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4 Measles, Mumps, and Rubella Vaccine INTRODUCTION Measles Measles is caused by a single-stranded, negative-sense nonsegmented RNA virus of the genus Morbillivirus and the family Paramyxoviridae that encodes at least eight structural proteins (Gershon, 2010a). The virus is easily inactivated by extremes of pH, heat, and sunlight (Strebel et al., 2008). As the only natural hosts for the wild virus, humans transmit measles through aerosolized respiratory fluids or droplet nuclei (Babbott and Gordon, 1954; de Jong, 1965). The incubation period of the measles virus is 10 to 12 days (CDC, 1998). The prodromal stage, during which the infected individual is most contagious, lasts 2 to 4 days and manifests as conjunctivitis, fever, malaise, and tracheobronchitis (Strebel et al., 2008). This period is followed by 4 days of fever as high as 105°F (Strebel et al., 2008). Rash is preceded by Koplik’s spots that appear on the lining of the cheeks and lips and may persist for 1 to 2 days after the onset of rash (Strebel et al., 2008). The rash, which occurs 14 days after exposure, starts on the head and spreads to the trunk and extremities over 3 to 4 days, before fading (Strebel et al., 2008). Individuals are infectious for as long as 4 days before and after the onset of rash (Strebel et al., 2008). Serious complications of measles include pneumonia, postinfectious en- cephalitis, subacute sclerosing panencephalitis (SSPE), and death (Johnson et al., 1984; Miller, 1987; Strebel et al., 2008). These complications are 103
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104 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY associated with a fever lasting more than 2 days after the onset of rash (Strebel et al., 2008). Measles-related mortality is highest for infants, young children, and adults with decreased risk in older children and adolescents (CDC, 1998). Other complications include acute otitis media, appendicitis, hepatitis, myocarditis, and thrombocytopenia (Kempe and Fulginiti, 1965). Although recognized as a disease for approximately 2,000 years, the first major advance in the study of measles was in 1846 when Parnum ob- served measles cases in the Faroe Islands. Parnum confirmed the infectious nature of measles, defined the 2-week incubation period, and noted that individuals infected with measles did not become ill after subsequent expo- sure to the virus (Strebel et al., 2008). In 1954, Enders and Peebles propa- gated measles virus in human renal tissues (Enders and Peebles, 1954). Nine years later, in 1963, the first live, attenuated vaccine was licensed for use in the United States (Enders, 1962). The Edmonston B virus strain that was passaged at 35–36°C through primary renal cells, primary human amnion cells, and embryonic chicken cells a total of 59 times was used in many vaccines (Strebel et al., 2008). In 1965 and 1968, the Schwarz and Moraten (more attenuated strain derived from Ender’s attenuated Edmon- ston measles virus) strains were also licensed in the United States. These strains were developed from the Edmonston B strain and were passaged at 32°C an additional 85 and 40 times, respectively (Strebel et al., 2008). The Schwarz and Moraten strains were shown to cause less severe and less fre- quent side effects (Andelman et al., 1963; Hilleman et al., 1968; Schwarz, 1964; Schwarz and Anderson, 1965; Schwarz et al., 1967; Strebel et al., 2008). Today, the only strain licensed in the United States is the more at- tenuated, live Ender’s Edmonston strain (Moraten strain) (CDC, 1998). Prior to the licensure of a measles vaccine, an average of 400,000 measles cases were reported each year, although the actual incidence was estimated to be 3.5 million based on the size of the annual birth cohort, and the fact that nearly 100 percent of the population was infected during child- hood (CDC, 1998). With the licensure of the vaccine, the measles burden has been reduced by more than 99 percent, and in 1998, the Centers for Disease Control and Prevention (CDC) indicated that 95 and 98 percent of children vaccinated at age 12 and 15 months, respectively, developed measles antibodies (CDC, 1998). Mumps Mumps is an acute viral infection caused by an enveloped, negative- sense RNA virus of the genus Rubulavirus (Litman and Baum, 2010). The virus is composed of 15,384 nucleotides that encode seven genes, one of which is the SH protein that has been used to identify at least 12 mumps virus strains (Jin et al., 2000; Plotkin and Rubin, 2008). Mumps is transmit-
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105 MEASLES, MUMPS, AND RUBELLA VACCINE ted by direct contact with infectious respiratory secretions, droplet nuclei, or fomites that are then transferred to the nose and mouth (Litman and Baum, 2010). The average incubation period of the mumps virus is 16 to 18 days but can range from 2 to 4 weeks (Litman and Baum, 2010). Fifteen to 20 percent of mumps infections are asymptomatic; 50 percent of cases have nonspecific symptoms such as anorexia, headache, fever, and malaise, or present primarily as respiratory infections; and only 30 to 40 percent dem- onstrate the classic salivary gland tenderness and enlargement (parotitis) (CDC, 1998). Asymptomatic infection is more common in adults, while parotitis occurs most often in children age 2 to 9 years (CDC, 1998). Children younger than 5 years old more commonly manifest symptoms of lower respiratory disease (Plotkin and Rubin, 2008). Complications of mumps infection are possible without the presence of parotitis. In 1958, Philip et al. (1959) observed testicular and mammary inflammation in 5 percent of postpubertal men and 31 percent of women over 15 years of age. Pancreatitis occurs in 4 percent of cases, and although it has not been proven, evidence suggests an association between mumps infection and diabetes mellitus (Sultz et al., 1975). Neurological complications are more common in adults and occur three times more often in men than in women (Plotkin and Rubin, 2008). These complications include mumps meningitis, cerebellar ataxia, transverse myelitis and poliomyelitis-like disease, cranial nerve palsies, hydroencephalitis, and encephalitis, which occurs in less than 0.3 percent of cases, but is responsible for more than 50 percent of mumps- related fatalities (Bray, 1972; Cohen et al., 1992; Kilham et al., 1949; Lahat et al., 1993; Oldfelt, 1949; Oran et al., 1995; Plotkin and Rubin, 2008; Timmons and Johnson, 1970). Hearing loss due to infection of the endolymph is also a potential complication of mumps infection (Tanaka et al., 1988). Short-term, high-frequency deafness occurs in approximately 4 percent of mumps cases, and permanent hearing loss occurs in only 1 per 20,000 cases and is usually unilateral (Litman and Baum, 2010; Plotkin and Rubin, 2008). Mumps arthropathy, more common in men than women, oc- curs most often in young adults (Plotkin and Rubin, 2008). It may manifest as arthralgias, polyarticular migratory arthritis, and monoarticular arthritis (Gordon and Lauter, 1984; Harel et al., 1990). Myocarditis is rare and gen- erally self-limited, although some fatal cases have been reported (Chaudary and Jaski, 1989; Roberts and Fox, 1965). Johnson and Goodpasture (1934) identified the causative agent of mumps in 1934, and in 1945 Habel and Enders successfully cultivated the virus in chick embryos (Enders, 1946; Habel, 1945). The first inactivated mumps vaccine was developed in 1946 and tested in humans in 1951 (Habel, 1946, 1951). The first live, attenuated vaccine was developed in the 1960s in the United States and former Soviet Union (Plotkin and Rubin,
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106 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY 2008; Weibel et al., 1967). In the United States, mumps vaccines are manu- factured using the Jeryl Lynn strain mumps virus that was isolated from the throat of Jeryl Lynn Hilleman in the 1960s (Plotkin and Rubin, 2008). The vaccine is currently licensed in the mono-, tri-, and tetravalent forms, although the monovalent, Mumpsvax (Merck and Co., Inc.), is no longer available in the United States. Prior to the licensing of a live-attenuated mumps vaccine, mumps outbreaks occurred every 2 to 5 years, with peak incidence from January through May (Anderson and Seward, 2008; Litman and Baum, 2010). Since the introduction of the vaccine, the incidence of mumps infection has been reduced greatly, evidenced by a 99 percent decrease in mumps infection from 1968 to 1995 (CDC, 1998). Rubella Rubella, also known as German measles, is caused by an enveloped, positive-sense RNA togavirus of the genus Rubivirus (Gershon, 2010b). The rubella virus genome consists of approximately 9,800 nucleotides, and the virus can be divided into two clades and at least seven genotypes (Zheng et al., 2003). Maturing by budding from the cell membrane (Murphy et al., 1968), rubella virus is relatively unstable and vulnerable to chemical in- activation, extremes of pH and heat, lipid solvents, and ultraviolent light (Gershon, 2010b). Rubella is spread through contact with infectious respiratory secre- tions, and replication occurs in the nasopharynx of the infected individual (Plotkin and Reef, 2008). Rubella infections are subclinical in 25 to 50 per- cent of cases (CDC, 1998). In those cases in which clinical illness develops, the beginning of the 12- to 23-day incubation period is largely asymptom- atic (CDC, 1998; Plotkin and Reef, 2008). By the end of the second week virus can be isolated from the blood and symptoms of conjunctivitis, low- grade fever, lymphadenopathy, and malaise are present (Plotkin and Reef, 2008). A rash follows spreading downwards from the face before fading within 1 to 3 days (Plotkin and Reef, 2008). Rubella illness in a child or adult is usually benign although arthritis and arthralgia has been observed in association with viral replication in the synovial cavity of the joints (Plotkin and Reef, 2008). Other complications of rubella include encepha- litis, Guillain-Barré syndrome (GBS), progressive rubella panencephalitis, and thrombocytopenia (Gershon, 2010b; Plotkin and Reef, 2008). Rubella virus infection during pregnancy can lead to congenital rubella infection in neonates. The disease outcome is directly correlated to the age of the fetus at the time of infection with younger fetuses experiencing more severe disease (Gershon, 2010b). Infections within the first 2 months of pregnancy can cause multiple congenital defects or spontaneous abortion in
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107 MEASLES, MUMPS, AND RUBELLA VACCINE 65 to 85 percent of women (Gershon, 2010b). Infections in the third month and fourth month are associated with a single defect in 30 to 35 percent and 10 percent of cases, respectively (Gershon, 2010b). Commonly associated defects include transient thrombocytopenia purpura and meningoencepha- litis, as well as permanent and developmental manifestations such as hear- ing loss, pulmonic stenosis, mental retardation, and behavioral disorders (Gershon, 2010b). Other less common manifestations include myocardial abnormalities, hepatitis, and seizure disorders (Gershon, 2010b). Studies have also shown that diabetes mellitus occurs 50 times more frequently in children with congenital rubella, and insulin-dependent diabetes has been reported in 40 percent of adults who were congenitally infected with rubella during the 1942 rubella epidemic (Gershon, 2010b). Clinically described as early as the 1700s, rubella was considered a dis- ease of children and young adults and was given little attention until 1941 when Gregg discovered an association between maternal rubella infection and congenital cataracts (Gregg, 1941). Parkman and colleagues and Weller and Neva isolated the causative agent of rubella in 1962 (Parkman et al., 1962; Weller and Neva, 1962). By 1970, three rubella virus strains were licensed for use in vaccines in the Untied States: Cendehill (grown in rabbit kidney), HPV-77 (grown in dog kidney), and HPV-77 (grown in duck em- bryo) (HPV-77DE) (Hilleman et al., 1969; Meyer et al., 1969; Prinzie et al., 1969). HPV-77DE was used as the rubella component of the first MMR vaccine, but was later replaced with RA 27/3 after studies showed RA 27/3 induced higher antibody levels, more persistent seropositivity, more resistance to reinfection, and greater herd immunity (Fogel et al., 1978; Gershon et al., 1980; Klock and Rachelefsky, 1973). Today, RA 27/3 is the only rubella virus strain available for use in vaccines in the United States. Measles-, Mumps-, and Rubella-Containing Vaccines In the United States, measles, mumps, and rubella (MMR) vaccine is a live, attenuated virus vaccine and is manufactured by Merck & Co., Inc. Although Merck is licensed to produce monovalent measles, mumps, and rubella vaccines—Attenuvax, Meruvax, and Mumpsvax, respectively— currently, these vaccines are no longer available in the United States. The combination vaccine, M-M-R II (Merck), contains greater than 1,000 TCID50 of a more attenuated line of measles virus derived from Ender’s attenuated Edmonston strain, greater than 12,500 TCID50 of Jeryl Lynn mumps virus, and greater than 1,000 TCID50 of Wistar Institute RA 27/3 rubella virus, in addition to sorbitol, sodium phosphate, sucrose, sodium chloride, hydrolyzed gelatin, human albumin, fetal bovine serum, and neomycin (Merck & Co., Inc., 2007). The vaccine does not contain a preservative. In 2005 the Food and Drug Administration (FDA) licensed the tetravalent measles, mumps,
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108 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY rubella, and varicella (MMRV) vaccine, ProQuad (Merck). ProQuad contains greater than 3.0 log10 TCID50 of a more attenuated line of measles virus derived from Ender’s attenuated Edmonston strain, greater than 4.3 log10 TCID50 of Jeryl Lynn mumps virus, greater than 3.0 log10 TCID50 of Wistar Institute RA 27/3 rubella virus, and greater than 3.99 log10 plaque-forming units (PFUs) of Oka/Merck varicella zoster virus (VZV)—the equivalent to that found in varicella virus vaccines (see Chapter 5) (Merck & Co., Inc., 2009). ProQuad also does not contain a preservative. The Advisory Committee on Immunization Practices (ACIP) recom- mends that all children receive two subcutaneous doses of the MMR or MMRV vaccine without preference. The first dose is scheduled between 12 and 15 months of age and is followed by a second dose between 4 and 6 years of age prior to kindergarten or first grade. The ACIP also recommends that adults born after 1956 and all women of childbearing age who are not pregnant receive at least one dose of the MMR vaccine in the absence of prior immunity (CDC, 1998). The vaccine is contraindicated in those with hypersensitivity to any component of the vaccine including gelatin, preg- nant women, those with allergies to neomycin, febrile respiratory illness or other active febrile infection, and the immunosuppressed. According to the National Immunization Survey, from 2005 to 2009 more than 90 percent of children aged 19 to 35 months had received at least one dose of the MMR vaccine (CDC, 2010). The committee focused on virus strains used in licensed U.S. vaccines. On occasion, the committee reviewed other virus strains that were suffi- ciently similar to U.S. strains. This will be noted in the text. The committee was not charged with reviewing the MMRV vaccine. MEASLES INCLUSION BODY ENCEPHALITIS Epidemiologic Evidence No studies were identified in the literature for the committee to evalu- ate the risk of measles inclusion body encephalitis after the administration of MMR vaccine. Weight of Epidemiologic Evidence The epidemiologic evidence is insufficient or absent to assess an association between MMR vaccine and measles inclusion body encephalitis.
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109 MEASLES, MUMPS, AND RUBELLA VACCINE Mechanistic Evidence The committee identified five publications reporting measles inclu- sion body encephalitis after the administration of measles or MMR vac- cine. Freeman et al. (2004) and Kim et al. (1992) demonstrated wild-type measles virus in their patients. These cases did not contribute to the weight of mechanistic evidence. Described below are three publications reporting clinical, diagnostic, or experimental evidence that contributed to the weight of mechanistic evidence. Bitnun et al. (1999) describe a 21-month-old boy presenting with sta- tus epilepticus, fever, irritability, and vomiting 9 months after receiving an MMR containing the Moraten strain of measles. Serology was positive for antimeasles IgM and IgG; the cerebrospinal fluid (CSF) was not positive for these antibodies. The patient died when ventilatory support was with- drawn 51 days after admission. Evaluation of the patient’s immune system revealed depressed proliferative responses to mitogens and antigens and de- pressed CD8 cell numbers. Measles hemagglutinin and matrix proteins were observed by immunohistochemical staining performed on biopsied brain tissue. Furthermore, intracytoplasmic and intranuclear inclusions with the appearance of paramyxovirus neucleocapsids were revealed by electron microscopy. Reverse-transcription polymerase chain reaction (RT-PCR) am- plified measles RNA from the patient’s brain tissue. PCR analysis of the N gene and sequence analysis of the F gene from viral material isolated in the biopsied brain tissue was identical to the Moraten measles vaccine strain. Baram et al. (1994) describe a 22-month-old girl who presented with focal and generalized myoclonic seizures, clumsiness, falling, head drop, and right arm jerk 4 months after receiving a measles, mumps, and rubella vaccine. The patient’s history included a febrile illness with rash at the age of 5 weeks. The patient died of aspiration pneumonia at 25.5 months of age, 3.5 months after the onset of symptoms. Upon autopsy, inclusion bodies were identified and found to contain helical nucleocapsid tubules. Measles virus was amplified, by PCR, from the patient’s brain. Poon et al. (1998) described a 2-year-old boy, diagnosed with human immunodeficiency virus (HIV), presenting with generalized convulsive sei- zures lasting 40 minutes 9 months after receiving a measles, mumps, and rubella vaccine. Despite treatment the patient continued to develop partial and generalized seizures. The patient presented with a fever, lymphade- nopathy, hepatosplenomegaly, and delayed language and motor skills upon physical and developmental examination. Tests were negative for herpes simplex virus, cytomegalovirus, respiratory syncytial virus, Toxoplasma, and cryptococal organisms. The patient died 4 months after admission for pneumonia. Electron microscopic observation of a fine-needle aspiration
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110 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY biopsy of the right temporal region showed intranuclear inclusions cor- responding to the configuration and size of measles virus. Weight of Mechanistic Evidence Measles inclusion body encephalitis is a complication of wild-type mea- sles infection that develops months to years after the initial acute measles infection (Reuter and Schneider-Schaulies, 2010). Furthermore, measles inclusion body encephalitis is confined to immunodeficient patients and is inevitably fatal (Reuter and Schneider-Schaulies, 2010). The committee considers the effects of natural infection one type of mechanistic evidence. In addition, the three publications described above presented clinical evidence sufficient for the committee to conclude the vaccine was a contrib- uting cause of measles inclusion body encephalitis after administration of a measles-containing vaccine. The publications reported either intranuclear inclusions corresponding to measles virus or the isolation of measles virus from the brain; vaccine strain measles virus was identified by PCR in one publication. The latencies between vaccination and the development of measles in- clusion body encephalitis in the publications described above were 4 and 9 months, suggesting persistent viral infection as the mechanism. Direct viral infection may also contribute to the symptoms of measles inclusion body encephalitis; however, the publications did not provide evidence linking this mechanism to MMR vaccine. The committee assesses the mechanistic evidence regarding an as- sociation between the measles vaccine and measles inclusion body encephalitis in individuals with demonstrated immunodeficiencies as strong based on one case presenting definitive clinical evidence. The committee assesses the mechanistic evidence regarding an as- sociation between the mumps or rubella vaccine and measles inclu- sion body encephalitis as lacking. Causality Conclusion Conclusion 4.1: The evidence convincingly supports a causal re- lationship between MMR1 vaccine and measles inclusion body encephalitis in individuals with demonstrated immunodeficiencies. 1 The committee attributes causation to the measles component of the vaccine.
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111 MEASLES, MUMPS, AND RUBELLA VACCINE ENCEPHALITIS AND ENCEPHALOPATHY Epidemiologic Evidence The committee reviewed 13 studies to evaluate the risk of encephalitis or encephalopathy after the administration of measles or MMR vaccine. Nine studies (Bino et al., 2003; D’Souza et al., 2000; Fescharek et al., 1990; Katz, 1969; Landrigan and Witte, 1973; Patja et al., 2000; Stetler et al., 1985; Vahdani et al., 2005; Weibel et al., 1998) were not considered in the weight of epidemiologic evidence because they provided data from passive surveillance systems and lacked unvaccinated comparison populations. One controlled study (Griffin et al., 1991) had very serious methodological limi- tations that precluded its inclusion in this assessment. The study by Griffin et al. (1991) was unable to find any cases of encephalopathy following MMR immunization, so no conclusions could be drawn from this analysis. The three remaining controlled studies (Makela et al., 2002; Ray et al., 2006; Ward et al., 2007) contributed to the weight of epidemiologic evi- dence and are described below. Makela et al. (2002) conducted a retrospective cohort study in 535,544 children (1 to 7 years of age) who received an MMR vaccination in Finland from November 1982 to June 1986. Vaccination data were collected from a National Public Health Institute cohort that included the child’s social secu- rity number, age at vaccination, and the year and month of vaccination. The nationwide hospital discharge register was linked to the vaccination data using the social security number of each child. The investigators reviewed the hospital discharge register for cases of encephalitis or encephalopathies (referred to as encephalitis) following vaccination; records with a defined cause unrelated to vaccination were excluded. Cases of encephalitis that occurred within 3 months of vaccination were validated with information from the patients’ medical records and the exact dates of vaccination were verified. The number of events observed within the 3-month postvaccina- tion risk period was compared to the events observed during the control period, which was defined as subsequent 3-month postvaccination intervals until 24 months was reached. A total of 199 children were hospitalized for encephalitis during the study period; 9 occurred within 3 months of MMR vaccination, 110 occurred after the 3 months following vaccination, and 80 occurred before MMR vaccination. The analysis did not find an increase of encephalitis hospitalizations within 3 months of vaccination (p = .28). The authors concluded that MMR vaccination does not increase the risk of encephalitis in children. Ray et al. (2006) conducted a case-control study in children (0 to 6 years of age) enrolled in four health maintenance organizations (HMOs) participating in the Vaccine Safety Datalink (VSD) from January 1981
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112 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY through December 1995. The cases were defined as patients hospitalized with a primary or secondary diagnosis of encephalopathy, encephalitis, or Reye syndrome, and who were enrolled in the HMO at least 60 days be- fore hospitalization (or since birth for patients under 60 days of age). The medical records of all cases were reviewed by a neurologist, who was blind to vaccination status, to confirm patients met the case definition. A total of 452 encephalopathy cases were identified and categorized according to whether the encephalopathy etiology was known, unknown, or suspected but unconfirmed. One to three controls were matched to each case on age (within 7 days), sex, HMO location, and length of enrollment in the HMO. Vaccination histories were obtained from the medical records and stratified into time windows; the cases and controls had similar vaccination rates. Odds ratios were calculated for MMR vaccination within the specified time windows and included all cases, cases with unknown or suspected but unconfirmed diagnoses, or cases with only suspected but unconfirmed diag- noses. None of the comparisons found a statistically significant increase in risk, meaning all 95% confidence intervals (CIs) for odds ratios included 1. In fact, most of the point estimates of the odds ratios in these comparisons were less than 1. The highest odds ratio point estimate was 1.23 (95% CI, 0.51–2.98) for cases of unknown or suspected encephalopathy within 90 days of MMR vaccination. The authors concluded that MMR vaccination is not associated with an increased risk of encephalopathy owing to the absence of a consistent time association between vaccination and encepha- lopathy onset. Ward et al. (2007) conducted a self-controlled case series study in children (2 to 35 months of age) residing in the United Kingdom or Ireland between October 1998 and September 2001. MMR vaccines with the Jeryl Lynn or RIT 4385 mumps component, and Moraten or Schwarz measles component were in use during the study period. The British Pediatric Surveillance Unit distributed monthly surveillance surveys to pediatricians in order to identify children with encephalitis, or suspected severe illness with fever and seizures. The questionnaires were reviewed by a physician to confirm patients met the case definition of severe neurologic disease (encephalitis or febrile seizures). Vaccination histories of confirmed cases were obtained from the child’s general practitioner by the Immunization Department, Health Protection Agency, Centre for Infections, London. The risk periods considered were 6–11 days and 15–35 days after MMR vaccination; each child was categorized as having been vaccinated or un- vaccinated, and with disease or without disease based on dates of vaccine administration and disease episodes during these time periods. A total of 107 children (12 to 35 months of age) with confirmed severe neurologic disease were included in the analysis for MMR vaccine. The relative risk of severe neurologic disease within 6 to 11 days after MMR vaccination was
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113 MEASLES, MUMPS, AND RUBELLA VACCINE 5.68 (95% CI, 2.31–13.97) and within 15 to 35 days after MMR vaccina- tion was 1.34 (95% CI, 0.52–3.47). While a significant increased risk of disease was observed during the 6 to 11 day postvaccination period, three of the six cases received MMR and meningococcal C conjugate vaccine on the same day, and four of the six cases reported complex febrile seizures combined with encephalopathy. The authors concluded that administration of MMR vaccine is associated with an increased risk of severe neurologic disease within 6 to 11 days of vaccination, but attributed the risk to the inclusion of cases with complex febrile seizures. Furthermore, the study included two vaccine formulations, one of which is not available in the United States, and the association of these vaccines with encephalitis was not analyzed separately. Weight of Epidemiologic Evidence Two of the three studies detailed above showed no significant increased risk of encephalopathy after MMR vaccination. Makela et al. (2002) found only 9 of the 199 cases were diagnosed within their defined risk period of 0–3 months, a rate no higher than during the control periods of this cohort study. All control periods were after vaccination, which weakens the results of this study. Of the three studies, the study by Ray et al. (2006) investigated the largest number of cases with 452 that were then matched to controls, and was the only study judged to have negligible limitations. The authors considered different risk intervals and different categories of diagnosis but did not find evidence of an increased risk. The last paper by Ward et al. (2007) showed a significant increase of neurologic disease—but the illnesses were predominantly complex febrile seizures with recovery except in one patient, not other forms of encephalopathy (the association of MMR vac- cination and seizures is discussed in a subsequent section). The study also combined assessments for two vaccine formulations, one of which is not available in the United States. Thus, two of the three studies—of which only one had negligible limitations—found no association between MMR vac- cine and encephalitis or encephalopathy. A third study did find an increase in risk, but the association was with febrile seizures, which are arbitrarily discussed in another section of the report. See Table 4-1 for a summary of the studies that contributed to the weight of epidemiologic evidence. The committee has limited confidence in the epidemiologic evi- dence, based on three studies that lacked validity and precision to assess an association between MMR vaccine and encephalitis or encephalopathy.
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228 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY Jayarajan, V., and P. A. Sedler. 1995. Hearing loss following measles vaccination. Journal of Infection 30(2):184-185. Jin, L., S. Beard, A. Hale, W. Knowles, and D. W. G. Brown. 2000. The genomic sequence of a contemporary wild-type mumps virus strain. Virus Research 70(1-2):75-83. Johnson, C. D., and E. W. Goodpasture. 1934. An investigation of the etiology of mumps. Journal of Experimental Medicine 59(1):1-19. Johnson, R. T., D. E. Griffin, R. L. Hirsch, J. S. Wolinsky, S. Roedenbeck, I. L. Desoriano, and A. Vaisberg. 1984. Measles encephalomyelitis—clinical and immunological studies. New England Journal of Medicine 310(3):137-141. Jorch, G., M. Kleine, and H. Erwig. 1984. Coincidence of virus encephalitis and measles- mumps vaccination [in German]. Monatsschrift Kinderheilkunde Organ der Deutschen Gesellschaft fur Kinderheilkunde 132(5):299-300. Joyce, K. A., and J. E. Rees. 1995. Transverse myelitis after measles, mumps, and rubella vac- cine. British Medical Journal 311(7002):422. Karavanaki, K., E. Tsoka, C. Karayianni, V. Petrou, E. Pippidou, M. Brisimitzi, M. Mavrikiou, K. Kakleas, I. Konstantopoulos, M. Manoussakis, and C. Dacou-Voutetakis. 2008. Prevalence of allergic symptoms among children with diabetes mellitus type 1 of different socioeconomic status. Pediatric Diabetes 9(4 Pt 2):407-416. Katz, S. L. 1969. The effect of live attenuated measles-virus vaccine on the central nervous system. International Archives of Allergy and Applied Immunology 36(Suppl.):125-133. Kaye, J. A., M. D. Melero-Montes, and H. Jick. 2001. Mumps, measles, and rubella vaccine and the incidence of autism recorded by general practitioners: A time trend analysis. British Medical Journal 322(7284):460-463. Kazarian, E. L., and W. E. Gager. 1978. Optic neuritis complicating measles, mumps, and rubella vaccination. American Journal of Ophthalmology 86(4):544-547. Kelso, J. M., R. T. Jones, and J. W. Yunginger. 1993. Anaphylaxis to measles, mumps, and rubella vaccine mediated by IgE to gelatin. Journal of Allergy and Clinical Immunology 91(4):867-872. Kempe, C. H., and V. A. Fulginiti. 1965. Pathogenesis of measles virus infection. Archiv fur Die Gesamte Virusforschung 16(1-5):103-128. Khetsuriani, N., P. Imnadze, L. Baidoshvili, L. Jabidze, N. Tatishili, G. Kurtsikashvili, T. Lezhava, E. Laurent, and R. Martin. 2010. Impact of unfounded vaccine safety concerns on the nationwide measles-rubella immunization campaign, Georgia, 2008. Vaccine 28(39):6455-6462. Ki, M., T. Park, S. G. Yi, J. K. Oh, and B. Y. Choi. 2003. Risk analysis of aseptic meningitis after measles-mumps-rubella vaccination in Korean children by using a case-crossover design. American Journal of Epidemiology 157(2):158-165. Kilham, L., J. Levens, and J. F. Enders. 1949. Nonparalytic poliomyelitis and mumps meningoencephalitis—differential diagnosis. Journal of the American Medical Associa- tion 140(11):934-936. Kim, T. M., H. R. Brown, S. H. Lee, C. V. Powell, P. Bethune, N. L. Goller, H. T. Tran, and J. S. Mackay. 1992. Delayed acute measles inclusion body encephalitis in a 9-year-old girl: Ultrastructural, immunohistochemical, and in situ hybridization studies. Modern Pathology 5(3):348-352. Kline, L. B., S. L. Margulies, and S. J. Oh. 1982. Optic neuritis and myelitis following rubella vaccination. Archives of Neurology 39(7):443-444. Klock, L. E., and G. S. Rachelefsky. 1973. Failure of rubella herd immunity during an epi- demic. New England Journal of Medicine 288(2):69-72. Konkel, G., C. Runge, U. Szillat, S. Wiersbitzky, R. Bruns, and U. Schmidt. 1993. Cerebral convulsions: Encephalitis following MMR, OPV, HiB or DPT vaccination? [in German]. Kinderarztliche Praxis 61(6):232-234.
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