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Committee to Review Adverse Effects of Vaccines; Institute of Medicine; Stratton K, Ford A, Rusch E, et al., editors. Adverse Effects of Vaccines: Evidence and Causality. Washington (DC): National Academies Press (US); 2011 Aug 25.

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Adverse Effects of Vaccines: Evidence and Causality.

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11Meningococcal Vaccine

INTRODUCTION

Meningococcal disease describes the clinical manifestations of invasive infection with the gram-negative bacteria Neisseria meningitides. N. meningitides (meningococcus) colonizes the human nasopharynx and is transmitted through direct contact with respiratory secretions or aerosolized droplets of respiratory fluids (Granoff et al., 2008). Carried by approximately 10 percent of the population, meningococcus is generally a communal organism and invasive disease relies on a combination of host factors and strain qualities (Granoff et al., 2008). In the United States in 2004, 1,400–2,800 cases of invasive meningococcal disease were reported (CDC, 2005).

Common symptoms of meningococcal infection include meningitis, headache, fever, stiffness of the neck, nausea, vomiting, photophobia, and altered mental status (Granoff et al., 2008). Meningococcemia (meningococcal sepsis) occurs in 10 to 20 percent of cases and is characterized by abrupt fever and a rash that may progress to purpura fulminans (Granoff et al., 2008). Meningococcemia is associated with hypotension, acute adrenal hemorrhage (Waterhouse-Friderichsen syndrome), and multiorgan failure (Granoff et al., 2008). Pneumonia is also associated with meningococcal disease and occurs in 6 to 15 percent of patients (Racoosin et al., 1998; Rosenstein et al., 1999). Additionally, conjunctivitis, otitis media, epiglottitis, arthritis, urethritis, and pericarditis may occur because of invasive infection; however, these developments are rare (Apicella, 2010; Miller et al., 1979; Rosenstein et al., 1999; Schaad, 1980).

The risk of meningococcal disease is higher among asplenic individuals and those with deficiencies in the terminal common complement pathway of the immune system (CDC, 2005). Additionally, prior viral infection, crowding, active and passive smoking, attending bars or nightclubs, and imbibing in alcohol are all associated with higher risk of meningococcal disease (CDC, 2005).

Prior to the development of antibiotics, approximately 70 to 85 percent of cases of meningococcal disease were fatal (Granoff et al., 2008). With the introduction of antibiotics, the case-fatality rate has dropped to nearly 30 percent worldwide and 10–14 percent in the United States (CDC, 2005; Granoff et al., 2008). Ten to 20 percent of meningococcal disease survivors experience permanent sequelae such as limb loss, hearing loss, neurologic disability, and scarring (Granoff et al., 2008).

Meningococcus has been grouped into at least 13 different groups based on serological differences in the surface polysaccharides (Apicella, 2010). Of these, five serogroups—A, B, C, W-135, and Y—are responsible for almost all instances of meningococcal disease (Granoff et al., 2008). Group A meningococcus produces the majority of disease in the “ meningitis belt” of sub-Saharan Africa but causes less than 0.3 percent of cases in the United States and Europe (Granoff et al., 2008). Serogroup W-135 was known to cause rare disease until demonstration of W-135 meningococcus in outbreaks in 2000 and 2001 during the Hajj in Mecca, Saudi Arabia (Granoff et al., 2008). In the United States, the majority of meningococcal disease is caused by serogroups B, C, and Y (Granoff et al., 2008). Serogroup B causes more than 50 percent of disease in infants less than 1 year old, and 75 percent of disease in individuals greater than 11 years is caused by serogroups C, Y, or W-135 (CDC, 2005).

Although various vaccines against meningococcal disease have been available for more than 30 years, currently there is no vaccine to protect against all five of the pathogenic serogroups. During the early 1900s, attempts were made to develop inactivated whole-cell vaccine, but this direction was abandoned due to ambiguous efficacy results and high rates of reactogenicity (Gates, 1918; Granoff et al., 2008; Sophian and Black, 1912; Underwood, 1940). The immunogenicity of exotoxin-containing culture filtrates was explored in the 1930s (Ferry and Steele, 1935; Kuhns et al., 1938). The development of antibiotics provided a more effective means to combat meningococcal infection. During the 1940s, it was demonstrated that inoculation with group-specific polysaccharides produced immunogenicity in mice (Scherp and Rake, 1945), but similar inoculation failed to produce the results in humans (Kabat et al., 1944; Watson and Scherp, 1958). It was later determined that the polysaccharide antigens capable of causing immunogenicity in humans were of a higher molecular weight than those used by Scherp and Rake (Gotschlich et al., 1972; Kabat and Bezer, 1958). In the late 1960s, Gotschlich and his colleagues developed a purification process capable of isolating heavier antigens, and this became the basis of current polysaccharide vaccines (Gotschlich et al., 1969). These vaccines, including the Food and Drug Administration–licensed Menomune (Sanofi Pasteur, Inc.), produce a T cell–independent response and therefore are not very effective in young children and do not produce a booster effect at any age (Granoff et al., 2008). In the 1980s, researchers demonstrated that by conjugating polysaccharides to protein carriers, a T cell–dependent immune response could be induced (Anderson et al., 1985; Robbins et al., 1996). This was significant because polysaccharide vaccines do not induce T-dependent immunity (Kelly et al., 2005, 2006) and therefore do not confer lasting immunity or significant reduction of meningococcus carriage or transmission. In 2005, a tetravalent conjugate vaccine was licensed in the United States and approved for use in persons 11–55 years old (CDC, 2005).

Currently, there are two types of meningococcal vaccines available in the United States: polysaccharide and conjugate. Meningococcal polysaccharide vaccines (MPSVs) are available worldwide in bivalent (A and C) and tetravalent (A, C, W-135, and Y) formulations, but only the tetravalent MPSV4 Menomune-A/C/Y/W-135 (Sanofi Pasteur) is licensed in the United States. Menomune contains 50 µg each of lyophilized powder that is reconstituted prior to administration with sterile, pyrogen-free distilled water without preservative in the single-dose presentation and with sterile, pyrogen-free distilled water and thimerosal, a mercury derivative added as a preservative in the multidose presentation (Sanofi Pasteur, Inc., 2009). Two quadrivalent conjugate vaccines, Menectra (Sanofi Pasteur) and Menveo (Novartis Vaccines and Diagnostics) are licensed in the United States. Menectra, licensed in 2005, contains 4 µg each of the capsular polysaccharide for the four serogroups conjugated to 48 µg of diphtheria toxoid (Sanofi Pasteur, Inc., 2011). It is provided in a single-dose vial and contains no added preservative or adjuvant (Sanofi Pasteur, Inc., 2011). Menveo, licensed in 2011, is composed of 10 µg of A and 5 µg each of C, Y, and W-135 oligosaccharides covalently bonded to the CRM197 protein (Novartis Vaccines and Diagnostics, 2010). The vaccine is supplied in two single-dose vials (A and C-Y-W-135) and contains no preservative or adjuvant (Novartis Vaccines and Diagnostics, 2010).

The Advisory Committee on Immunization Practices currently recommends routine vaccination of persons 11 to 12 years of age and individuals at increased risk of meningococcal disease including college freshman living in dormitories, military recruits, and asplenic individuals (CDC, 2005). MCV4 is preferred for persons 11 to 55 years of age; however, MPSV4 is recommended for individuals between 2 and 10 years and those greater than 55 years old (CDC, 2005). In 2009, the National Immunization Survey estimated that 53.6 percent of adolescents between 13 and 17 years of age had received at least one dose of the MCV4 vaccine (CDC, 2010).

ENCEPHALITIS AND ENCEPHALOPATHY

Epidemiologic Evidence

The committee reviewed one study to evaluate the risk of encephalitis or encephalopathy after the administration of meningococcal vaccine. This one controlled study (Ward et al., 2007) contributed to the weight of epidemiologic evidence and is described below.

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. 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 0–3 and 0–7 days after meningococcal C conjugate vaccination; each child was categorized as having been vaccinated or unvaccinated, and with disease or without disease based on dates of vaccine administration and disease episodes. A total of 50 children (2 to 11 months of age) and 107 children (12 to 35 months of age) with confirmed severe neurologic disease were included in the analysis. The analysis was stratified by age group: 2–11 and 12–35 months. No cases were observed in the 0–3 day risk period for both age groups. For the 0–7 day risk period, no cases were observed for the 2- to 11-month age group but one case was observed for the 12- to 35-month age group.

The study did not find a significant association with any manifestation of encephalopathy. The relative risk of severe neurologic disease in the 0–7 day risk period after meningococcal C conjugate vaccination was estimated at 1.28 (95% CI, 0.17–9.75). As evidenced by the wide confidence interval, the sample size is not large enough to get a more precise estimate of the relative risk. The authors concluded that administration of meningococcal C conjugate vaccine is not associated with an increased risk of severe neurologic disease within 0 to 7 days of vaccination.

Weight of Epidemiologic Evidence

The committee has limited confidence in the epidemiologic evidence, based on one study that lacked validity and precision, to assess an association between meningococcal vaccine and encephalitis or encephalopathy.

Mechanistic Evidence

The committee did not identify literature reporting clinical, diagnostic, or experimental evidence of encephalitis or encephalopathy after administration of meningococcal vaccine.

Weight of Mechanistic Evidence

T cells and complement activation may contribute to the symptoms of encephalitis or encephalopathy; however, the committee did not identify literature reporting evidence of these mechanisms after administration of meningococcal vaccine.

The committee assesses the mechanistic evidence regarding an association between meningococcal vaccine and encephalitis or encephalopathy as lacking.

Causality Conclusion

Conclusion 11.1: The evidence is inadequate to accept or reject a causal relationship between meningococcal vaccine and encephalitis.

Conclusion 11.2: The evidence is inadequate to accept or reject a causal relationship between meningococcal vaccine and encephalopathy.

ACUTE DISSEMINATED ENCEPHALOMYELITIS

Epidemiologic Evidence

No studies were identified in the literature for the committee to evaluate the risk of acute disseminated encephalomyelitis (ADEM) after the administration of meningococcal vaccine.

Weight of Epidemiologic Evidence

The epidemiologic evidence is insufficient or absent to assess an association between meningococcal vaccine and ADEM.

Mechanistic Evidence

The committee identified one publication reporting ADEM after administration of a meningococcal vaccine. The publication did not present evidence beyond temporality (Py and Andre, 1997). The publication did not contribute to the weight of mechanistic evidence.

Weight of Mechanistic Evidence

The symptoms described in the publication referenced above are consistent with those leading to a diagnosis of ADEM. Autoantibodies, T cells, and molecular mimicry may contribute to the symptoms of ADEM; however, the publication did not provide evidence linking these mechanisms to meningococcal vaccine.

The committee assesses the mechanistic evidence regarding an association between meningococcal vaccine and ADEM as lacking.

Causality Conclusion

Conclusion 11.3: The evidence is inadequate to accept or reject a causal relationship between meningococcal vaccine and ADEM.

TRANSVERSE MYELITIS

Epidemiologic Evidence

No studies were identified in the literature for the committee to evaluate the risk of transverse myelitis after the administration of meningococcal vaccine.

Weight of Epidemiologic Evidence

The epidemiologic evidence is insufficient or absent to assess an association between meningococcal vaccine and transverse myelitis.

Mechanistic Evidence

The committee did not identify literature reporting clinical, diagnostic, or experimental evidence of transverse myelitis after administration of meningococcal vaccine.

Weight of Mechanistic Evidence

Autoantibodies, T cells, and molecular mimicry may contribute to the symptoms of transverse myelitis; however, the committee did not identify literature reporting evidence of these mechanisms after administration of meningococcal vaccine.

The committee assesses the mechanistic evidence regarding an association between meningococcal vaccine and transverse myelitis as lacking.

Causality Conclusion

Conclusion 11.4: The evidence is inadequate to accept or reject a causal relationship between meningococcal vaccine and transverse myelitis.

MULTIPLE SCLEROSIS

Epidemiologic Evidence

The committee reviewed one study to evaluate the risk of multiple sclerosis (MS) after the administration of meningococcal vaccine. This one study (Laribiere et al., 2005) was not considered in the weight of epidemiologic evidence because it provided data from a passive surveillance system and lacked an unvaccinated comparison population.

Weight of Epidemiologic Evidence

The epidemiologic evidence is insufficient or absent to assess an association between meningococcal vaccine and MS.

Mechanistic Evidence

The committee did not identify literature reporting clinical, diagnostic, or experimental evidence of MS after administration of meningococcal vaccine.

Weight of Mechanistic Evidence

Autoantibodies, T cells, and molecular mimicry may contribute to the symptoms of MS; however the committee did not identify literature reporting evidence of these mechanisms after administration of meningococcal vaccine.

The committee assesses the mechanistic evidence regarding an association between meningococcal vaccine and MS as lacking.

Causality Conclusion

Conclusion 11.5: The evidence is inadequate to accept or reject a causal relationship between meningococcal vaccine and MS.

GUILLAIN-BARRÉ SYNDROME

Epidemiologic Evidence

The committee reviewed two studies to evaluate the risk of Guillain-Barré syndrome (GBS) after the administration of meningococcal vaccine. One study (Ball et al., 2001) was not considered in the weight of epidemiologic evidence because it provided data from a passive surveillance system and lacked an unvaccinated comparison population.

The one remaining controlled study (De Wals et al., 2008) contributed to the weight of epidemiologic evidence and is described below.

De Wals et al. (2008) conducted a retrospective cohort study on residents of Quebec, Canada, during the 2001 immunization campaign using meningococcal C vaccine. According to the Provincial Meningococcal Vaccine Registry, a total of 1,428,463 individuals (aged 2 months to 20 years) received at least one dose of vaccine from November 2000 through December 2002. The vaccination records were linked to hospital discharge records using information from the provincial database. Medical records were reviewed for patients who had diagnostic codes for GBS in the hospital discharge records; the authors classified cases as confirmed, possible, or probable. The risk period for observed GBS incidence was defined as 6 or 8 weeks following vaccination. The control period for expected GBS incidence included all other time observed during the study period. The analysis included 33 patients with GBS, of whom 19 received a meningococcal C vaccine. Only 2 cases had GBS onset within 8 weeks of vaccination, which was compared to 3.1 expected cases; the 6-week period included 1 observed case and 2.5 expected cases. The month- and age-adjusted incidence ratio of confirmed, probable, or possible cases of GBS within 8 weeks of meningococcal C vaccination was 0.65 (95% CI, 0.01–2.41) and within 6 weeks of vaccination was 0.40 (95% CI, 0.02–2.21). The authors concluded that meningococcal C vaccination does not appear to be associated with an increased risk of GBS, but they noted the limited power of the study to detect a small increased risk.

Weight of Epidemiologic Evidence

The committee has limited confidence in the epidemiologic evidence, based on one study that lacked validity and precision, to assess an association between meningococcal C vaccine and GBS.

Mechanistic Evidence

The committee identified one publication reporting GBS after administration of meningococcal vaccine. The publication did not provide evidence beyond temporality and did not contribute to the weight of mechanistic evidence (Pritchard et al., 2002).

Weight of Mechanistic Evidence

The symptoms described in the publication referenced above are consistent with those leading to a diagnosis of GBS. Autoantibodies, complement activation, immune complexes, T cells, and molecular mimicry may contribute to the symptoms of GBS; however, the publication did not provide evidence linking these mechanisms to meningococcal vaccine.

The committee assesses the mechanistic evidence regarding an association between meningococcal vaccine and GBS as lacking.

Causality Conclusion

Conclusion 11.6: The evidence is inadequate to accept or reject a causal relationship between meningococcal vaccine and GBS.

CHRONIC INFLAMMATORY DISSEMINATED POLYNEUROPATHY

Epidemiologic Evidence

No studies were identified in the literature for the committee to evaluate the risk of chronic inflammatory disseminated polyneuropathy (CIDP) after the administration of meningococcal vaccine.

Weight of Epidemiologic Evidence

The epidemiologic evidence is insufficient or absent to assess an association between meningococcal vaccine and CIDP.

Mechanistic Evidence

The committee identified one publication reporting CIDP after administration of meningococcal vaccine. The publication did not provide evidence beyond temporality, which was determined to be too long (Datie et al., 2003). Long latencies between vaccine administration and development of symptoms make it impossible to rule out other possible causes. The publication did not contribute to the weight of mechanistic evidence.

Weight of Mechanistic Evidence

The symptoms described in the publication referenced above are consistent with those leading to a diagnosis of CIDP. Autoantibodies, T cells, and molecular mimicry may contribute to the symptoms of CIDP; however, the publication did not provide evidence linking these mechanisms to meningococcal vaccine.

The committee assesses the mechanistic evidence regarding an association between meningococcal vaccine and CIDP as lacking.

Causality Conclusion

Conclusion 11.7: The evidence is inadequate to accept or reject a causal relationship between meningococcal vaccine and CIDP.

ANAPHYLAXIS

Epidemiologic Evidence

The committee reviewed three studies to evaluate the risk of anaphylaxis after the administration of meningococcal vaccine. These three studies (Ball et al., 2001; Bentsi-Enchill et al., 2007; Yergeau et al., 1996) were not considered in the weight of epidemiologic evidence because they provided data from passive surveillance systems and lacked unvaccinated comparison populations.

Weight of Epidemiologic Evidence

The epidemiologic evidence is insufficient or absent to assess an association between meningococcal vaccine and anaphylaxis.

Mechanistic Evidence

The committee identified four publications reporting anaphylaxis after administration of meningococcal vaccine. Two publications did not provide evidence including the time frame between vaccination and the development of symptoms (Makela et al., 1977; Peng and Jick, 2004). One publication reported the concomitant administration of vaccines making it difficult to determine which, if any, vaccine could have been the precipitating event (Ball et al., 2001). These publications did not contribute to the weight of mechanistic evidence.

Described below is one publication reporting clinical, diagnostic, or experimental evidence that contributed to the weight of mechanistic evidence.

Yergeau et. al. (1996) performed a retrospective descriptive study of adverse events reported to a central passive surveillance system after meningococcal vaccination in the province of Quebec, Canada, from December 1992 through March 1993. Meningococcal vaccines in use during the study period included groups A, C, Y, and W135 or only groups A and C. The authors reported one case of anaphylaxis developing 30 minutes postvacccination in a 12-year-old girl. The patient presented with decreased blood pressure, dyspnea, and bronchospasm despite two doses of adrenalin. The patient made a full recovery.

Weight of Mechanistic Evidence

The publication described above presented clinical evidence sufficient for the committee to conclude the vaccine was a contributing cause of anaphylaxis after administration of meningococcal vaccine. The clinical description established a strong temporal relationship between administration of the vaccine and the anaphylactic reaction.

The committee assesses the mechanistic evidence regarding an association between meningococcal vaccine and anaphylaxis as strong based on one case presenting temporality and clinical symptoms consistent with anaphylaxis.

Causality Conclusion

Conclusion 11.8: The evidence convincingly supports a causal relationship between meningococcal vaccine and anaphylaxis.

CHRONIC HEADACHE

Epidemiologic Evidence

The committee reviewed one study to evaluate the risk of chronic headache after the administration of meningococcal vaccine. This one study (Laribiere et al., 2005) was not considered in the weight of epidemiologic evidence because it provided data from a passive surveillance system and lacked an unvaccinated comparison population.

Weight of Epidemiologic Evidence

The epidemiologic evidence is insufficient or absent to assess an association between meningococcal vaccine and chronic headache.

Mechanistic Evidence

The committee did not identify literature reporting clinical, diagnostic, or experimental evidence of chronic headache after administration of meningococcal vaccine.

Weight of Mechanistic Evidence

The committee assesses the mechanistic evidence regarding an association between meningococcal vaccine and chronic headaches as lacking.

Causality Conclusion

Conclusion 11.9: The evidence is inadequate to accept or reject a causal relationship between meningococcal vaccine and chronic headache.

CONCLUDING SECTION

Table 11-1 provides a summary of the epidemiologic assessments, mechanistic assessments, and causality conclusions for meningococcal vaccine.

TABLE 11-1. Summary of Epidemiologic Assessments, Mechanistic Assessments, and Causality Conclusions for Meningococcal Vaccine.

TABLE 11-1

Summary of Epidemiologic Assessments, Mechanistic Assessments, and Causality Conclusions for Meningococcal Vaccine.

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Copyright 2012 by the National Academy of Sciences. All rights reserved.
Bookshelf ID: NBK190008

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