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Many bacteria, such as certain Neisseria and Haemophilus or
Escherichia coli, are able to withstand the bactericidal activity
of complement and phagocytes. This bacterial self protection is
brought about by encapsulation. Bacterial capsules thus enable the
pathogenic bacteria to survive in the host by counter action or
evasion of the nonspecific host defense in the early pre immune
phase of an infection. It is only in the late immune phase of the
infection, when specific anticapsular antibodies are formed and
enforce the host's defense system, that this protective action is
overcome. Encapsulated bacteria are then killed and eliminated.
Interestingly, some capsules can not or only inefficiently be
handled by the immune system. The ensuing lack of antibody
formation results in a prolonged susceptibility of the host to the
pathogenic bacteria exhibiting such capsules. It was found that
bacterial capsules consist of acidic poly saccharides. From this it
followed that the role of the capsules in the interaction of
encapsulated bacteria with the host may be due to the chemistry of
the capsular polysaccharides. This led to intensive studies of
capsular polysaccharides in many laboratories. Our increasing
knowledge of the structural features of capsular polysaccharides
prompted not only immuno chemical studies analyzing the
interactions of these poly saccharide antigens and characterizing
the epitopes, but also investigations into their biosynthesis.
These studies were complemented and supported by genetic analyses.
Today many interdisciplinary investigations of capsular
polysaccharides are in progress.
The great majority of bacterial infections are initiated by the
adhesion of pathogenic bacteria to cells and mucosal surfaces of
the host. The sequela of adhesion may range from the action of
toxins outside target cells to their penetration into or through
tissue. Besides the consequences of bacterial adhesion related in
infection, the result may be colonization of mucosal surfaces with
normally harmless bacteria, which in stress situations may become
virulent, a phenomenon known as nosocomial infections. With very
few exceptions, adhesion is carbohydrate speci fic. It is mediated
by bacterial recognition proteins that are, according to the
phenomenon studied, termed adhesins or hem agglutinins; the term
"lectin" is sometimes also used. The chemical nature of the ad he
sins and their organization on the bacterial surface have been
studied intensively in many laboratories. The application of
genetic and biochemical techniques has led to substantial progress
in the molecular characterization of adhesins in recent years. We
now know that adhesins may occur as structural subunits of fimbriae
and that they may form fimbriae which can be considered as mono- or
multifunctional linear adhesin polymers. Other adhesins do not form
recognizable structures and are tenta tively called nonfimbrial.
Adhesins may even be components of bacterial cell walls.
Adhesin-receptor specificities have been unravelled. The study of
the distribution of receptors in tissue has created implications
about the possible susceptibility to infections.
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