Vaccination of patients deficient in a late complement component with tetravalent meningococcal capsular polysaccharide vaccine

Platonov, Alexander E.; Белобородов, В Б; Pavlova, L. I.; Vershinina, I. V.; Käyhty, Helena

doi:10.1111/j.1365-2249.1995.tb03600.x

Cited by 38 publications

(8 citation statements)

References 27 publications

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“…Eighteen patients with late complement defects who were given the quadrivalent polysaccharide vaccine were followed for 2 years. Two episodes of meningococcal disease occurred in two patients at 9 and 12 months following administration of the vaccine (350). One of the patients was presumed to have group C disease based on the observation of a significant increase in anti-group C polysaccharide antibody titers.…”

Section: Roles Of Natural Antibody and Opsonophagocytosis In Protectimentioning

confidence: 99%

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

2010

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SUMMARY The complement system comprises several fluid-phase and membrane-associated proteins. Under physiological conditions, activation of the fluid-phase components of complement is maintained under tight control and complement activation occurs primarily on surfaces recognized as “nonself” in an attempt to minimize damage to bystander host cells. Membrane complement components act to limit complement activation on host cells or to facilitate uptake of antigens or microbes “tagged” with complement fragments. While this review focuses on the role of complement in infectious diseases, work over the past couple of decades has defined several important functions of complement distinct from that of combating infections. Activation of complement in the fluid phase can occur through the classical, lectin, or alternative pathway. Deficiencies of components of the classical pathway lead to the development of autoimmune disorders and predispose individuals to recurrent respiratory infections and infections caused by encapsulated organisms, including Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. While no individual with complete mannan-binding lectin (MBL) deficiency has been identified, low MBL levels have been linked to predisposition to, or severity of, several diseases. It appears that MBL may play an important role in children, who have a relatively immature adaptive immune response. C3 is the point at which all complement pathways converge, and complete deficiency of C3 invariably leads to severe infections, including those caused by meningococci and pneumococci. Deficiencies of the alternative and terminal complement pathways result in an almost exclusive predisposition to invasive meningococcal disease. The spleen plays an important role in antigen processing and the production of antibodies. Splenic macrophages are critical in clearing opsonized encapsulated bacteria (such as pneumococci, meningococci, and Escherichia coli) and intraerythrocytic parasites such as those causing malaria and babesiosis, which explains the fulminant nature of these infections in persons with anatomic or functional asplenia. Paramount to the management of patients with complement deficiencies and asplenia is educating patients about their predisposition to infection and the importance of preventive immunizations and seeking prompt medical attention.

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Section: Roles Of Natural Antibody and Opsonophagocytosis In Protectimentioning

confidence: 99%

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

2010

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“…Saudi Arabia (2003) 6 months-4 years 377 Sporadic nd 0-12% 0.7-1.0 [140] USA 12-22 months 27 Sporadic <1 19% ≤ 0.2 [124] Finland (1981)(1982)(1983)(1984)(1985)(1986)(1987)(1988)(1989)(1990)(1991)(1992) 6-23 months 118 Sporadic nd (2.5-3 log 2 ) nd [123] USA (1982-1983) 2-12 years 70 Sporadic <1 [107] nd GMT 0.04 [127] USA 2-3 years 77 Sporadic <1 [107] <5% 0.1 [105] USA 2-10 years 1375 Sporadic <1 53% nd [103] UK (2003-2004) 2-3 years Sporadic 1.5 48% nd [108,126] France 3-13 years 21 Sporadic nd 57% nd [100] Saudi Arabia (2003) 5-9 years 240 Sporadic nd 13% 0.3 [92,105] Yugoslavia 14-17 years 60 Sporadic nd (4.3 log 2 ) n d [99] USA 11-18 years 88 Sporadic <1 [107] 65% nd [104] The Netherlands 11-62 years 46 Sporadic nd GMT 29 37 [106] USA 18-49 years 25 Sporadic <1 [107] 15% 0.2 [105] USA >17 years 30 Sporadic <1 [107] (<1 log 2 ) n d [140] Austria 19-27 years 40 Sporadic nd (<3.3 log 2 ) n d [101] USA (1997-1998) 18-55 years 90 Sporadic <1 [107] 40% 0.5 [102] USA 25-43 years 30 Sporadic <1 [107] (3 log 2 ) n d [141] Russia 33-42 years 15 Sporadic nd nd 2 [142] *Ranges describe variation within age groups. GMT: Geometric mean titer; Ig: Immunoglobulin; nd: Not determined; SBA: Serum bacterial antibody.…”

Section: Carriage-induced Immunitymentioning

confidence: 99%

“…Among adolescents and adults, polysaccharide vaccine results in good immunogenicity [99,101,106,140,141,142] with 95% of persons vaccinated showing a fourfold or more rise in SBA pre to post-vaccination [104]. Similarly, conjugate vaccination resulted in high seroconversion (> fourfold rise in SBA titers) with 100% of persons vaccinated having protective antibody titers [102,104].…”

Section: Immunogenicitymentioning

confidence: 99%

Meningococcal serogroup W135 in the African meningitis belt: epidemiology, immunity and vaccines

Mueller¹,

Borrow²,

Gessner³

2006

Expert Review of Vaccines

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In the sub-Saharan African meningitis belt there is a region of hyperendemic and epidemic meningitis stretching from Senegal to Ethiopia. The public health approaches to meningitis epidemics, including those related to vaccine use, have assumed that Neisseria meningitidis serogroup A will cause the most disease. During 2001 and 2002, the first large-scale epidemics of serogroup W135 meningitis in sub-Saharan Africa were reported from Burkina Faso. The occurrence of N. meningitidis W135 epidemics has led to a host of new issues, including the need for improved laboratory diagnostics for identifying serogroups during epidemics, an affordable supply of serogroup W135-containing polysaccharide vaccine for epidemic control where needed, and re-evaluating the long-term strategy of developing a monovalent A conjugate vaccine for the region. This review summarizes the existing data on N. meningitidis W135 epidemiology, immunology and vaccines as they relate to meningitis in sub-Saharan Africa.

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“…The capsule helps prevent bacteria from desiccation and is important in infection because it provides protection from the host immune response by interfering with both complement-mediated killing (1)(2)(3) and the adhesion of monocytes and neutrophils to the bacteria (4,5). Consequently, capsules are an important virulence factor for numerous pathogenic bacteria including those that cause disease in livestock, like Pasteurella multocida, and bacteria such as Escherichia coli and Neisseria meningitidis, which cause bacterial meningitis and sepsis in humans (6).…”

mentioning

confidence: 99%

Functional and Structural Characterization of Polysaccharide Co-polymerase Proteins Required for Polymer Export in ATP-binding Cassette Transporter-dependent Capsule Biosynthesis Pathways

Larue

Ford

Willis

et al. 2011

Journal of Biological Chemistry

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Neisseria meningitidis serogroup B and Escherichia coli K1 bacteria produce a capsular polysaccharide (CPS) that is composed of ␣2,8-linked polysialic acid (PSA). Biosynthesis of PSA in these bacteria occurs via an ABC (ATP-binding cassette) transporter-dependent pathway. In N. meningitidis, export of PSA to the surface of the bacterium requires two proteins that form an ABC transporter (CtrC and CtrD) and two additional proteins, CtrA and CtrB, that are proposed to form a cell envelope-spanning export complex. CtrA is a member of the outer membrane polysaccharide export (OPX) family of proteins, which are proposed to form a pore to mediate export of CPSs across the outer membrane. CtrB is an inner membrane protein belonging to the polysaccharide co-polymerase (PCP) family. PCP proteins involved in other bacterial polysaccharide assembly systems form structures that extend into the periplasm from the inner membrane. There is currently no structural information available for PCP or OPX proteins involved in an ABC transporter-dependent CPS biosynthesis pathway to support their proposed roles in polysaccharide export. Here, we report cryo-EM images of purified CtrB reconstituted into lipid bilayers. These images contained molecular top and side views of CtrB and showed that it formed a conical oligomer that extended ϳ125 Å from the membrane. This structure is consistent with CtrB functioning as a component of an envelope-spanning complex. Cross-complementation of CtrA and CtrB in E. coli mutants with defects in genes encoding the corresponding PCP and OPX proteins show that PCP-OPX pairs require interactions with their cognate partners to export polysaccharide. These experiments add further support for the model of an ABC transporter-PCP-OPX multiprotein complex that functions to export CPS across the cell envelope. Capsular polysaccharides (CPSs)2 are produced by many bacteria and form a layer (the capsule) that coats the surface of the cell. The capsule helps prevent bacteria from desiccation and is important in infection because it provides protection from the host immune response by interfering with both complement-mediated killing (1-3) and the adhesion of monocytes and neutrophils to the bacteria (4, 5). Consequently, capsules are an important virulence factor for numerous pathogenic bacteria including those that cause disease in livestock, like Pasteurella multocida, and bacteria such as Escherichia coli and Neisseria meningitidis, which cause bacterial meningitis and sepsis in humans (6).CPSs vary significantly in carbohydrate composition and glycosidic linkages. Despite the diversity of structures, the majority of CPSs produced by Gram-negative bacteria are assembled via either an ATP-binding cassette (ABC) transporter-dependent biosynthesis pathway or a Wzy-dependent biosynthesis pathway (for review, see Refs. 7,8). These pathways are fundamentally different in the topology of the polysaccharide polymerization reaction at the inner membrane. In Wzy-dependent pathways, polymer repeat units are assembled at...

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Vaccination of patients deficient in a late complement component with tetravalent meningococcal capsular polysaccharide vaccine

Cited by 38 publications

References 27 publications

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

Meningococcal serogroup W135 in the African meningitis belt: epidemiology, immunity and vaccines

Functional and Structural Characterization of Polysaccharide Co-polymerase Proteins Required for Polymer Export in ATP-binding Cassette Transporter-dependent Capsule Biosynthesis Pathways

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