Diphtheria

Diphtheria is an acute, toxin-mediated disease caused by the bacterium orynebacterium diphtheriae. Toxin production (toxigenicity) occurs only when the bacillus is itself infected (lysogenized) by a specific virus (bacteriophage) carrying the genetic information for the toxin (tox gene). Only toxigenic strains can cause severe disease.

 

 Simplified version: The diphtheria is a bacteria, and a virus called a bacteriophage, inserts itself into the diphtheria bacteria, and takes over the bacterial genes to make toxin. The Diphtheria bacteria isn’t the problem. It’s whether the bacteriophage that converts the bacterial genes into a toxin is around or not. That is the determinant of clinical disease, not the presence of the bacteria.


You can pick up diphtheroids anywhere. Diphtheria is still around as it is ubiquitous. Clinical disease is more likely to been seen in poverty stricken areas, because it’s a toxin-mediated disease, and more likely to be seen where people have insufficient vitamin C and other micronutrients. . Even when the bacteriophage is around, many people might carry diphtheria or even be infected, but rarely get clinical diphtheria. The toxin can’t be produced in the presence of iron. So people who have iron deficiency are more likely to have clinical diphtheria.

 

Diphtheria was on the decline long ago due to improved living conditions. One of the reasons that it’s not found using regular swabs is that it requires a specialized media not normally used in a laboratory. It can be declared “eradicated” because it is not generally looked for. However when they do, they find it.
It is common to present evidence that shows that the diphtheria vaccine doesn’t prevent infection, carriage or spread. To say that people who had not been vaccinated might have died is ludicrous. If you look at some of the older studies you’d see it just isn’t so. According to the 1999 CDC MMWR:
 
 
 
 
 
 
 

 

Circulation of toxigenic strains of C. diphtheriae persists in parts of both developed and developing countries where diphtheria is not being reported. For example, a focus of toxigenic C. diphtheriae was found in South Dakota in 1996 with molecular analysis of strains suggesting local persistence since the 1970s; and a recent serological study in rural Kenya showed high diphtheria immunity among unvaccinated persons, suggesting continued circulation.

Eradication is not currently feasible because preliminary evidence suggests that circulation of toxigenic C. diphtheriae might persist, even in populations with fairly high childhood immunization coverage, and might be difficult to detect; and sustainable reservoirs for the toxin gene might exist in nonhuman mammals. Future feasibility depends on understanding prevention of continued circulation and evidence that circulation of the toxin gene in the animal reservoirs is not sustained indefinitely.

Seven factors could hinder eradication: the phage carrying the toxin gene can occasionally be found in nondiphtheria Corynebacterium species infecting animals (this may represent an ineradicable reservoir for reintroduction of toxin gene into non-toxigenic C. diphtheriae strains); infection with a toxigenic strain can either be direct or in situ by a phage carrying the toxin gene, infecting a commensal non-toxigenic C. diphtheriae strain; an asymptomatic carrier state exists, even among immune persons, and circulation appears to be able to continue under some settings, even in populations with fairly high childhood immunization rates; immunity to diphtheria is not life-long (a minimum of three doses is required for effective primary immunization, and periodic booster doses are required throughout adult life to maintain protective titres — in addition, immune persons are not distinguishable from susceptible persons except by serological or Schick testing; in countries with low incidence, both the clinician and the laboratory can easily miss the diagnosis of diphtheria, and empirical antibiotic treatment can prevent recovery of the organism; limited epidemiological, clinical, and laboratory expertise is available on diphtheria; and political will may be lacking because the disease burden is low in developed countries and is perceived to be relatively low in developing countries.

 

You can develop natural immunity to Diphtheria without being vaccinated.   It was clearly shown in Russia because they found that the key to fighting diphtheria had nothing to do with antibodies but with production of interferon. The people who got diphtheria in Russia were vaccinated with twice the number of doses but the CDC conveniently overlooked this fact.

What the Russians found was that, in terms of toxic diphtheria, it wasn’t the antoxin antibodies in the blood that was important; it was how well the person was able to initiate the interferon cascade. If a person had difficulty producing interferon, they would get diphtheria and die regardless of vaccination status or even antibody status. That was why the majority of people who got severe diphtheria or died of diphtheria in Russia were immunodeficient, the homeless and alcoholics. The Russians have researched and understand that nutrition, immunity and the innate immune system are the most important things to have working well. One Russian study looked at children with an immunodeficiency and found that:

 

 “Thymomegalia is registered in every third child in some regions [of Russia].” In this paper the authors confirm that after DPT-immunization of the children with thymomegalia the anti-diphtheria antibodies is not being produced at all or in an insufficient quantity.”

 

(Ref: Kuz’menko L. G., Arziamova V. V. Nedostatochnost’ produktsii protivodifteriinyh antitel u detei s timomegaliei pri immunizatsii vaktsinoi AKDS (The insufficiency of the anti-diphtheria antibodies production after immunization with DPT vaccine) Detskie infektsii (Children infections), 2004, 2(7), с. 24-26.)

 

Yet, we are told that it’s very important for immunodeficient children who can’t make antibodies to have these vaccines. But what use is the antitoxin antibodies from vaccines if immunodeficient kids can’t make antibodies?  It makes no sense.

 Thymomegalia is registered in every third child in some regions [of Russia]. In this paper the authors confirm that after DPT-immunization of the children with thymomegalia the anti-diphtheria antibodies is not being produced at all or in an insufficient quantity.

It is known that DPT vaccination even in healthy children not only produces a specific immune response, but causes the allergic reorganization in the body, lowers the specific resistance… The children with modified reactivity from the high-risk groups react to DPT-vaccination by the long-term suppression of resistance, by developing postvaccinal complications, by defective immune response, by high morbidity… It was demonstrated the DPT-vaccinations (from the first to the third shot) in the most children with thymomegalia of the 1st grade by their first year of life caused the complicated course of the vaccinal process, namely allergic complications, acute respiratory diseases, the lack or inferior immune reaction to diphtheria or pertussis toxins and enlarging the thymus up to 2nd-3rd grade. The result of the three shots was the factual absence of immunity to whooping cough, low anti-diphtheria and high anti-tetanus… immunity.”

(Ref: Adishcheva N. I. Kliniko-immunologicheskie pokazateli vaktsinal’nogo protsessa AKDS u detei s uvelicheniem timusa I stepeni (Clinical-immunological characteristics of the vaccinal process in children with 1st grade thymomegalia Abstract of PhD thesis. Tomsk, 1996, pp. 2 and 24.)
Did you know there is 8 times the amount of diphtheria toxin in the children’s vaccines vs. the adult versions?

 

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Pneumococcal (Prevnar)

Pneumococcal disease is caused by a common bacterium, the pneumococcus, or also known as Streptococcus pneumoniae, which can attack different parts of the body. From the CDC Pink Book

 
Pneumococci are common inhabitants of the respiratory tract and may be isolated from the nasopharynx of 5% to 70% of healthy adults. Rates of asymptomatic carriage vary with age, environment, and the presence of upper respiratory infections. Only 5%–10% of adults without children are carriers. In schools and orphanages, 27%–58% of students and residents may be carriers. On military installations, as many as 50%–60% of service personnel may be carriers. The duration of carriage varies and is generally longer in children than adults. In addition, the relationship of carriage to the development of natural immunity is poorly understood.

Prevnar (PCV7) was licensed in 2000 for children under age 2 or for older high risk children. It was marketed to prevent invasive pneumococcal infections that can cause earaches, meningitis, blood poisoning and pneumonia, even though the chance of an infant contracting invasive pneumococcal disease was determined to be about 0.15%. Prevnar was also promoted as the ‘prevention of ear infections vaccine’ even though the package insert showed the vaccine decreases ear infections by only 9%.

Prevnar covers only 7 strains out of over 90. These strains are: 4, 9V, 14, 19F, and 23F and oligosaccharide from 18C, 6B. Prevnar was invented due to the routine use of Hib vaccine. Pneumococcal infections increased by filling the void left by the Hib vaccine.

There are two vaccines for adults and children over the age of 2 called Pneumovax and Pnu-Immune which cover 23 different strains of Streptococcus pneumoniae bacteria. The conjugate vaccine is used in the children’s version, Prevnar, and the polysaccharide vaccine is used in adult version.

Pneumococcus bacteria do not generally cause severe disease. Why it does cause more severe disease in some people is not widely understood.  The high risk groups would include: persons aged 65 and older; individuals with weak immune systems due to cancer, leukemia, Hodgkin’s disease or human immunodeficiency virus (HIV); persons with sickle cell disease or without a functioning spleen; individuals who have a chronic illness such as lung, heart, and kidney disease, diabetes and alcoholism; persons living in special environments or communities, such as Alaskan Natives and certain American Indian populations; and residents of chronic or long-term care facilities. (Facts About Pneumococcal Disease)

Efficacy and Safety Studies:

 

There used to be an FDA transcript and a chart that showed the low efficacy for AOM, but it appears to have been removed.  Here is an excerpt of what it said:
 

In summary, the Committee concluded that data derived from two efficacy trials are adequate to demonstrate efficacy of Prevnar® against AOM caused by vaccine serotype.   
However, the committee expressed concern about the low efficacy (7%) of the vaccine against AOM regardless of etiology and concluded that substantial clinical benefit of Prevnar in reducing AOM regardless of etiology had not been demonstrated. The Committee cautioned against including an indication statement as proposed by the sponsor into the label and suggested using qualifying language if an indication for AOM regardless of etiology were to be added. Committee members cautioned against promoting prevention of AOM as a benefit of Prevnar in direct-to-consumer advertising because of concerns about unrealistic public expectations.  

The Committee was concerned that promoting Prevnar as an “AOM vaccine” could potentially compromise confidence in the existing recommendations for the vaccine and trust in the labeling that FDA puts on a vaccine.

 What about the safety of Prevnar? 

 

In the clinical trials, the pneumococcal vaccine was compared against an experimental meningococcal vaccine. This means the clinical trial had no real placebo because the reaction profile was unknown for both experimental vaccines, which would compromise the scientific validity of the safety trial. Children in the Prevnar trial group had more seizures, irritability, high fevers, amongst other reactions. There were 12 deaths reported in the Prevnar group but were dismissed as “Sudden Infant Death Syndrome.” (REF: Wyeth-Lederle Product Manufacturer Insert Pneumococcal 7- Valent Conjugate Vaccine (PREVNAR). Issued February 2000. www.fda.gov/cber/label/prevnarLB.pdf). Also see: Prevnar -a critical review of a new vaccine.

 

While the Pneumococcal vaccine may have reduced incidence rates, there has been a trade-off due to serotype replacement  The strains not covered in the current vaccine for children are proliferating. According to Science Daily:

The incidence of IPD caused by strains not included in the vaccine rose by 40%. One of the non-vaccine strains, 19A showed an increase of 264%… Disease caused by non-PCV7 serotypes, especially 19A, is emerging and accounts for nearly all IPD.

According to The Journal of Infectious Diseases 2008; 197:1016–1027: Emergent Streptococcus pneumoniae Serotype 19A in the United States 2005:

Conclusions.  PCV7 ineffectiveness against serotype 19A, antibiotic resistance, clonal expansion and emergence, and capsular switching have contributed to the genetic diversity of 19A and to its emergence as the predominant invasive pneumococcal serotype in the United States.

Another problem with the widespread use of Prevnar has been the emergence of antibiotic resistant bacterial strains. The introduction of Prevnar appears to have caused many strains to become highly resistant. A vaccine-resistant virulent strain of strep is causing ear infections in children that cannot be treated with antibiotics safe for use in children.

 

Michael E. Pichichero and Janet R. Casey of the University of Rochester in New York documented the emergence of an antibiotic-resistant strain of another bacterium known as Streptococcus pneumoniae, which causes common ear infections. Although all 11 children identified in the Rochester area with the microbe so far were successfully treated, five required an antibiotic approved only for adults, and one child was left with permanent hearing loss.

The researchers attributed the emergence of the strain to a combination of the overuse of antibiotics and the introduction of a vaccine that protects against the infection.

“The use of the vaccine created an ecological vacuum, and that combined with excessive use of antibiotics to create this new superbug,” Pichichero said.

 

Prevnar has not reduced the number of cases of meningitis. It has merely changed them to other types of meningitis.

Children with Bacterial Meningitis Presenting to the Emergency Department during the Pneumococcal Conjugate Vaccine Era. Volume 15 Issue 6 Page 522-528, June 2008 Academic Emergency Medicine 15 (6) , 522–528.

 Conclusions: Although now a rare infectious disease in United States, bacterial meningitis still causes substantial morbidity in affected children. Despite the introduction of PCV7, S. pneumoniae remains the most common cause of bacterial meningitis in U.S. children, with approximately half of cases due to nonvaccine serotypes.

 What is the answer to that? A new vaccine for Meningitis for toddlers and adolescents! This will simply try and fool Mother Nature and further mess with the bacterial balance of the body. This will not just affect those who choose to vaccinate because the strains not covered by the vaccine are in higher concentrations in those vaccinated, which will facilitate the spread of the bacteria to everyone.

 

MRSA is also a strain of the bacterium that usually causes staph infections that used to be easily treatable with common antibiotics in the penicillin family. Resistant strains of the organism have been increasing.

 

Natural immunity to pneumococcus may be more important for protecting against the disease than the vaccine according to research published in 2005. The researchers found that another mechanism, other than antibody protection, confers protection against the bacteria. What provides this protection? Researchers don’t quite know.

 these observations make a strong case for the importance of one or more factors other than [the development of] antibodies” is necessary to confer protection against pneumococcal disease.” So, children have an element of natural protection, beyond the perceived benefit of the pneumococcal vaccine, we do not understand.

Interesting!

 

If we are trading one disease for another, how do we stop it, and stop the need for more and more vaccines?  Is it already too late?  Stay tuned for more on pneumococcus…

 

Cumulative weekly number of reports of Invasive Pneumococcal Disease due to any of the serotypes NOT IN Prevenar™ : Children aged < 2 Years in England and Wales by Epidemiological Year: July-June (2003- To Date)

 

Source:

http://www.hpa.org.uk/webw/HPAweb&HPAwebStandard/HPAweb_C/1207821645727?p=1203409671876