The 1976 Swine Flu Vaccination Program

I recently read an article written by the David J. Sencer, the director of the Center for Disease Ccontrol in 1976. I found it interesting what with all of the recent publicity about the H1N1 vaccine. I have written a brief summary and added some links to the original article and to the CDC’s H1N1 factsheet.

http://www.cdc.gov/ncidod/EID/vol12no01/pdfs/05-1007.pdf
http://www.cdc.gov/h1n1flu/general_info.htm

In 1976 at Fort Dix Army base more than 200 soldiers became infected with a swine flu strain (H1N1) similar to the virus that caused the 1918 outbreak in which an estimated 50 million people died worldwide. It was decided that mass quantities of the vaccine would be needed to vaccinate the entire population to prevent a pandemic like that of 1918. The director of the CDC recommended that the federal government contract private pharmaceutical companies to produce the vaccine. A nationwide immunization program was launched by the federal government at a cost of $137million. Before any vaccine was released however, the vaccine manufacturers required that the federal government underwrite them against claims of adverse reactions prior to any vaccine delivery. The federal government agreed and the vaccinations began.

Soon cases of Guillain-Barré Syndrome were identified in patients days or weeks after receiving the vaccination. By December of 1976 more than 40 million people had been vaccinated against H1N1, of which about 500 people developed GBS. According to the NIH Guillain-Barré syndrome is a disorder in which the body's immune system attacks part of the peripheral nervous system by destroying the myelin sheath that surrounds the axons of many peripheral nerves. Sometimes it destroys the axons themselves. It usually occurs a few days or weeks after a viral infection. While there is no known cure for GBS there are treatments that can lessen the severity and speed recovery.

Statistically the number of GBS cases in the vaccinated population was higher than what would be found in the normal population in 1976 (according to the CDC about 1 more case per 100,000 that were vaccinated). As a result federal health officials decided that even the idea that GBS could be linked with the vaccine warranted ending the vaccine program immediately, so that the possibility could be investigated. In the Media the vaccination program was considered a debacle, and the director of the CDC was fired. In addition, the anticipated H1N1 pandemic of 1976 failed to happen.

According to the CDC the link between flu vaccine and GBS has been studied and in most cases no link was found. However in two studies it is suggested that 1 more person out of 1 million people vaccinated with the seasonal flu are likely to develop GBS. (http://www.cdc.gov/h1n1flu/vaccination/factsheet_gbs.htm )

Any thoughts?


More information on Guillain-Barré from the NIH at http://www.ninds.nih.gov/disorders/gbs/gbs.htm

Mystery Colors in Lymph Tissue

Since we recently discussed tattoo inks that elicit type 4 immune responses, I thought I'd mention another interesting phenomenon that arises from tattooing:
A patient presented with a lump in the right armpit that had been there for 6 months. After investigation, there could be no conclusion made about the cause of the lump. This necessitated an excision biopsy. The resulting H&E stained sample is shown above. Beyond some hyperplasia, the only noticeable defect was a black "discoloration". Immediately, it was suspected that the black spots were metastases of malignant melanoma (which is notorious for its dark pigmentation). However, after more vigorous examination and a specific, stain-based testing, they determined that this was not a melanoma. In fact, this black color was due to a tattoo that the patient had gotten 30 years previously. It has been well documented that tattoo inks end up in spleen and lymph tissue. However, it had not previously been reported that such an old tattoo could cause enlargement of a lymph node (it had been assumed that such an effect occurs within the immediate timeframe of recieving the tattoo).

Presumably, the presence of tattoo inks in immune tissues is due to uptake in the skin by antigen presenting cells which then migrate to the lymph nodes or spleen. It is interesting to note that tattoos are not only sometimes the victims of attack by the immune system within the skin, but can also cause some interesting pathology within tissues of the immune system. Since tattoo inks are not regulated, its frightening to wonder what sort of unintended chemistry might find its way into some of your body's most important defensive tissues.

That said, I'll probably still get a tattoo when I pass my comprehensive exam.


CM Jack, A Adwani and H Krishnan. Tattoo pigment in an axillary lymph node simulating metastatic malignant melanoma. International Seminars in Surgical Oncology. 2005, 2:28

Are you choosing who you are attracted to or is it your MHC region?

We know that there are many genes in the MHC I and II regions and that they are highly polymorphic. Combinations of these genes and polymorphisms are important because they are related to the number of peptides that can be presented to t-cells.
It has been shown in fish (arctic charr) that they can discriminate between MHC identical siblings and siblings with different MHC genotypes (Olsen, et al, 1997). Fish chose swimming in water scented with a sibling who had the same MHC genotypes over water in siblings who did not. In mice it has been shown that MHC genes influence individual body odor in mice and that mice also prefer MHC-dissimilar mates (Chaix, et al, 2008).
In humans, there have also been studies looking at odor preference and MHC region, although there have been no studies that have linked odor preference and attraction. In several “sweaty t-shirt” experiments women were asked their preference to smells found on t-shirts that had been worn by males with different MHC genes. Females significantly preferred the odor of males with dissimilar MHC regions to their own. Another study looked at the genetic similarity at the MHC region between spouses, which included 30 European American couples from Utah and 30 African American couples in which there was found an association between mate selection and MHC dissimilarity in the European American couples(Chaix, et al, 2008).
So if you have problems in your relationships it may not be your fault!

Alzheimer vaccine

Neuropathological analysis ofAD-affected brains reveals extensive atrophy due to neuronal loss, and accumulation of neurofibrillary tangles and neuritic plaques, surrounded by a tract of neuroinflammation (i.e. astrocytosis and activated microglia). Neuritic plaques consist of deposits of variously sized peptides collectively called b-amyloid (Ab), which is widely believed to be the key player in the pathogenesis of AD. Within this context, reducing AD amyloidosis represents one of the main therapeutic strategies under investigation for AD. Examples of this approach include the Ab vaccine (which reduces brain amyloidosis by several mechanisms), inhibitors of secretases, Ab-disaggregants, non-steroidal anti-inflammatory agents, cholesterol-lowering compounds and estrogen, all of which are known to reduce the production and/or accumulation of Ab .

Potential roles of insulin and IGF-1 in Alzheimer’s disease

Aging is characterized by a significant decline of metabolic and hormonal functions, which often facilitates the onset of severe age-associated pathologies. One outstanding example of this is the reported association of deranged signaling by insulin and insulin-likegrowth- factor 1 (IGF-1) with Alzheimer’s disease (AD).
Recent compelling biological data reveal effects of insulin and IGF-1 on molecular and cellular mechanisms underlying the pathology of AD.Emerging evidence suggests that insulin and IGF-1 have important functions in the brain, including metabolic, neurotrophic, neuromodulatory and neuroendocrine actions.Insulin, IGF-1, their receptors and IGF-1-binding proteins (IGFBPs) are all present in rodent and human brain.It is now known that insulin and IGF-1 are actively
transported across the blood–brain barrier and possibly even produced locally in the brain.
In addition to the physiological activities in the brain, a wealth of data points to a potential role of the insulin– IGF-1 pathway in the pathogenesis of age-related neurodegenerative diseases, such as Alzheimer’s disease.In particular, AD patients show changes in insulin and IGF-1 levels and their response to insulin is defective.

Alzheimer disease and Vit E

Many lines of evidence suggest that oxidative stress is important in the pathogenesis of Alzheimer disease. In particular, b-amyloid, which is found abundantly in the brains of Alzheimer disease patients, is toxic in neuronal cell cultures through a mechanism involving free radicals. Vitamin E prevents the oxidative damage induced by b-amyloid in cell culture and delays memory deficits in animal models.

AD and Type 2 Diabetes may have common link...

Various recent studies have delineated out a possible connection and predictor for the development of both Alzheimer's Disease and Type 2 Diabetes. As the both have an inflammatory component to them, the studies have linked them to a common duo of enzymes, butyrylcholinesterase and acetylcholinesterase. Both work to degrade and break down acetylcholine. Acetylcholine has been known to have anti-inflammatory actions. So, by degrading the anti-inflammatory biochemical, you ultimately have a double negative which results in an anti-anti-inflammatory or pro-inflammatory condition in the body. It is this pro-inflammatory condition which is believed to be the cause of both AD and Type 2 Diabetes.

Another common link that is extremely nascent in its research is the common link of Insulin Degrading Enzyme (IDE) in both AD and Type 2 Diabetes. Some research has shown that the dysfunction of IDE in some shape is present in both Type 2 Diabetes and AD.

I think this proves interesting because it connects two conditions that on the surface may not have ever seemed connected. To me, it reaffirms the fact that when we look at solving any conditions/disease within the body that we need to ensure we have take a holistic approach, particularly when inflammation is a common component.

A reference for the first study, titled "Elevated butyrylcholinesterase and acetylcholinesterase may predict the development of type 2 diabetes mellitus and Alzheimer’s disease" by Allam A. Rao, Gumpeny R. Sridhar and Undurti N. Das, is: http://www.sciencedirect.com.ezproxy1.library.arizona.edu/science?_ob=MImg&_imagekey=B6WN2-4NWW6SJ-2-1&_cdi=6950&_user=56761&_orig=search&_coverDate=12%2F31%2F2007&_sk=999309993&view=c&wchp=dGLzVzz-zSkWA&md5=047efd6e6ff36de91df59d9f0f740212&ie=/sdarticle.pdf