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Bacteria with polysaccharide capsules (such as some members of the Haemophilus influenzae, Neisseria meningitides and Streptococcus pneumoniae families) are frequent pathogens in early life, in part due to the inability of the immature immune system to mount a protective immune response. The polysaccharide capsule is both a virulence factor, allowing the organism to evade the binding of potentially lethal complement components and, paradoxically, a target for protective antibody. B cells derived from the immature immune system (below 2 years of age) are unable to make antibodies to native polysaccharides due to reasons not yet fully elucidated. Nasophrayngeal colonisation with encapsulated bacteria is a common feature of early childhood and in the absence of protective immunity may lead to blood borne diseases such as meningitis, local spread causing otitis media or pneumonia, or transmission via nasal secretions to other susceptible individuals.
Efforts to prevent infection with encapsulated bacteria in early childhood using vaccines containing purified capsular polysaccharides have failed due to the poor immunogenicity of these compounds in the very young. Rabbits also fail to respond to purified polysaccharides. However, it was work in these animals in the 1920s that led to the discovery that conjugation of a polysaccharide to a protein carrier rendered the polysaccharide moiety immunogenic in previously unresponsive rabbits.1 This work laid the foundation for the development of conjugate vaccines for use in humans, but it was only in the 1970s that work began seriously on the prototype vaccine for use in humans, a H influenzae type b (Hib) conjugate.
Perspective on the papers by Ladhani et al (see p 665) and McVernon …