The role of E. Coli. virulence factors adhesins and hemolysins during a urinary tract infection
Uropathogenic strains of Escherichia coli are characterized by the expression of distinctive bacterial properties, products, or structures referred to as virulence factors because they help the organism overcome host defenses and colonize or invade the urinary tract. Virulence factors of recognized importance in the pathogenesis of urinary tract infection (UTI) include adhesins (P fimbriae, certain other mannose-resistant adhesins, and type 1 fimbriae), the aerobactin system, hemolysin, K capsule, and resistance to serum killing. This review summarizes the virtual explosion of information regarding the epidemiology, biochemistry, mechanisms of action, and genetic basis of these urovirulence factors that has occurred in the past decade and identifies areas in need of further study. Virulence factor expression is more common among certain genetically related groups of E. coli which constitute virulent clones within the larger E. coli population. In general, the more virulence factors a strain expresses, the more severe an infection it is able to cause. Certain virulence factors specifically favor the development of pyelonephritis, others favor cystitis, and others favor asymptomatic bacteriuria. The currently defined virulence factors clearly contribute to the virulence of wild-type strains but are usually insufficient in themselves to transform an avirulent organism into a pathogen, demonstrating that other as-yet-undefined virulence properties await discovery. Virulence factor testing is a useful epidemiological and research tool but as yet has no defined clinical role. Immunological and biochemical anti-virulence factor interventions are effective in animal models of UTI and hold promise for the prevention of UTI in humans.
Escherichia coli, the predominant aerobic, coliform species in the healthy colon, is not a primary pathogen, but it can cause disease when it escapes from its usual gastrointestinal habitat. Invasion of the bloodstream is the most serious manifestation of E. coli infection and is commonly found among patients with urinary tract infection (UTI), biliary tract infection, or other intraperitoneal infection. E. coli is the species that most commonly causes bacteremia and sepsis in association with these infections [1, 2]. E. coli on the perineal skin can gain access to the urinary tract and proliferate there, especially when urine flow is disrupted by mechanical obstruction or neurologic dysfunction . In the alimentary tract, E. coli typically ascends from the duodenum and may colonize the biliary tract .
Bacterial adherence to uroepithelial cells by fimbrial or nonfimbrial adhesins is considered to be an important pathogenic factor for UTI. The known fimbriae or adhesins of E. coli include P-, S-/F1C-, and type-1 fimbriae as well as afimbrial adhesins [3, 5]. Both host and E. coli virulence factors can contribute to the development of upper UTI, and less virulent strains can cause upper UTI in hosts with predisposing factors, such as diabetes with poor glycemic control, immunosuppression, or urinary tract obstruction . The presentation of acute cholangitis (AC) may be similar to that of UTI. E. coli is the most commonly observed pathogen in studies of biliary bacteriology, on the basis of results of cultures of choledochal bile obtained from patients with or without AC or from patients with choledocholithiasis [7–10]. The incidence of bacteremia among patients with AC has varied from 0% to 75%, and E. coli has remained the pathogen most frequently associated with the disease [11–15]. Sakurai et al.  found that adherence of E. coli to the epithelium of the human gallbladder correlated with the degree of epithelial damage. They also found that secondary bacterial infection is more likely to occur in patients with contaminated bile than in those without contaminated bile.