Rubella and CRS

Rubella and Congenital Rubella Syndrome

 

     Rubella had a natural virulence cycle of every 6-9 years and was once a disease of school-aged child that was typically caught between the ages of 5-9 year old. 80% thus developed natural antibodies to Rubella and protected them into adulthood, while 15% remained susceptible to the disease. The goal of the Rubella vaccine program was to prevent fetal infection, or CRS, in women in the childbearing years who had not acquired natural immunity in childhood.  Unfortunately, the original goal has not been obtained. The exact opposite is occurring as young adult women in their childbearing years now have the highest rate of Rubella incidence. Is this a new phenomenon occurring in today’s generation? No. To spite the large Rubella vaccine program, since 1969 there has been a shift in incidence and a shift in age susceptibility.

 
 
 
 
 
 
 

 

              

“During the 1990s, the characteristics (ie, age distribution, sex, and race/ethnicity) of rubella cases changed significantly. In 1990, incidence was higher among children younger than 15 years than among persons aged 15 to 44 years… since the mid 1990s, incidence has increased among persons aged 15 to 44 years and decreased among children younger than 15 years. In 1990, children younger than 15 years accounted for 69% of cases. Since 1996, the highest percentage of cases occurred among persons aged 20 to 29 years, with a high in 1999 of 49%.  

  

     According to a 1980 Pediatrics study, the susceptibility rate of 6th graders was 15% in those vaccinated. (2) The susceptibility rate has remained the same rate as in the pre-vaccine era, even after the late 1970’s initiative to re-immunize all females during the child bearing years.

 

 

      

     Has the Rubella vaccine reduced Congenital Rubella Syndrome? You be the judge. Rubella was not a nationally notifiable disease until 1966. Rubella vaccine was licensed and recommended in 1969 for girls and boys in infancy and/or the preschool years, and then eventually recommended for adolescents. Since 1969, Rubella cases have declined, yet CRS cases increased after the introduction of the vaccine. In 1966, the pre-vaccine era, there were 11 cases of CRS. In 1969, after the introduction of the vaccine, there were 31 CRS cases. By 1970, there was an increase of 77 cases and in 1971, 68 cases. During the 1980’s, CRS cases declined once again but still remained higher than the pre-vaccination era. In 1992, there were 11 cases of CRS which is the same exact number of cases in 1966 before the Rubella vaccine was routinely used.  In 2000, there were 9 cases of CRS and in 2006, one case.

 

     As you can see, the Rubella vaccine has had little impact on reducing the number of CRS cases over the last 40 years since its introduction, yet it increased CRS cases in some years. There are even incidences were women had high levels of antibodies to Rubella before pregnancy, yet the babies had CRS. There are also some women who will never seroconvert (show positive antibodies) no matter how many times they are vaccinated.

      

     What has vaccination really accomplish if immunity wanes from infancy, if vaccinated young women are made more susceptible when they need immunity the most, and the increase in congenital rubella syndrome? Yet, natural immunity in early childhood can protect for a lifetime. Think about this statement made in 1964, before there was a Rubella vaccine implemented, by Dr. Hugh Paul in The Control Of Diseases:

     “The disease (rubella) cannot be prevented, and in view of its very mild character, and the possibility that it may have catastrophic effects if contracted by an expectant mother, it is questionable if it should be prevented in childhood and adolescence even if this were possible.  It has been suggested that female children should be deliberately exposed to infection in order to achieve a life-long immunity from the disease and possibly from malformation in the offspring in later life.  This idea is not an unreasonable one… Rubella does not kill, and even complications are uncommon.” 

 

      

 

 

 

 

 

 

 

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Mumps

      The Mumps vaccine was developed for the protection of adult males who may not have acquired mumps in childhood and gained natural immunity. In the pre-vaccine era, and for more than 10 years after the recommended Mumps vaccine, children typically caught Mumps between 5-9 years of age. The shift in incidence from childhood to adolescents was seen in 1985 to 1988. Then in 1992, there was another shift as Mumps was increasing and occurring in adolescents and young adults (10-19 years old) and exceeded all other age groups. The exact opposite of what the vaccine was intended for has been occurring; despite large vaccine coverage rates in childhood.  It should also be noted that the seasonal pattern of Mumps from 1988-1993 was consistent with the pre-vaccine era.

 

     During the 2005-2006 outbreaks, 51% had received 2 doses of Mumps vaccine, yet the incident rate was highest in those aged 18-24 years. Even after the ACIP made new recommendations in the 1980’s, adolescents and adults in 1982, 1986, and 1987 had the highest infection rates. During the 1989-1991 outbreaks amongst children in primary and secondary school, the majority were vaccinated. From 1988-1993, 75% of Mumps cases were seen in adolescents over 15 years of age and young adults. This trend has continued.

      “The shift in higher risk for mumps to these other age groups (i.e., from younger children of school ages to older children, adolescents, and young adults) — which occurred after the routine use of mumps vaccine was initiated — has persisted despite minimal fluctuations in disease incidence that occurred in recent years among the various age groups.” ( The resurgence of Mumps in Young Adults and Adolescents. John D. Shanley, M.D. Shanley_07 [1] pdf, pg. 1-4.)

 

     Young adults in high school and colleges were the primary target of the 2006 Mumps outbreak, even though most (84%) had received 2 doses of MMR. The ACIP then recommended yet another Mumps ‘booster’ vaccine, and for CSTE to update its case definition.  2010 was the goal set for elimination of Mumps in the United States. That year appears to be no longer attainable.

          “Despite a high coverage rate with two doses of Mumps-containing vaccine, a large Mumps outbreak occurred, characterized by 2-dose vaccine failure, particularly among Midwestern college adults who probably received the second dose as school children.  A more effective Mumps vaccine or changes in vaccine policy may be needed…” 

      The Mumps vaccine program has essentially put all adult males at a greater risk, since it can be cause more complications in adulthood.  If the vaccine had only been offered to susceptible males and females after puberty, who had not acquired a natural case in childhood, we might very well see a different picture than we see today.  

Pertussis (Whooping Cough)

     In the pre-vaccine era, 93% of Pertussis cases occurred in children between 1-5 years old. Since the 1980’s, the high incidence rate shifted to children over 5 years of age and older. In 2005, booster vaccines were recommended for adolescents and adults between the ages of 11-64 years old.

 

      From 1985-1987, 25% of reported cases were in children 10 years of age and over. From 1995-1998, that number increased to 42%. The largest majority of cases have been in the vaccinated populations. During the 1980’s, 1990’s and 2000’s, the number of adolescents and adults acquiring Pertussis has increased to spite high vaccination rates. (1) (2) (3) (4) (5)

              “Although pertussis incidence remains highest among young infants, rates are also on the rise in adolescents and adults and there may be significant under-reporting in these age groups, especially those with mild or atypical infection. Compared with surveillance data from 1994 to 1996, the pertussis incidence rate among adolescents and adults increased 62% and 60%, respectively, from 1997 to 2000.”

 

     There has also been an increase in babies under 1 year acquiring Pertussis. The number of cases in babies under 3 months of age from 1990-1997 did not lower. From 1999-2000, 48% of cases were in this age group. In 2001, 62% were under 3 months old. (6)

 

     According to a 2000 CDC MMWR report: “Despite record high vaccination coverage levels with 3 doses of DTaP among U.S. children aged 19–35 months, pertussis continues to cause fatal illness among vulnerable infants. During 1980–1998, the average annual incidence of reported pertussis cases and deaths among U.S. infants increased 50%. The increased morbidity and mortality occurred primarily among infants aged <4 months, who were too young to have received the recommended three DTaP vaccinations at ages 2, 4, and 6 months.” (7)

 

 

     Pertussis has always been endemic despite a vaccine.  It has a natural circulation every 2-5 years. This has not changed since the introduction of the vaccine, and thus indicates that the vaccine may prevent some disease, but has had little impact on transmission amongst the population. The efficacy of the DTaP is roughly 85% effective but waning immunity occurs after 2-5 years. In a case controlled study, it was found that infants of adolescent Mothers, aged 15-19 years, were 6 times more likely to acquire Pertussis compared to infants of older Mothers aged 20-29 years. Death from Pertussis is rare today. The majority of deaths, 90%, are in babies under 6 months of age. DTaP is also a reactive vaccine which means it does not prevent carriage or transmission of the disease. Therefore, vaccinated adolescents, adults and children can serve as reservoirs and transmitters to unprotected infants. (8) (9)

 

 

     Some epidemiologists believe B. Pertussis has mutated by changing its DNA and genetic coding.  Scientists in the Netherlands observed changes in the structure of the circulating wild-type bacteria when compared with those who were vaccinated. The differences were the outer membrane protein pertactin and the pertussis toxin itself. Similar genetic changes have been observed in Poland, Finland and the U.S. Any changes would thus render mutated bacteria immune to vaccination. As far as changing its character, many new cases lack the common ‘whoop’, yet 30% of cases were infected. Some cases were misdiagnosed as atypical asthma.(10) (11)

 

 

     In 2005, Tdap vaccines were recommended for adolescents over age 9 and adults under age 65 due to waning immunity from the DTaP vaccine given in infancy or childhood. There are no pertussis vaccines approved for children 7–9 years of age or for persons older than 64 years. The efficacy is similar and ‘inferred’ to that of DTaP. It is unknown if immunizing adolescents and adults will actually reduce the risk of transmission to infants. Nor is it known how long this vaccine may provide some people with protection. (12)

 

     

In the early 1900’s, it was questioned whether the control of Whooping Cough was even practicable. It has and remains to this day a more severe disease in infancy than in any other age group. A vaccine has not changed that fact. Generations passed have always known that the proper care in treatment of whooping cough would not lead to fatality, and most fatalities were the result of other complications mainly in the immune suppressed. (15)

 

 

Footnotes: 

 

       1.        Medscape Today. Epidemiology and Transmission of Disease. http://www.medscape.com/viewarticle/549508_2

 

2.        CDC MMWR, September 05, 1997 / 46(35);822-826. Pertussis Outbreak Vermont, 1996.  http://www.cdc.gov/mmwr/preview/mmwrhtml/00049244.htm

 

3.        The New England Journal of Medicine. Vol. 331:16-21. July 7, 1994. The 1993 Epidemic of Pertussis in Cincinnati — Resurgence of Disease in a Highly Immunized Population of Children.  http://content.nejm.org/cgi/content/full/331/1/16

 

4.        CDC MMWR, March 27, 1987 / 36(11);168-71. Epidemiologic Notes and Reports Pertussis Surveillance — United States, 1984 and 1985. http://www.cdc.gov/mmwR/preview/mmwrhtml/00000893.htm

 

5.        See #1

 

6.        CDR Weekly 21, June 2001. Enhanced surveillance of laboratory confirmed cases of Bordetella pertussis, England and Wales: 1999 to January-March quarter 2001. www.hpa.org.uk/cdr/archives/2001/cdr2501.pdf

 

7.        CDC, MMWR. July 19, 2002 / 51(28);616-618 Pertussis Deaths — United States, 2000. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5128a2.htm

 

8.        Medscape Today. Epidemiology and Transmission of Disease. http://www.medscape.com/viewarticle/549508_2

 

9.        Clinical Infectious Diseases.Epidemiological, Clinical, and Laboratory Aspects of Pertussis in Adults. 01 JUNE 1999 Supplement, Volume 28, Number S2.  James D. Cherry. http://www.journals.uchicago.edu/toc/cid/28/s2

 

8.        Medscape Today. Epidemiology and Transmission of Disease. http://www.medscape.com/viewarticle/549508_2

 

9.        Clinical Infectious Diseases.Epidemiological, Clinical, and Laboratory Aspects of Pertussis in Adults. 01 JUNE 1999 Supplement, Volume 28, Number S2.  James D. Cherry. http://www.journals.uchicago.edu/toc/cid/28/s2

 

10.     See #9.

 

11.     Emerging Infectious Diseases. Changes in Predominance and Diversity of Genomic Subtypes of Bordetella pertussis Isolated in the United States, 1935 to 1999.Terri Hawes Hardwick, et al. http://www.cdc.gov/ncidod/EID/vol8no1/01-0021.htm

 

12.     Adacel Tdap Package Insert. www.fda.gov/cber/label/adacelLB.pdf

 

13.     IS THE CONTROL OF MEASLES AND WHOOPING-COUGH PRACTICABLE? Am J Public Health (N Y). 1916 March; 6(3): 265–268. FRANCiS GEORGE CURTIS, M. D., Chairman, Board of Health, Newton, Mass. Read at a General Session of the American Public Health Association, Rochester, N. Y., September 10, 1915.

 

14.   Whooping Cough. Am J Public Health Nations Health. 1936 May; 26(5): 523–524.

 

15.     A STATISTICAL STUDY OF WHOOPING COUGH. FREDERICK S. CRUM, PH. D., Am J Public Health (N Y). 1915 October; 5(10): 994–1017.