Serum bactericidal antibody response to serogroup C polysaccharide meningococcal vaccination in children with primary antibody deficiencies (2023)

Table of Contents
Vaccine Abstract Introduction Section snippets Subjects Characteristics of the patients Age distribution Discussion Acknowledgements References (43) The loss of IgM memory B cells correlates with clinical disease in common variable immunodeficiency J Allergy Clin Immunol Scientific challenges for the quality control and production of group C meningococcal conjugate vaccines Vaccine Meningococcal surrogates of protection–serum bactericidal antibody activity Vaccine Development and phase 1 clinical testing of a conjugate vaccine against meningococcus A and C Vaccine Meningococcal serogroup C-specific IgG antibody responses and serum bactericidal titres in children following vaccination with a meningococcal A/C polysaccharide vaccine FEMS Immunol Med Microbiol Development of natural immunity to Neisseria meningitides Vaccine A review of vaccine research and development: meningococcal disease Vaccine Common variable immunodeficiency: clinical and immunological features of 248 patients Clin Immunol Primary immunodeficiency diseases: an update from the International Union of Immunological Societies Primary Immunodeficiency Diseases Classification Committee Meeting in Budapest J Allergy Clin Immunol Update on primary immunodeficiency diseases J Allergy Clin Immunol Frequency and clinical manifestations of patients with primary immunodeficiency disorders in Iran: update from the Iranian primary immunodeficiency registry J Clin Immunol Primary immunodeficiency in Iran: first report of the national registry of PID in children and adults J Clin Immunol Immunologic disorders: general considerations The primary immunodeficiencies N Engl J Med Agammaglobulinemia Pediatrics Primary hypogammaglobulinaemia: a survey of clinical manifestations and complications Q J Med Prevention of meningococcal disease Am Fam Physician Time of hope for the eventual elimination of meningococcal strains A, C, Y, and W-135 in the United States Am Fam Physician Prevention and control of meningococcal disease. Recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR Recomm Rep The meningococcal vaccine—public policy and individual choices N Engl J Med Meningococcal vaccines Cited by (35) Use and interpretation of diagnostic vaccination in primary immunodeficiency: A working group report of the Basic and Clinical Immunology Interest Section of the American Academy of Allergy, Asthma & Immunology Recombinant outer membrane secretin PilQ <inf>406-770</inf> as a vaccine candidate for serogroup B Neisseria meningitidis B-cell-T-cell activation and interaction in common variable immunodeficiency Evaluation of Immunoglobulin Levels and Infection Rate in Patients with Common Variable Immunodeficiency After Immunoglobulin Replacement Therapy Association of IL-4 and IL-10 gene promoter polymorphisms with common variable immunodeficiency Evaluation of liver diseases in Iranian patients with primary antibody deficiencies Recommended articles (6) HHV-6-positivity in diseases with demyelination Serum interleukin 6 and 10 levels in Takotsubo cardiomyopathy: Increased admission levels may predict adverse events at follow-up Characterization, crystal structures, electrochemical and antibacterial studies of four new binuclear cobalt(III) complexes derived from o-aminobenzyl alcohol Postencephalitic parkinsonism and selective involvement of substantia nigra in childhood Increased plasma IL-6, IL-8, TNF-alpha, and G-CSF in Japanese narcolepsy Transcriptome Analysis of Adrenocortical Cells in Health and Disease FAQs Videos

Vaccine

Volume 25, Issue 29,

20 July 2007

, Pages 5308-5314

Author links open overlay panel, , , , , , , , , ,

Abstract

Primary antibody deficiencies are characterized by decreased serum levels of immunoglobulin isotypes and increased susceptibility to infection by various microorganisms including encapsulated bacteria. This study was performed in order to evaluate bactericidal antibody response of these patients to polysaccharide meningococcal vaccine. Twenty-four antibody deficient children of mean age 11.2±3.5 years, and 15 sex and age-matched healthy volunteers were enrolled. All subjects received meningococcal polysaccharide vaccine A+C; blood samples were collected before vaccination and 3 weeks after vaccination. Following vaccination, the serum bactericidal antibody (SBA) geometric mean titre was significantly increased compared to the prevaccination level in the patient group (8.98 versus 1.63, P<0.001) and the control group (12.13 versus 1.26, P<0.001). All controls had a protective SBA response (SBA titre of ≥8 post-vaccination or rise of ≥4-fold from pre- to post-vaccination), whereas only 16 of 24 patients (66.6%) had a protective response (P=0.014). The non-responder patients included 5 cases with common variable immunodeficiency, two cases with hyper IgM syndrome, and one case with IgG subclass deficiency. This study indicates that some patients with primary antibody deficiencies can produce protective post-vaccination titres similar to the normal population, despite the common perception that patients with primary antibody deficiencies respond poorly to vaccination. This supports the use of polysaccharide-containing vaccines in these patients.

Introduction

Primary immunodeficiency disorders (PID) are characterized by various defects of the immune system, and increased susceptibility to infections [1], [2], [3], [4]. Since Bruton described agammaglobulinemia for the first time in 1952 [5], more than 100 different types of PID have been identified [3], [6].

Patients with primary antibody deficiencies (PAD) are the most common group amongst those with PID, and are characterized by decreased serum levels of immunoglobulin isotypes and increased susceptibility to certain infections [1], [7], [8], [9]. This group comprises 20 different disorders, ranging from a severe reduction in all serum immunoglobulin isotypes with absent B cells, to specific antibody deficiencies with normal immunoglobulin concentrations and B cell counts [1], [7]. Patients with PAD are susceptible to pyogenic infections, especially infections caused by encapsulated bacteria such as Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis[8], [9].

Meningococcal infection is a devastating disease, which can result in severe complications and death despite the use of antibiotics [10], [11], [12]. Globally, there is an incidence of at least 1 per 100,000 persons per year, a mortality rate of 10–14% and a morbidity rate of 11–19% [11], [12], [13]. It is estimated that 5–15% of the population are asymptomatic carriers who may transmit the organism by contact from person to person [14], [15]. Although only a small proportion of normal persons colonized with N. meningitidis will develop meningitis [14], there is an increased susceptibility to meningitis in PAD patients, with an incidence of approximately 4 per 1000 cases per year [1], [7], [16], [17], [18], [19].

The polysaccharide vaccine against meningococcus serogroups A and C was the prototype vaccine for this infection, and has been in use for 30 years. This vaccine, which is available worldwide, is safe, inexpensive and effective against the serotypes A and C [14], [20]. The plain polysaccharide vaccines are T-cell independent [10], [21], [22]. Although conjugate vaccines for serogroups other than serogroup B are available, they are not deployed worldwide.

This study was performed in order to evaluate bactericidal antibody response of patients with PAD to polysaccharide meningococcal vaccine. This is the first time that the bactericidal antibody response to this vaccine has been investigated in this group of patients.

Section snippets

Subjects

In this study, 24 pediatric cases of PAD (16 male and 8 female; mean age: 11.2±3.5 years) were recruited as the patient group and 15 sex and age-matched healthy volunteers (9 male and 6 female; mean age: 12.6±2.7 years) were selected as control group. All patients who had been under regular follow-up in the Children's Medical Center Hospital, a referral center for patients with PID in Tehran, Iran [23], were selected for this study. Diagnosis of PAD is based on standard criteria, which have

Characteristics of the patients

The patient group comprised 16 cases with common variable immunodeficiency (CVID), 3 with hyper IgM syndrome (HIgM), 2 with selective IgA deficiency (SIgAD), 1 with isolated IgG subclass deficiency (IgGSD) and 2 with IgA with IgG subclass deficiency (IgAIgGSD) (Table 1). The serum immunoglobulin levels and B- and T-lymphocyte populations of the patients are shown in Table 2.

Age distribution

All the patients were children at the time of study (median: 11.8; age range: 4–16 years). The median age of first

Discussion

PID are a heterogeneous group of disorders, characterized by hypogammaglobulinemia and an increased susceptibility to severe and recurrent infections [1], [2], [3], [4]. In this study, we evaluated the bactericidal antibody response of patients with PAD to polysaccharide meningococcal vaccine.

More than half of our patients had at least one pathognomonic clinical manifestation during their first year of life. This long diagnosis lag may be due to a lack of awareness about such diseases among

Acknowledgements

This research has been supported by Immunology, Asthma and Allergy Research Institute, Tehran University of Medical Sciences and Health Services grant.

The authors would like to thank all colleagues in Immunology, Asthma and Allergy Research Institute, especially Miss Shokouhi Shoormasti, Mrs. Faridani, and Mr. Siavashi for their kind assistance in preparing the samples for this study. Also, thanks to all colleagues in the Department of Bacterial Vaccine and Antigen Production, Pasteur Institute

References (43)

  • R. Carsetti et al.

    The loss of IgM memory B cells correlates with clinical disease in common variable immunodeficiency

    J Allergy Clin Immunol

    (2005)

  • L. Jodar et al.

    Scientific challenges for the quality control and production of group C meningococcal conjugate vaccines

    Vaccine

    (2004)

  • R. Borrow et al.

    Meningococcal surrogates of protection–serum bactericidal antibody activity

    Vaccine

    (2005)

  • P. Costantino et al.

    Development and phase 1 clinical testing of a conjugate vaccine against meningococcus A and C

    Vaccine

    (1992)

  • R. Borrow et al.

    Meningococcal serogroup C-specific IgG antibody responses and serum bactericidal titres in children following vaccination with a meningococcal A/C polysaccharide vaccine

    FEMS Immunol Med Microbiol

    (2000)

  • A.J. Pollard et al.

    Development of natural immunity to Neisseria meningitides

    Vaccine

    (2001)

  • M.P. Girard et al.

    A review of vaccine research and development: meningococcal disease

    Vaccine

    (2006)

  • C. Cunningham-Rundles et al.

    Common variable immunodeficiency: clinical and immunological features of 248 patients

    Clin Immunol

    (1999)

  • L. Notarangelo et al.

    Primary immunodeficiency diseases: an update from the International Union of Immunological Societies Primary Immunodeficiency Diseases Classification Committee Meeting in Budapest

    J Allergy Clin Immunol

    (2006)

  • F.A. Bonilla et al.

    Update on primary immunodeficiency diseases

    J Allergy Clin Immunol

    (2006)

  • N. Rezaei et al.

    Frequency and clinical manifestations of patients with primary immunodeficiency disorders in Iran: update from the Iranian primary immunodeficiency registry

    J Clin Immunol

    (2006)

  • A. Aghamohammadi et al.

    Primary immunodeficiency in Iran: first report of the national registry of PID in children and adults

    J Clin Immunol

    (2002)

  • E.R. Stiehm et al.

    Immunologic disorders: general considerations

  • F.S. Rosen et al.

    The primary immunodeficiencies

    N Engl J Med

    (1995)

  • O.C. Bruton

    Agammaglobulinemia

    Pediatrics

    (1952)

  • R.A. Hermaszewski et al.

    Primary hypogammaglobulinaemia: a survey of clinical manifestations and complications

    Q J Med

    (1993)

  • S.R. Kimmel

    Prevention of meningococcal disease

    Am Fam Physician

    (2005)

  • R.K. Zimmerman

    Time of hope for the eventual elimination of meningococcal strains A, C, Y, and W-135 in the United States

    Am Fam Physician

    (2005)

  • O.O. Bilukha et al.

    Prevention and control of meningococcal disease. Recommendations of the Advisory Committee on Immunization Practices (ACIP)

    (Video) October 2017 ACIP Meeting - Pneumococcal Vaccines; Anthrax; RSV; Evidence based Recommendations

    MMWR Recomm Rep

    (2005)

  • P.A. Offit et al.

    The meningococcal vaccine—public policy and individual choices

    N Engl J Med

    (2003)

  • D.M. Granoff et al.

    Meningococcal vaccines

  • (Video) February 2019 ACIP Meeting - Meningococcal Vaccines

    Cited by (35)

    • Use and interpretation of diagnostic vaccination in primary immunodeficiency: A working group report of the Basic and Clinical Immunology Interest Section of the American Academy of Allergy, Asthma & Immunology

      2012, Journal of Allergy and Clinical Immunology

      A major diagnostic intervention in the consideration of many patients suspected to have primary immunodeficiency diseases (PIDDs) is the application and interpretation of vaccination. Specifically, the antibody response to antigenic challenge with vaccines can provide substantive insight into the status of human immune function. There are numerous vaccines that are commonly used in healthy individuals, as well as others that are available for specialized applications. Both can potentially be used to facilitate consideration of PIDD. However, the application of vaccines and interpretation of antibody responses in this context are complex. These rely on consideration of numerous existing specific studies, interpolation of data from healthy populations, current diagnostic guidelines, and expert subspecialist practice. This document represents an attempt of a working group of the American Academy of Allergy, Asthma & Immunology to provide further guidance and synthesis in this use of vaccination for diagnostic purposes in consideration of PIDD, as well as to identify key areas for further research.

    • Recombinant outer membrane secretin PilQ <inf>406-770</inf> as a vaccine candidate for serogroup B Neisseria meningitidis

      2012, Vaccine

      Secretin PilQ is an antigenically conserved outer membrane protein which is present on most meningococci. This protein naturally expressed at high levels and is essential for meningococcal pilus expression at the cell surface. A 1095bp fragment of C-terminal of secretin pilQ from serogroup B Neisseria meningitidis was cloned into prokaryotic expression vector pET-28a. Recombinant protein was overexpressed with IPTG and affinity-purified by Ni-NTA agarose. BALB/c mice were immunized subcutaneously with purified rPilQ406–770 mixed with Freund's adjuvant. Serum antibody responses to serogroups A and B N. meningitidis whole cells or purified rPilQ406–770 and functional activity of antibodies were determined by ELISA and SBA, respectively. The output of rPilQ406–770 was approximately 50% of the total bacterial proteins. Serum IgG responses were significantly increased in immunized group with PilQ406–770 mixed with Freund's adjuvant in comparison with control groups. Antisera produced against rPilQ406–770 demonstrated strong surface reactivity to serogroups A and B N. meningitidis tested by whole-cell ELISA. Surface reactivity to serogroup B N. meningitidis was higher than serogroup A. The sera from PilQ406–770 immunized animals were strongly bactericidal against serogroups A and B. These results suggest that rPilQ406–770 is a potential vaccine candidate for serogroup B N. meningitidis.

    • B-cell-T-cell activation and interaction in common variable immunodeficiency

      2010, Human Immunology

      Common variable immunodeficiency (CVID) is a heterogeneous group of disorders, characterized by hypogammaglobulinemia and normal or low numbers of B cells, which predispose patients to recurrent infections. Peripheral blood mononuclear cells from 19 patients with CVID, and age- and sex-matched controls, were subjected to an in vitro assay of B-cell–T-cell activation and interaction, using anti-immunoglobulin (Ig)-D conjugated to dextran (α-δ-dex), as a polyclonal T independent type 2 antigen mimic, with and without anti-CD3/anti-CD28, as polyclonal T-cell stimuli. Stimulation of lymphocytes with either anti-CD3 or anti-CD3 plus anti-CD28 induced T-cell activation and proliferation in CVID patients who were similar to age- and sex-matched controls, but B cells of patients were significantly less activated when peripheral blood mononuclear cells were stimulated with polyclonal T-cell agonists alone. Comparison of CD86 expression in the patients with matched controls revealed that patients had low B-cell activation in response to T-cell stimuli (bystander T-cell help). In conclusion, this sample of CVID patients exhibits a defect of T-cell “help” to B cells, and/or B-cell response to T-cell help.

    • Evaluation of Immunoglobulin Levels and Infection Rate in Patients with Common Variable Immunodeficiency After Immunoglobulin Replacement Therapy

      2010, Journal of Microbiology, Immunology and Infection

      Common variable immunodeficiency (CVID) is characterized by decreased serum levels of IgG and increased susceptibility to recurrent infections. The aim of this study was to evaluate the IgG subclass levels of CVID patients.

      Twenty-four CVID patients who had been under regular intravenous immunoglobulin replacement therapy for 96.13 ± 54.83 months were enrolled in this study. Serum IgG and IgG subclass levels, and clinical outcomes for these patients were evaluated after this period of treatment.

      Mean serum IgG levels were significantly increased from 272.91 ± 185.58 mg/dL at the time of diagnosis to 455.29 ± 200.23 mg/dL after treatment, while there was no significant difference in the serum levels of IgM and IgA. Decreased serum levels of IgG1 were detected in 75% of the patients studied. Decreased serum levels of IgG2, IgG3 and IgG4 were also detected in 6, 11, and 11 patients, respectively. All patients experienced recurrent infectious diseases either before, or after, diagnosis.

      Although serum IgG levels in the patients significantly increased after regular intravenous immunoglobulin replacement therapy, serum IgM and IgA levels remained diminished over time. Furthermore, a number of cases had low levels of IgG subclasses, in spite of normal total IgG levels, which could explain why some patients had continued infections, even after immunoglobulin replacement therapy.

    • Association of IL-4 and IL-10 gene promoter polymorphisms with common variable immunodeficiency

      2010, Immunobiology

      Common variable immunodeficiency (CVID) is a heterogeneous group of disorders, characterized by severe reduction in serum IgG and IgA with normal or low number of B-cells. Interleukin (IL)-4 and IL-10 levels could be altered in CVID patients, while cytokine production could be affected with polymorphisms of gene promoter regions.

      The allele and genotype frequencies of IL-4 and IL-10 gene promoter polymorphic sites were investigated in 30 CVID patients in comparison with controls.

      (Video) Oct 20, 2022 ACIP Meeting - Public comment & Meningococcal Vaccines

      IL-10 GA genotype was the most frequent genotype at position −1082 in CVID patients, whereas IL-10 AA genotype was significantly decreased in the patient group at the same position. For IL-4, TG (−1098) and TC (−33) genotypes were significantly overrepresented in CVID group, while frequencies of IL-4 TT (−1098) and CC (−33) were significantly decreased in the patient group. Frequency of IL-10 ACA and IL4 GCC haplotypes in CVID patients were significantly higher than controls, whilst frequency of IL-10 ACC and IL-4 TCC significantly decreased in the patient group.

      Considering low frequency of IL-10 ACC low producing haplotype, high production of IL-10 could be explained in CVID patients. High production of IL-4 could also be expected based on haplotypes frequencies of this cytokine gene polymorphisms.

    • Evaluation of liver diseases in Iranian patients with primary antibody deficiencies

      2009, Annals of Hepatology

      Citation Excerpt :

      Because of high incidence of liver involvement, it is advised to perform a biochemical liver profile, including serum concentrations of amino transaminases must be performed at least twice yearly in all patients with primary antibody deficiency.43 The presence of autoantibodies like smooth muscle antibody (SMA) is usual in PID specially in T-cell deficiencies that can reflect dysregulation in immune system and may involve the liver.5,14,16,30,44 Triggering of autoimmune inflammatory processes by hepatotropic viruses is one possible mechanism by which such chronic liver disease may develop.14,44

      Introduction. Patients with primary antibody deficiency (PAD) can complicate with liver disease. This study was performed in order to study the prevalence and causes of hepatobiliary diseases in Iranian patients with PAD.

      Material and methods. Sixty-two patients with PAD were followed-up and signs and symptoms of liver disease were recorded. All patients were screened for hepatitis C virus (HCV-RNA) and those patients with any sign of liver disease or gastrointestinal complaints were tested for Cryptosporidium parvum.

      Results. Clinical evidences of liver disease, including hepatomegaly, were documented in 22 patients (35.5%). Eight patients (13%) had clinical and/or laboratory criteria of chronic liver disease. Only one patient was HCV-RNA positive; he had stigmata of chronic liver disease and pathologic evidence of chronic active hepatitis with cirrhosis. Cryptosporidium parvum test was positive for one patient with hyper-IgM syndrome. In liver biopsy of patients with liver involvement, one had histological findings related to sclerosing cholangitis, and five had mild to moderate chronic active hepatitis with unknown reason.

      Conclusions. Chronic active hepatitis is the most common pathologic feature of liver injury in Iranian patients with PAD. Liver disease in PAD usually accompanies with other organ involvements and could increase the mortality of PAD. Whether this high rate of liver disease with unknown origin (75%) is the result of an unidentified hepatotropic virus or other mechanisms such as autoimmunity, is currently difficult to understand.

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    FAQs

    What serogroup is meningococcal polysaccharide? ›

    Meningococcal group A polysaccharide is group-specific polysaccharide antigens extracted and purified from Neisseria meningitidis serogroup A. N. meningitidis is a bacteria that causes endemic and epidemic diseases including meningitis and meningococcemia.

    What are the reactions to the meningitis vaccine? ›

    Soreness, redness, or swelling where the shot is given, tiredness, fatigue, headache, muscle or joint pain, fever, chills, nausea, or diarrhea can happen after meningococcal B vaccination. Some of these reactions occur in more than half of the people who receive the vaccine.

    What is serogroup B meningococcal vaccine? ›

    Meningococcal B vaccine can help protect against meningococcal disease caused by serogroup B. A different meningococcal vaccine is available that can help protect against serogroups A, C, W, and Y.

    What are the side effects of meningococcal B vaccine in infants? ›

    The meningococcal B vaccine is safe and effective, although all medications and vaccines can have side effects. Babies who get the meningococcal B vaccine are more likely to develop a high temperature (fever). Other common side effects include irritability, pain, redness and swelling at the injection site.

    What is meningococcal group C vaccine? ›

    Conclusions: Group C meningococcal polysaccharide vaccine is indicated in adults and children over 2 years old to protect them from meningococcal disease due to group C when exposed to high risk of infection.

    Who gets meningococcal polysaccharide vaccine? ›

    All 11 to 12 year olds should get a MenACWY vaccine, with a booster dose at 16 years old. Teens and young adults (16 through 23 years old) also may get a MenB vaccine. CDC also recommends meningococcal vaccination for other children and adults who are at increased risk for meningococcal disease.

    Should I give my child the meningococcal vaccine? ›

    Who should get the meningococcal vaccines? All children ages 11 through 12 years should receive meningococcal vaccine (MenACWY) followed by a booster dose at age 16 years. Vaccination is also recommended for all adolescents ages 13 through 18 years who did not receive a dose at age 11-12 years.

    Is there an immune response to meningitis vaccine? ›

    Vaccines that help protect against meningococcal disease work well but cannot prevent all cases. As part of the licensure process, MenACWY and MenB vaccines showed that they produce an immune response. This immune response suggests the vaccines provide protection, but data are limited on how well they work.

    What are rare side effects of meningococcal vaccine? ›

    In rare cases, a meningococcal vaccine may cause a severe allergic reaction. Signs of this include: Hoarseness, wheezing, trouble breathing, or swallowing. Hives, itching, skin warmth, or redness.

    What is the difference between meningococcal vaccine and meningitis B vaccine? ›

    The MenACWY vaccine is very effective at protecting against four strains of the bacteria, while the MenB vaccine protects against a fifth strain.

    Who is at risk because of a serogroup B meningococcal disease outbreak? ›

    Babies, teens, and young adults have higher rates of meningococcal disease than people of other ages do. Other factors, such as having certain medical conditions, can increase your risk for getting this disease, no matter how old you are.

    Should my baby have meningococcal B vaccine? ›

    Some people are at higher risk of getting meningococcal disease. The following high-risk groups (listed below) are recommended for meningococcal vaccine: all infants and young children, particularly those aged less than 2 years. adolescents aged 15 to 19 years.

    What are the cons of meningococcal vaccine? ›

    MenB vaccines are safe. However, as with any vaccine, side effects can occur.
    • Soreness, redness, or swelling where the shot was given.
    • Feeling tired (fatigue)
    • Headache.
    • Muscle or joint pain.
    • Fever or chills.
    • Nausea or diarrhea.

    What are the issues with meningococcal vaccine? ›

    The most common side effects are usually mild and go away on their own. Severe allergic reactions following vaccination are rare, but can be life threatening. Symptoms of a severe allergic reaction can include hives, swelling of the face and throat, difficulty breathing, a fast heartbeat, dizziness, and weakness.

    How many years is the meningococcal vaccine good for? ›

    Meningitis vaccines are thought to only last for about five years, according to the Center for Young Women's Health. Adults can also get the meningitis vaccine if their doctors recommend it.

    Why is meningitis C vaccine discontinued? ›

    However, based on the decline of diseases know as invasive meningococcal A, C, W and Y, a dose of MenC-containing vaccine for infants is no longer recommended.

    What is the difference between meningococcal B and C? ›

    The meningococcal C (Men-C) vaccine protects against infection from meningococcal bacteria, type C. The meningococcal quadrivalent vaccine protects against 4 types of meningococcal bacteria: types A, C, Y and W-135. The meningococcal B (Men-B) vaccine protects against infection from meningococcal bacteria, type B.

    Is meningococcal C the same as meningitis? ›

    The meningitis C vaccine offers protection against a type of bacteria called meningococcal group C bacteria, which can cause meningitis. Babies are offered a combined Hib/MenC vaccine at 1 year of age.

    Should I vaccinate against meningococcal B? ›

    Vaccination is a safe and effective way to protect yourself from meningococcal disease. Meningococcal disease is most commonly caused by types A, B, C, W and Y. Vaccines can protect against all these types, but different vaccines protect against different types.

    Do college students need meningitis B vaccine? ›

    The MenACWY vaccine is recommended for college freshman living in a dormitory. The vaccine has been recommended for 11-12 year olds since 2005, so it is possible that incoming freshmen have already received a dose. If you received a dose before age 16, you should get a booster before you go to college.

    What are the first signs of meningococcal? ›

    Symptoms may include:
    • Fever and chills.
    • Fatigue (feeling tired)
    • Vomiting.
    • Cold hands and feet.
    • Severe aches or pain in the muscles, joints, chest, or abdomen (belly)
    • Rapid breathing.
    • Diarrhea.
    • In the later stages, a dark purple rash.

    Is meningitis vaccine worth it? ›

    The CDC recommends that people have a vaccination against meningitis. Guidelines suggest that all children receive the MenACWY vaccine at 11–12 and the booster at 16.

    Do you need meningococcal vaccine every 5 years? ›

    For patients who received their most recent dose at age 7 years or older, administer the booster dose 5 years later. Administer boosters every 5 years thereafter throughout life as long as the person remains at increased risk for meningococcal disease.

    What age is meningitis C vaccine given? ›

    The Hib/MenC vaccine is offered to all babies at the age of 1 year as part of the NHS vaccination schedule. The vaccine: boosts the protection your baby has already gained from their 1st course of Hib vaccine, which they received in the 6-in-1 vaccine at 8, 12 and 16 weeks old.

    How likely is it to get meningitis after vaccination? ›

    Like with any vaccine, meningococcal vaccines are not 100% effective. This means there is still a chance someone can develop meningococcal disease after vaccination. People should know the symptoms of meningococcal disease since early recognition and quick medical attention are extremely important.

    Who is generally at highest risk for meningitis Why? ›

    Although meningitis affects all ages, young children are most at risk. Newborn babies are at most risk from Group B streptococcus, young children are at higher risk from meningococcus, pneumococcus and Haemophilus influenzae.

    Can you still get meningitis after vaccine? ›

    Vaccines help protect against all three serogroups (B, C, and Y) of Neisseria meningitidis bacteria most commonly seen in the United States. Like with any vaccine, meningococcal vaccines are not 100% effective. This means there is still a chance you can develop meningococcal disease after vaccination.

    Can meningococcal cause brain damage? ›

    Between 10-15 percent of cases are fatal, with another 10-15 percent causing brain damage and other serious side effects. If meningococcal meningitis is diagnosed, people in close contact with an infected individual should be given preventative antibiotics.

    Which of the following is a potential long term complication from meningococcal disease? ›

    It can cause long-term problems, like loss of limbs or brain damage, and be deadly.

    How long do meningitis B vaccine side effects last? ›

    As with all vaccines, side-effects can occur and are usually short-lived (24 – 48 hours). The most common side-effects include tenderness and swelling at the injection site, fever, irritability, vomiting and/or diarrhoea.

    What age is meningococcal B vaccine given? ›

    Administer MenB vaccines at 16 through 18 years of age to maximize protection when adolescents are at highest risk. CDC recommends vaccine providers who choose to administer the MenB vaccine series give it in later adolescence. The preferred age at which to administer MenB vaccine is between 16 to 18 years.

    Are serogroup B meningococcal or MenB vaccines? ›

    A serogroup B meningococcal (Men B) vaccine series may be administered to adolescents and young adults 16 through 23 years of age to provide short term protection against most strains of serogroup B meningococcal disease. The preferred age for Men B vaccination is 16 through 18 years of age.

    Which group has the highest rate of meningococcal infection? ›

    Anyone can get meningococcal disease, but rates of disease are highest in children younger than 1 year old, with a second peak in adolescence. Among adolescents and young adults, those 16 through 23 years old have the highest rates of meningococcal disease.

    What is the most common meningococcal serogroup? ›

    Disease and epidemiology

    Meningococcal disease is most commonly caused by serogroups A, B, C, W and Y. disease (IMD). The highest incidence of meningococcal disease is in children aged <2 years and adolescents aged 15–19 years.

    Why do babies get meningococcal vaccine? ›

    Vaccines are essential to protect against meningitis. Infants and young children are especially at risk of the condition, as their immune systems are not fully developed and able to fight it off. Although viral meningitis is rarely life threatening, it can still make infants and young children very ill.

    Does meningitis vaccine last a lifetime? ›

    For children under the age of 7 years, administer a booster dose 3 years after completion of the primary series and every 5 years thereafter. For children 7 years old or older and adults, administer a booster dose 5 years after completion of the primary series and every 5 years thereafter.

    What is the cost of meningococcal vaccine? ›

    This vaccine may also be needed for career or travel purposes and can be purchased. The price for one-dose is approximately $160. Talk to your health care provider or check with your private health insurance if you are not eligible for the free vaccine.

    What serotype is meningococcal? ›

    Meningococcal disease is a serious and potentially life-threatening infection caused by the bacterium Neisseria meningitidis. N. meningitidis can be classified into 12 serogroups based on its capsular polysaccharide; serogroups A, B, C, W, X, and Y are the primary causes of meningococcal disease worldwide.

    What is meningococcal polysaccharide vaccine group A? ›

    Meningococcal polysaccharide diphtheria conjugate vaccine is an active immunizing agent used to prevent infection by certain groups of meningococcal bacteria. The vaccine works by causing your body to produce its own protection (antibodies) against the bacteria.

    Is meningococcal a group B? ›

    Meningitis and sepsis caused by meningococcal group B bacteria can affect people of any age but are most common in babies and young children. While most young children recover from MenB, around 1 in 20 die from the infection.

    What are the 4 strains of meningococcal vaccine? ›

    The meningococcal quadrivalent vaccine protects against 4 types of meningococcal bacteria: types A, C, Y and W-135. The meningococcal B (Men-B) vaccine protects against infection from meningococcal bacteria, type B.

    What are the 2 types of meningococcal? ›

    There are two major types of meningococcal disease: Meningococcal meningitis and meningococcemia. Meningococcal meningitis is an infection of the tissue (called the “meninges”) that surrounds the brain and spinal cord. Meningococcemia is an infection of the blood and may also involve other parts of the body.

    What are the 4 strains of meningococcal? ›

    Six serogroups (types) of Neisseria meningitidis — A, B, C, W, X, and Y —cause most disease worldwide. Three of these serogroups (B, C, and Y) cause most of the illness seen in the United States. View, download, or print communication resources to learn more about meningococcal disease and how to prevent it.

    What age do you get meningococcal polysaccharide vaccine? ›

    All 11 to 12 year olds should receive a meningococcal conjugate vaccine. Since protection wanes, CDC recommends a booster dose at age 16 years. The booster dose provides protection during the ages when adolescents are at highest risk of meningococcal disease.

    What is the difference between meningitis and meningococcal vaccine? ›

    Meningitis is a dangerous inflammation of the lining of the brain and spinal cord. Two meningitis vaccines protect against four types of meningococcal disease. An additional type of vaccine protects against serotype B, which also causes meningitis.

    Is meningococcal polysaccharide vaccine a meningitis shot? ›

    MENINGOCOCCAL POLYSACCHARIDE VACCINE (muh ning goh KOK kal vak SEEN) is a vaccine to protect from bacterial meningitis. This vaccine does not contain live bacteria. It will not cause a meningitis. This medicine may be used for other purposes; ask your health care provider or pharmacist if you have questions.

    Which deficiency predisposed meningococcal infection? ›

    Complement deficiency has been identified as a major predisposing factor for meningococcal disease.

    Who is at highest risk for meningococcal meningitis? ›

    This disease occurs more often in people who are: Teenagers or young adults. Infants younger than one (1) year of age. Living in crowded settings, such as college dormitories or military barracks.

    Should my child get meningococcal vaccine? ›

    Who should get the meningococcal vaccines? All children ages 11 through 12 years should receive meningococcal vaccine (MenACWY) followed by a booster dose at age 16 years. Vaccination is also recommended for all adolescents ages 13 through 18 years who did not receive a dose at age 11-12 years.

    Why does the meningitis shot hurt so bad? ›

    SIRVA, or shoulder injury related to vaccine administration, can happen when a meningitis vaccine is administered too high or too deeply into the shoulder. As a result, the injection causes inflammation in the shoulder joint, causing extreme shoulder pain and reduced range of motion.

    Videos

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