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According to the ministry’s epidemiology department, the number of people of all ages who died from complications of the flu in the last few months was 27 – double that of last year – and that hardly any of them had gone to their health fund to be vaccinated. In addition, 61 Israelis have been hospitalized with severe complications of the flu since the beginning of the season.
Although the shot – which should have been given in late September to all children over the age of six months and to all adults – is free, only about 19% of the population – or 1.63 million of the more than 8 million Israelis above the age of six months – has been vaccinated.
and that hardly any of them had gone to their health fund to be vaccinated.
originally posted by: Phage
So, maybe if more people had been vaccinated fewer would have died. Highly likely fewer would have gotten ill.
originally posted by: hopenotfeariswhatweneed
Since we are arguing a small percentage of people have complications with vaccines therefor they should be no longer used, can we also remove seat belts since a small percentage of people have complications with seat belts...
originally posted by: Phage
a reply to: ElectricUniverse
I'm not sure infectious disease follows arithmetic rules but apparently Israel has a better medical system than the US. It's "universal" there, isn't it? Sounds sort of socialistic.
It has nothing to do with "their socialist healthcare" since very few people get complications from the flu,
originally posted by: Phage
And health care has nothing to do with that?
Interesting. I guess they just have stronger constitutions than Americans.
You have a strange way of looking at statistics. But I would think that, in general, people who have better access to health care are less likely to suffer complications and/or death of disease.
Only those 2,200 people would get "health care" related to the flu.
originally posted by: projectvxn
Try reading all of my responses before asking me leading questions.
Communicable disease is no ones right to spread.
New Canadian studies suggest seasonal flu shot increased H1N1 risk
Filed Under: H1N1 2009 Pandemic Influenza; Influenza Vaccines
By: Maryn McKenna | Apr 06, 2010
Apr 6, 2010 (CIDRAP News) –
In a lengthy article published today in Public Library of Science Medicine (PLoSMed), researchers detail the results of four supplementary studies that were launched after an April 2009 school outbreak provided the first signal of an association between seasonal flu shots and pandemic flu illness. The studies, which took in about 2,700 people, found overall that the likelihood of needing medical attention for pandemic flu was 1.4 to 2.5 times greater among people who were vaccinated the previous fall.
]The Canadian researchers add, however, that their results may signal a heretofore-undetected biological mechanism of interaction, one that could occur again in the rare instance of a pandemic strain arising after a flu season has already begun. The 2009 pandemic strain surfaced in the last weeks of the 2008-09 flu season, months after vaccines for that season had been administered.
"Our results may seem counterintuitive, but they cannot be dismissed on the basis that no biological mechanism can plausibly explain them," the Canadian researchers write. "If these observations do reflect a real biological effect . . . they raise important questions that warrant further scientific observation."
Biomed Res Int. 2015;2015:675149. doi: 10.1155/2015/675149. Epub 2015 Feb 1.
A new mechanism of vitamin C effects on A/FM/1/47(H1N1) virus-induced pneumonia in restraint-stressed mice.
Cai Y1, Li YF1, Tang LP1, Tsoi B1, Chen M1, Chen H1, Chen XM1, Tan RR1, Kurihara H1, He RR1.
It is well known that vitamin C could protect against influenza infection, but little is known about the mechanisms. This study aimed to investigate the influence and possible mechanisms of vitamin C on pneumonia induced by influenza virus in stressed mice. Results showed that restraint stress significantly increased the mortality and the severity of pneumonia in mice caused by A/FM/1/47(H1N1) virus infection, which was attenuated by oral administration of vitamin C (125 and 250 mg/kg). Moreover, vitamin C administration significantly decreased expression of susceptibility genes, including mitochondrial antiviral signaling (MAVS) and interferon regulatory factor 3 (IRF3), and increased expression of NF-κB. These work in conjunction to induce type I interferons (IFNs) and elicit innate antiviral response as key factors in RIG-I-mediated signal transduction pathway. The above effects of vitamin C were further found to relate with inhibition of excess CORT synthesis by regulating steroid hydroxylating enzymes in adrenal gland. In conclusion, the protective effects of vitamin C on influenza virus-caused pneumonia might be related to its inhibition of CORT synthesis, which reduces the susceptibility to influenza viral infection in restraint-stressed mice. These findings provide a new mechanism for the effects of vitamin C on influenza virus-induced pneumonia in restraint-stressed mice.
Nutrition. 2010 Jan;26(1):128-32. doi: 10.1016/j.nut.2009.09.015.
Combined inhalational and oral supplementation of ascorbic acid may prevent influenza pandemic emergency: a hypothesis.
Banerjee D1, Kaul D.
Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India. firstname.lastname@example.org
Occurrence of influenza pandemics is a worldwide phenomenon and a significant cause of mortality and morbidity throughout the globe. It is due to mutations in the influenza virus genetic material creating antigenic drift of pathogenic viral proteins resulting in emergence of new influenza virus strains. Therefore, the vaccines available for prevention of influenza offer no protection against influenza pandemics caused by new virus strains. Moreover, the existing drugs used to combat influenza may be ineffective to treat influenza pandemics due to the emergence of drug resistance in the pandemic virus strain. Therefore, a working strategy must be developed to combat influenza pandemics. In this review we have addressed this problem and reviewed the published studies on ascorbic acid in the common cold and influenza and laboratory studies on the effect of ascorbic acid on influenza virus. We have also correlated the clinical and laboratory studies and developed a hypothesis to prevent influenza pandemics.
J Manipulative Physiol Ther. 1999 Oct;22(8):530-3.
The effectiveness of vitamin C in preventing and relieving the symptoms of virus-induced respiratory infections.
Gorton HC, Jarvis K.
A total of 463 students ranging in age from 18 to 32 years made up the control group. A total of 252 students ranging in age from 18 to 30 years made up the experimental or test group.
Investigators tracked the number of reports of cold and flu symptoms among the 1991 test population of the facility compared with the reports of like symptoms among the 1990 control population. Those in the control population reporting symptoms were treated with pain relievers and decongestants, whereas those in the test population reporting symptoms were treated with hourly doses of 1000 mg of Vitamin C for the first 6 hours and then 3 times daily thereafter. Those not reporting symptoms in the test group were also administered 1000-mg doses 3 times daily.
Overall, reported flu and cold symptoms in the test group decreased 85% compared with the control group after the administration of megadose Vitamin C.
Vitamin C in megadoses administered before or after the appearance of cold and flu symptoms relieved and prevented the symptoms in the test population compared with the control group.
J Pharm Pharmacol. 2016 Mar;68(3):406-20. doi: 10.1111/jphp.12529. Epub 2016 Feb 21.
Red ginseng and vitamin C increase immune cell activity and decrease lung inflammation induced by influenza A virus/H1N1 infection.
Kim H1,2, Jang M1, Kim Y1, Choi J1, Jeon J1, Kim J3, Hwang YI1, Kang JS1,2, Lee WJ1.
Because red ginseng and vitamin C have immunomodulatory function and anti-viral effect, we investigated whether red ginseng and vitamin C synergistically regulate immune cell function and suppress viral infection.
Administration of red ginseng and vitamin C enhanced the activation of immune cells like T and NK cells, and repressed the progress of viral lytic cycle. It also reduced lung inflammation caused by viral infection, which consequently increased the survival rate.
© 2016 Royal Pharmaceutical Society, Journal of Pharmacy and Pharmacology.
originally posted by: projectvxn
a reply to: ElectricUniverse
For the overwhelmingly vast majority, they are safe.
J Biomed Sci. 2002 Jul-Aug;9(4):359-64.
Abnormal measles-mumps-rubella antibodies and CNS autoimmunity in children with autism.
Singh VK1, Lin SX, Newell E, Nelson C.
1Department of Biology and Biotechnology Center, Utah State University, Logan, Utah 84322, USA. email@example.com
Autoimmunity to the central nervous system (CNS), especially to myelin basic protein (MBP), may play a causal role in autism, a neurodevelopmental disorder. Because many autistic children harbor elevated levels of measles antibodies, we conducted a serological study of measles-mumps-rubella (MMR) and MBP autoantibodies. Using serum samples of 125 autistic children and 92 control children, antibodies were assayed by ELISA or immunoblotting methods. ELISA analysis showed a significant increase in the level of MMR antibodies in autistic children. Immunoblotting analysis revealed the presence of an unusual MMR antibody in 75 of 125 (60%) autistic sera but not in control sera. This antibody specifically detected a protein of 73-75 kD of MMR. This protein band, as analyzed with monoclonal antibodies, was immunopositive for measles hemagglutinin (HA) protein but not for measles nucleoprotein and rubella or mumps viral proteins. Thus the MMR antibody in autistic sera detected measles HA protein, which is unique to the measles subunit of the vaccine. Furthermore, over 90% of MMR antibody-positive autistic sera were also positive for MBP autoantibodies, suggesting a strong association between MMR and CNS autoimmunity in autism. Stemming from this evidence, we suggest that an inappropriate antibody response to MMR, specifically the measles component thereof, might be related to pathogenesis of autism.
Copyright 2002 National Science Council, ROC and S. Karger AG, Basel
Selection of Abstracts Regarding
Immune and/or Mitochindrial Dysfunction,
Sulfation and/or Detoxification Deficits in Autism
Updated August, 2011
Jyonouchi H, Geng L, Streck DL, Toruner GA. Children with autism spectrum disorders (ASD) who exhibit chronic gastrointestinal (GI) symptoms and marked fluctuation of behavioral symptoms exhibit distinct innate immune abnormalities and transcriptional profiles of peripheral blood (PB) monocytes. J Neuroimmunol. 2011 Jul 29.
Division of Allergy/Immunology and Infection Diseases, Department of Pediatrics, University of Medicine and Dentistry of New Jersey (UMDNJ)-New Jersey Medical School (NJMS), 185 South Orange Ave, Newark, NJ, United States.
Innate/adaptive immune responses and transcript profiles of peripheral blood monocytes were studied in ASD children who exhibit fluctuating behavioral symptoms following infection and other immune insults (ASD/Inf, N=30). The ASD/Inf children with persistent gastrointestinal symptoms (ASD/Inf+GI, N=19), revealed less production of proinflammatory and counter-regulatory cytokines with stimuli of innate immunity and marked changes in transcript profiles of monocytes as compared to ASD/no-Inf (N=28) and normal (N=26) controls. This included a 4-5 fold up-regulation of chemokines (CCL2 and CCL7), consistent with the production of more CCL2 by ASD/Inf+GI cells. These results indicate dysregulated innate immune defense in the ASD/Inf+GI children, rendering them more vulnerable to common microbial infection/dysbiosis and possibly subsequent behavioral changes.
Ratajczak HV. Theoretical aspects of autism: causes--a review. J Immunotoxicol. 2011 Jan-Mar;8(1):68-79.
Autism, a member of the pervasive developmental disorders (PDDs), has been increasing dramatically since its description by Leo Kanner in 1943. First estimated to occur in 4 to 5 per 10,000 children, the incidence of autism is now 1 per 110 in the United States, and 1 per 64 in the United Kingdom, with similar incidences throughout the world. Searching information from 1943 to the present in PubMed and Ovid Medline databases, this review summarizes results that correlate the timing of changes in incidence with environmental changes. Autism could result from more than one cause, with different manifestations in different individuals that share common symptoms. Documented causes of autism include genetic mutations and/or deletions, viral infections, and encephalitis following vaccination. Therefore, autism is the result of genetic defects and/or inflammation of the brain. The inflammation could be caused by a defective placenta, immature blood-brain barrier, the immune response of the mother to infection while pregnant, a premature birth, encephalitis in the child after birth, or a toxic environment.
Giulivi C, Zhang YF, Omanska-Klusek A, Ross-Inta C, Wong S, Hertz-Picciotto I, Tassone F, Pessah IN. Mitochondrial dysfunction in autism. JAMA. 2010 Dec 1;304(21):2389-96.
AL-Ayadhi and Mostafa Journal of Neuroinflammation
Serum antinucleosome-specific antibody as a marker of autoimmunity in children with autism
Laila Yousef AL-Ayadhi 1 and Gehan Ahmed Mostafa 1,2*
Increasing evidence of autoimmune phenomena in some individuals with autism could represent the
presence of altered or inappropriate immune responses in this disorder. The role of the nucleosome in the induction of antibody response in some autoimmune-mediated tissue damage may provide novel targets for treatment. Due to the paucity of studies investigating the frequency of systemic auto-antibodies in autism, we are the first to investigate the frequency of antinucleosome-specific antibodies in a group of autistic children.
Serum antinucleosome-specific antibodies were measured by ELISA in 60 autistic children, between the ages
of 3 and 12 years, in comparison to 60 healthy children. Autistic severity was assessed using the Childhood Autism
Rating Scale (CARS).
Autistic children had significantly higher serum antinucleosome-specific antibodies than healthy children
( P < 0.001 ). The seropositivity of antinucleosome-specific antibodies was found in 46.7% of autistic children. Autistic
children with a family history of autoimmunity (40%) had a significantly higher frequency of serum
antinucleosome-specific antibodies (83.3%) than patients without such a history (22.2%, P < 0.001 ).
Serum levels of antinucleosome-specific antibodies were increased in some autistic children. However,
these data should be treated with caution until further investigations are performed with a larger subject population to determine whether these antibodies have a role in the induction of autoimmunity in a subgroup of autistic children.
The role of immunotherapy in children with autism should be also studied.
Keywords: Antinucleosome-specific antibodies, Autism, Autoimmunity, Family history of autoimmunity
J Neuroimmunol. 2004 Jul;152(1-2):176-82.
Autoantibody repertoires to brain tissue in autism nuclear families.
Silva SC1, Correia C, Fesel C, Barreto M, Coutinho AM, Marques C, Miguel TS, Ataide A, Bento C, Borges L, Oliveira G, Vicente AM.
1Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6, 2781-196 Oeiras, Portugal.
The hypothesis of an immune dysfunction in autism spectrum disorders has previously been put forward without, however, compelling evidence of a direct relation to its etiology or pathogenesis. To further understand if autoimmunity could play a significant role in autism, we analyzed autoantibody repertoires to brain tissue extract in the plasma of 171 autism children, their parents, and 54 controls, by quantitative immunoblotting. Multiparametric analysis revealed significant differences between patients and controls, and showed that one single reactivity in Section 32 of the blot had the most power to discriminate between these samples. Family correlation coefficients and heritability estimates did not provide any evidence that this reactivity was genetically determined. While the molecular weight of the target protein suggested that it might be an isoform of Myelin Basic Protein (MBP), inhibition assays with human MBP argued against this hypothesis. The study evidences the widespread occurrence of autoreactivities to brain tissue in autism patients, which may represent the immune system's neuroprotective response to a previous brain injury occurred during neurodevelopment. The molecular identification of the target protein in Section 32 will contribute to the understanding of the role of immune responses against brain antigens in autistic patients.
Eurosurveillance, Volume 18, Issue 49, 05 December 2013
Case of vaccine-associated measles five weeks post-immunisation, British Columbia, Canada, October 2013
M Murti ()1, M Krajden2, M Petric2, J Hiebert3, F Hemming1, B Hefford4, M Bigham1, P Van Buynder1
Fraser Health Authority, Surrey, British Columbia, Canada
Public Health Microbiology and Reference Laboratory British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada
National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada
1-1400 George St., White Rock, British Columbia, Canada
Citation style for this article: Murti M, Krajden M, Petric M, Hiebert J, Hemming F, Hefford B, Bigham M, Van Buynder P. Case of vaccine-associated measles five weeks post-immunisation, British Columbia, Canada, October 2013. Euro Surveill. 2013;18(49):pii=20649. Available online: www.eurosurveillance.org...
Date of submission: 15 November 2013
We describe a case of vaccine-associated measles in a two-year-old patient from British Columbia, Canada, in October 2013, who received her first dose of measles-containing vaccine 37 days prior to onset of prodromal symptoms. Identification of this delayed vaccine-associated case occurred in the context of an outbreak investigation of a measles cluster.
In this report we describe a case of measles-mumps-rubella (MMR) vaccine-associated measles illness that was positive by both PCR and IgM, five weeks after administration of the MMR vaccine. Based on our literature review, we believe this is the first such case report which has implications for both public health follow-up of measles cases and vaccine safety surveillance.
Laboratory testing for measles was performed on specimens collected on the day of rash onset. Measles RNA was detected in the nasopharyngeal swab by the RT-PCR assay . Acute and convalescent measles specific IgM and IgG antibodies were detected in the blood by ELISA (Enzygnost Anti-Measles Virus IgM and IgG (Dade Behring, Marburg, Germany): IgM detectable (0.213), IgG 1294 mIU/mL, and IgM detectable (0.246), IgG 2,413 mIU/mL, respectively. Virus genotype was determined by the National Microbiology Laboratory in Winnipeg, Canada as vaccine strain, genotype A, MVs/British Columbia/39.13 [A] (VAC) . Other virology testing found no detectable Parvovirus B19 specific IgG or IgM antibody, and detectable human herpesvirus (HHV)-6 specific IgG antibody but no detectable HHV-6 DNA.
Paediatr Child Health. 2012 Apr; 17(4): e32–e33.
Differentiating the wild from the attenuated during a measles outbreak
Lindsay Nestibo, BN RN,1 Bonita E Lee, MD FRCPC MSC (Epi),2 Kevin Fonseca, PhD D(ABMM),3 Jennifer Beirnes,4 Marcia M Johnson, MD MHSc FRCPC,5 and Christopher A Sikora, MD MSc MPH CCFP FRCPC6
1Communicable Disease Control, Alberta Health Services;
2Paediatric Infectious Disease, University of Alberta;
3Provincial Laboratory for Public Health;
4National Microbiology Laboratory, Public Health Agency of Canada;
5Population and Public Health Division, Alberta Health Services;
6School of Public Health, University of Alberta, Edmonton, Alberta
Correspondence: Dr Christopher A Sikora, University of Alberta, Suite 104 West Tower, Coronation Plaza, 14310–111 Avenue, Edmonton, Alberta T5M 3Z7. Telephone 780-342-0252, e-mail
In the spring of 2010, there was heightened awareness of measles infection in the physician community as a result of a public health notification related to several imported measles cases in Alberta. During this period, a 15-month-old child presented to his paediatrician’s office with irritability, a fever (38.8°C), a cough and conjunctivitis. The child had a five-day history of illness that began with an elevated temperature and a raised, sandpaper-like rash that originated at the occiput, and eventually spread to and covered the torso. There was mild cervical lymphadenopathy, and no rhinitis or Koplik spots. The child was not immunocompromised and had no significant medical history. Just 12 days before presentation to his paediatrician, the child was immunized with the M-M-R II vaccine (Merck Canada Inc). A thorough investigation by the Division of Population and Public Health, Alberta Health Services, revealed no significant travel history and no contact with any known measles patients in the preceding four weeks. All other members of the household were healthy and previously immunized with an MMR vaccine.
Two weeks after the resolution of symptoms, the National Microbiology Laboratory reported the measles virus in both samples as being genotype A – 100% identical to Genbank entry #FJ2111583 (the Edmonston-Enders vaccine strain).
Complications of Measles
Some people may suffer from severe complications, such as pneumonia (infection of the lungs) and encephalitis (swelling of the brain). They may need to be hospitalized and could die.
As many as one out of every 20 children with measles gets pneumonia, the most common cause of death from measles in young children.
About one child out of every 1,000 who get measles will develop encephalitis (swelling of the brain) that can lead to convulsions and can leave the child deaf or with intellectual disability.
For every 1,000 children who get measles, one or two will die from it.