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.