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Capsular Serotyping of Streptococcus pneumoniae by Latex Agglutination
Published on: September 25, 2014
Defective antipneumococcal polysaccharide antibody response in children with recurrent respiratory tract infections
L A Sanders1, G T Rijkers, W Kuis
1Department of Immunology, University Hospital for Children and Youth, Het Wilhelmina Kinderziekenhuis, Utrecht, The Netherlands.
Insights
Patients with recurrent infections may have impaired immune responses to pneumococcal polysaccharides. Long-term follow-up is crucial to differentiate temporary delays from persistent defects, which can indicate developing humoral immunodeficiency.
Area of Science:
- Immunology
- Pediatrics
- Infectious Diseases
Background:
- Recurrent pyogenic infections are linked to impaired responses to polysaccharide antigens.
- Investigated deficient pneumococcal polysaccharide responses in patients with recurrent infections.
Purpose of the Study:
- To assess the immune response to pneumococcal polysaccharide vaccine in children with recurrent infections.
- To identify potential underlying immunodeficiencies.
Main Methods:
- 45 patients (1.7-17.1 years) received 23-valent pneumococcal polysaccharide vaccine.
- Antibody levels to seven pneumococcal serotypes measured by ELISA pre- and post-vaccination.
- Protein antigen booster immunization administered.
Main Results:
- 14% (5/35) of patients with normal immunoglobulin levels had low antipneumococcal antibodies and failed to respond to vaccination.
- 10 patients had diagnosed humoral immunodeficiency, with 7 failing to respond to pneumococcal vaccination.
- Appropriate response to protein antigens was observed in patients with polysaccharide response defects.
Conclusions:
- A defective immune response to polysaccharide antigens requires long-term follow-up.
- Distinguishing transient maturational delay from persistent impaired response is essential.
- Impaired polysaccharide response may precede humoral immunodeficiency disease.
Background:
Recurrent pyogenic infections are known to occur in patients with an impaired response to polysaccharide antigens. We investigated the occurrence of deficient responses to pneumococcal capsular polysaccharides in patients with recurrent respiratory tract and recurrent systemic infections.
Methods:
Forty-five patients, 1.7 to 17.1 years of age, were immunized with 23-valent pneumococcal polysaccharide vaccine. Antibody levels to seven pneumococcal serotypes (3, 4, 6A, 9N, 14, 19F, 23F) were determined by ELISA before and after immunization. In addition, patients received a booster immunization with diphtheria toxoid, tetanus toxoid, and poliomyelitis virus vaccine.
Results:
Thirty-five patients had normal serum immunoglobulin levels. Five of these patients (14%) had low antipneumococcal preimmunization antibody levels and failed to respond to pneumococcal vaccination, whereas the response to booster immunization with protein antigens was appropriate. Three patients were younger than 3 years old, and one had a family history of IgG2 deficiency. Low IgG developed in a fifth patient during follow-up. Ten patients had a humoral immunodeficiency. Seven of these patients failed to respond to pneumococcal vaccination.
Conclusions:
We conclude that a defective immune response to polysaccharide antigens in patients requires long-term follow-up to distinguish transient maturational delay from a persistent selective impaired response to polysaccharide antigens, which on occasion may precede the development of humoral immunodeficiency disease.
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