Bacteria

Escherichia coli, Proteus, Klebsiella, Enterobacter and Staphylococcus saprophyticus are the most common etiologic agents in UTI. E. coli dominate in both outpatient and hospitalized populations and are the most extensively characterized regarding mechanisms of virulence.

The population structure of E. coli is clonal, i.e. genetic elements occur in nonrandom, relatively stable combinations. Uropathogenic E. coli are a selected subset of the E. coli flora at large. The pyelo-nephritogenic clones are identified by a limited number of surface antigen serotypes (0:K:H:F = lipo-polysaccharide (LPS), capsular polysaccharide, flagellar and fimbrial antigens) and intracellular iso enzyme patterns (electrophoretic types), and by the expression of molecules which damage the host tissues. Adherence is mediated by bacterial surface lectins, which may be associated with fimbriae. The lectins bind the bacteria to host receptor molccules consisting of oligosaccharide sequences in glycoproteins or glycolipids. The P fimbrial lectins recognize the Galal-4Gal)3 and GalNAc epitopes within the globoseries of glycolipid receptors. S Fimbrial lectins recognize sialic acid residues, and type I fimbriae bind mannose residues found, for example, on the Tamm Horsfall protein and secretory immunoglobulin A (IgA), and connective tissue proteins such as collagen and laminin.

LPS is the endotoxin of E. coli, which contains the lipid A moiety responsible for eliciting a wide array of inflammatory host responses. Hemolysin participates in the destruction of host cells through its lytic activity. The capsular polysaccharides protect bacteria against attack by complement and neutrophils, and aerobactin facilitates the trapping of free iron required for the bacterial oxidative metabolism, especially in environments with limited oxygen supply. These characteristics are all designated as virulence factors, since they occur more frequently in acute pyelonephritis than in screening bacteriuria strains.

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