assistant Professor
Medical College of Georgia
Father of child with autism
“…we haven’t connected. So I think part of what’s missing here, we’ve got to stop all this battling and we’ve got to honor each other’s perspective…”
“On a personal note, seeing a room packed full of autism and health professionals hang on every word of a long demanding speaking schedule that addressed toxic triggers has done more to melt my cynicism than anything has done in a long time. Looking out on the crowd I had hope for the first time in ages that we parents might not be alone in our fight forever, and that I may get to stop having to be a doctor and a lawyer and journalist and an activist and the town crier and just get to be a mom to my boys.
I have long recognized that my role in this community is to be the challenger. To guide (and sometimes push hard) people toward what is needed or being neglected. It was an incredible experience to spend the day with divisions of CDC and the AAP, whose parent orgs I have been sharply criticizing for years, and to NOT have anything critical to say! To see people getting it right. For there to be no BS to have to call out and enjoy watching doctors and parents learn from one another and connect with one another.”
Swine Flu May Be Human Error; WHO Investigates Claim
By Jason Gale and Simeon Bennett
Bloomberg.com
May 13 (Bloomberg) -- The World Health Organization is investigating a claim by an Australian researcher that the swine flu virus circling the globe may have been created as a result of human error.
Adrian Gibbs, 75, who collaborated on research that led to the development of Roche Holding AG’s Tamiflu drug, said in an interview that he intends to publish a report suggesting the new strain may have accidentally evolved in eggs scientists use to grow viruses and drugmakers use to make vaccines. Gibbs said he came to his conclusion as part of an effort to trace the virus’s origins by analyzing its genetic blueprint.
“One of the simplest explanations is that it’s a laboratory escape,” Gibbs said in an interview with Bloomberg Television today. “But there are lots of others.”
The World Health Organization received the study last weekend and is reviewing it, Keiji Fukuda, the agency’s assistant director-general of health security and environment, said in an interview May 11. Gibbs, who has studied germ evolution for four decades, is one of the first scientists to analyze the genetic makeup of the virus that was identified three weeks ago in Mexico and threatens to touch off the first flu pandemic since 1968.
A virus that resulted from lab experimentation or vaccine production may indicate a greater need for security, Fukuda said. By pinpointing the source of the virus, scientists also may better understand the microbe’s potential for spreading and causing illness, Gibbs said.
Possible Mistake
“The sooner we get to grips with where it’s come from, the safer things might become,” Gibbs said by phone from Canberra yesterday. “It could be a mistake” that occurred at a vaccine production facility or the virus could have jumped from a pig to another mammal or a bird before reaching humans, he said.
Gibbs and two colleagues analyzed the publicly available sequences of hundreds of amino acids coded by each of the flu virus’s eight genes. He said he aims to submit his three-page paper today for publication in a medical journal.
“You really want a very sober assessment” of the science behind the claim, Fukuda said May 11 at the WHO’s Geneva headquarters.
The U.S. Centers for Disease Control and Prevention in Atlanta has received the report and has decided there is no evidence to support Gibbs’s conclusion, said Nancy Cox, director of the agency’s influenza division. She said since researchers don’t have samples of swine flu viruses from South America and Africa, where the new strain may have evolved, those regions can’t be ruled out as natural sources for the new flu.
No Evidence
“We are interested in the origins of this new influenza virus,” Cox said. “But contrary to what the author has found, when we do the comparisons that are most relevant, there is no evidence that this virus was derived by passage in eggs.”
The WHO’s collaborative influenza research centers, which includes the CDC, and sites in Memphis, Melbourne, London and Tokyo, were asked by the international health agency to review the study over the weekend, Fukuda said. The request was extended to scientists at the Food and Agriculture Organization in Rome, the World Organization for Animal Health in Paris, as well as the WHO’s influenza network, he said.
“My guess is that the picture should be a lot clearer over the next few days,” Fukuda said. “We have asked a lot of people to look at this.”
Virus Expert
Gibbs wrote or co-authored more than 250 scientific publications on viruses during his 39-year career at the Australian National University in Canberra, according to biographical information on the university’s Web site.
Swine flu has infected 5,251 people in 30 countries so far, killing 61, according to WHO data. Scientists are trying to determine whether the virus will mutate and become more deadly if it spreads to the Southern Hemisphere and back. Flu pandemics occur when a strain of the disease to which few people have immunity evolves and spreads.
Gibbs said his analysis supports research by scientists including Richard Webby, a virologist at St. Jude Children’s Research Hospital in Memphis, who found the new strain is the product of two distinct lineages of influenza that have circulated among swine in North America and Europe for more than a decade.
In addition, Gibbs said his research found the rate of genetic mutation in the new virus was about three times faster than that of the most closely related viruses found in pigs, suggesting it evolved outside of swine.
Gene Evolution
“Whatever speeded up the evolution of these genes happened at least seven or eight years ago, so one wonders, why hasn’t it been found?” Gibbs said today.
Some scientists have speculated that the 1977 Russian flu, the most recent global outbreak, began when a virus escaped from a laboratory.
Identifying the source of new flu viruses is difficult without finding the exact strain in an animal or bird “reservoir,” said Jennifer McKimm-Breschkin, a virologist at the Commonwealth Science and Industrial Research Organization in Melbourne.
“If you can’t find an exact match, the best you can do is compare sequences,” she said. “Similarities may give an indication of a possible source, but this remains theoretical.”
The World Organization for Animal Health, which represents chief veterinary officers from 174 countries, received the Gibbs paper and is working with the WHO on an assessment, said Maria Zampaglione, a spokeswoman.
Genetic Patterns
The WHO wants to know whether any evidence that the virus may have been developed in a laboratory can be corroborated and whether there are other explanations for its particular genetic patterns, according to Fukuda.
“These things have to be dealt with straight on,” he said. “If someone makes a hypothesis, then you test it and you let scientific process take its course.”
Gibbs said he has no evidence that the swine-derived virus was a deliberate, man-made product.
“I don’t think it could be a malignant thing,” he said. “It’s much more likely that some random thing has put these two viruses together.”
Gibbs, who spent most of his academic career studying plant viruses, said his major contribution to the study of influenza occurred in 1975, while collaborating with scientists Graeme Laver and Robert Webster in research that led to the development of the anti-flu medicines Tamiflu and Relenza, made by GlaxoSmithKline Plc.
Bird Poo
“We were out on one of the Barrier Reef islands, off Australia, catching birds for the flu in them, and I happened to be the guy who caught the best,” Gibbs said. The bird he got “yielded the poo from which was isolated the influenza isolate strain from which all the work on Tamiflu and Relenza started.”
Gibbs, who says he studies the evolution of flu viruses as a “retirement hobby,” expects his research to be challenged by other scientists.
“This is how science progresses,” he said. “Somebody comes up with a wild idea, and then they all pounce on it and kick you to death, and then you start off on another silly idea.”
To contact the reporters on this story: Jason Gale in Geneva at j.gale@bloomberg.net; Simeon Bennett in Singapore atsbennett9@bloomberg.net.
Last Updated: May 13, 2009 01:36 EDT
Luke 4:16-20
And he came to Nazareth, where he had been brought up. And as was his custom, he went to the synagogue on the Sabbath day, and he stood up to read.
And the scroll of the prophet Isaiah was given to him. He unrolled the scroll and found the place where it was written,
“The Spirit of the Lord is upon me,
because he has anointed me
to proclaim good news to the poor.
He has sent me to proclaim liberty to the captives
and recovering of sight to the blind,
to set at liberty those who are oppressed,
to proclaim the year of the Lord’s favor.”
And he rolled up the scroll and gave it back to the attendant and sat down. And the eyes of all in the synagogue were fixed on him. And he began to say to them, “Today this Scripture has been fulfilled in your hearing.”
Matthew 5:3
Blessed are the poor in spirit, for theirs is the kingdom of heaven.
Media Advisory - News Conference
What:
1) On Wednesday 6th May 2009 a formal complaint will be filed with the General Medical Council of the UK against four senior doctors, all highly regarded members of the UK medical establishment. It is alleged, and supported by documentary evidence, that Dr. Richard Horton, Editor of The Lancet, Dr. David Salisbury of the Dept. of Health, Professor Arie Zuckerman, former Dean of the Medical School, Royal Free Hospital, and Dr. Michael Pegg, Chair of the Ethics Committee of the Royal Free gave false testimony on oath in the GMC hearings involving Dr. Andrew Wakefield, Professor John Walker-Smith, and Professor Simon Murch.
2) At the same time parents of 4 children involved in the original Lancet study, on which the major allegations have been based, will make public statements regarding the GMC hearings.
When: Wednesday May 6, 2009
Time: 11:30am – 12:30pm
Where: The Kingsway Hall Hotel, 66 Great Queen Street, London, WC2B 5BX,
www.kingswayhall.co.uk
Who: U.S. attorney James Moody, director of U.S. charities Safe Minds and the National Autistic Association, acting on behalf of 13 American and British autism organisations, states:
“Dr. Richard Horton, Editor of The Lancet, Dr. David Salisbury of the Dept. of Health, Professor Arie Zuckerman, former Dean of the Medical School at the Royal Free Hospital, and Dr. Michael Pegg, Chair of the Ethics Committee of the Royal Free, should be investigated for supplying false testimony. Furthermore, the current GMC hearing against Drs. Wakefield. Murch and Walker-Smith should be terminated. This unwarranted attack on scientists and doctors who came to the aid of desperately ill children has deterred others from helping similarly affected children, and distracted attention from the public health crisis caused by the substantial rise in autism diagnoses.”
Three families representing four of the 12 children included in the original Lancet publication will speak out publicly for the first time about the GMC hearings to clarify the details of their childrens’ involvement in the case series, and express their families’ support of the doctors they consider to be wrongly under investigation by the GMC. A letter from the families to the GMC expressing support of the doctors being investigated will be read by those who are able to be present.
Contact: James Moody - autismandvax@aol.com; tel: 001 202-298-4766.
Induction of metallothionein in mouse cerebellum and cerebrum with low-dose thimerosal injection.
Cell Biol Toxicol. 2009 Apr 9.
Minami T, Miyata E, Sakamoto Y, Yamazaki H, Ichida S.
Department of Life Sciences, School of Science & Engineering, Kinki University, 3-4-1 Kowakae, Higashi-osaka, Osaka, 577-8502, Japan, minamita@life.kindai.ac.jp.
Thimerosal, an ethyl mercury compound, is used worldwide as a vaccine preservative. We previously observed that the mercury concentration in mouse brains did not increase with the clinical dose of thimerosal injection, but the concentration increased in the brain after the injection of thimerosal with lipopolysaccharide, even if a low dose of thimerosal was administered. Thimerosal may penetrate the brain, but is undetectable when a clinical dose of thimerosal is injected; therefore, the induction of metallothionein (MT) messenger RNA (mRNA) and protein was observed in the cerebellum and cerebrum of mice after thimerosal injection, as MT is an inducible protein. MT-1 mRNA was expressed at 6 and 9 h in both the cerebrum and cerebellum, but MT-1 mRNA expression in the cerebellum was three times higher than that in the cerebrum after the injection of 12 microg/kg thimerosal. MT-2 mRNA was not expressed until 24 h in both organs. MT-3 mRNA was expressed in the cerebellum from 6 to 15 h after the injection, but not in the cerebrum until 24 h. MT-1 and MT-3 mRNAs were expressed in the cerebellum in a dose-dependent manner. Furthermore, MT-1 protein was detected from 6 to 72 h in the cerebellum after 12 microg/kg of thimerosal was injected and peaked at 10 h. MT-2 was detected in the cerebellum only at 10 h. In the cerebrum, little MT-1 protein was detected at 10 and 24 h, and there were no peaks of MT-2 protein in the cerebrum. In conclusion, MT-1 and MT-3 mRNAs but not MT-2 mRNA are easily expressed in the cerebellum rather than in the cerebrum by the injection of low-dose thimerosal. It is thought that the cerebellum is a sensitive organ against thimerosal. As a result of the present findings, in combination with the brain pathology observed in patients diagnosed with autism, the present study helps to support the possible biological plausibility for how low-dose exposure to mercury from thimerosal-containing vaccines may be associated with autism.
"We believe that adversomics (the immunogenetics and immunogenomics of vaccine adverse events at the individual and population level, respectively) is critical to understanding and preventing serious adverse vaccine-related events, developing the next generation of vaccines, and to improving public confidence in vaccine safety."
"Nonetheless, the field of adversomics is growing due to scientific interest in understanding the basis for vaccine reactions, “push” from the growing field of individualized medicine, and consumer demand for safer vaccines."
Adversomics: The Emerging Field of Vaccine Adverse Event Immunogenetics
Gregory A. Poland, MD,* Inna G. Ovsyannikova, PhD,† and Robert M. Jacobson, MD‡
Key Words: genetic association, immunogenetics, vaccine adverse events
(Pediatr Infect Dis J 2009;28: 431–432)
Vaccines have enabled tremendous decreases in infectious diseases, eradication of smallpox, saved lives, and remain among the most effective and cost-effective of our public health initiatives.1 At the same time, as an ever larger number of vaccines are administered globally, increasing concerns about adverse events and reactions have been raised and threaten the public health successes attributable to vaccines. For example, the controversy surrounding measles-mumps-rubella (MMR) vaccine and thimerosal are emblematic of public concerns and perceptions regarding vaccine safety and vaccine adverse reactions (AEs). With current and future technologic advances such as high throughput whole-genome scanning, transcriptomics, epigenetics, proteomics, and new biostatistical approaches to understanding huge databases of information, we can better understand associations and mechanisms by which genetically- mediated individual variations in vaccine response and reactivity occur. Armed with such knowledge, the ability to predict such AEs, or to design new vaccine approaches that minimize or eliminate serious vaccine-related reactions could be devised, consistent with a more personalized or individual approach to vaccine practice which we have called adversomics (the immunogenetics and immunogenomics of vaccine adverse events at the individual and population level, respectively).
CURRENT KNOWLEDGE
Immune, inflammatory, idiosyncratic, and other responses to a vaccine are determined by a host of known and unknown factors, including individual characteristics (age, gender, race, medical condition, etc.), the quality and quantity of vaccine antigen(s), the number of doses administered, route of immunization, and host genetics. Although tremendous work has gone into understanding genetic susceptibility to infectious diseases,2 attention now needs to turn toward understanding genetic susceptibility to vaccine-related AEs. Indeed in the case of live vaccines, one might simplistically envision administration of such vaccines as an “infection” and conceptually study the susceptibility to such reactions in the same manner. To further develop this construct, we have hypothesized that adverse reactions and events may not be random, but may in fact be, in part, genetically predetermined. For example, early studies demonstrated that certain populations are unusually susceptible to measles vaccine reactions with post-vaccine febrile reactions among 11 different Amerind populations 0.4°C higher than in Caucasian populations.3 It was speculated that genetic differences in Amerinds were associated with intensified reactions to measles vaccine. Studies of Native American children revealed higher risks for invasive Haemophilus influenzae type b infection than white children. Decreased IgG2 and IgG4 antibody responses to H. influenzae type b polysaccharide vaccine were observed in healthy Apache children, compared with white children, potentially explaining the higher incidence of H. influenza type b infections in Apache populations. 4 Later studies revealed specific Km and
Gm genetic allotypes associated with poorer immune response.5
More recent studies have investigated the role of cytokines in the pathogenesis of AEs associated with live viral vaccines. A large study of AEs, including fever, lymphadenopathy, and localized or generalized rash, after smallpox immunization was associated with increased levels of IFN-!, TNF-", IL-2, IL-5, and IL-10, whereas individuals who did not report an AE demonstrated increased IFN-! levels only during the acute phase compared with baseline levels after immunization.6 Concerns regarding myopericarditis after smallpox vaccine has resulted in studies which are examining possible genetic associations.7,8
Additional insights into identification of genetic markers that affect immune and physiological responses to viral vaccines emerged from a study which examined the genetic basis for adverse events after smallpox vaccination.9 The hypothesis was that subjects experiencing AEs exhibited unique genetic polymorphisms associated with AE reactions in response to smallpox vaccination. To test the hypothesis 346 smallpox (Dryvax) immunized individuals were genotyped for single-nucleotide polymorphisms (SNPs) in 19 candidate genes and assessed for the development of fever associated with the receipt of vaccine. This study showed that fever following smallpox vaccination was associated with specific haplotypes on the IL1 gene complex, and in the IL18 and IL4 genes. Importantly, these findings raise the possibility that the same genetic polymorphisms linked to fever after smallpox vaccine may also influence fever risk after other live virus vaccines, including MMR.9,10 For example, a small percentage of children who get vaccine-induced fever after MMR will develop febrile seizures. Knowledge of a genetic association could allow the development of predictive tests or preventive therapies that could be administered with vaccine to prevent such AEs.
In another study 131 healthy volunteers from 2 independent smallpox vaccine studies were genotyped across 386 genes and assessed for local and systemic AEs.11 The authors reported that genetic polymorphisms in genes expressing an enzyme previously associated with adverse reactions to a variey of pharmacologic agents (ie, the methylenetetrahydrofolate reductase, MTHFR, gene) and an immunologic transcription factor (ie, the interferon regulatory factor-1, IRF1, gene) were associated with local and systemic AEs (an oral temperature !38.3°C, generalized skin eruptions, or enlarged or tender regional lymph nodes) after smallpox vaccination.
Our own laboratory has done extensive work in identifying genetic associations with HLA, cytokine, cytokine receptor, innate receptors, innate immune response genes, and signaling molecules and both humoral and cell-mediated immune responses.12,13 This work has been fundamental to identifying and understanding associations between genetic polymorphisms and variations in immune responses. Such methods must now be turned toward understanding adverse events associated with vaccination. An example is that epidemiologic studies have quantified the risk of immune thrombocytopenic purpura (ITP) and anaphylaxis, attributable to the MMR vaccine in the second year of life as 1 case per 40,000 vaccinated children.14,15 Recently France et al demonstrated that 76% of ITP cases in children ages 12 to 23 months were related to MMR vaccination.15 Identification of a genetic association between MMR vaccine and ITP would be important and would inform attempts at developing preventive strategies or improved vaccines. A further example is the expanding recommendations for the use of seasonal influenza vaccine and the potential use of pandemic vaccines globally; studies of the genetic susceptibility to Guillain-Barre Syndrome (GBS) would be important.16
SUMMARY
We believe that adversomics (the immunogenetics and immunogenomics of vaccine adverse events at the individual and population level, respectively) is critical to understanding and preventing serious adverse vaccine-related events, developing the next generation of vaccines, and to improving public confidence in vaccine safety. Significant difficulties in the growth of the field of vaccine immunogenetics include the difficulty of studying large enough numbers of subjects (rare AEs are, by definition, rare), lack of research funding, the complexity and extensive polymorphic nature of immune response genes, statistical issues of multiple comparisons and statistical power, issues of multigenic and other gene interactions such as complementation and epigenetic DNA modifications, and gender, racial, and ethnic differences. Nonetheless, the field of adversomics is growing due to scientific interest in understanding the basis for vaccine reactions, “push” from the growing field of individualized medicine, and consumer demand for safer vaccines. The capability to reproduce statistical associations in independent population-based studies remains essential to assessing the generalization of such studies. Clearly more comprehensive studies are needed to determine if there are
associations between genetic variations among individuals and susceptibility to serious adverse events in response to vaccination. These factors combined with technologic ability will lead to a new era in vaccinology and better, safer vaccines.
REFERENCES
1. Centers for Disease Control and Prevention. Ten
Great Public Health Achievements—United States,
1900–1999. MMWR. 1999;48:241–243.
2. Kaslow R, et al. eds. Genetic Susceptibility to
Infectious Diseases. New York, NY: Oxford University
Press; 2008:1– 447.
3. Black FL, et al. Intensified reactions to measles
vaccine … J Infect Dis. 1971;124:306 –317.
4. Siber GR, et al. Impaired antibody response to
Haemophilus influenzae type b polysaccharide…
N Engl J Med. 1990;323:1387–1392.
5. Goldblatt D, et al. Association of Gm allotypes
with the antibody response … J Immunol. 1994;
153:5316 –5320.
6. Rock MT, et al. Adverse events after smallpox
immunizations … J Infect Dis. 2004;189:1401–
1410.
7. Halsell JS, et al. Myopericarditis following smallpox
vaccination … JAMA. 2003;289:3283–3289.
8. Wilson CB, et al. Vaccine safety–vaccine benefits
… Nat Rev Immunol. 2001;1:160 –165.
9. Stanley SL, et al. The immunogenetics of smallpox
vaccination. J Infect Dis. 2007;196:212–219.
10. Usonis V, et al. Reactogenicity and immunogenicity
of a new live …. Pediatr Infect Dis J.
1999;18:42– 48.
11. Reif DM, et al. Genetic basis for adverse events
after smallpox vaccination. J Infect Dis. 2008;
198:16 –22.
12. Poland GA, et al. Heterogeneity in vaccine immune
response … Clin Pharmacol Ther. 2007;
82:653– 664.
13. Poland GA, et al. Vaccine immunogenetics ….
Vaccine. 2008;26:6183– 6188.
14. Stratton KR, et al. Adverse events associated with
childhood vaccines other than pertussis and rubella
… JAMA. 1994;271:1602–1605.
15. France EK, et al. Risk of immune thrombocytopenic
purpura … Pediatrics. 2008;121:e687–
e692.
16. Juurlink DN, et al. Guillain-Barre syndrome after
influenza vaccination in adults … Arch Intern
Med. 2006;166:2217–2221.
Concise Reviews The Pediatric Infectious Disease Journal • Volume 28, Number 5, May 2009
432 ©
We have never argued that people shouldn't be immunized for the most serious threats including measles and polio, but surely there's a limit as to how many viruses and toxins can be introduced into the body of a small child. Veterinarians found out years ago that in many cases they were over-immunizing our pets, a syndrome they call Vaccinosis. It overwhelmed the immune system of the animals, causing myriad physical and neurological disorders. Sound familiar? If you can over-immunize a dog, is it so far out to assume that you can over-immunize a child? These forward thinking vets also decided to remove thimerosal from animal vaccines in 1992, and yet this substance, which is 49% mercury, is still in human vaccines. Don't our children deserve as much consideration as our pets?
“A baby’s body is bombarded with immunologic challenges—from bacteria in food to the dust they breathe. Compared to what they typically encounter and manage during the day, vaccines are literally a drop in the ocean”, and Dr. Offits studies theoretically show an infant could handle up to 100,000 vaccines at one time … safely.
"The figure of 100,000 is correct, and probably a little conservative".
Minnesota Department of Health
News Release
April 14, 2009
Contact information
Polio virus associated with oral vaccine reported in Minnesota resident
Patient who died had weakened immune system, multiple other health conditions
State health officials are investigating a case of infection associated with the polio virus in a Minnesotan who died last month.
The patient was infected with a virus strain found in the oral polio vaccine. The oral vaccine, which is no longer used in the U.S., contained live polio virus. The injected polio vaccine now in use contains only inactivated virus.
The patient died with symptoms that included paralytic polio, but it is not known to what extent the polio may have contributed to the death. The patient had a weakened immune system and multiple health problems. The patient most likely acquired the vaccine-derived polio virus from someone who had received the live-virus, oral poliovirus vaccine (OPV) before the use of OPV was discontinued nine years ago.
Infection from polio virus can cause a wide range of symptoms. Most infections result in no or mild symptoms, but in rare cases can severely affect the neurologic system, resulting in paralysis.
Minnesota Department of Health officials are emphasizing that there is no risk to the general public from this case. Only people who have had direct, close contact with the patient, such as certain health care workers, may be at risk of infection. Adhering to recommended infection control guidelines and being vaccinated protect against polio. At this time, no additional cases of infection with the polio virus have been reported in connection with the patient.
"We are working closely with our local and national partners to investigate this case," said Minnesota State Epidemiologist Dr. Ruth Lynfield. "It's important to note that while there is no risk to the general public, many people still have vivid memories of a time when polio was a major public health concern before the first vaccines were introduced in the 1950s. This is a very rare occurrence and does not signal a resurgence of polio."
MDH staff are working with hospital staff to determine if there might be health care workers at risk for disease. Hospital staff are notifying all health care workers who may have been exposed. "Only unvaccinated people or people with deficient immune systems who have had direct, ungloved contact with the patient's bodily secretions are at any risk for disease," said Dr. Aaron DeVries, Medical Epidemiologist at MDH. Health officials will follow up with health care workers to make sure their immunizations are up to date and they are showing no signs of disease. "If you don't hear from a public health or health care official, you're not at risk," DeVries said.
This type of polio infection is very rare, officials stressed. In rare instances, a person who has either never been vaccinated or has certain immunodeficiencies can acquire the polio virus from someone who has been vaccinated and is excreting the virus in their stool. Sometimes these infections result in illness, as happened in this situation. Only 45 cases of vaccine-derived polio disease in persons with immunodeficiencies have been reported in the world since 1961.
This is the second instance of a polio infection caused by a vaccine strain of virus in the United States since 2000, when use of live-virus oral polio vaccine was discontinued in the U.S. All polio vaccinations in the U.S. are now done with an injected, killed-virus vaccine. The other instance of vaccine-derived polio infection also occurred in Minnesota, in 2005, but was very different from this case. It occurred in an unimmunized child from a community that had high levels of non-immunization and that case was not associated with neurological symptoms.
"We suspect that one reason why Minnesota has detected both cases in the United States in the last 10 years is because of the high level of cooperation among astute clinicians, a network of clinical laboratories and the Minnesota Department of Health, which in turn has a Public Health Laboratory that looks for such rare agents as polio virus," Lynfield said.
Naturally-occurring polio has been eradicated in the western hemisphere. The last case of naturally-occurring (not from vaccine) paralytic polio disease occurred in the United States in 1979.
Although members of the general public are not at risk, MDH officials say this unusual case should serve as a reminder to make sure that all of your immunizations are current and that children receive immunizations as recommended.
"It's always a good idea to check with your physicians or health care providers to be certain all of your vaccinations are current," DeVries said. "Make sure you're protected and your children are protected."
Most people in the United States have been vaccinated against polio and healthy people have developed full immunity to the disease. An estimated 94 percent of Minnesota's two-year-olds have had the full primary series of three polio shots, which are usually administered in infancy.
NOTE TO EDITORS/REPORTERS: According to Minnesota laws, the Minnesota Department of Health is unable to provide any further identifying information regarding the patient. In addition, the family has expressed their strong desire to maintain their privacy and confidentiality, so we are asking media to refrain from attempts to identify, locate or interview the family. Health officials are also concerned that doing so could interfere with the continuing investigation.
-MDH-
For more information, contact:
Doug Schultz
MDH Communications
651-201-4993
Dr. Aaron Devries
Epidemiologist
651-201-5414
Ockham's Razor and autism: The case for developmental neurotoxins contributing to a disease of neurodevelopment
M. Catherine DeSoto
Department of Psychology, University of Northern Iowa, Baker Hall, Cedar Falls, IA 50614-0505, United States
Received 16 January 2009;
accepted 7 March 2009.
Available online 21 March 2009.
Abstract
Much professional awareness regarding environmental triggers for ASD has been narrowly focused on a single possible exposure pathway (vaccines). Meanwhile, empirical support for environmental toxins as a broad class has been quietly accumulating. Recent research has shown that persons with ASD have comparatively higher levels of various toxins and are more likely to have reduced detoxifying ability, and, that rates of ASD may be higher in areas with greater pollution. This report documents that within the state with the highest rate of ASD, the rate is higher for schools near EPA Superfund sites, t (332) = 3.84, p = .0001. The reasons for the rise in diagnoses likely involve genetically predisposed individuals being exposed to various environmental triggers at higher rates than in past generations.
Keywords: Autism; Developmental disorders; Toxins; Pollution; Heavy metals; Environmental contaminants
Paid for by Obama for America
BARACK OBAMA: SUPPORTING AMERICANS WITH AUTISM SPECTRUM DISORDERS
More than one million Americans have Autism Spectrum Disorders (ASD), a complex condition that impacts communication, socialization, and behavior. And more cases of ASD are being recognized across the country at an alarming pace. Barack Obama believes that we must do more to help support Americans with ASD, their families, and their communities. Throughout his career, Barack Obama has worked with families affected by ASD to raise awareness and to provide support to parents and families living with ASD. As president, Obama will build on these many years of advocacy and ensure that his administration prioritizes ASD research, public awareness, and lifelong support services. Obama will seek to increase federal ASD funding for research, treatment, screenings, public awareness, and support services to $1 billion annually by the end of his first term in office. Obama will also continue to work with parents, physicians, providers, researchers, and schools to create opportunities and effective solutions for people with ASD.
Record of Leadership on ASD Research and Care: As an Illinois state senator, Barack Obama sponsored legislation that became law to create an ASD diagnosis education program, an initiative designed to promote the implementation of evidence-based practices. The goal of the project is to offer educational opportunities at all levels of care, including physicians, early intervention (EI) specialists, psychologists, teachers, day care providers, parents, respite workers, and speech and language therapists. Obama has personally worked side-byside with Illinois families affected by ASD to support efforts to build the Therapeutic School and Center for Autism Research. This school and research center will bring together education, academic research, early intervention programs, and training to prepare its students for independent living.
In the U.S. Senate, Obama is a cosponsor of a measure that would expand federal funding for life-long services for people with ASD, authorizing approximately $350 million in new federal funding for key programs related to treatments, interventions and services for both children and adults with ASD.
Appoint Federal ASD Coordinator to Oversee All Federal ASD Efforts: Barack Obama will ensure all federal ASD activities occur in an efficient manner that prioritizes both research and supports for families affected by ASD. Obama will appoint a Federal ASD Coordinator to oversee federal ASD research and federal efforts to improve awareness of ASD and improve the training of medical professionals to identify and treat ASD. By establishing one top-level point person to coordinate ASD efforts in the White House, Obama will ensure that ASD receives the recognition and priority it deserves in the federal government. The Federal ASD Coordinator will also be tasked with eliminating bureaucratic obstacles that may be delaying implementation of important ASD measures and ensuring that all federal ASD dollars are being spent in a manner that prioritizes results. The Coordinator will work with state task forces on ASD to ensure effective communication and
collaboration among federal, state, and local agencies.
Fully Fund the Combating Autism Act and Federal Autism Research Initiatives: Barack Obama supported the Combating Autism Act of 2006, which was signed into law in December 2006. The Combating Autism Act authorizes increased federal funding for ASD research and efforts to boost public awareness and early diagnosis of ASD. Since the bill has been enacted, however, federal funding for ASD has not increased to the levels Paid for by Obama for America authorized by the Combating Autism Act. As a U.S. Senator, Obama has worked to fully fund the Combating Autism Act and as president, he will ensure that his administration addresses the growing impact of ASD and other special needs on American families. President Obama will fully fund the Combating Autism Act, which provides nearly $1 billion in autism-related funding over 5 years, and work with Congress, parents and ASD experts to determine how to further improve federal and state programs.
Support Special Needs Education for Children with ASD: Barack Obama understands that children with special needs – students with visual, hearing, physical, sensory, and mental impairments – require meaningful resources to succeed both inside and outside the classroom. Obama is a strong supporter of the Individuals with Disabilities Education Act (IDEA) and supports full federal funding of the law to truly ensure that no child is left behind. The current underfunding of IDEA causes school districts throughout the country to deny necessary services to students with ASD and other special needs. Obama will also work to change IDEA’s definition of “autism” to Autism Spectrum Disorders to ensure that all children diagnosed with ASD disorders receive the support they need.
Support Universal Screening: While roughly 90 percent of infants in the United States are currently screened for various potentially disabling or life-threatening conditions, fewer than half the states screen all infants for the full recommended panel of 29 disorders. Many of these conditions, if caught early, can be treated before they result in permanent impairments or even death. Barack Obama believes we should screen all infants, and also that we must set a national goal to provide re-screening for all two-year-olds, the age at which some conditions, including ASD, begin to appear. These screenings will be safe and secure, and available for every American that wants them. Part of Obama's early childhood intervention plan will be directed at coordinating fragmented community programs to help provide all children access to screening for disabilities as infants and again as two-year olds. Achieving universal screening is essential so that disabilities can be identified early enough for those children and families to get the special supports and resources they need.
Work Together: As part of his commitment to open the doors of our government to the American people, Barack Obama is committed to facilitating open dialogue among Americans with special needs and their families, federal and state agencies, regional centers, resource centers, research institutions, school districts, first
responders, and community members.