Acute pyelonephritis results from bacterial invasion of the renal parenchyma. In all age groups, episodes of bacteriuria occur commonly, but most are asymptomatic (ABU) and do not lead to infection. Infection isinfluenced by bacterial factors and host factors.
Most bacterial data are derived from research with
which accounts for 70-90% of uncomplicated UTIs and 21-54% of complicated UTIs. A subset of
(UPEC),also termed extraintestinal pathogenic
(ExPEC), accounts for most clinical isolates from UTIs. UPECderives commonly from the phylogenetic groups B2 and D, which express distinctive O, K, and H antigens.
genes encode several postulated virulence factors (VFs), including adhesins, protectins, siderophores,and toxins, as well as having the metabolic advantage of synthesizing essential substances.Adhesins have specific regions that attach to cell receptor epitopes in a lock-and-key fashion. Mannose-sensitive adhesins (usually type 1 fimbriae) are present on essentially all
. They contribute to colonization(eg, bladder, gut, mouth, vagina) and possibly pathogenesis of infection; however, they also attach topolymorphonuclear leukocytes (PMN), leading to bacterial clearance. Mannose-resistant adhesins permit thebacteria to attach to epithelial cells, thereby resisting the cleansing action of urine flow and bladder emptying.They also allow the bacteria to remain in close proximity to the epithelial cell, enhancing the activity of other VFs.The P fimbriae family of adhesins are epidemiologically associated with prostatitis, pyelonephritis (70-90% of strains), and sepsis. This same family of adhesins in associated with less than 20% of ABU strains. TheAFA/Dr family is associated with diarrhea, UTI, and particularly pyelonephritis in pregnancy. The S/F1C familyis associated with neonatal meningitis and UTI. Siderophores are involved iron uptake, an essential element for bacteria, and possibly adhesion. Protectins include lipopolysaccharide (LPS) coatings (resist phagocytosis),Tra T and Iss (both resist action of complement), and Omp T (cleave host defense proteins, such asimmunoglobulins).Toxins, including alpha hemolysin, cytotoxic necrotizing factor-1, cytolethal distending toxin, and secretedautotransporter toxin, affect various host cell functions; LPS shed from a membrane or released by bacteriallysis leads to cytokine release. No single VF is sufficient or necessary to promote pathogenesis. It seems that amultiple VFs are necessary to ensure pathogenesis, although adhesins play an important role.Bacterial strains producing ABU may provide, in some instances (controversial), a measure of protectionagainst symptomatic infections from UPEC and other organisms; but, it may also cause increased morbidityand mortality. Once bacteriuria is established, these strains appear to stop producing adhesins, allowing themto survive and persist without producing an inflammatory reaction. The frequency of ABU in preschool girls isless than 2%; in pregnant women, 2-9.5%; in women aged 65-80 years, 18-43%; in men aged 65-80 years,1.5-15.3%; in women older than 80 years, 18-43%; and in men older than 80 years, 5.4-21%. There isconsiderable morbidity associated with ABU in pregnancy, renal transplantation, and genitourinary surgery (seeTable 1).Table 1. Asymptomatic Bacteriuria: Incidence, Morbidity, Screening, and Treatment