Mumps Epidemiology and Immunity: The Anatomy of a Modern Epidemic

Pediatric Infectious Disease Journal. 27(10) Supplement:S75-S79, October 2008.
Anderson, Larry J. MD; Seward, Jane F. MB, BS, MPH

The success of the measles, mumps, and rubella 2-dose vaccination program led public health officials in 1998 to set a goal to eliminate endemic transmission of mumps virus by 2010 in the United States. The large outbreak of mumps in the spring of 2006 has led public health officials to re-evaluate this goal and to recognize that the transmission and epidemiology of mumps in highly vaccinated populations may be different than anticipated. During 2006, a total of 6584 confirmed and probable cases of mumps were reported to the Centers for Disease Control and Prevention and most of these, 5865, occurred between January 1 and July 31. The peak of the outbreak was in April and seemed to be focused on college campuses in 9 midwestern states with Iowa having the highest attack rate. College campuses with mumps outbreaks included ones with 77% to 97% of students having had 2 doses of a mumps vaccine. Diagnosing mumps proved to be problematic in vaccinated persons (ie, laboratory tests seemed to be insensitive and some apparent mumps cases had mild nonclassic illness). The outbreak demonstrated that mumps can sometimes transmit efficiently in highly vaccinated populations and the clinical and laboratory diagnosis of mumps in vaccinated persons is more difficult than in naive persons. The reason for this mumps outbreak is not clear but probably results from multiple factors contributing to an overall increase in susceptibility and/or transmission.

(C) 2008 Lippincott Williams & Wilkins, Inc.



     In the pre-vaccination era, Measles was a common childhood illness usually acquired before the age of 10 years old, and thus attained permanent immunity.  At least 95% of American children had Measles by the time they were 15 years old. Measles was rare in infants under the age of one as they were protected by their Mother’s natural immunity from childhood and through breastfeeding.

     As the Measles vaccination program increased, the epidemiology of Measles shifted. Measles cases began occurring in late adolescents, young adults, and babies under one year of age. This is not a new trend.  During the Measles outbreaks in 1976-1977, 60% of those cases occurred in children over age 10 and 26% occurred in children over age 15. This trend has continued to spite high vaccine coverage rates in developed and developing countries. It has also led to longer intervals between epidemic years; known as the “honeymoon effect’. In the 1984 Measles outbreak, 58% of school-age children who had been vaccinated caught Measles.

     A.W. Hedrich researched and published a study in 1933 on the patterns of Measles in Baltimore, Maryland from 1900-1931.  He surmised that the majority of children under 15 years of age who would catch Measles would not go above 53%, and would not drop below 32% during those 32 years.  At least 47% of children in Baltimore would not have Measles each time an outbreak ended. (2)  Hedrich’s research showed that the number of people in a community had nothing to do with the decline in virulence of the virus when an outbreak comes to an end. Measles is endemic and occurs whenever nature says it’s time. Epidemics have continued to occur even with high vaccine rate coverage, and occur in both vaccinated and unvaccinated.

     Where infants are concerned, vaccinated Mothers today do not have the full natural immunity to protect their infants.  In 1992 alone, 22.2% of measles cases were in infants less than 12 months of age. This was an increase from 19.2% in 1991 and 17.0% in 1990. In 1990, 27.9% of reported cases occurred in children 1-4 years of age, and 30.1% in 1991. In Texas alone, 75% of the cases were in children younger than 5 years old, and 35% in children less than 12 months old. In Kentucky, the opposite happened. Measles made up 49% of the cases in children 5-19 years old.

   According to the CDC’s Pink Book Measles Chapter, it is admitted that infants are now more at risk from Measles during outbreaks than in the pre-vaccination era.

     In addition, measles susceptibility of infants younger than 1 year of age may have increased. During the 1989–1991 measles resurgence, incidence rates for infants were more than twice as high as those in any other age group. The mothers of many infants who developed measles were young, and their measles immunity was most often due to vaccination rather than infection with wild virus. As a result, a smaller amount of antibody was transferred across the placenta to the fetus, compared with antibody transfer from mothers who had higher antibody titers resulting from wild-virus infection. The lower quantity of antibody resulted in immunity that waned more rapidly, making infants susceptible at a younger age than in the past.”



     According to a 1999 issue in Pediatrics:   “Infants whose mothers were born after 1963 are more susceptible to measles than are infants of older mothers. An increasing proportion of infants born in the United States may be susceptible to measles.” Mothers who had infants born after 1963, had a measles attack rate of 33%, compared with 12% for infants of older mothers.  The difference in infant’s immunity levels between the vaccinated Mothers and the unvaccinated Mothers can also be seen in the 1995 Pediatrics Journal.

      Even the World Health Organization has admitted that the vaccinated have a 14 times greater chance of contracting the disease than the unvaccinated.  ( National Health Federation Bulletin, (Nov. ‘69).

     Another issue worth mentioning is that without the circulating wild virus producing a boosting effect for older adults, and infants not as protected by maternal antibodies, the disease becomes more dangerous. A disease that a 5 year old could once recover from in 1-2 weeks has the potential to kill an infant, adolescent or adult. Measles used to have a natural virulence of every 3-4 years. The vaccine has caused longer intervals between exposures.


     “But the last generation to have routinely suffered through most of these diseases is crossing through mid-life and the first generation to have avoided them is hovering around 40.”

     Before vaccination became commonplace, adults often came in contact with youngsters suffering from mumps, measles and the other childhood diseases. That remained the case in the early days of vaccine administration when these diseases still commonly circulated.”

     “If people had protection – natural or vaccine-acquired – those exposures were actually helpful. They acted as a sort of natural booster shot, reminding the immune system to be on guard for this threat.  Some experts now wonder whether these unrecorded natural boosts may have led the medical community to overestimate the durability of immunity generated by childhood vaccinations. These days, few people are getting natural boosting to these diseases.”

     The Measles vaccine has made the disease rarer in childhood, but more dangerous when it does occur, due to the age shift. There can also be a higher case fatality rate in infant and adult infections.  When considering the risks or benefits of the vaccine, consider this:  Once a population is exposed to measles in childhood, few infants or adults will contract it as they will have acquired immunity for life.  The vaccine simply can not do that. All it has done is decrease the virulence, the circulation cycle of the disease, and pushed the disease incidence to older persons and infants when the disease can be more harmful and deadly.

   According to the American Journal of Epidemiology, it was projected, based on a computer model:

        “However, despite short-term success in eliminating the disease, long-range projections demonstrate that the proportion of susceptibies in the year 2050 may be greater than in the prevaccine era. Present vaccine technology and public health policy must be altered to deal with this eventually.” So the end result will be the same number (or more) of susceptibles, but “distributed evenly throughout all age groups”. Since adults and infants have higher risk of Measles complications and fatality, the Measles eradication plan has resulted in higher risk to the overall population. Obviously the public health policy solution is more and more vaccination, more boosters for children and adolescents, and adults as well. A very short-sighted, questionable and expensive campaign to eliminate a self-limiting childhood disease.”

     It should also be noted that in the pre-vaccine era, 10% of the population was always susceptible to Measles. After the Childhood Immunization Initiative from 1977-1979, it was admitted that at least 5 % would not develop Measles antibodies, and Measles would continue to occur despite high vaccination rates and it has. Those susceptible are those who have primary and secondary vaccine failure, adults who escaped natural Measles because of decreasing transmission in the late 1960’s, lack of virulence to boost natural immunity, infants under one year of age to decreased maternal antibodies, and waning immunity in the vaccinated. Therefore in the future, we may very well see a higher risk than 10% susceptible to Measles and spread out to all age groups in the overall population.

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.” 











      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)





       1.        Medscape Today. Epidemiology and Transmission of Disease.


2.        CDC MMWR, September 05, 1997 / 46(35);822-826. Pertussis Outbreak Vermont, 1996.


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.


4.        CDC MMWR, March 27, 1987 / 36(11);168-71. Epidemiologic Notes and Reports Pertussis Surveillance — United States, 1984 and 1985.


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.


7.        CDC, MMWR. July 19, 2002 / 51(28);616-618 Pertussis Deaths — United States, 2000.


8.        Medscape Today. Epidemiology and Transmission of Disease.


9.        Clinical Infectious Diseases.Epidemiological, Clinical, and Laboratory Aspects of Pertussis in Adults. 01 JUNE 1999 Supplement, Volume 28, Number S2.  James D. Cherry.


8.        Medscape Today. Epidemiology and Transmission of Disease.


9.        Clinical Infectious Diseases.Epidemiological, Clinical, and Laboratory Aspects of Pertussis in Adults. 01 JUNE 1999 Supplement, Volume 28, Number S2.  James D. Cherry.


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.


12.     Adacel Tdap Package Insert.


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.