Natural immunity is virtually ALWAYS superior both in strength and duration to vaccine immunity. (I use the term virtually because there are always rare instances when natural immunity fails or wanes or when vaccine immunity doesn’t, but overall, it is no contest)
One of my primary objections to universal vaccination for typically benign childhood illnesses; the denial of natural immunity and the epidemiological shifts which often (usually) occur, placing the most vulnerable populations at risk.
Here is some of the info I have compiled on this subject. Not all, but probably ENOUGH, lol! Gotta get to bed.
First, I want to do Pertussis, since the immunological pathways on this one are unclear, and the claim is often made that the natural infection confers only fleeting immunity, same as the vaccine, notoriously, does.
IMO, this is an unsupportable hypothesis, based on the recent/current epidemiology observed and the evidence from clinical and case studies.
“Despite extensive research, no serologic correlates of immunity have been identified for pertussis.”http://gsbs.utmb.edu/microbook/ch031.htm
“Infection induces substantial immunity, although the protective antigens have not been identified conclusively. …
A case of whooping cough confers substantial immunity, which usually lasts for many years..”http://www.aafp.org/afp/970915ap/pertussis.html
“Immunity following natural infection is complete and lifelong.8 (Bass JW. Pertussis: current status of prevention and treatment. Pediatr Infect Dis 1985;4:614-9.) …..Children who have a history of pertussis, either culture-positive disease or typical symptoms with an epidemiologic link to a culture-proved case, do not need additional pertussis vaccination.26 (Centers for Disease Control and Prevention. Update: Vaccine side effects, adverse reactions, contraindications, and precautions-recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 1996; 45(RR-12):22-31. )”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“During 1988 and 1989 the prevalence of serum IgG antibodies to pertussis toxin in a sample of 3,875 unvaccinated, apparently healthy persons between the ages of 1 year to 19 years was estimated by enzyme-linked immunosorbent assay…The overall prevalence of IgG antibodies was 80.8%, with a steady increase from 33.5% among 1- to 3-year-old children to 95% among 17- to 19-year-old individuals. The prevalence of natural immunity was 50% and 75% at the ages of 4 and 6 years, respectively..20.8% of children had antibodies to pertussis toxin even though they had no history of whooping cough.”http://www.clinipath.net/~subinews/page20.html
“In the prevaccine era, whooping cough occurred mainly in the 1-5 year age group. Use of the vaccine has shifted the peak incidence to early adolescence, but with the majority of cases spread across the adult age group. Lack of natural immunity and diminished vaccine immunity in adults means less infants < 1 year acquire maternal immunity, making them more prone to infection at an age when the mortality is highest. ..IgA found only after natural infection, not vaccination.”http://www.chestjournal.org/cgi/content/full/115/5/1254
“Investigations of outbreaks have documented that adults develop infection with B pertussis and transmit the organism to susceptible children or other adults. Thus, previously immunized adults and adolescents are the main sources of transmission of B pertussis…
The period of immunity induced by the pertussis vaccine tends to wane within 5 to 10 years and is shorter than that induced by the disease itself.. Furthermore, in vaccinated populations, adults maintain the ability to transmit B pertussis and are now the primary source of infection to susceptible children who may develop severe disease..”http://www.aafp.org/afp/970915ap/pertussis.html
“Vaccination provides protection against both colonization and disease for only two to three years. Protection then declines steadily until, 10 to 12 years after vaccination, patients have little or no immunity against the infection.
Thus, adolescents and adults, despite complete childhood vaccination, are susceptible to infection and can spread the disease to infants and young children. ..”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“Several changes in the epidemiology have occurred in the most recent six-year period. The incidence of whooping cough in children has decreased by at least 50%, but the proportion of cases occurring in infants younger than 12 weeks of age has doubled to 30% of all cases. Formerly most young infants acquired their illness from siblings or other children, but in the recent period adults in the household were the most common source of infection to neonates and young infants.”http://www.hc-sc.gc.ca/pphb-dgspsp/p...29s3_1e.html#1
“There is good evidence that vaccine efficacy decreases with time, possibly from 100% at 1 year down to 46% at 7 years(5). This is why there was a trend toward increased pertussis incidence among older children, adolescents, and adults in the 1990s. In Finland, the whole cell pertussis vaccine has been available since 1952 and is given at 3, 4, 5, and 24 months, with about 98% coverage. In the 1990s there was a 5-fold increase in the incidence of pertussis among infants, who get the disease mainly from adolescents and adults. In 1999, 29% of laboratory confirmed cases in Finland were aged 20 years or older. ..
(in the US)
From the early 1990s there has been an increase in the number of reported pertussis cases, ranging from < 5,000 cases per year in 1990 to 7,867 cases in 2000, and yet rates of immunization – vaccine given at 2, 4, 6, 15 to 18 months and 4 to 5 years – have remained high, in the 90%+ range for at least three doses of either acellular or whole cell vaccine. As well, the number of deaths (which occur predominantly in infants) has been increasing since the late 1990s. ..”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“Pertussis or whooping cough is an acute infection of the respiratory tract caused by Bordetella pertussis. Despite wide-scale vaccination in many countries, this disease is reemerging throughout the world in both adults and children. Emergence has been explained by many factors: wane of vaccine and natural immunity, increase of asymptomatic carriers, and/or natural selection of non-vaccine strains.”http://www.who.int/vaccines/en/pertussis.shtml
“..following previous infection, occasional exposure to B. pertussis strains circulating in the community may be required to sustain high-level immunity. “http://www.cdc.gov/ncidod/eid/vol6no5/srugo.htm
“We demonstrated B. pertussis infection in fully vaccinated children ages 2-3 years and 5-6 years who had contact with an infected child. We investigated whether younger or recently vaccinated children may be protected from classical clinical illness but remain susceptible to infection and become asymptomatic carriers. ..Conclusions; The effects of whole-cell pertussis vaccine wane after 5 to 10 years, and infection in a vaccinated person causes nonspecific symptoms (3-7). Vaccinated adolescents and adults may serve as reservoirs for silent infection and become potential transmitters to unprotected infants (3-11). The whole-cell vaccine for pertussis is protective only against clinical disease, not against infection (15-17). Therefore, even young, recently vaccinated children may serve as reservoirs and potential transmitters of infection…. Our results indicate that children ages 5-6 years and possibly younger, ages 2-3 years, play a role as silent reservoirs in the transmission of pertussis in the community”http://www.rnzcgp.org.nz/NZFP/Issues.../or_cullen.htm
“We have assumed that the immunity gained when infection precedes vaccination is lifelong, while that gained when infection follows the loss of vaccine-induced immunity lasts only as long as the original vaccine-induced immunity. This assumption is certainly defensible given the observed increase in adult pertussis in vaccinated communities, but it is not universally accepted.”
“A nationally representative cross-sectional health examination survey that included venipuncture was conducted among 21,288 U.S. participants aged 6 years and older from 1988 through 1994. Serologic evidence of varicella-zoster virus infection was measured by enzyme immunoassay of varicella-zoster virus-specific IgG antibody. The seroprevalence of IgG antibody to varicella-zoster virus increased from 86.0% in children aged 6 through 11 years to 99.6% in adults aged 40 through 49 years. Immunity to varicella remained at 99% or higher in Americans aged 50 years and older. …Future varicella serosurveys in Americans will provide essential information to interpret the population impact of varicella vaccine. “http://en.wikipedia.org/wiki/Chicken_pox
“Once someone has been infected with the disease, they usually develop protective immunity for life, and cannot get it again. As the disease is more severe if contracted by an adult, parents have been known to ensure their children become infected before adulthood….The long-term duration of protection from varicella vaccine is unknown, but there are now persons vaccinated more than thirty years ago with no evidence of waning immunity, while others have become vulnerable in as few as 6 years. Assessments of duration of immunity are complicated in an environment where natural disease is still common, which typically leads to an overestimation of effectiveness, and we are only now entering an era in the US where the long-term efficacy of varicella vaccine can be accurately gauged…Catching chickenpox as a child through conventional means tends to result in lifelong immunity, and exposure of adults to children so infected protects adults from other varicella-related diseases, like shingles . Second episodes of chickenpox are rare, but do occur, in both vaccine and naturally acquired immunity, but far more often from the vaccine; in one study, 30% of children had lost the antibody after five years, and 8% had already caught "wild" chickenpox in that five year period…Yet another issue under direct investigation from the CDC is the possibility that the vaccine has a high failure rate from the outset. Large outbreaks of chickenpox have occurred at schools which required their children to be vaccinated”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“it is unknown how universal immunization will influence the epidemiology of varicella infections. The duration of immunity, both conferred and passive reinoculation, remains a concern and must continue to be evaluated in the population of vaccinees”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“It is concluded that OKA/Merck varicella-zoster vaccination leads to antibody persistence for 2 years ..”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“…immunity of at least two years' duration is conferred upon the vaccinated subjects.”.http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“At a mean of 5 years after vaccination, 93% of children and 94% of adults had IgG antibodies to VZV as determined by ELISA. VZV antibody concentrations were significantly higher at 5 years than at 1 year after immunization in children and adults. Cell-mediated immunity to VZV was detected in 87% of children and 94% of adults at 5 years. “http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“Varivax has been found to be 95% to 100% effective in conferring immunity for at least 10 years”http://www.merckfrosst.ca/e/health/v...npox/home.html
How long will VARIVAX® III protect patients for?
The length of protection with VARIVAX® III is unknown at the present time and the need and timing for a booster dose is currently under evaluation.
However, according to the National Advisory Committee on Immunization (NACI), “In actual use, it is estimated that the vaccine will offer 70% to 90% protection against varicella of any severity and 95% protection against severe varicella for at least 7 to 10 years after vaccination…”.http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“In order to know the rate of occurrence of varicella among vaccinees (breakthrough varicella: BV), questionnaire postcards were sent to 593 healthy children who had received varicella vaccine (Oka strain) from March 1987 to December 1989. The questionnaire survey was repeated once a year until January 1996. The annual attack rate from the 1st to 3rd questionnaire was approximately 12%: however, from the 5th to 8th one it was 1-4%. To February 1996, the cumulative attack rate was 157/459 (34.2%). This rate was comparable to that among vaccinees who had confirmed seroconversion; namely, 51/132 (38.6%). These rates are much higher than those reported by other authors. All BV cases were clinically mild; even subjects who had received the vaccine 7 years prior to the disease showed mild symptoms. The high incidence may be partly explained by the regional epidemiology of varicella. The decrease in annual incidence with time after vaccination may be due to the following reasons: some vaccinees remained free from BV owing to reinforcement of their immunity from subclinical infection of varicella-zoster virus (VZV) and others from diminution of opportunity for exposure to VZV with increasing age. Varicella vaccine seems to be effective in modifying the symptoms of varicella, but not potent enough in protecting from VZV infection.”http://www.ncbi.nlm......&dopt=Abstr..._uids=15243919
Since licensure in the United States, studies have shown that varicella vaccine's overall effectiveness ranges from 44% to 100%, with substantial protection against moderate and severe varicella; however, breakthrough illness has been documented in up to 56% of vaccinated individualshttp://www.ncbi.nlm......&dopt=Abstr..._uids=15138400
a period of > or =4 years since vaccination was a risk factor for breakthrough diseasehttp://www.ncbi.nlm......&dopt=Abstr..._uids=14993534
CONCLUSIONS: A chickenpox outbreak occurred in a school in which 97% of students without a prior history of chickenpox were vaccinated. Students vaccinated >5 years before the outbreak were at risk for breakthrough disease. Booster vaccination may deserve additional consideration.http://www.ncbi.nlm......&dopt=Abstr..._uids=14970064
CONCLUSIONS: Although varicella vaccine is effective, its effectiveness decreases significantly after 1 year, although most cases of breakthrough disease are mild. If administered at younger than 15 months, the vaccine's effectiveness was lower in the first year after vaccination, but the difference in effectiveness was not statistically significant for subsequent years.http://www.ncbi.nlm......&dopt=Abstr..._uids=12477940
The index case occurred in a healthy child who had been vaccinated three years previously and who infected more than 50 percent of his classmates who had no history of varicella. The effectiveness of the vaccine was 44.0 percent (95 percent confidence interval, 6.9 to 66.3 percent) against disease of any severity and 86.0 percent (95 percent confidence interval, 38.7 to 96.8 percent) against moderate or severe disease. Children who had been vaccinated three years or more before the outbreak were at greater risk for vaccine failure than those who had been vaccinated more recentlyhttp://www.cmaj.ca/cgi/content/full/168/5/589
Other factors related to primary failure of the varicella vaccine are a history of asthma, lower age at vaccination, and simultaneous or closely spaced varicella and MMR vaccine administration,2 although none of these was a risk factor in the New Hampshire outbreak. Higher doses of vaccine may provide better protection.7 Secondary failure is due to waning immunity with the passage of time.http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“Widespread use of the varicella vaccine in the United States has led to important changes in the epidemiology of the infection..Data from the United States Centers for Disease Control and Prevention have shown a dramatic decline in the incidence of varicella (76 to 87% from 1995 to 2000), with the greatest decline observed in preschool children, as well as a reduction in the number of hospitalizations for cases of varicella. However, as the proportion of children in the United States who have received the varicella vaccine has increased there have been several recent reports in which the effectiveness of the vaccine was substantially lower than expected. In particular, reports during outbreaks of varicella in children have noted increases in breakthrough disease in children who were vaccinated before the age of 15 months, in children with asthma, in those who received the varicella vaccine soon after the measles, mumps, and rubella vaccine (<28 days), and in children who received the vaccine more than 3 years before the development of disease.”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“In all scenarios the model pointed out an initial decrease of case frequency observed in the first 3-5 years, followed by a series of epidemic peaks, variable in number and size by vaccination strategy. Moreover, as the number of cases among infants decreases, the number of cases among adults increases. Such event is minimised only by very high vaccination coverage (80% in the first year of life and 50% at 12 years of age).”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“Vaccination of adolescents and adults will protect at-risk individuals, but will not have a significant impact on the epidemiology of the disease on a population basis. On the other hand, extensive use as a routine vaccine in children will have a significant impact on the epidemiology of the disease. If sustained high coverage can be achieved, the disease may virtually disappear. If only partial coverage can be obtained, the epidemiology may shift, leading to an increase in the number of cases in older children and adults. “http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“A nationally representative cross-sectional health examination survey that included venipuncture was conducted among 21,288 U.S. participants aged 6 years and older from 1988 through 1994. Serologic evidence of varicella-zoster virus infection was measured by enzyme immunoassay of varicella-zoster virus-specific IgG antibody. The seroprevalence of IgG antibody to varicella-zoster virus increased from 86.0% in children aged 6 through 11 years to 99.6% in adults aged 40 through 49 years. Immunity to varicella remained at 99% or higher in Americans aged 50 years and older. …Future varicella serosurveys in Americans will provide essential information to interpret the population impact of varicella vaccine. “
“In 1995, varicella vaccination was introduced into the infant immunization schedule of the United States. Currently, many other countries are considering mass varicella vaccination. Mass vaccination has two dangers: it could increase the number of varicella cases in adults, where severity is greater, and increase cases of zoster. A deterministic, realistic, age-structured model (RAS) was built to study these concerns…The model predicts that, although an upward shift in the age at infection occurs, the overall morbidity due to varicella is likely to decrease following mass infant vaccination. On the other hand, cases of zoster may significantly increase in the first 50 years following vaccination. The model predicts that, in a population similar to England and Wales (50 m people), varicella vaccination with 90% coverage would prevent 0.6 m inpatient days due to varicella but would generate an extra 1.1 m inpatient days due to zoster over the first 65 years. Thus, under base-case model assumptions, the gain in reduction of varicella morbidity from infant vaccination is offset in the short-term by the increases in zoster morbidity (using inpatient days as a proxy). Paradoxically, less effective vaccines or vaccine programmes can be more effective in reducing overall morbidity (varicella + zoster) by allowing the virus to circulate more, which produces a smaller shift in the age at infection and a smaller increase in zoster cases. Copyright 2003 Wiley-Liss, Inc.”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“recent evidence suggests that an increase in zoster incidence appears likely, and the more effective vaccination is at preventing varicella, the larger the increase in zoster incidence. Targeted vaccination of susceptible adolescents and/or the contacts of high-risk individuals can be effective at preventing disease in these individuals with minimal risk to the community. However, targeted strategies would not prevent most disease (including most severe disease), and will not lead to a long-term reduction in the incidence of zoster. “http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum
Aust N Z J Public Health. 2005 Dec;29(6):544-51.
Modelling the impact of vaccination on the epidemiology of varicella zoster virus in Australia.
“…Infant vaccination is predicted to reduce the incidence of varicella. However, zoster incidence is expected to increase initially, assuming exposure to varicella boosts immunity to zoster. Accumulated morbidity from both varicella and zoster is predicted to remain above that expected without vaccination for the first 70 years of an infant program (assuming 90% coverage with boosting for 20 years). However, after 70 years the net health savings from vaccination are predicted to increase substantially. CONCLUSIONS AND IMPLICATIONS: Infant vaccination is expected to be a successful long-term commitment to reducing morbidity associated with VZV infection in Australia.”(My Note:That’s right folks, after only 70 short years, universal CP vaccination is predicted to result in lower overall incidence of CP/shingles!!! (calculating in the increased incidence rate for shingles, which, BTW, carries 5 times the rate of death as CP, among the naturally immune who lose their immunity due to universal vaccination, of course, and assuming 90% coverage and boosting for 20 yrs, of course, big assumptions, btw. What a deal, huh?http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum
Int J Toxicol. 2005 Jul-Aug;24(4):205-13.
Medical Veritas International (MVI), Pearblossom, California 93553, USA. firstname.lastname@example.org
“The universal varicella program has proven effective in terms of reducing the number of reported verified varicella cases by 85%, from 2,934 in 1995 to 412 in 2002. Prior to this dramatic reduction, immunologic boosting due to exogenous exposures to wild-type varicella-zoster virus (VZV) in the community (1) caused mean serum anti-VZV levels among vaccines to increase with time after vaccination and (2) served as a mechanism that helped suppress the reactivation of herpes zoster (HZ), especially among individuals with a previous history of wild-type varicella.That immunologic boosting might play a significant role in both varicella and the closely related HZ epidemiology is evidenced by (1) a decline in vaccine efficacy by over 20%, from 95.7% (95% C.I., 82.7% to 98.9%) in 1999 to 73.9% (95% C.I., 57.9% to 83.8%) in 2001 and (2) an unexpectedly high cumulative (2000 to 2003) true incidence rate of 223 (95% C.I. 180-273) per 100,000 person-years (p-y) among children <10 years old with a previous history of varicella. Because capture-recapture methods demonstrate a likely lower bound of 50% underreporting, the actual rate is likely double or 446 per 100,000 p-y, approaching the HZ rate reported among older adults. Other recent studies based on VASP data have mitigated against discovery of the above trends that challenge several initial assumptions inherent to the universal varicella program, namely, (1) a single dose confers long-term immunity and (2) there is no immunologically mediated link between varicella and HZ incidence. As vaccinated children replace those with a prior history of wild-type varicella in the <10 age group, increasing HZ incidence among this cohort will be of less concern in the near future. However, previous scientific studies, including the present preliminary results from active surveillance indicate that HZ may be increasing among adults. It may be difficult to design booster interventions that are cost-effective and meet or exceed the level of protection provided by immunologic boosting that existed naturally in the community in the prelicensure era.”
(My note: the CDC KNEW or strongly suspected the potential problems with CP vaccination before it recommended it for universal use. Read the following carefully and note all the UNKNOWNS they admit to. Seems a pretty damn reckless choice to push ahead given all the unknowns, all of which are being borne out currently. Don’t hold your breath for a contraction of the recommendation. Instead, we get a booster for kids/adults and a new shingles vax for older adults. SURPRISE!!! http://www.cdc.gov/mmwr/preview/mmwrhtml/00042990.htm
July 12, 1996
In Japan, antibodies to VZV were present in 97% of children 7-10 years after vaccination, and titers were comparable to those in children who had natural varicella infection 7-10 years earlier (85). A subsequent 20-year follow-up study revealed that antibody levels were higher than those observed 10 years earlier (86). These higher levels might have resulted from asymptomatic boosting of vaccine-induced immunity by exposure to wild-type VZV, because less than 20% of children in Japan were vaccinated during 1991-1993.
Current data concerning vaccine efficacy and persistence of antibody in vaccinees are based on research that has been conducted when natural VZV infection has been highly prevalent and has not been affected by wide use of the vaccine. Thus, the extent to which the protection provided by vaccination has been increased by boosting from exposure to natural virus and whether longer term immunity may wane as the circulation of natural VZV decreases are unknown. …
As the use of varicella virus vaccine increases, the epidemiologic features of the disease are expected to change. The circulation of wild-type VZV is not currently affected by the use of the vaccine. Under present conditions, antibody to varicella has been demonstrated to persist for 6-10 years following vaccination in children; however, the extent to which longer-term immunity may wane is unknown. The importance of immunologic boosting following exogenous reexposure to VZV to the long-term persistence of both humoral and cell-mediated immunity to varicella is unknown. The significance of the loss of natural boosting in relation to the incidence of herpes zoster in persons who were vaccinated or exposed to wild-type virus is also unknown. Increased antibody levels have been observed in vaccinees following exposure to natural varicella; however, opportunities for immunologic boosting will be greatly reduced with widespread use of the vaccine. Revaccination 4-6 years after initial vaccination also has resulted in a boost in antibody levels. In addition, the changes in epidemiology of varicella resulting from the widespread use of vaccine in younger children are expected to decrease the circulation of wild-type virus and may establish a population of older children who were neither vaccinated nor exposed to wild-type virus, eventually resulting in a population of adults who are susceptible to varicella. …
The need for any changes in vaccine use will be determined by both postmarketing surveillance (conducted by the manufacturer of the vaccine) and ongoing surveillance (conducted by CDC). Presently, only 4%-5% of expected cases of varicella are reported annually to NNDSS. “
“Measles causes serious morbidity in infants, with the highest risk among those who are 6 to 12 months of age. In the United States, measles vaccine has been given at age 12 to 15 months to minimize interference by passive antibodies and to achieve the high seroprevalence required for herd immunity. Infants of mothers with vaccine-induced immunity may lose passively acquired antibodies before 12 months, leaving them susceptible to measles infection.”http://pediatrics.aappublications.or...ract/104/5/e59
“Infants whose mothers were born after 1963 had a measles attack rate of 33%, compared with 12% for infants of older mothers…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.”http://www.personalmd.com/news/a1998081109.shtml
“Because such protective (maternal) antibodies have traditionally persisted through the first year of life, the recommended vaccination age in the US was set at 12 to 15 months.
However, most infants are now born to mothers who were immunized against measles rather than mothers who have antibodies due to infection with the measles virus themselves. Studies have shown that vaccine-induced antibodies are passed from mother to infant, but are lost earlier than disease-induced antibodies. Among the infants studied, only 52% of 6-month-old infants and 35% of 9-month-old infants had antibodies present before vaccination. No 12-month-old infants did.
"As a result, more infants younger than 12 months now lack... measles immunity, leaving them unprotected and in the highest-risk group for life-threatening complications," according to the report. “
SOURCE: The Journal of the American Medical Association 1998;280:527-532.http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
““After more than 20 years of measles immunisation in the developing world, the epidemiology of measles is radically changed, and the absence of measles epidemics might lead to waning immunity due to less clinical and subclinical infections boosting the antibody level. An increasing proportion of mothers are vaccinated, thus transferring a lower maternal antibody level to their infants who will be susceptible to measles at a younger age.”http://cdli.asm.org/cgi/content/full/6/6/868
”With an increasing proportion of women with vaccine-acquired immunity, a further shift to the left of the seroprevalence curve in the infant population is expected to occur. As predicted by Wilkins and Wehrle (37), by the time most infants are born to vaccinated mothers, vaccination recommendations must be adapted, because of the premature loss of maternally derived antibodies (4, 18, 21, 23). Studies that have been conducted in Africa (8), Israel (9), and Turkey (1) have shown that most infants of well-vaccinated populations become susceptible to clinical measles after 6 months of age. The consequences of a shift from long-lasting passive immunity in infancy to early loss of maternally derived vaccine-induced antibodies are evident from investigations of an epidemic of measles in the United States in 1992 which showed that 22.2% of all cases were in infants aged less than 1 year (5). “http://www.ncbi.nlm.nih.gov/entrez/q..._uids=10023894
“As measles vaccination coverage increases, the circulation of wild measles will decrease, and vaccine-induced antibody is less likely to be boosted. Thus, new epidemics, albeit milder in form, may occur in vaccinated areas which should be recognised in campaigns to eradicate measles.”
Reinfection with rubella may occur in as many as 80% of vaccinated subjects, but only in about 3% of those who have had a previous rubella infection (25). The risk of fetal infection after rubella reinfection in early pregnancy has been estimated to be less than 5% (26), which is comparable to the risk of any adverse outcome in a pregnancy.http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“The loss rates of rubella IgG during the follow-up periods were 14.3 and 15.8%, respectively. Among vaccinated groups, the loss rate was 18.8%, which was significantly higher than 13.8% of the mixture of natural and vaccine-induced immunity groups.
..Under this higher rubella antibody loss rate, in order to prevent congenital rubella syndrome, the immunization for women at childbearing age appears necessary until rubella can be eliminated or controlled”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“The immunity to rubella of 115 girls aged 10 to 14 years was tested in 1978. The proportion of girls found to be immune was 80%, similar to rates in the prevaccination era. Nearly half of the immunity was from documented vaccination, and the other half was presumably from infection with wild rubella virus. The vaccination failure rate was 12%. Because of declining immunity to rubella of women of child-bearing age, detecting low levels of immunity in these women is becoming increasingly important. Immunization of 12- to 15-month-old children has not been effective. Vaccinating all girls 10 to 12 years old would likely be the most effective method of preventing an increase in the incidence of congenital rubella syndrome in the next decade.”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
The main epidemiological values characterizing rubella in Moscow were calculated on the basis of a new mathematical model. Quantitative estimates of the intensity of infection in different age groups of the population were obtained. It has been established that the risk of infection in children is especially high in comparison with adult population. That is why 98% of the population aged 15 are immune. The probability of falling ill with rubella was determined for persons with different antibody levels. The cases of congenital rubella in Moscow are rare due to the low risk of infection in adults and to their immunity acquired in childhood. Consequently, there is no necessity for vaccination against rubella in Moscow at the present time, but it should be recommended to organize constant epidemiological surveillance of congenital rubella.http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
The rare occurrence of rubella embryopathy in Mali stimulated us to investigate the rubella immunity of the population. Sera from females from Hamburg (n = 97) between 16 and 42 years old were in 84,5% seropositive (hemolysin-in-gel test) whilst a sample of Malien females (n = 99) were positive in 92,9%. Our investigations showed that the Malien children were significantly (p = less than 0.001) earlier infected by rubella than in Hamburg (Mali: children under 8 years [n = 196] in 46.9%; Hamburg [n = 151] in 20.5%). In Mali 7-8 years old children were already in 87.5% seropositive (Hamburg: only in 46.7%). The early immunity in childhood is due to the bigger African family in comparison with the smaller European family. The height of rubella serum titers was in grown-ups identical, but the relationship was vice versa in both studied newborn populations. Newborns from Mali showed lower rubella antibody titers than their mothers (newborns from Hamburg had a tendency to higher titers). Similar relationships were found already in the amount of neutralizing polioantibodies in newborns from both countries. A rubella immunisation in Mali seems not to be indicated.http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
Serologic responses and patterns of antibody persistence in children given HPV-77 DE-5 or RA27/3 vaccine were compared with those in children who had experienced natural infection. ….Natural infection with wild virus was shown to induce more vigorous immune responses than did either vaccine: antibody titers were higher, decreases were smaller, and none fell to less than 1:8 (HAI) or less than 1:4 (NT).”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“Following earlier work we show that certain vaccination programmes could actually increase the incidence of serious cases. At first sight, this may seem inconceivable. Mathematical analysis, however, reveals that this is indeed a real possibility. Implementing a vaccination programme that is not sufficiently intensive to eradicate the infection in the population will ultimately lead to a new steady state in which the force of infection is lower than in the period before the start of the programme. As a consequence those who are not (effectively) vaccinated have a higher chance of contracting the infection at an older age. For many viral infections, the chance of serious complications is greater if the infection is acquired at an older age.”http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
Six hundred and fifty-three teenagers (aged 11-13 year) living in Siena and its surroundings (Tuscany, Italy) were the sample for serological screening intended to ascertain immunity to rubella. It was found that 324 of the teenagers (49.62%) lacked antibodies and, hence, were unprotected against the infection. Out of the 324 girls, 196 (around 3/5) were vaccinated using live vaccine. Post-vaccinal complications, with clinical signs of rubella infection, were recorded in almost one third of the vaccinees. Virus isolation from the blood was, in every case, not possible after either 10 or 30 days from vaccination. The serological findings, expressed in hemagglutination inhibition antibodies, could be summarized in the following way: (i) antibodies at low titre were found in only eight out of 184 girls (4.35%) ten days after vaccination; (ii) serological conversion was recorded in 187 out of 188 girls (99.47%) 30 days after vaccination; (iii) the titres were moderately high but much lower than those recorded for the natural infection. The results are discussed in the context of their implications for the strategies of rubella vaccination as far as the safety and the effectiveness of the vaccine are concerned, with emphasis on the duration of the protective immunity.http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“Although the Amish make up less than 0.05% of the United States population, nearly all rubella reported in the United States in 1991 occurred in this population. In early 1991 a large rubella outbreak in a Tennessee Amish community that had experienced no rubella for 17 years afforded an opportunity to describe the epidemiology of rubella in this unique population. Structured interviews were conducted with 54 Amish families. Of 383 persons in the sample 85 (22%) had rubella. Illnesses were mild; 16% of cases lacked fever and 20% of cases reported no symptoms except rash. Children < 17 years of age were 7 times more likely than older individuals to be affected (77 of 214 vs. 8 of 165). All pregnant women in the community were > 20 years of age; none developed rubella. No congenital rubella syndrome was recognized. Although rubella is increasingly a disease of adolescents and young adults, in this outbreak, rubella was again a childhood disease. Illness in this community-based investigation was mild; rubella may be difficult to diagnose and report. Immunity after remote natural infection was durable since the community's last outbreak. Pregnant women probably were protected by the age distribution of immunity..”
“Approximately 50 percent of patients who contract hepatitis B develop no symptoms after exposure. However, the exposure ensures that they will have life-time immunity. An additional 30 percent develop only flu-like symptoms, and again, this group will acquire life-time immunity. The remaining 20 percent exposed to hepatitis B will develop the symptoms of the disease. 95 percent of this 20 percent will fully recover, with life-time immunity. Therefore, less than five percent of people who contract Hepatitis B will become chronic carriers of the infection.”http://www.arens.com/brian/hbv.htm
“Hepatitis B is a virus that causes the liver to become inflamed. Most people fight off the infection themselves. However, approximately 5-10% of those people who are infected with the virus will become carriers, an estimated 5-10% of those people infected each year will progress to chronic liver disease, cirrhosis and possibly liver cancer…..
About 90% of adults recover from hepatitis B in a few months, clearing the virus from their system and developing an immunity. They will never get hepatitis B again..”http://www.cdc.gov/epo/mmwr/preview/...l/00033405.htm
The duration of vaccine-induced immunity has been evaluated in long- term follow-up studies of both adults and children (48,51). Only the plasma-derived hepatitis B vaccine has been evaluated because it has had the longest clinical use; however, on the basis of comparable immunogen- icity and short-term efficacy, similar results would be expected with recombinant vaccines. The magnitude of the antibody response induced by the primary vaccination series is predictive of antibody persistence, and a logarithmic decline of antibody levels occurs over time. Among young adults (homosexual men and Alaskan Eskimos) who initially responded to a three- dose vaccine series, loss of detectable antibody has ranged from 13% to 60% after 9 years of follow-up. For children vaccinated after the first year of life, the rate of antibody decline has been lower than for adults (51). The peak antibody titers for infants are lower than those for children immunized after 12 months of age, but the rate of antibody decline is comparable with that observed for adults in the same population.
Long-term studies of healthy adults and children indicate that immuno- logic memory remains intact for at least 9 years and confers protection against chronic HBV infection, even though anti-HBs levels may become low or decline below detectable levels (48,51,52). In these studies, the HBV infections were detected by the presence of anti-HBc. No episodes of clinical hepatitis were reported and HBsAg was not detected, although brief episodes of viremia may not have been detected because of infrequent testing. The mild, inapparent infections among persons who have been previously vaccinated should not produce the sequelae associated with chronic HBV infection and should provide lasting immunity. In general, follow-up studies of children vaccinated at birth to prevent perinatal HBV infection have shown that a continued high level of protection from chronic HBV infections persists at least 5 years (52,53).http://www.ncbi.nlm.nih.gov/entrez/q...604&query_hl=1
Pediatr Infect Dis J. 2004 Jul;23(7):650-5.
Duration of hepatitis B immunity in low risk children receiving hepatitis B vaccinations from birth.
RESULTS: Of low risk infants receiving a plasma-derived vaccine, 41% (42 of 102) of those whose primary response was unknown and 24% (4 of 17) who had initially responded retained protective titers (> or = 10 mIU/mL) of anti-HBs at 9 and 13 years, respectively. Of those who did not have protective antibody titers, 61% (33 of 54) and 67% (8 of 12), respectively, responded to a booster dose. In children of HBsAg-positive mothers, 31% retained protective anti-HBs at 12 years, and 90% (9 of 10) with nonprotective titers responded to a booster. In low risk children initially receiving a recombinant vaccine, 12.5% (26 of 208) and none (0 of 36) retained protective anti-HBs titers at 5 and 7 years of age, respectively. Of those who did not have protective titers, 90% (120 of 134) and 91% (32 of 35), respectively, responded to a booster. CONCLUSIONS: Anti-HBs disappeared by 5 years of age in most children who were vaccinated with hepatitis B vaccine from birth. Although most children showed immunologic memory, one-third failed to demonstrate an anamnestic response to a booster dose. Additional long term studies of low risk infants are needed to determine duration of protection and the necessity for or timing of booster doses.
(NOTE: the vaccine is estimated below to confer immunity for at least 15 yrs, but to wane faster in those vaxed before they were 4 yrs old. HELLO! The US vaxes at BIRTH and a few more times before age 4. Which suggests a duration of immunity far less than 15 yrs.
Further, assuming even a 15 yr duration of immunity, that means MILLIONS of children will reach the age of highest risk of exposure/infection (which is most often associated with sexual activity and iv drug use, which, if it occurs, is most likely to occur in the late teen and adult years) LACKING IMMUNITY and vulnerable to infection AND to infecting their newborns (who are MOST prone, after adults, to become chronic carriers/suffer serious effects). OTOH, had they gained natural immunity as children, when the infection is LEAST likely to result in serious effects, they would likely be immune for life, with no adverse events. See the pattern here? So similar to other epidemiological shifts wrought by the mass vaccination of children.
Universal hep b vaccination of infants/children will, imo and based on the data to date, result in huge increases in chronic hep b (as opposed to benign hep b) since more adults and infants will end up infected for the first time, and they are, repeat after me, those at highest risk of complications.)http://my.webmd.com/content/Article/101/106142.htm
Feb. 28, 2005 -- The hepatitis B vaccine works for at least 15 years -- longer than once thought…The vaccine "strongly protected against [hepatitis B] infection for at least 15 years in all age groups," they report.
However, the benefits faded fastest in people vaccinated when they were 4 years old or younger. Researchers will keep an eye on those patients to see if they need additional doses of the vaccine or booster shots in the future. ..The news comes from a study of Alaska natives, who have high rates of hepatitis B, with most cases starting in early childhood.
A total of 1,578 people participated.
In the early 1980s, participants were fully vaccinated against hepatitis B. All were at least six months old, and some were in their 20s or older.
After 15 years, the researchers were still in touch with almost half of the group. The vaccine's protection against infection was still going strong in 84% of those people….The vaccine's effectiveness waned the most in people vaccinated before their fifth birthday. "It is important that we continue to follow this group in order to determine when and if booster doses will be necessary," says the study….”
A link to the abstract:http://www.ncbi.nlm.nih.gov/entrez/q...627&query_hl=1
(Note, this study deals with the plasma derived vaccine, not the recombinant version currently in use, but it is generally assumed that duration will be similar.)
““The immunity of infants is derived passively from their mothers, and disappears during the first year of life. After that time immunity is acquired as a result of infections, which are usually subclinical. (Burnet, 1972 p. 194).” (NOTE, maternal immunities are likely weaker and of less duration in vaccinated as opposed to naturally immune mothers, as is the case with measles and some other infections)http://www.astdhpphe.org/infect/dip.html
“In the United States, the diphtheria threat is shifting from children to adults and adolescents. Cases are occurring in persons who have not been immunized or in vaccinated persons who did not receive periodic booster doses to maintain their immunity.”http://www.nlm.nih.gov/medlineplus/e...cle/001608.htm
“Protective immunity is not present longer than 10 years after the last vaccination”http://www.who.int/vaccines/en/diptheria.shtml
“The public health burden of diphtheria has been low in most developing countries because most children have acquired immunity through subclinical or cutaneous infection. “http://www.cdc.gov/nip/publications/pink/dip.pdf
“Skin infections are quite common
in the tropics and are probably responsible for the high levels
of natural immunity found in these populations…The overall case-fatality rate for diphtheria is 5%-10%, with higher death rates (up to 20%) in persons <5 and >40 years of age.
…The current age distribution
of cases corroborates the finding of inadequate levels of circulating
antitoxin in many adults (up to 60% with less than protective
levels)….Because of waning antitoxin titers, most individuals have antitoxin
levels below the optimal level 10 years after the last dose….”