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 specific. 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 tentatively 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.