Disease Risk – Mumps

 

Risk to a child from Mumps if not vaccinated until after the age of 5:

Case Fatality Rate: The WHO reports the case fatality rate worldwide at 1 in 10,000 cases.[1]  In the USA, an average of one death per year occurred from 1980-1999.[2]

Rate of Long Term Sequelae or Injury: Mumps can cause encephalitis (2 per 100,000 cases) and deafness (5 in 100,000 cases)[1][2][3]. In 80% of the deafness cases, the hearing loss is reported to be unilateral (affecting one ear).[2]  Infection in older males can also result in sterility, but this is not a risk to the under five population.

Incidence Rate: From 2004 – 2008 the average number of mumps cases per year was 1682 with typical years resulting in around 500 cases and periodic larger outbreaks (6,500 cases in 2006).[4]

Incremental Risk in highly vaccinated population (if a child does not vaccinate by age 5):

In the mumps outbreak in the USA in 2006 [5], mumps outbreaks occurred primarily on college campus in the Midwest.  A total of 6584 cases and 85 hospitalizations were reported in 2006; no deaths occurred.  No large outbreaks were reported at primary or secondary schools. In the 18-24 years age group, the incidence of mumps was higher than in all the other age groups combined by a factor of 3.7. Of the patients with known vaccination status, less than 4% of those under the age of 30 years were unvaccinated. Only about 3.3% of the cases occurred in children under age 5, with an incidence rate of approximately 40/10,000 for age <1 and 180/10,000 for ages 1-4. Neither vaccination status nor race or ethnic group was significantly associated with complications.

Approximately 3.5% of cases occurred in the under five population in the USA 2006 mumps outbreak [5]. Based on the average number of cases from 2004 – 2008 (1682), the average number of cases in children under five would be 59.  The WHO reports the case fatality rate worldwide at 1 in 10,000 cases [1].  Assuming that the risk of death is only to unvaccinated children, and assuming a max vaccination rate of 96% [5], then the cumulative risk of death to the child over the first five years of life was calculated to be 0.00036 per 10,000 children or a 1 in 27,911,286 risk.

Encephalitis occurs at a rate of 2 in 100,000 cases and deafness results in 5 in 100,000 cases [3].  Assuming that the risk of encephalitis or deafness is only to unvaccinated children, and assuming a max vaccination rate of 96% [5], then the cumulative risk of permanent injury to the child over the first five years of life was calculated to be 0.00025 per 10,000 children or a 1 in 39,873,265 risk.

Incremental Risk in population with low vaccination (if a child does not vaccinate by age 5):

Assuming that infection levels increased to USA pre-vaccine levels in 1964, when there were approximately 212,000 cases per year [3] in a population of 192,000,000 [7], then the incidence rate would be 11 per 10,000 each year.

The WHO reports the case fatality rate worldwide at 1 in 10,000 cases [1].  The cumulative risk of death to the child over the first five years of life was calculated to be 0.00552 per 10,000 children or a 1 in 9,056,604 risk.

Encephalitis occurs at a rate of 2 in 100,000 cases and deafness results in 5 in 100,000 cases [3].  The cumulative risk of permanent injury to the child over the first five years of life was calculated to be 0.00386 per 10,000 children or a 1 in 12,938,006 risk.

 

 

References:

[1] http://www.who.int/immunization_monitoring/diseases/mumps_surveillance/en/index.html

[2] Mumps in Emergency Medicine. http://emedicine.medscape.com/article/784603-overview#a0199

[3] Centers for Disease Control and Prevention: Epidemiology and Prevention of Vaccine-Preventable Disease. Atkinson W, Wolfe S, Hamborsky J, McIntyre L. eds. 11th edition. Washington D.C.: Public Health Foundation, 2009.

[4] Center for Disease Control and Prevention.  Notifiable Diseases/Deaths in Selected Cities Weekly Information.  MMWR2009; 58(45): 1276-1287.

[5] Recent Resurgence of Mumps in the United States.  N Engl J Med 2008; 358:1580-1589, April 10, 2008.  http://www.nejm.org/doi/full/10.1056/NEJMoa0706589

[6] CDC.  MMWR on Mumps.  MMWR 32(42): 545.

[7] http://www.census.gov/popest/archives/1990s/popclockest.txt

 

Disease Risk – Measles

 

Risk to a child from Measles if not vaccinated until the age of 5:

Measles (also known as Rubeola or morbilli) is a viral infection of the respiratory system.  It is classically characterized by initial fever followed by a rash that covers most of the body.  Measles is highly infectious and is spread through aerosolized droplets from infected persons.  It is contagious from 2-4 days prior to and 2-5 days after the onset of the rash.  Prior to vaccination, 90% of the population in the US contracted measles by the time they turned 15.  Although it is generally a mild illness, it can be accompanied by very serious complications (pneumonia, encephalitis, SSPE) or death in a small number of cases. [1]    Measles can be very serious in immunocompromised persons.

The severity of the disease is hard to judge due to inconsistent documentation and conclusions by various authors worldwide.  In a 1967 study by authors from the CDC they state:  “For centuries the measles virus has maintained a remarkably stable ecological relationship with man.  The clinical disease is a characteristic syndrome of notable constancy and only moderate severity.  Complications are infrequent, and, with adequate medical care, fatality is rare. Susceptibility to the disease after the waning of maternal immunity is universal; immunity following recovery is solid and lifelong in duration.”[2]   In 2004, we find CDC authors telling a very different story about the exact same time period:  “Nevertheless, in the late 1950s, serious complications due to measles remained frequent and costly. As a result of measles virus infections, an average of 150,000 patients had respiratory complications and 4000 patients had encephalitis each year; the latter was associated with a high risk of neurological sequelae and death. These complications and others resulted in an estimated 48,000 persons with measles being hospitalized every year.”[3](Orenstein).   Following the reference chain, we see these estimates are mainly based on a study from cases between 1929-1953 [4].  Miller performs a UK based study in 1964 and observes:  “In the meantime it can be said that the results reflect complication rates under the present conditions of medical practice, and on these grounds measles can scarcely be regarded as a mere inconvenience.”[5]   A subsequent study from Denmark by Tidstrom (1968) makes the following observation:  “Encephalitis is a rare complication in measles and, concerning mortality rate and sequelae, is not so severe as considered previously.” [6]

Factors Not Considered: There is considerable evidence that the risk from severe measles disease is highly variable depending on factors influenced by economic and living conditions.  Morbidity and mortality due to measles is far higher in the developing world.  In a study from the UK, Maclure found that the risk of hospitalization from measles in children living in deprived households was over 10 times higher than in areas where households were not deprived.[7]  For measles, overcrowding and unemployment were more correlated with measles hospitalization than vaccination rates.  In the developing world, the majority of complications occur in the younger children.  Gordon et al describe that in Guatemala, nutritional supplements reduced the annual mortality rate by 65% while medical care reduced it by almost 70% [8].

Case Fatality Rate: The CDC Pink book lists several causes of death from measles including:  Death from pneumonia, acute encephalitis, and subacute sclerosing panencephalitis (SSPE).[1]

Determining an accurate case fatality rate is very difficult given that reported incidence of measles is deemed unreliable and varies over time.  During epidemics, it is assumed that more cases are reported.  It was assumed prior to mass vaccination in 1963, only 1 in 10 cases were reported.[9] (Bellini)   Today, it is assumed that most cases are reported and these assumptions heavily affect the case fatality calculations.  There is also evidence that during epidemics that many subclinical cases occur.  [9,10]

The most recent study of the pre-vaccine era is the Tidstrom study from Denmark in 1968.  Tidstrom is insightful because it analyses measles data over 15 years, and it separately analyzes two distinct periods where treatment of respiratory failure were fundamentally changed following a severe poliomyelitis epidemic in 1952.[6]  The study covers a 15 year period during which there were 298,700 births (estimated total child population of 577,477 children < 15) with 157,300 notifications (~27%) and a total of 4874 patient hospitalizations.  This study provides a unique view into the effects of more modern medical protocols when treating measles encephalitis.  The difference was quite striking.  In the period prior to 1952, there were 5 deaths among 21 patients (24%) of encephalitis.  In the period following 1952, there was only one death among 47 patients (2.1%) from encephalitis.  Tidstrom notes that the latter rate of 2.1% was consistent with a Swedish publication showing one death among 38 patients (2.6%).  Consistent with most other studies, pneumonia was the most frequent complication resulting 1,268 hospitalized cases (26%) and 12 deaths (0.9%).  Unlike the case fatality rate from encephalitis, the case fatality rate from pneumonia was surprisingly consistent across the entire 15 year period of study.  There were 4 other deaths (2%) of the 4874 hospitalizations from a variety of different complications and pre-existing conditions.  Tidstrom notes that most of the numbers are consistent with other studies from that era, with the exception of a lower encephalitis rate.  She explains this:  “The frequency of encephalitis was 0.043% of the notified cases in the City and County of Copenhagen. The incidence of encephalitis as a complication in measles is reported to range from 0.1% to 0.25%. The variations may be caused by varying criteria for the diagnosis. Some authors classify every symptom from the central nervous system as due to encephalitis, which means that cases with secondary lymphocytic meningitis without other signs of central nervous disturbances than pleocytosis are included.”

In 1964, Miller published a study from a postal follow-up of ~53,000 notified measles cases in England and Wales.  The Miller (1964) study was mainly focused on complications and notes a total number of 12 deaths (0.022 per 1000 notifications) which is higher but in a similar ballpark to the case fatality rate from Tidstrom (0.014 per 1000 notifications).  However, Miller (1964) notes that there is evidence that half of the deaths occur in persons with serious or chronic disease or disability.  So if you take that into consideration, the Tidstrom numbers based on healthy patients are higher.  This analysis uses the case fatality data from Tidstrom (1968) with a heavier weighting of notifications to population based on the notifications percentages from ages 1-4 (measles vaccine doesn’t protect children < 1 year old)  from Miller (1964).

SSPE is a progressive fatal disease caused by persistent measles infection.  SSPE occurs an average 7-10 years post measles infection.  The main risk factor for SSPE is the development of measles infection at an early age (before 2 years of age)[9].  Bellini et al[9] did a rigorous SSPE follow-up case study after the large measles outbreak from the US in 1989-1991.  They concluded that SSPE rates were traditionally underestimated and calculated a rate of 6.5-11 cases of SSPE per 100,000 cases of measles.  This analysis needs to determine the individual risk that is vaccine preventable.  Although Bellini et al concluded that vaccination prevents more cases of SSPE than previously thought, an examination of the cases shows that this protection is entirely due to herd immunity, not directly due to vaccination.  In every case they document, the patient contracted the disease prior to vaccination, or post-vaccination (indicating vaccine failure in that individual).  For the purposes of this analysis, the risk of SSPE is not considered directly vaccine preventable.

Rate of Long Term Sequelae: Miller (1964) discusses many complications of measles but notes that a subsequent study would have to follow-up the cases and determine the rates of long term sequelae.  Tidstrom (1968) performs a follow-up of 95% of the hospitalized encephalitis cases (59 of 62) over the study period.  Forty five patients were examined by Tidstrom and 14 answered questions by mail.  Tidstrom notes that 68% had a complete recovery, 3 had serious defects and 16 had mild defects.  Three of the 15 mild defects were classified as “dubious”.  This analysis will use a long term sequelae rate of 16/59 or 27% of encephalitis cases.

Incremental Risk in Population with Low Rates of Vaccination (if a child does not vaccinate by age 5): As described above, this analysis calculates the risk of death and long term sequelae based on Tidstrom (1968) case rates, with adjusted weightings by age provided by the Miller (1964) study.  This analysis uses a weighted notification rate of 54% (based on Tidstrom population weighted by Miller notifications).  The cumulative fatality rate was 0.5284 per 10,000 or 1 in 18,924.  The cumulative risk of long term sequelae was 0.6309 per 10,000 or 1 in 15,851.

Incremental Risk in Highly Vaccinated Population (if a child does not vaccinate by age 5): Calculations of vaccine preventable risk are very difficult in highly vaccinated populations due to the lack of good statistics regarding vaccinated population counts, and percentage of vaccinated incidence.  As described above, in the case of measles, the reduction of risk is due to herd immunity.  The CDC declared measles eradicated in the US around the year 2000.  Statistics show that the measles cases have dropped to less than 0.1% of the rates pre-vaccination.  Taking 0.1% of the risk from populations with low rates of vaccination, yields a fatality rate of 0.00053 per 10,000 or 1 in 18,923,686.   The cumulative risk of long term sequelae was 0.00063 per 10,000 cases or 1 in 15,851,399.

 

References:

[1] Centers for Disease Control and Prevention: Epidemiology and Prevention of Vaccine-Preventable Disease. Atkinson W, Wolfe S, Hamborsky J, McIntyre L. eds. 11th edition. Washington D.C.: Public Health Foundation, 2009.

[2] D. J. Sencer, H. B. Dull, and A. D. Langmuir.  Epidemiologic basis for eradication of measles in 1967.  Public Health Rep. 1967 March; 82(3): 253–256.

[3]  Orenstein WA, Papania MJ, Wharton ME.  Measles elimination in the United States.  J Infect Dis. 2004 May 1;189 Suppl 1:S1-3.

[4]  MILLER HG, STANTON JB., GIBBONS JL.  Para-infectious encephalomyelitis and related syndromes; a critical review of the neurological complications of certain specific fevers.  Q J Med. 1956 Oct;25(100):427-505.

[5]  MILLER DL., FREQUENCY OF COMPLICATIONS OF MEASLES, 1963. REPORT ON A NATIONAL INQUIRY BY THE PUBLIC HEALTH LABORATORY SERVICE IN COLLABORATION WITH THE SOCIETY OF MEDICAL OFFICERS OF HEALTH.  Br Med J. 1964 Jul 11;2(5401):75-8.

[6]  Tidstrom B.  Complications in measles with special reference to encephalitis.  Acta Med Scand. 1968 Nov;184(5):411-5.[7]  Maclure A, Stewart GT.  Admission of children to hospitals in Glasgow: relation to unemployment and other deprivation variables.  Lancet 1984 Sep 22;2(8404):682-5.

[7]  Maclure A, Stewart GT.  Admission of children to hospitals in Glasgow: relation to unemployment and other deprivation variables.  Lancet 1984 Sep 22;2(8404):682-5.

[8]  GORDON JE, JANSEN AA, ASCOLI W.  MEASLES IN RURAL GUATEMALA.  J Pediatr. 1965 Apr;66:779-86.

[9]  Bellini WJ, Rota JS, Lowe LE, Katz RS, Dyken PR, Zaki SR, Shieh WJ, Rota PA.  Subacute sclerosing panencephalitis: more cases of this fatal disease are prevented by measles immunization than was previously recognized.  J Infect Dis. 2005 Nov 15;192(10):1686-93. Epub 2005 Oct 12.

[10] Miller C, Andrews N, Rush M, Munro H, Jin L, Miller E.  The epidemiology of subacute sclerosing panencephalitis in England and Wales 1990-2002.  Arch Dis Child. 2004 Dec;89(12):1145-8.

 

 

Disease Risk – Influenza

 

Risk to a child from Influenza (Flu) if not vaccinated until after the age of 5:

Incidence Rates:

The first live attenuated influenza vaccine was licensed in 2003. Among children 0–4 years of age, hospitalization rates have varied from 100 per 100,000 healthy children to as high as 500 per 100,000 for children with underlying medical conditions. [1]

Case Fatality Rate: In 2006/07 there were 29 deaths in children under age five and 41 in 2007/08 for an average of 35 flu deaths per year in that age group during that two year period [2].  In 2008 per the US Census the total population of children under 5 in the United States was 21 million [3].

Rate of Long Term Sequelae or Injury: The most frequent complication of influenza is pneumonia, most commonly secondary bacterial pneumonia (e.g., Streptococcus pneumoniae, Haemophilus influenzae, or Staphylococcus aureus). Primary influenza viral pneumonia is an uncommon complication with a high fatality rate. [1]  If these complications do not result in death, the patient typically does not have permanent injury.  Influenza-related encephalitis is rare, occurring at a population incidence of 0.21 per million population.[4]

Incremental Risk in Population with Low Rates of Vaccination (if a child does not vaccinate by age 5):

According to an 2008 appraisal of all comparative studies by The Cochrane Collaboration [5], the efficacy of the influenza vaccine in children under two was similar to placebo; in other words, the vaccine is not effective in children under two.  The researchers concluded that “… at present we could find no convincing evidence that vaccines can reduce mortality, hospital admissions, serious complications and community transmission of influenza” and that “Decision makers’ attention to the vaccination of very young children is not supported by the evidence summarized in our review.”

This analysis is an evidence-based review.  Since there is no credible evidence that influenza vaccination reduces death or permanent injuries in children ages 0 – 4, this analysis concludes that the incremental cumulative risk of not vaccinating is zero.

Incremental Risk in Highly Vaccinated Population (if a child does not vaccinate by age 5):

There is no credible evidence of herd immunity due to influenza vaccination.  As explained above in “Incremental Risk in Population with Low Rates of Vaccination”, there is no credible evidence that influenza vaccination reduces death or permanent injuries in children ages 0 – 4.  Therefore, this analysis concludes that the incremental cumulative risk of not vaccinating is zero.

 

References:

 

[1] Centers for Disease Control and Prevention: Epidemiology and Prevention of Vaccine-Preventable Disease. Atkinson W, Wolfe S, Hamborsky J, McIntyre L. eds. 11th edition. Washington D.C.: Public Health Foundation, 2009.

[2] Center for Disease Control and Prevention.  Notifiable Diseases/Deaths in Selected Cities Weekly Information.  MMWR 2009; 58(45): 1276-1287.

[3] United States Census Bureau.  The 2010 Statistical Abstract; Table 78: Live Births, Deaths, Marriages and Divorces: 1960 to 2007.

[4] Hjalmarsson A, Blomqvist P, Brytting M, Linde A, Skoldenberg B. Encephalitis after influenza in Sweden 1987-1998: a rare complication of a common infection. Eur Neurol. 2009; 61(5):289-94. Epub 2009 Mar 17.

[5] Smith S, Demicheli V, Di Pietrantonj C, Harnden AR, Jefferson T, Matheson NJ, Rivetti A. Vaccines for preventing influenza in healthy children.  Cochrane Database Syst Rev. 2006 Jan 25;(1):CD004879

Disease Risk – Hib

 

Risk to a child from Haemophilus influenzae b (Hib) if not vaccinated until the age of 5:

Factors not considered:

1)      The vaccine failure rate after immunization for Hib is rare at an estimated 2.2 per 100,000 vaccinees [1] and consequently is not considered in this analysis.

2)      The question of overall invasive Hi disease risk changes when employing a mass vaccination strategy involving only a single serotype is one that has been debated and there is at least one study indicating a clear trend toward invasive disease through serotype replacement [2].  However, the complexity of introducing serotype replacement into the disease and vaccine risk assessment precludes it from being included in the analysis at this time resulting in a bias toward higher vaccine efficacy assessment.  The risk of Invasive Hi disease has a large variability in different populations with numerous known risk factors.  For this analysis we have to use average risk rates from large studies but we encourage readers to understand the different risk factors (i.e. breast feeding, socio-economic conditions etc) that can substantially raise or lower individual risks from invasive Hi disease.

Case Fatality Rate: The CDC pink book lists the risk of death from Hib Meningitis at 2-5% [3].  In Schoendorf et al (1994) [4] they document that prior to Hib vaccination in the US from 1980-1987, the fatality rate of Hi Meningitis was dropping despite consistent levels of hospitalizations due to meningitis.  This indicates that medical care was reducing the case fatality rate of this disease.  In 1987, the rate had dropped to about 2% of Meningitis cases.  Meningitis occurs consistently in approximately 50% of Invasive Hi disease cases[5] meaning that the overall fatality case rate from invasive Hi disease had dropped to 1% due to modern medical care.

Rate of Long Term Sequelae or Injury: The CDC pink book lists the case rate of hearing impairment or other neurologic sequelae from Hib Meningitis as 15%-30%.[3]  This number is unreferenced and non-specific as to whether the sequelae is long or short term.  Ladhani et al (2010) performed a unique modern long term follow-up study in the UK of cases of invasive Hib disease following vaccine failure.[6] They found that the rates of long term sequelae in the study group were consistent with invasive Hib cases prior to vaccination at a rate of approximately 10.4%.

Incidence Rates: Prior to vaccination, the vast majority of cases were in children < 12 months of age with the peak incidence rates occurring around 6-7 months of age.[3]  In times of readily circulating virus, infants would receive passive protection through transplacentally acquired maternal IgG antibodies and breastfeeding.[3]  Vaccine protection is typically provided through two or three shots providing full protection at about 6 months of age.    Infants < 6 months are generally considered unprotected by vaccines.[3]  Post vaccination, the vast majority of cases were found in children < 6 months of age, likely due to a loss of maternal immunity and lack of vaccine protection.  In both the pre-vaccine and post-vaccine eras, the incidence rates of invasive meningitis are approximately 5 times higher in the first year of life compared to each of the next 4 years.  Given that the distribution of cases within the first year has changed and depends highly on the state of maternal immunity and breastfeeding status, this analysis will assume a relatively even split between incidence rates from 0-6 months, and 6-12 months of age.  Given that vaccination will only provide protection for infants greater than 6 months of age, only the cases in the first year would be vaccine preventable for this analysis.

Risk in Population with Low Rates of Vaccination: There are varying incidence rates of Hib meningitis from the pre-vaccine era.  This analysis used national mortality and hospital discharges data provided in Schoendorf et al (1994)[4].  The Schoendorf study documented a relatively consistent hospitalization rate in the years immediately prior to vaccination (1980-1987).  The average hospitalization rate for Hib meningitis was calculated for the 8 years at 39.515 per 100,000.  Based on the age distribution noted above, we calculated a meningitis rate of 109.76 per 100,000 for year 0 and 21.95 per 100,000 for years 1-4.  The meningitis rates were doubled to calculate the yearly Invasive Hib disease incidence rate (meningitis occurs in 50% of invasive Hi disease).  The cumulative incremental rate of invasive Hib disease from ages 0-4 was then calculated to be 28.5 per 10,000 or 1 in 350.  (50% of year 0 rate was used because vaccination wouldn’t protect infants < 6 months).  The cumulative risk of death was calculated to be 0.285 per 10,000 or 1 in 35,078.  The cumulative risk of permanent injury was calculated to be 2.96 per 10,000 or 1 in 3,372.

Risk in Highly Vaccinated Population: Post vaccination rates of invasive Hib disease are very low.  This analysis used the incidence rate from 2008 MMWR[7].  Unfortunately, serotyping in the US has over 30% rate of undetermined cases.  The province of Ontario consistently determines most of the serotypes found across the province which was documented in Adam et al (2010).  Using these numbers, they found Hib occurred in about 10% of the cases.  This analysis took the US Serotype B values of 0.42 and 0.29 (year 0 and years 1-4) and adjusted them up to 10% of the total Invasive Hi cases to 0.613 for year 0 and 0.421 for years 1-4.  The cumulative incremental rate of invasive Hib disease from ages 0-4 was then calculated to be 0.199 per 10,000 or 1 in 50,239.  (50% of year 0 rate was used because vaccination wouldn’t protect infants < 6 months).  The cumulative risk of death was calculated to be 0.00199 per 10,000 or 1 in 5,023,903.  The cumulative risk of permanent injury was calculated to be 0.0207 per 10,000 or 1 in 483,067.

 

References:

[1] Heath PT, Booy R, Azzopardi HJ, Slack MP, Bowen-Morris J, Griffiths H, et al.  Antibody concentration and clinical protection after Hib conjugate vaccination in the United Kingdom. JAMA 2000;284:2334–40.

[2] Adam HJ, et al. Changing epidemiology of invasive Haemophilus influenzae in Ontario, Canada: Evidence for herd effects and strain replacement due to Hib vaccination. Vaccine (2010), doi:10.1016/j.vaccine.2010.03.075

[3] Centers for Disease Control and Prevention: Epidemiology and Prevention of Vaccine-Preventable Disease. Atkinson W, Wolfe S, Hamborsky J, McIntyre L. eds. 11th edition. Washington D.C.: Public Health Foundation, 2009.

[4] Schoendorf, K., Adams, W., Kiely, J., Wenger, J.  National Trends in Haemophilus influenzae Meningitis Mortality and Hospitalization Among Children, 1980 through 1991.  Pediatrics.  1994; 93: 663-668.

[5] Peltola H. Worldwide Haemophilus influenzae type b disease at the beginning of the 21st century: global analysis of the disease burden 25 years after the use of the polysaccharide vaccine and a decade after the advent of conjugates. Clinical Microbiology Reviews 2000;13:302–17.

[6] Ladhani S, Heath PT, Aibara RJ, Ramsay ME, Slack MPE, Hibberd ML, Pollard AJ, Moxon ER, Booy R.  Long-term complications and risk of other seious infections following invasive Haemophilus influenza serotype b disease in vaccinated children.   Vaccine 2010;28:2195-2200.  doi:10.1016/j.vaccine.2009.12.057

[7] CDC. Reported cases and incidence* of notifiable diseases,† by age group — United States, 2008. MMWR 57 (No.54);32.

Disease Risk – Hepatitis B

 

Risk to a child from Hepatitis B if not vaccinated until after the age of 5:

Incidence Rates:  Universal infant vaccination for Hepatitis B began in the United States in 1991.

In the United States, the most important routes of transmis­sion are sexual contact and unsanitary needles during injection-drug use. Fecal-oral transmission does not appear to occur. Perinatal transmission from mother to infant at birth is very efficient. Beyond perinatal transmission, only 5% of newly acquired Hepatitis B infection are known to be caused by a factor other than high-risk sexual activity or injection-drug use (i.e., occupa­tional, household, travel, and healthcare-related). [3]

Nationwide surveillance data showed that in the pre-vaccine era from 1983 to 1987, 161 children 1 to 4 years of age were reported with acute hepatitis B [4].  During 1990–2007, incidence of acute hepatitis B in the United States among persons aged <15 years declined from 1.2 cases per 100,000 population in 1990 to 0.02 cases per 100,000 population in 2007.[5]

As many as 90% of infants who acquire HBV infection from their mothers at birth become chroni­cally infected. Of children who become infected with HBV between 1 year and 5 years of age, 30% to 50% become chronically infected.[3]

Case Fatality Rate: Approximately 25% of persons with chronic HBV infection die prematurely from cirrhosis or liver cancer.[3]  While most acute HBV infections in adults result in complete recovery, fulminant hepatitis occurs in about 1% to 2% of acutely infected persons (case-fatality rate 63% to 93%). [3]

Rate of Long Term Sequelae or Injury: Chronic active hepatitis develops in more than 25% of carriers (a.k.a. chronic HBV infection) and often results in cirrhosis.

Incremental Risk in Population with Low Rates of Vaccination (if a child does not vaccinate by age 5): The incremental cumulative risk of permanent-injury to a child not vaccinated by age five was calculated to be 0.3 per 10,000 or 1 in 33,000.  The cumulative risk of death is the first five years of life was calculated to be 0.0035 per 10,000 or 1 in 2,849,000.  The cumulative risk of premature death later in life from Hepatitis B liver damage was calculated to be 0.075 per 10,000 or 1 in 133,000.  Incorporating both risks, the cumulative risk of either acute death in first five years or premature death later in life was calculated to be 0.0785 per 10,000 or 1 in 127,000.

Incremental Risk in Highly Vaccinated Population (if a child does not vaccinate by age 5): The incremental cumulative risk of permanent-injury to a child not vaccinated by age five was calculated to be 0.00125 per 10,000 or 1 in 8,000,000.  The cumulative risk of death is the first five years of life was calculated to be 0.0000585 per 10,000 or 1 in 171,000,000.  The cumulative risk of premature death later in life from Hepatitis B liver damage was calculated to be 0.0125 per 10,000 or 1 in 8,000,000.  Incorporating both risks, the cumulative risk of either acute death in first five years or premature death later in life was calculated to be 0.00131 per 10,000 or 1 in 7,642,000.

 

References:

[1] Centers for Disease Control and Prevention.  Notifiable Diseases/Deaths in Selected Cities Weekly Information.  MMWR2009; 56(53): 1-94.

[2] United States Census Bureau.  The 2010 Statistical Abstract; Table 78: Live Births, Deaths, Marriages and Divorces: 1960 to 2007.

[3] Centers for Disease Control and Prevention: Epidemiology and Prevention of Vaccine-Preventable Disease. Atkinson W, Wolfe S, Hamborsky J, McIntyre L. eds. 11th edition. Washington D.C.: Public Health Foundation, 2009.

[4] Centers for Disease Control and Prevention. Shapiro CN, McCaig LF, Gensheimer KF, Levy ME, Stoddard JJ, Kane MA, Hadler SC. Hepatitis B virus transmission between children in day care. Pediatr Infec Dis J. 1989 Dec; 8(12):870-5.

[5] Centers for Disease Control and Prevention. Surveillance for Acute Viral Hepatitis – United States, 2007. MMWR. May 22, 2009 / 58(S S03);1-27.  http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5803a1.htm

Disease Risk – Hepatitis A

 

Risk to a child from Hepatitis A if not vaccinated until after the age of 5:

Case Fatality Rate: Case fatality rates for Hepatitis A are generally quite low, are heavily weighted toward older adults, and vary widely with risk factors. [1][2] Previous reports have shown a case-fatality rate of only 0.01% to 0.03% [3] but an increased risk of death with age – up to 2% in adults [1].  Because the risk of death is higher in adults, for the purposes of this analysis the case fatality rate of 0.01% is used.

Complications: Although Hepatitis A can result in serious illness (with adults being at higher risk) permanent injury from Hepatitis A is rare enough that it is not generally listed.

Incremental Risk in Population with Low Rates of Vaccination (if a child does not vaccinate by age 5): Prior to the induction of the vaccine, the US average was 10 cases per 100,000 across all age groups.  The case fatality rate is the same as in the analysis for the High-vaccination population.  The estimated case fatality rate would be 0.0001.The 5-year cumulative risk of death for a child under 5 is 0.0005 per 10,000, or 1 in 20 million.

Incremental Risk in Highly Vaccinated Population (if a child does not vaccinate by age 5): Since the introduction of the vaccine, incidence rates have decreased from 10 cases per 100,000 to approximately 2.5 per 100,000 in the 2-18 year old age range [1].  If we assume that all cases are in unvaccinated population (59.6% unvaccinated [4]) the estimated case rate is 4.19 per 100,000.  Using the case fatality rate of 0.01% for ages 0-5, the case fatalities per year is estimated to be 0.00042 per 100,000 or 0.000042 per 10,000 per year. The 5-year cumulative risk of death for a child under 5 is 0.000209 per 10,000, or 1 in 48 million.

 

References:

[1] Centers for Disease Control and Prevention: Epidemiology and Prevention of Vaccine-Preventable Disease. Atkinson W, Wolfe S, Hamborsky J, McIntyre L. eds. 11th edition. Washington D.C.: Public Health Foundation, 2009.

[2] Serious Hepatitis A:  An Analysis of Patients Hospitalized during an Urban Epidemic in the United States.  Willner I, Uhl M, Howard S, Williams E, Riely C, Waters B.  Annals of internal medicine Volume 128, Number 2, 1998.

[3] Melnick JL.  History and epidemiology of hepatitis A virus.  J Infect Dis.  1995 171(Suppl 1);s2-s8

[4] CDC. National, State, and Local Area Vaccination Coverage Among Children Aged 19-35 Months—United States, 2008. MMWR 58(33);921-926.

Disease Risk – Diphtheria

 

Risk to a child from Diphtheria if not vaccinated until the age of 5

Diphtheria is an infectious disease caused by the bacterium Corynebacterium diphtheriae. It primarily affects the mucous membranes of the respiratory tract (respiratory diphtheria), although it may also affect the skin (cutaneous diphtheria) and lining tissues in the ear.  Prior to vaccination, diphtheria was endemic.  In historical times, classical naso-pharyngeal Diphtheria resulted in relatively high rates of mortality in young children although like most diseases morbidity and case fatality rates differed significantly between communities, likely reflecting differences in standards of living.[1]  The Diphtheria vaccine is toxoid-based and thus does not protect the individual from infection, but instead from the effects of the toxin produced by the bacteria.  Mass vaccination initiated in the 1940’s combined with improved living conditions has gradually resulted in only a handful of annual cases of diphtheria infection from North America.[2]  However, because vaccination does not confer immunity to the disease, the pathogen still exists and outbreaks can recur if living and health conditions decline sufficiently as witnessed in the former Russian republics in the 1990’s.

Case Fatality Rates: The case fatality rates largely vary depending on the age of the patient and the type of diphtheria infection.  Dixon observed that case fatality rates have remained relatively constant over time but that local variations between locations could be quite drastic[1].  The CDC lists case fatality rates of up to 20% in persons younger than 5 and older than 40.  Using data from the recent outbreaks in Russia, the highest case fatality rate was 13% for unvaccinated children < 18 years while the rate for fully vaccinated children was 0.5%.[3]  This analysis will use a rate of 13%.

Rates of Long Term Sequelae or Injury: Although there are several complications that can occur from Diphtheria infection, there is little documentation regarding long term sequelae.  This analysis will use a long term sequelae rate of 0.

Incremental Risk in Highly Vaccinated Population (if a child does not vaccinate by age 5): In the past five years there has not been a single reported case of diphtheria within the United States[1].  Diphtheria is no longer circulating within the United States and so the risk posed to an individual child electing not to receive the diphtheria vaccine is zero provided that herd immunity, adequately clean water supply and basic sanitation are maintained.

Incremental Risk in Population with Low Rates of Vaccination (if a child does not vaccinate by age 5): The most recent outbreak of Diphtheria in modern times occurred in the former Russian republics during the 1990s.  In populations with low rates of vaccination, diphtheria outbreaks occur in waves so this analysis uses the incidence rates over the peak 5 years ending in 1996.[4]  The 5 year incidence rates per 100,000 population used are:  1.93, 6.55, 16.04, 16.98 and 6.81 (ending in 1996).  The cumulative risk of death over the 5 years is calculated to be 6 per 100,000 or 1 in 15,925.

References:

[1] Dixon, JMS.  Diphtheria in North America.  J Hyg. Camb (1984), 93, 419-432

[2] Centers for Disease Control and Prevention: Epidemiology and Prevention of Vaccine-Preventable Disease. Atkinson W, Wolfe S, Hamborsky J, McIntyre L. eds. 11th edition. Washington D.C.: Public Health Foundation, 2009.

[3]  Vitek CR, Brisgalov SP, Bragina VY, Zhilyakov AM, Bisgard KM, Brennan M, Kravtsova ON, Lushniak BD, Lyerla R, Markina SS, Strebel PM.  Epidemiology of epidemic diphtheria in three regions, Russia, 1994-1996.  Eur J Epidemiol. 1999 Jan;15(1):75-83.

[4]  Vitek CR, Wharton M.  Diphtheria in the former Soviet Union: reemergence of a pandemic disease.  Emerg Infect Dis. 1998 Oct-Dec;4(4):539-50.

 

Disease Risk Analysis

This disease risk analysis calculates the incremental risk of permanent injury or death from vaccine-preventable diseases if a parent theoretically decided to delay a child’s vaccines until age 5. To make a full comparison of disease risks for that child, the incremental risk is calculated for two cases:  1) a high-vaccinated population in which most other children are vaccinated such that herd immunity provides some protection for the unvaccinated, and 2) a low-vaccinated population in which enough children are unvaccinated that there is no herd immunity and thus a greater risk of the disease (see SmartVax Discussion on Herd Immunity). To be able to perform the analysis, several assumptions were made as to how to calculate incremental risk (see Assumptions for Weigh The Risks Analysis).

Note: SmartVax does not promote a view that no child should be vaccinated.  The SmartVax disease risk analysis was performed for the purpose of demonstrating that if vaccines contribute to autism, then the current vaccine-injury risks could be numerically much higher than even the worse-case disease risks.  This finding highlights the need for comprehensive, unbiased research into how vaccines could contribute to autism.

This “Disease Risks in Low-Vaccinated Population Compared to Autism Risk” table demonstrates that the risk of autism is much higher than the incremental risk of injury or death from diseases if a child is not vaccinated until age 5 in a low-vaccinated population:

low-vax-disease-risk-versus-autism

This “Disease Risks in a High-Vaccinated Population” table includes the analysis of incremental disease risk in a highly-vaccinated population, in which there is some protection benefit from herd immunity.

high-vax-disease-risk

Links to the Disease Risk analysis for these vaccine-preventable diseases:

Disease Risk – Hepatitis B Disease Risk – Pertussis Disease Risk – Hepatitis A
Disease Risk – Polio Disease Risk – Hib Disease Risk – Measles
Disease Risk – Rotavirus Disease Risk – Pneumococcal disease Disease Risk – Mumps
Disease Risk – Diphtheria Disease Risk – Influenza Disease Risk – Rubella
Disease Risk – Tetanus Disease Risk – Varicella

Vaccine-Induced Deaths

 

A May 2011 published study by Neil Z Miller and Gary S Goldman (Infant mortality rates regressed against number of vaccine doses routinely given) found that nations that require more vaccine doses tend to have higher infant mortality rates as demonstrated in this diagram:

Infant Mortality Rate and number of vaccine doses

The Miller/Goldman study discusses the origination of the SIDS diagnosis shortly after an increase in infant vaccines in the 1960’s, and how the supposed decrease in SIDS deaths in the 1990’s was actually due to infant deaths being re-classified as other Sudden Unexpected Infant Deaths. The study describes the plausibility of vaccine-induced SIDS; however, the research is not sufficient to quantify an incremental risk of SIDS from vaccines.

In October 2010, the BBC aired a documentary called “The Vaccine Detectives” about the scientific research by Dr. Peter Aaby in Guinea-Bissau.  Dr. Aaby’s research shows that the DTP vaccine (diphtherisa-tetanus-pertussis) significantly increases the mortality risk in infants in Guinea-Bissau.  Aaby’s research also found a gender-specific difference in vaccine-injury risk, finding a significantly increased mortality risk to girls of combining the DTP and measles vaccines.  Dr. Aaby’s work indicates that much of the conventional wisdom on vaccination could be wrong, and could lead to a significant overhaul of vaccination strategies (for more, see this article by Dr. Mercola summarizing the documentary or view Part One and Part Two of the documentary at BBC: The Vaccine Detectives). Research is not available to determine how or whether this quantitative increased mortality risk from vaccination in developing countries could be applied to determine an increased risk of vaccine-induced deaths in the United States.

Because insufficient research has been performed on vaccine-induced deaths in the United States, this Weigh The Risks analysis does not calculate an increased risk of vaccine-induced death to children under age 5.  Instead, information is provided below to discuss the plausibility of a quantitative increased risk of vaccine-induced death.

SIDS (Sudden Infant Death Syndrome) is the designation given to infant deaths of unknown cause.  SIDS is believed to be related to an inability to breathe properly enough to maintain life.  Data shows a decrease in SIDS deaths based on advice to have children sleep on their backs rather than on their front.  Data shows increased risk of SIDS if infant sleeps in the bed with the mother, presumably because there is a higher chance of breathing being obstructed by sheets or the mother’s body.  Recent research suggests that fans operating in the infant’s room to circulate the air can also decrease the risk of SIDS.

A search on the Internet will find numerous anecdotal stories from parents who believe that their child’s death was caused by vaccines but was categorized as a SIDS death.  Because the current vaccination paradigm does not incorporate the possibility of vaccine-induced death, the current practice does not allow an infant’s death to be defined as a vaccine-induced death and instead dictates that the death be labeled as a SIDS death.  Further, procedures do not call for autopsies to be performed after SIDS deaths for the purposes of looking for evidence that the death was vaccine-induced.  So as to the argument that there isn’t direct evidence that vaccines cause SIDS death, technically the answer is correct – but it is because procedurally the collection of such evidence is systematically avoided.

The CDC does maintain a reporting system called VAERS (Vaccine Adverse Event Reporting System), a voluntary system for doctors to report anecdotal stories from parents about adverse vaccine reactions including injuries and deaths.  However, VAERS is not a reliable source for direct scientific evidence.  A report of an infant death the night after vaccines were administered does not necessarily mean that the death was caused by vaccines.  Further, VAERS is plagued by inconsistent reporting by different doctors (it is a voluntary system) and by systemic under-reporting of adverse events overall.  The CDC themselves estimated that less than 1/10th of adverse events are reported to VAERS, and caution against the use of VAERS as direct scientific evidence of causality.

Epidemiological studies (indirect studies) on a vaccine-SIDS link have assumed that if a vaccine were to cause a SIDS death, then the death would occur within a very short window after vaccine administration.  The time window in the studies has typically been either 1 week or 3 weeks after vaccine administration.  Generally, these studies have not found an association between vaccines and SIDS.  These studies are complicated by the fact that infants are typically receiving more vaccines every 1-2 months through the first 6 months of life.  There have been no epidemiological studies that compare SIDS rates in a vaccinated group versus an unvaccinated group of children.

But vaccine-induced death is plausible.  The Manitoba asthma study showed that vaccine-induced chronic asthma didn’t become clinically apparent until months or years later, and that much of these cases could be avoided simply by delaying the Diptheria-Pertussis-Tetanus vaccine series from 2/4/6 months to 5/7/9 months.  Based on this study, it is plausible to hypothesize that:

  • For children who are clinically diagnosed with asthma months or years later, there may be a sub-clinical reduction in breathing capability (e.g. preliminary chronic asthma)that begins several weeks or months after vaccines are administered
  • For a subset of children with genetic susceptibility, vaccine-induced asthma may exhibit itself as an acute asthma attack several weeks or months after the vaccines are administered.
  • In either of the above cases, the asthma might combine with other factors to contribute to a SIDS death (i.e. vaccines might increase the risk of SIDS).

But plausibility does not equal causality, and the absence of an epidemiological study of SIDS rates in vaccinated vs. unvaccinated children does not mean that such a study would necessarily find that SIDS occurs more frequently in vaccinated children.  Thus for the purposes of this Weigh The Risks analysis, vaccine-induced deaths is not quantified.

It is worth noting also that there is scientific evidence that children with autism have a higher premature death rate.  If vaccines are scientifically proven to cause some cases of autism, then a calculation could then be performed to determine a long-term death rate from vaccine-induced autism.

Vaccine-Induced Allergies

A study published in the journal Pediatrics in June 2011 found that 8.0% of American children have food allergies, with 38.7% of those children (or 3.1% of all children) having a history of severe reactions.  Historically, the words “allergy” and “anaphylaxis” were coined to describe vaccine-injuries (see The words “allergy” and “anaphylaxis” were invented to describe vaccine-injuries).
RISK OF VACCINE INDUCED ALLERGIES
Every vaccination will produce allergy antibodies.  And the more potent a vaccine with aluminum or toxoid additives (adjuvants), the greater the risk for allergy and life threatening anaphylaxis to any of the injected ingredients. This is a medically recognized risk of vaccination.[1]  This risk of anaphylaxis and allergy has become a reality for a rising number of children over the last 20 years as vaccines have increased in number and potency.

Allergic sensitization occurs when a protein(s) that is ingested, inhaled or injected, manages to evade enzymatic modification or detoxification and gain access to the bloodstream.  If it persists in the blood, the protein is deemed a threat and the body sets up a defense that includes antibodies such as IgE (immunoglobulin epsilon) – on subsequent exposure to the protein this antibody triggers the release of histamine. Histamine causes inflammation and the contraction of smooth muscle.  Symptoms include hives, constricted airways, vomiting, diarrhea, a drop in blood pressure and even death.

Anaphylaxis following vaccination with the conjugate vaccine Hib B, for example, has increased in recent years complicating routine immunization.[2] [3]  But a potentially more profound and yet little discussed allergic concern is the use of foods in pediatric injections (vaccines, Vitamin K1, etc.) and their role in the creation of food allergies.

 

FOOD ALLERGIES

See also:  Peanut allergies

Pediatric injections have historically contained food proteins including those from beef, egg, pork, fish, dairy, legumes such as soybean and castor bean, and more. Mice injected with pertussis and egg protein resulted in egg allergy.[4]  Could this happen to humans?

Starting in 1994 and continuing through the 1990s, an outbreak of gelatin allergy in Japanese and American children was identified as having been caused by pediatric vaccination.  In that year, changes to the vaccination schedule in Japan meant that: the DTP was replaced by an acellular version containing gelatin; the age at which it was administered to children was dropped from 2 years to 3 months; and this new vaccine was given before the live virus MMR vaccine that also contained gelatin. When children began reacting with anaphylaxis to the MMR vaccine as well as gelatin containing foods (yoghurt, jello, etc.) doctors investigated. Finally, they concluded that the aluminum adjuvant in the DTaP had helped sensitize children to the “minute amounts” of “poorly hydrolyzed” beef and pork gelatin in the vaccine.[5]  Removal of gelatin from the DTaP vaccines was “an ultimate solution for vaccine-related gelatin allergy”[6] Subsequently, new cases of anaphylaxis following the MMR vaccine in Japanese children decreased.

A similar association was found in the US.[7]  Gelatin continues to be used in other vaccines.

Given the recognized history of vaccine induced allergy in children, has vaccination also precipitated the current increase of peanut allergy in children?  Since 1997 prevalence of this life threatening allergy has increased from .4% of children under 18 to an estimated 1.4% in 2008.

PEANUT ALLERGY  

Peanut allergy was first documented in several post-WWII studies of adults and children injected with the new ‘wonder drug’ penicillin.  At this time, a challenge existed in that a dose of penicillin would last just a few hours.  To prolong the action of this drug, army doctor Cpt. Monroe Romansky mixed it with what was available during wartime — peanut oil and beeswax.  It was a simple solution — the body would metabolize the oil and slowly release the drug into the bloodstream. Unfortunately, Romansky’s formula also sensitized a handful of children and adults to peanuts.[8] To reduce this side effect, the peanut oil was refined to remove as much sensitizing protein as possible.  And yet, according to the FDA most “highly refined” peanut oil contains trace intact proteins 0.014 to 16.7 µg protein/ml oil.[9]  Regardless, with its relative safety in penicillin, peanut oil was adopted into common use within the pharmaceutical industry.

In 1964, Merck announced that it had patented a revolutionary peanut oil vaccine adjuvant.  This news was reported in 1964 and 1966 in The New York Times[10] with follow up in medical literature through the early 70s. Merck’s Adjuvant 65-4 provoked such high levels of antibodies – 64 times higher than the same vaccine in an aqueous solution — that any vaccine to which it was added could produce many years worth of immunity. Was this potency safe?  A 1973 WHO report co-written by Adjuvant 65-4 inventor Maurice Hilleman found the use of peanut oil was relatively safe if properly injected to avoid “severe adverse reactions”.[11] But the safety of the adjuvant was challenged by others including D. Hobson in the Postgraduate Medical Journal (March, 1973).  Hobson documented the power of this adjuvant to sensitize recipients to vaccine proteins. This adjuvant created allergies.

Peanut allergy in children and adults grew slowly until the late 1980’s when its prevalence began to accelerate in children in certain westernized countries such as the US, Canada, the UK, and Australia.  This rise is documented by ER records, two cohort studies from the Isle of Wight and eye-witness accounts. In the early 1990s, teachers in the affected countries were taken aback by a sudden surge of food allergic kindergarten children.

The rise in life-threatening food anaphylaxis in children coincided with significant changes to the pediatric injection and vaccination schedules of the affected countries: injection of the Vitamin K1 prophylaxis (containing legume oil) became routine in the mid-1980s; the novel conjugate vaccine Hib B that was soon rolled into an unprecedented 5 vaccines in one needle and delivered to babies without benefit of long term study.  The injected adjuvants and toxoids and food proteins designed to provoke the immune system also increased the risk of provoking allergy.  Allergy is an evolved defense against acute toxicity.

There are precedents recent and historical (see  The Words Allergy and Anaphylaxis were Invented to Describe Vaccine-Injuries) for the causal link between vaccines and mass allergy.

ALLERGY & ANAPHYLAXIS WERE INVENTED TO DESCRIBE VACCINE-INJURIES

The terms “allergy” and “anaphylaxis” were created following a strange illness that affected up to 50% of vaccinated children at the close of the 1800s.  This illness was simply called “serum sickness” and followed the first mass administration of diphtheria anti-toxin sera.  Austrian pediatrician Clemens von Pirquet studied the illness at length and observed that the symptoms of this sickness resembled those in people who were hypersensitive to pollens and bee stings.  To better describe this ‘altered reactivity’ to the sera he created the Latin derived word allergy in 1906.

In 1901, another doctor Charles Richet had stumbled on the same phenomenon during attempts to vaccinate dogs to a jellyfish poison.  He began by injecting dogs with trace amounts of the poison to create a level of tolerance to it.  However, when he injected the animals a second time, he provoked a violent reaction that quickly killed the dogs.  For this reaction he used a Latin term ana-phylaxis or anti-protection, because the outcome was the opposite of the protection that the vaccine was supposed to provide.

Richet experimented further.  He quickly discovered that any protein including those from foods injected into the bloodstream results in sensitization and anaphylaxis on subsequent exposure to the food. Richet injected minute quantities of milk and meat proteins into cats, rabbits and horses and showed that anaphylaxis is a universal immune system defense.

Prior to the advent of vaccination, mass allergy such as serum sickness was unknown.  At the dawn of the 20th century, doctors identified the problem of allergy as an outcome of mass vaccination – on which government relied.  The dilemma of serum-induced allergy was summarized by allergist Warren Vaughan in 1941:

“Serum disease, as this is called, is a man-made malady.  If we had no curative serums and if there were no such thing as a hypodermic syringe with which to introduce the material under the skin, there would be no serum disease.  Instead multitudes would still be dying from diphtheria and lockjaw … Thus, we find ourselves in somewhat of a dilemma, faced with the necessity for choosing the lesser of two potential evils.”    Warren Vaughan, Strange Malady (1941)

As vaccine ingredients became better refined to reduce the sensitizing proteins, prevalence of serum sickness decreased.  With the 20th century expansion of vaccination programs and schedules to include food proteins and adjuvants, however, other unforeseen problems arose to take its place.  One of these was a rise in food allergy.

 

 


 

[1] D. O’Hagan (ed.), “Induction of Allergy to Food Proteins,” and “Real and Theoretical Risks of Vaccine Adjuvants,” Vaccine Adjuvants (NJ, Humana Press, 2000) 10 & 32.

[2] M.R. Nelson, et al., “Anaphylaxis complicating routine childhood immunization: haemophilus influenza b conjugated vaccine,” Pediatric Asthma, Allergy & Immunology, 14, 4 (Dec. 2000): 315-321.

[3] M. Flora Martin-Munoz, “Anaphylactic reaction to diphtheria-tetanus vaccine in a chid: specific IgE IgG determinations and cross-reactivity studies,” Vaccine, 20, 27-38 (Sept. 2002): 3409-3412.

[4] U. Kosecka, et al. “Pertussis adjuvant prolongs intestinal hypersensitivity, “ International Archives of Allergy & Immunology, 119, 3 (July, 1999): 205-11.

[5] Nakayama T, Aizawa C, Kuno-Sakai H. “A clinical analysis of gelatin allergy and determination of its causal relationship to the previous administration of gelatin-containing acellular pertussis vaccine combined with diphtheria and tetanus toxoids,” Journal of Allergy & Clinical Immunolology (Feb., 1999): 321-5.

[6] H. Kuno-Sakai, M. Kimura, “Removal of gelatin from live vaccines and DTaP – an ultimate solution for vaccine-related gelatin allergy,” Biologicals, 31 (2003): 245-249.

[7] V. Pool, et al. “Prevalence of anti-gelatin IgE antibodies in people with anaphylaxis after measles-mumps-rubella vaccine in the United States,” Pediatrics, 110, 6 (Dec. 2002): e71.

[8] G. Hildick-Smith, et al., “Penicillin Regiments in Pediatric Practice: Study of Blood Levels,” Pediatrics (Jan. 1950): 97-113.

[9] Threshold Working Group, Approaches to Establish Thresholds for Major Food Allergens and for Gluten in Food. III, IV, V, (FDA , March, 2006)

[10] Stacy V. Jones, “Peanut oil used in new vaccine; product patented for Merck said to extend immunity,” The New York Times, Business Financial Section (Sept. 19, 1964) 31.

Anon, “Peanut Oil Additive is Found to Improve Flu Shot’s Potency,” The New York Times (Nov. 11, 1966).

[11] M.R. Hilleman, et al., “Imunological Adjuvants Report of a WHO Scientific Group”, World Health Organization Technical Report Series, No. 5959 (Geneva, WHO, 1976) 11.