Host parasite interaction in urinary tract infection.

The last decade has provided new insight into the mechanisms of host-parasite interactions in the urinary tract. Reduction of host resistance appears to reduce the requirement for bacterial virulence, whereas the resistant host becomes infected with bacteria of high virulence. In the resistant host, bacterial virulence can be defined as the sum of properties required to colonize the urinary tract and induce tissue reactions. The ability to attach to uroepithelial cells is the single property most frequently associated with pyelonephritogenic clones. Attachment to the Gal alpha 1-4Gal beta-containing receptors promotes localization of bacteria to the kidney and the induction of lipopolysaccharide-mediated inflammation. Other virulence factors, defined by increased frequency in acute pyelonephritis compared with asymptomatic bacteriuria, include haemolysin and aerobactin production. Among the factors which influence the natural resistance to urinary tract infection are urinary flow and reactivity to endotoxin. The resistance induced by natural exposure to infection or immunization may be protective in experimental models, but the importance of this is not yet defined. The localization, severity and sequelae of urinary tract infection are determined by the balance between bacterial virulence and host resistance. Although disease is a result of the interaction between bacterial virulence and host resistance, these components are discussed separately for clarity.