Putting the Herd (Immunity Debate) to Rest

Understanding infectious systems (and debating them) requires a person to be able to reason about highly complex biological structures, of which, contain hundreds of demographic and epidemiological variables.[*]

It seems commonplace in debates/discussions concerning herd immunity that extrapolating demands on others are made – particularly to maintain specific elimination thresholds (one example easily comes to mind: non-medical vaccine exemptions should be void to maintain herd immunity). 


Elimination Thresholds and the Dynamics of Immunity

Two authentic hazards arise when debates concerning herd immunity/vaccination rates place consistent emphasis on maintaining elimination thresholds (ie 90-95% vaccination rates)

(1) the debate begins to distract from the fundamental extreme dynamics of epidemic theory, particularly to herd immunity[* pg297]  

(2) the debate portrays a human life as a instrument in medicine that can/should be utilized in a societal defense against viruses/bacteria/disease. (the dismissal pertaining to an individual’s choice regarding a medical procedure)

For this post, I will only be addressing the first point (the complexities relating to the influences on herd immunity). To learn more about the second issue you can read this post.

I feel the need to address this particular point because in common debates regarding herd immunity (pertaining to national vaccination programs) a fundamental cornerstone of epidemiology is continually dismissed: the extreme dynamic consequences of the intrinsic nonlinearity of host-agent systems.[*] 

In laymens terms – this shit is complex.


Does Herd Immunity Exist?

Absolutely.

There is no denying that herd immunity is an extremely potent natural phenomenon which is altered by a multitude of influences (which I am going to attempt to list briefly a little later). In the presence of a national vaccine program, it is purposefully manipulated with the intention that the recognized gains will out weigh any known disadvantage(s) that might occur (financially, safety, policy, etc). [*]

In the United States, we rely on the ACIP to examine new (and current) vaccination campaigns of which must be weighed very cautiously. To intentionally modify the current existing herd immunity against a non-fatal, acute childhood disease can carry unfortunate characteristics such as protecting one population while actually placing another group at higher risk than before (ex varicella campaign).[*][*][*][*]


On the other hand, there are campaigns that historically have provided success. So far, the only infection to be eradicated worldwide is smallpox (variola major -WHO 1977). This accomplishment generated much optimism in the philosophy of eradication thresholds that other infectious diseases (such as measles and pertussis) were targeted.  Unfortunately, this thinking may have been misguided for many reasons: smallpox was unique given its low communicability, the high average age of infection, the ease of diagnosis and the stability of vaccine storage conditions.[*]


It is also important to reveal, that there are complete absences of herd immunity seen in several diseases (some of which we currently vaccinate against such as rubella, diphetheria, pertussis).[*]

The blanket justification of herd immunity in support of elimination thresholds for vaccination on the current US vaccine schedule has the very real potential in becoming a crude and one-dimensional debate.


The Fundamentals

When speaking of herd immunity in relationship to a national vaccination campaign, one must be specific to which disease they are discussing and they must show an understanding to the intricate nature of influences of immunity within the individual and within a community.

To begin, a foundation must be understood. Epidemic theory considers three variables: agent, host and environment (each of which has many components/interactions/influences in-and-of themselves).

Agent
An agent is any infectious pathogen. These vary in biological makeup, size, transmission, and habitat. In the construction of mathematical models of epidemics and herd immunity, all possible variations in all aspects of the agent's behavior (particularly in relation the host and the environment) must be taken into account.[*]

Host
The classification of a host is relevant when an agent invades a foreign entity (aka the host) resulting in a defensive immune response with the purpose of protection. Immunity attained can range from temporary to permanent. [*] 


What is of particular study is the host’s response with antibodies specific to the infectious antigen. These seropositive individuals are those who have current infections or who have experienced an infection in the past – moving them from the category of ‘infected’ to ‘recovered’.[*]    

Of course, when referring to the context of herd immunity, one must consider both the individual hosts and the population as a whole.

Environment
Consideration and concern is given to the environment and vicinity in which both the host and agent dwell. This can range from geographical heterogeneity to seasonal variations (again, for both host and agent).



Mathematical Modeling – SIR Model

Epidemiology gives birth to herd immunity theory when the first mathematical model examined how infectious agents affected large populations over time.[*][*][*]

Obviously, for ethical reasons and financial reasons (hopefully the former out weighs the later), experimentation or field trials are prohibitive – making mathematical modeling critical in making theoretical predictions of how a disease will spread and can be useful for evaluating control strategies (particularly in the case of a bio-weapon attacks).[*][*]

The Mass Action Principle (SIR) has been widely applied and accepted in epidemic theory since 1927 – when Kermack and McKendrick published 3 papers outlining and describing a mathematical model in which they considered a fixed population with 3 compartments: susceptible; infected; recovered (SIR).[*][*][*]

Susceptibles (S) – Individuals that are susceptible have, in the case of the basic SIR model, never been infected, and they are able to catch the disease. Once they have it, they move into the Infected compartment.[*]

Infected (I) – Infected individuals can spread the disease to susceptible individuals. The time they spend in the infected compartment is the infectious period, after which they enter the recovered compartment. [*]

Recovered (R) – immune to the disease or otherwise removed from the population. Individuals in the recovered compartment are assumed to be immune for life. [*]

In the SIR model, vaccination is equivalent to complete removal (aka transfer to the Recovered compartment). It is assumed that vaccinated individuals can not infect or be infected. [*] 

The above described SIR model is helpful although it is written using an equation that implies a deterministic model (no randomness with a continuous time). [*]

To account for this, the SIR model is the basis for other similar models (SEIS, MSIR, MSEIRS) that make small adjustments in its parameters that attempt to alleviate certain ‘real-world’ problems, for example:[*][*] 

SEIS  - considers the exposed or latent period of the disease (a person is not immediately infected).

MSEIRS – considers an infection that does not leave a lasting immunity in which individuals that have recovered will return to being susceptible again, moving back into the S compartment.

MSIR – considers a disease where an individual is born with a passive immunity from the mother.

Although mathematical equations are very useful in understanding basic principles and the interplay between variables, their assumptions can lead to oversimplification.[*][*]

My concern centers on the simplicity of many mathematical models, particularly in the face of such biological complexity. Especially useful tools in modern complex theories incorporate multiple algorithms and concepts of TCS (theoretical computer science), however these tools are not yet utilized and relatively unknown in epidemiology.[*][*]



Complexities of the Herd

There are several assumptions made in the formulation of the above mentioned equations. These assumptions have benefits and disadvantages.

Benefits may include being utilized for a general guide to risk assessment or a supportive piece to compare alternative policies/intervention – a wide-ranging compass to help make epidemiological decisions.

However, it is clear that to make the forecast more realistic, it is necessary to introduce more details in the disease dynamics. Models that incorporate even the most elaborate derivations omit important features.[* pg 296]

Here are a handful of features to begin to take into consideration that influence the dynamics of disease, immunity, transmission, and recovery.[*]


Geographical heterogeneity
This refers to gender (i.e. male-female ratios), age, and factors correlated with residence. Because of existing heterogeneity, estimated elimination thresholds vary between local communities – significant local differences in population dynamics arise which, consequently adjust estimates.[*][*]

Areas of similar dynamics and variation pertaining to heterogeneity:

• Age-Structured populations

• Variable infectivity

• High contact probabilities

• Persistence of pathogens within hosts

• Variations in infection risk by age group

• Limitation of application to a closed population (no immigration or emigration)[*]

• Demographic turnover (birth or death).[*]

Host genetic factors
A particularly new dynamic gaining more comprehension is the role of host genetic factors – this dynamic is critical because mathematical models rely on and individual within the population as having an equal probability as every other individual of contracting and transmitting a disease.[*][*][*]
Research is continuing to learn strategies to identify host genes responsible for resistance/susceptibility to particular agents and the relationship between vaccine efficacy and genetics.

Areas of similar dynamics and variation pertaining to host genetic/immuno factors:

• intra-host dynamics

• Maternal immunity

Spatial epidemiology
The most fundamental of these is the problem of defining the spatial location of the entities being studied. For example,

In regards to the study on human health, spatial position of humans can pertain to the area or point with where an individual/group live, or with a point located where they work, or by using a line to describe their weekly trips. Each variation has dramatic effects analysis and on the conclusions obtained.[*]

Other issue arise in the application of spatial analysis which includes the limitation of mathematical knowledge problems in computer based calculations.[*] 


Antigenic shift
Antigenic shift is contrasted with antigenic drift (a natural mutation over time). The issue with antigenic shift concerns our lack ability to forecast ability of viruses to alter their genetic makeup (quickly creating mutant antigens) and bypassing the antibody barrier a host/community.[*]


Phylodynamics
Viral phylodynamics examines how epidemiological, immunological, and evolutionary processes impact viral genetic variation.

Dynamics of transmission is considered at the level of cells within an infected host, individual hosts within a population, or entire populations of hosts.[*]

Currently, it is understood that viruses within similar hosts, such as hosts that reside in the same geographic region, are expected to be more closely related genetically if transmission occurs more commonly between them.[*]

Areas of similar dynamics and variation pertaining to phylodynamics:

• pathogen population genetics

• evolution and spread of resistance to immunity/medication

• Strain (biology) structure and interactions

Seasonal variations
There are several biologically distinct mechanisms in which seasonality and climate change impacts host-pathogen interactions. Strong pressures on population dynamics are exerted by temperature, rainfall, seasonality and climate change – responses can range from simple annual cycles to more complex multiyear fluctuations.[*][*]

Although scientists are only beginning to understand how seasonal external drivers influence the majority of host–parasite systems, empirical evidence strongly supports the strength and mechanisms of which seasonality alters the spread and persistence of infectious diseases. [*][*]

To present two examples for further understanding:

Agent: rotavirus.
Seasonal affects: winter peaks; timing shifts with latitude[*]

Agent: meningococcal meningitis
Seasonal affect: wind speed and low humidity affect respiratory/aerosol transmission[*]

Areas of similar dynamics and variation pertaining to seasonal variation:

• alterations in immune system defenses (weakened during winter and during harsh weather)

• periparturient rise (pregnant women lowering their own immunity to prevent harming the fetus)

• diseases that are cyclical in nature

• diseases that are seasonal in nature

Ending the Debate on Herd Immunity 

Agent-Host-Environment: This relationship is complex and depends on such factors as a precise course of infection (not only with an individual but within the demography of the host population). Other factors include duration of immunity (natural or artificially acquired), maternally derived protection, age-related changes in the intimacy of contacts – not to mention a prevailing level of genetic and spatial heterogeneity in both susceptibility and resistance to infection.[*]

There is no denying that mathematical models aid in defining details associated with infectious systems. Adjustments made to incorporate dynamic influences have the ability to make useful generalities and estimates – particularly to elimination thresholds and the course of infection within a population.[*] 

However, the science and intuition built on decades of practical epidemiological experience still often fail to predict outcomes/implications of vaccination programs.[*]

Each vaccination campaign entails a massive disruption of the previous balance which results in a destabilization of epidemiologic patterns for many years.[* p297]

...are vaccinated individuals the ones stepping outside the herd?

Herd immunity existed prior to vaccination.

Preceding national vaccination programs, epidemiological patterns of immunity/disease existed for the greater good. With each national vaccine campaign, epidemiology is modified (benefiting some and disadvantaging others).

While it is perceived beneficial that some vaccinated diseases have diminished over time (such as measles, chicken pox, rubella), it is very likely that these infections existed in a precise biological niche that was very much intentional – benefits in which our understanding can not yet comprehend.[*]

How exactly can the herd immunity debate end? 

(1) Accepting that the encompassing complexity of infectious disease (and nature in general) is not something human understanding will be able comprehend in entirety. Yes, artifical modification (via vaccine) can impart benefits – but it also exposes populations/individuals to disadvantages (many of which cannot be forecasted in advance) – implementation of vaccine programs must not be taken lightly nor forced upon a population without individual consent. 

(2) Above all else, voluntary consent married with adequate comprehension of each vaccine is fundamental as national vaccine campaigns develop and progress. This is whatshould be the underlying principle in discussions on herd immunity – NOT mandatory vaccination.

This post is dedicated to those families that have been deliberately and maliciously accused of ‘free riding’ off of vaccine-induced/artificial herd immunity – especially those who have been told this by a medical professional in hopes of altering a consent of vaccination.

I like to believe all parents are doing the best they can. Please choose what works best for your family while honoring the rights of others to make that same choice.

Chickenpox Party-RSVP?

 

The infamous chicken pox party.
 
Even if you choose to vaccinate per the CDC’s recommended schedule (see 2013 update here), there is a likely chance you are aware of what a pox party is.
 
Here is the history, the rational and why I choose not to RSVP.
 
 
Welcome to the Party
 
 
“Chicken Pox Party” (aka Pox Party) - This term refers to when parents intentionally expose their otherwise healthy child to the varicella virus in hopes they contract the disease to promote natural immunity.
 
A person does not necessarily have to have a party. Some parents attempt to collect some type of infected material such as saliva, the elusive licked lollipop, or piece of clothing from the infected child/person.
 
However, it is unlikely that these particular methods will transmit the chickenpox virus effectively or reliably. This is because the varicella virus cannot survive for very long on the surface of such items. 
 
 
History
 
 
Forms of controlled inoculation are not new at all. Small pox and rubella are a few examples of diseases that where purposely transmitted in children earlier in history.
 
 
Chicken pox parties, in particular, were popular in the 1980’s prior to the national vaccination program included in the CDC’s list as of 1995. These gatherings would normally consist of family members or groups of children that play together/live near each other. These “pox parties” were among people that the families knew well.
 
 
The Purpose
 
 
If you decline the varicella vaccine for your child or if you aren't exposed to the wild-type strain, there is a risk (as with any disease), that your child may contract the disease later in life.
 
The purposeful infection of chickenpox is typically organized by parents on the main premise that contracting chicken pox at a younger age is less severe than if the disease is caught in adulthood.
 
It is well documented that complications in chickenpox are more likely to occur adults then in children. Considering that adults (13 yrs of age or older) only account for 5 percent of chickenpox cases each year, they account for a disproportionate number of deaths (55 percent).[1]
 
(On a side note, other diseases listed as being more severe later in life are measles and influenza. Flu-party anyone?)
 
 
 
RSVP, Regrets Only Please
 
While I can comprehend and appreciate the reasoning of a chickenpox party, I would not seek out and partake in one.  While we have chosen to decline this vaccine, there are several reasons why I would also decline this invite.
 
 
 
Reason 1
 
You cannot predict who will have a moderate or severe reaction.
 
Although it may be less common, children still have the potential to have a reaction from the varicella virus. Holding the full intention in making your healthy child sick with this virus, what if something did happen? 
 
 
Reason 2
 
A child depends on their parents completely to keep them safe and healthy. How is intentionally making your child sick fulfilling this obligation? Even if it is in hopes of the rare occasion they may contract chickenpox in adulthood and have a terrible, life-altering reaction from it.
 
 
One of the arguments people present concerning the use of vaccines is that they are unnatural. For me, a part of seeking out a disease to intentionally make a child sick carries something to be said about being unnatural as well.  
 
 
Reason 3
 
Is the significant risk real in adulthood?
 
 
Prior to the introduction of the varicella vaccine in 1995, there were approximately 4,000 annual cases of adult chicken pox resulting in 50 deaths from the disease.[2][3]
 
After the vaccine was introduced, there are approximately 1 in 2,254 annual cases in the United States (that’s 0.04 percent).[4]
 
 
Complications from adult chickenpox are still fairly rare considering 90 percent of cases occurring children younger then 10 years of age. This risk in adulthood largely accounts for adults with eczema, compromised immune systems, and those taking steroid medications.[5]
 
 
Bacterial superinfection of the skin is the most common serious complication of chickenpox in adults (but is still very rare).[6][7]
 
In my opinion, this does not give me a reason to deliberately seek out an infectious disease and hope my daughter contracts it in her youth. Moving from a 0.04 percent of potential risk to 100 percent potential risk doesn’t add up for me.
 
Reason 4 
 
 
The effectiveness of both the vaccine and wild-type chickenpox in youth to defer future attacks in adulthood relies heavily on the incidence of wild-type chickenpox within the community to act as boosters throughout life. This is noted in the package insert for the chickenpox vaccine as well as other peer-reviewed journals.
 
This means that if chickenpox is not common and you have been exposed to the virus while in your childhood (either by vaccine or naturally), you risk developing it again in adulthood or even suffering from the more severe disease of shingles.
 
Would this mean that once you have successfully given your child chickenpox, they would be reliant on attending chicken pox parties throughout their lives or require booster vaccines? That’s not something I would want.
 
 
Reason 5
 
Shingles.
 
By infecting a child with chickenpox intentionally, a parent is also placing their child at risk of suffering from shingles later in life.
 
Don’t get me wrong, this is a concern for children who contract chickenpox naturally and via vaccine administration.[8]
 
Here is the concern with Shingles:
 
The nationwide-mass varicella vaccination program has the medical community bracing for a major increase of herpes-zoster (shingles). This is, again, due to the lack of wild-type boosting properties of chickenpox that has been lost over the last decade.[8][9]
 
The highest increase of shingles has been seen among those 25 to 44 years and over 65 years of age. [8]
 
Shingles is a very painful rash that can turn into agonizing blisters. The painful (not itchy) rash can disrupt sleep and eating habits which has the potential in resulting in a condition called postherpetic neuralgia (PHN) which causes severe pain even when the rash clears. 
 
 

Are There Benefits?

 
 
Sure there are, and don’t get me wrong, I’m definitely not a proponent for the varicella vaccine. If I had to choose one over the other I would choose the wild-type strain naturally contracted.
 
 
However, we are in a precarious situation. Since the wild-type strain of chickenpox is extremely limited. When a parent exposes a child to the virus (which will lay dormant in their nervous system) in hopes of them having a more mild reaction then they would in adulthood - we are setting them up in an environment that does not offer boosters throughout life.
 
Again, they would then have two choices in adulthood - seek out more wild-strain chicken pox parties or get a booster vaccine (Chickenpox or shingles).
 
Another possible benefit of exposure in childhood would be that a woman gains the ability to pass on antibodies to her newborn which is more susceptible to adverse reactions from the virus (something that has not been documented on happening in vaccine induced immunity).
 
 
Conclusion
 
Every part of my being is passionate with making my daughters as healthy and happy as possible...the act of intentionally getting them sick “just in case” doesn’t seem to coincide with that (for me).
 

If my daughters became infected with chickenpox (or measles or whatever) naturally, I would welcome the implications that comes with it (natural immunity, stronger immune response, etc), but I couldn't devise a plan to purposefully infect my little ladies with disease. Nah, couldn’t do it.

References

 
[1] Schoenstadt, A. Adult Chickenpox-Diagnosing and Treating Adult Chickenpox. MedTV Website. Oct 2006
 
[2] Adult Chicken Pox on Disease.com Website
 
[3]   Schoenstadt, A. Chickenpox and Death. MedTV Website. Oct 2006
 
[4] Prevalence and Incidence of Chickenpox. Right Diagnosis website. Source statistic for calculation
 
[5] Infectious Diseases-Chickenpox. Medicalook Website
 
[6] Shingles and chickenpox (Varicella-zoster virus) – complications. University of Maryland Medical Center website.
 
[7] Nnama, H. (reviewed by D Fisher). Compications from Adult Chickenpox. Jul 2010
 
[8] Schmid, D. S., Jumaan, A., Impact of Varicella Vaccine on Varicella-Zoster Virus Dynamics. Clinical Microbiology Reviews. Vol 23 (1): 202-217. Jan 2010
 
[9] Brisson, M., Gay, N. J., Edmunds, W.J., Andrews, N.J. Exposure to varicella boosts immunity to herpes-zoster:implications for mass vaccination against chickenpox. Vaccine. Vol 20 Issues 19-20: 2500-2507. Jun 2002
 

 

Chickenpox Vaccine Virus Reverting Back to Virulence

Background: There are two live virus vaccines for chickenpox licensed in the U.S. -  Varivax and ProQuad (MMRV). Both are manufactured by Merck. [1]

These are live viruses that are attenuated. Attenuated refers to a virus that is altered in some way to make it less virulent or less harmful. This can be done by passing the virus through tissue culture, embryonated eggs or live animals.[2]

The purpose is to have the virus mutate in way that it is significantly different then the original, hence when introduced to the host it will not grow well (replicating very slowly) and, in theory, lack the ability to get a person sick.

The initial mutations (or possible deletions) that are a result from the attenuated process are desirable. But there is risk or reversion –  reverting back to becoming virulent/harmful.

****

It is understood that administering the chicken pox vaccine carries a *small* risk of actually exhibiting the clinical chicken pox disease.[3] In the past, this was believed to be the result of a deficient immune response (the child was was not capable of “fighting” off the attenuated virus). Now, with updated research, scientists are beginning to see that children may be getting sick because the virus strain in the vaccine is reverting back to a virulent virus and specific vaccine lots are to blame.  

it was feasible that the occurrence of rash would have proved to be determined by the host genotype and immune status irrespective of the viral genotype. In that case, the virus recovered from the rash would have been a random selection of the genotypes in the vaccine. We observed the converse: four residues were strongly and consistently selected in vivo during viral spread and the formation of skin rashes.[4]

The rashes were caused by at least seven different vaccine batches.[4]

The observed differences in sequence data from V-Oka-Biken and the two GlaxoSmithKline vaccine lots were unexpected.[5]

Chicken pox is unique in this case – it has scientists asking themselves why should the varicella vaccine virus experience reversion while other attenuated vaccines (such as poliovirus) stay attenuated? They believe it is because of the unique epidemiology of skin rashes.

The explanation appears to be in the central importance of skin rashes in the epidemiology of the virus: infectious virions are shed from the rash vesicles.[4]

After immunization, vOka virus replicates locally, then infects peripheral blood mononuclear cells and may be carried to distant sites including the skin, lungs, brain, and visceral organs.[4]

What exactly does this mean? Scientists really don’t know…at least I have not read an explanation.

According to a publication from the Proceedings of the National Academy of Sciences of the United States of America (PNAS) regarding the implimentation of a national vaccine program against chickenpox:

40 million patients have consequently created a highly replicated evolutionary experiment[4]

Most countries (such as the United Kingdom) where vaccination in not undertaken, are waiting it out to determine what happens here in the States; where mass vaccination is routine.[6]

China, for example, vaccinates 1 out of 5 children – imparting the benefits of the wild-type varicella to aid in the ‘herd immunity’. In the United States, where universal varicella vaccination has been practiced, the majority of children no longer receive exogenous (outside) boosting, thus, their cell-mediated immunity to VZV (varicella zoster virus) wanes--necessitating booster chickenpox vaccinations.[7]

The United Kingdom has expressed concern over starting a vaccination program against chicken pox that has the potential to disadvantage the middle-aged and elderly. Especially since the morbidity of shingles in later life is greater that that associated with chickenpox in childhood.[7]

There are six known wild-type strains of chicken pox; in most cases, acquiring one will result in an immunity to all strains of the virus. Could the introduction of a nationwide vaccine program against chickenpox increase this number? Could it make a potentially more virulent strain(s)? Could these strains have unique pathogenic qualities? 

These data illustrate, to our knowledge, the first detailed genomic analysis of a V-Oka variant (V-Oka-zoster) isolated from a zoster patient following vaccination with GlaxoSmithKline V-Oka vaccine.Conceivably, genomic mutations or reversions to wild type, particularly those that confer amino acid substitutions, could affect virulence and restore wild-type pathogenicity. [7]

Further more, VZV (varicella) strains with unique pathogenic qualities could emerge.[7]

Ironic.

The attempt to eliminate, in most cases, a mild childhood disease has repercussions that no scientist thought was possible - the emergence of an even more dangerous strain caused by the very vaccine trying to alleviate it.

Persons that are exposed to the wild-type virus after the vaccine can still contract chicken pox resulting in harboring both the attenuated vaccine oka strain as well as the wild-type (natural) strain which are both subject to reactivation as shingles.



Shingles

The dilemma of increasing cases of shingles was already evident from the beginning – though the implementation of our national immunization program was still executed.

In an analysis published in IJT, the effectiveness of the chicken pox vaccine is heavily dependent on natural boosting– as chickenpox declines, so does the effectiveness of the vaccine. Seems the solution to this, in the United States, is more boosters, of course.

The old school of thought is that the incidence of shingles increases with age due to older individual’s immune response declining. Now, it is understood that the increase of shingles with age is due to the fact that older people receive fewer natural boosts to their immunity (as their contact with children decline).

For chicken pox, the greater good theory (the possibility of injuring a few to help many via vaccination) doesn’t even hold true in this case, for the amount of lives saved vaccinating against varicella, that many lives would be lost to shingles.

any deaths prevented by vaccination will be offset by deaths from increasing shingles disease.[5]

What is the answer to a possible shingles epidemic? An adult vaccination program against shingles.

Using a shingles vaccine to control shingles epidemics in adults would likely fail because adult vaccination programs have rarely proved successful[5]

Conclusion

40 million patients have consequently created a highly replicated evolutionary experiment[4]

An acknowledged mutating (vaccine-made) virus, reverting to a new virulent strain of varicella...

A nationally implemented vaccine program to eliminate chicken pox to only be replaced by an increase death rate of shingles...

Can you imagine if the amount of time, effort and money put in place to eliminate this mild childhood illness was diverted into efforts to ease malnutrition and hunger in our country (or heaven forbid worldwide), how many lives would be enhanced?

Something to ponder…

I would like to include some comments from the article posted in 2005 on the News Medical forum, referencing Goldman’s publication in the International Journal of Toxicology, Universal Varicella Vaccination: Efficacy Trends and Effect on Herpes Zoster: [9]



Carrier Sinclair PharmD

As a pharmacist I have been seeing an increasing number of patients with the shingles. What concerns me the most is the young ages that I have been seeing with the shingles. At first I thought that maybe it was a mis-diagnosis but as I saw more and more children being treated for the shingles I started thinking that it might have something to do with the chicken-pox vaccines. I was glad to find this article because it has answered some of my questions.

Thanks,
Carrie Sinclair

Marcella

My now 3 year old received the chicken pox vaccination at 12 months and was just diagnosed yesterday with shingles.  It is absolutely absurd for a 3 year old to have to deal with shingles.  From all the research I have been doing it seems it is widely known that children who get chicken pox under one year of age are more susceptible to shingles as children...so why are we vaccinating children with a live form of the virus at 12 months (that's a bit close to the cutoff)?  I now have to deal with keeping my 3 year old away from my 9 month old so he does not give him chicken pox.  I definately think more research should be done and the chicken pox vaccine be only recommended and not mandatory for children to start school.  Our pediatrician commented yesterday that she has seen a lot more shingles cases in young children since the vaccine started.  I believe the vaccine is totally defeating it's purpose if our children now have to deal with shingles outbreaks at such a young age.  I will definately wait longer before my now 9 month old gets the vaccine; he will not be getting it at 12 months. 

Liz

My child received her C.P. booster shot 5 weeks ago. This time she got a mild case of C.P. Two weeks later I got shingles. Why? My older children had full blown C.P. I had C.P. My immunity system was  NOT compromised. I believe the vaccines are being made with a new strain of the C.P. family, which makes no sense to me at all. This very well could explain the children's developing shingles, and their reaction when exposed to traditional chicken pox, they have half an immunity so they react with shingles. A different strain is different.

Gb

People contributing this feedback are linking chicken pox vaccine with shingles -- not from idle speculation -- but from real experience.  It is NOT to be downplayed!

My own son had the vaccine and developed shingles a few months later on his eye.  We treated it for several years, and then he developed a gbm brain tumor as an 11 year old.  There are links between the chicken pox vaccine to the shingles virus and then to brain neoplasms in the scientific literature.  People should be careful what they expose their children to for the "greater good" at least until new vaccines have had a chance to be studied for impact.

References:

[1] National Vaccine Information Center (NVIC) Website. Varicella Zoster (Chickenpox)

[2] P Provost, D Krah, P Friedman. Process For Attenuated Varicella Zoster Virus Vaccine Production – Patent 5360736. Merck & Co.,Inc. Filed June 1992

[3] Merck & Co. Inc. Varivax (Varicella Virus Vaccine Live) Package Insert

[4] M Quinlivan, A Gershon, B Mahmoud, S Steinberg, P LaRussa, N Richard, J Breuer. Natural selection for rash-forming genotypes of the varicella-zoster vaccine virus detected within immunized human hosts. Proceedings of the NationalAcademy of Sciences of the United States of America (PNAS). Vol 104 No 1 208-212. Jan 2007.

[5] The Vaccines and other Biologicals department (May 2003). "Varicella vaccine". WHO.

[6] P D Welsby. Chickenpox, chickenpox vaccination, and shingles. Postgraduate Medical Journal. Vol 82(967) 351-352. May 2006.

[7] A Sauerbrei, E Rubtcova, P Wutzler, DS Schmid, V Loparev. Genetic Profile of an Oka Varicella Vaccine Virus Variant Isolated from an Infant with Zoster. Journal of Clinical Microbiology. Vol 42(12) 5604-5608. Dec 2004.

[8] G Goldman, Medical Veritas International (MVI). Universal Varicella Vaccination: Efficacy Trends and Effect on Herpes Zoster. International Journal of Toxicology. Vol 24(4). July 2005

[9] Chicken pox vaccine associated with shingles epidemic. Sept 2005 http://www.news-medical.net/news/2005/09/01/12896.aspx