Klebsiella pneumoniae infections occur in humans of all ages, however the highest risk groups appear to be infants, the elderly and the immunocompromised. One or more virulence factors may contribute to pathogenicity in humans. In this article we review three factors that may mediate virulence: cell wall receptors, capsular polysaccharide, and endotoxin. First, the presence of cell wall receptors enables K. pneumoniae to attach to the host cell, thereby altering the bacterial surface so that phagocytosis by polymorphonuclear leukocytes and macrophages is impaired and invasion of the non-phagocytic host cell is facilitated. Second, invasion of the host cell is also facilitated by the large polysaccharide capsule surrounding the bacterial cell; in addition this capsule acts as a barrier and protects the bacteria from phagocytosis. Third, K. pneumoniae produces an endotoxin that appears to be independent of factors that determine receptors and capsular characteristics. Marked interspecies differences in endotoxin production may correlate with virulence. Although some or all of these factors may ultimately determine virulence, the interaction of these factors in vivo has made it difficult to assess the relative contribution of any one of these virulence factors. The pathogenic mechanisms of K. pneumoniae that ultimately determine virulence remain unclear and will require further study.