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11
Meningococcal Vaccine
INTRODUCTION
Meningococcal disease describes the clinical manifestations of inva-
sive 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 aerosol-
ized droplets of respiratory fluids (Granoff et al., 2008). Carried by ap-
proximately 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 (meningo-
coccal 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 ad-
renal hemorrhage (Waterhouse-Friderichsen syndrome), and multiorgan
failure (Granoff et al., 2008). Pneumonia is also associated with meningo-
coccal 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 inva-
sive infection; however, these developments are rare (Apicella, 2010; Miller
et al., 1979; Rosenstein et al., 1999; Schaad, 1980).
599
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600 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
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). Sero-
group 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, at-
tempts were made to develop inactivated whole-cell vaccine, but this direc-
tion 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 immuno-
genicity 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
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MENINGOCOCCAL VACCINE
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 polysac-
charide vaccines (MPSVs) are available worldwide in bivalent (A and C)
and tetravalent (A, C, W-135, and Y) formulations, but only the tetra-
valent 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 dis-
tilled 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 adju-
vant (Novartis Vaccines and Diagnostics, 2010).
The Advisory Committee on Immunization Practices currently recom-
mends routine vaccination of persons 11 to 12 years of age and individuals
at increased risk of meningococcal disease including college freshman liv-
ing 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
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602 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
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 epi-
demiologic 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 Surveil-
lance 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 vac-
cination; each child was categorized as having been vaccinated or unvac-
cinated, 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 neu-
rologic disease within 0 to 7 days of vaccination.
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603
MENINGOCOCCAL VACCINE
Weight of Epidemiologic Evidence
The committee has limited confidence in the epidemiologic evi-
dence, based on one study that lacked validity and precision, to
assess an association between meningococcal vaccine and encepha-
litis or encephalopathy.
Mechanistic Evidence
The committee did not identify literature reporting clinical, diagnostic,
or experimental evidence of encephalitis or encephalopathy after adminis-
tration 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 as-
sociation between meningococcal vaccine and encephalitis or en-
cephalopathy as lacking.
Causality Conclusion
Conclusion 11.1: The evidence is inadequate to accept or re-
ject a causal relationship between meningococcal vaccine and
encephalitis.
Conclusion 11.2: The evidence is inadequate to accept or re-
ject a causal relationship between meningococcal vaccine and
encephalopathy.
ACUTE DISSEMINATED ENCEPHALOMYELITIS
Epidemiologic Evidence
No studies were identified in the literature for the committee to evalu-
ate the risk of acute disseminated encephalomyelitis (ADEM) after the
administration of meningococcal vaccine.
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604 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
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 ad-
ministration 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 con-
sistent with those leading to a diagnosis of ADEM. Autoantibodies, T cells,
and molecular mimicry may contribute to the symptoms of ADEM; how-
ever, the publication did not provide evidence linking these mechanisms to
meningococcal vaccine.
The committee assesses the mechanistic evidence regarding an as-
sociation 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 evalu-
ate 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.
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MENINGOCOCCAL VACCINE
Mechanistic Evidence
The committee did not identify literature reporting clinical, diagnostic,
or experimental evidence of transverse myelitis after administration of me-
ningococcal 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 as-
sociation 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 epidemio-
logic 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.
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606 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
Weight of Mechanistic Evidence
Autoantibodies, T cells, and molecular mimicry may contribute to the
symptoms of MS; however the committee did not identify literature report-
ing evidence of these mechanisms after administration of meningococcal
vaccine.
The committee assesses the mechanistic evidence regarding an as-
sociation 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 epidemio-
logic 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 resi-
dents of Quebec, Canada, during the 2001 immunization campaign using
meningococcal C vaccine. According to the Provincial Meningococcal Vac-
cine 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 Decem-
ber 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 inci-
dence 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 menin-
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MENINGOCOCCAL VACCINE
gococcal 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 in-
creased 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 evi-
dence, 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 adminis-
tration 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 consis-
tent with those leading to a diagnosis of GBS. Autoantibodies, complement
activation, immune complexes, T cells, and molecular mimicry may con-
tribute 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 as-
sociation 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 evalu-
ate the risk of chronic inflammatory disseminated polyneuropathy (CIDP)
after the administration of meningococcal vaccine.
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608 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
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 adminis-
tration 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 publica-
tion did not contribute to the weight of mechanistic evidence.
Weight of Mechanistic Evidence
The symptoms described in the publication referenced above are con-
sistent 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 me-
ningococcal vaccine.
The committee assesses the mechanistic evidence regarding an as-
sociation 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 anaphy-
laxis 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.
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MENINGOCOCCAL VACCINE
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 ex-
perimental 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 menin-
gococcal 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 postvac-
cination 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 administra-
tion of the vaccine and the anaphylactic reaction.
The committee assesses the mechanistic evidence regarding an asso-
ciation between meningococcal vaccine and anaphylaxis as strong
based on one case presenting temporality and clinical symptoms
consistent with anaphylaxis.
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610 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
Causality Conclusion
Conclusion 11.8: The evidence convincingly supports a causal rela-
tionship 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 me-
ningococcal vaccine.
Weight of Mechanistic Evidence
The committee assesses the mechanistic evidence regarding an as-
sociation 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.
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TABLE 11-1 Summary of Epidemiologic Assessments, Mechanistic Assessments, and Causality Conclusions for
Meningococcal Vaccine
Studies Contributing Cases Contributing
Epidemiologic to the Epidemiologic Mechanistic to the Mechanistic
Vaccine Adverse Event Assessment Assessment Assessment Assessment Causality Conclusion
Meningococcal Encephalitis Limited 1 Lacking None Inadequate
Meningococcal Encephalopathy Limited 1 Lacking None Inadequate
Meningococcal Acute Disseminated Insufficient None Lacking None Inadequate
Encephalomyelitis
Meningococcal Transverse Myelitis Insufficient None Lacking None Inadequate
Meningococcal Multiple Sclerosis Insufficient None Lacking None Inadequate
Meningococcal Guillain-Barré Syndrome Limited 1 Lacking None Inadequate
Meningococcal Chronic Inflammatory Insufficient None Lacking None Inadequate
Disseminated
Polyneuropathy
Meningococcal Anaphylaxis Insufficient None Strong 1 Convincingly Supports
Meningococcal Chronic Headache Insufficient None Lacking None Inadequate
611
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612 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
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