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Introduction

More than 80% of human urinary tract infections (UTI) are due to the bacterium, Escherichia coli, but urinary infections due to Proteus mirabilis are also well documented. P. mirabilis once attached to urinary tract, infects the kidney more commonly than E. coli. P. mirabilis belongs to Enterobacteriaceae and is a gram-negative motile swarmer bacterium. P. mirabilis are often found as free living organisms in soil and water but they are also parasitic in the upper urinary tract of human beings (Walker KE et al 1999).

Urinary tract infection due to Proteus mirabilis is not traditional and mostly reported in individuals with structural abnormalities of the urinary tract and is frequently isolated from the urine of elderly patients undergoing long-term catheterization and women with repeated UTI. Bacteria are attached to the penetrated tissue, resist host defenses and induce change to host tissue. Obviously establishment of P. mirabilis in the human urinary tract involves a host-parasitic immunological interaction and failure of host defense mechanisms favors the parasites

To be able to invade and successfully establish on the uroepithelial cells of the host, P. mirabilis produces several virulence factors e.g., pore-forming hemolysins (Fraser GM et al 2002), proticine 3, leukocidin, endotoxin, IgA and IgG proteases (Walker KE et al 1999), urease (Jones BD and Mobley HL 1988), deaminase, adhesins (Svanborg EC and de Man P 1987), polysaccharide capsules (Gygi D et al 1995), Pili/fimbriae (Bahrani FK et al 1993a, 1994b; Li X et al 1999a, 2001b, 2002c; Li X and Mobley HL 1998; Massad G et al 1994a, 1996b), peritrichous flagella (Belas R 1994;Belas R and Flaherty D 1994 and Furness RB et al 1997), the ability to form biofilms (Rather PN et al 1999; Sturgill et al 2002) and swarming ability. The above mentioned virulence factors enable the pathogens to overcome the various defense mechanisms of the host. During infections, tones are formed due to the action of urease. This enzyme hydrolyzes urea, which is present in urine at copious amount (Griffith DP et al 1976), generating ammonia and carbon dioxide. Ammonia so formed raises the pH, and normal soluble ions precipitate to form stones, usually composed of magnesium ammonium phosphate (struvite) caliculi and calcium phosphate (apatite). Translocation of bacteria from the epithelial surface to into deeper bladder tissues is resisted by the humoral and cellular mediated immune responses of the host.

Two processes in P. mirabilis that are likely to be are swarming and biofilm formation. Pathogenic as well as non-pathogenic bacteria prefer to live in colonies (Costerton JW et al 1987). Colonies of bacteria found on the surface of host epithelial tissues are called microcolonies. Colonies of bacteria exhibit high degree of organization and are characterized by distinguishable patterns of development called swarmers. The formation of swarming colonies by P. mirabilis is particularly well documented (Belas R 1996;Bisset KA 1973;Doughlas CW and Bisset KA 1976 and Rauprich O et al 1996). The products of large number of genes are believed to take part in the swarming process (Allison C and Hughes C 1991). The swarming process is very critical to the virulence of P. mirabilis because the expression of virulence determinants such as urease, hemolysin and the IgA metalloprotease are specific to the swarmer bacteria (Sturgill et al 2002). Biofilms are the congregated slimy mats of microbial communities that serve as a protective device for bacteria and also increase the ability of bacteria to resist both the actions of antibiotics and host responses. Biofilm formation by P. mirabilis is an important factor in the establishment of infections, which leads to a significant challenge to cure the biofilm-associated infections

Extensive research studies demonstrate that control of biofilm formation and inhibition of swarming by P. mirabilis may play an important role for prevention of virulence factors. P-nitrophenylglycerol (PNPG) is a potent anti-swarming agent that could inhibit swarming pattern. It is found that PNPG also inhibits the expression of virulence factors such as protease, urease, hemolysin and flagellum in P. mirabilis. In the presence of PNPG the invasion of human urothelial cells by P. mirabilis is also dramatically reduced. It suggests that PNPG could be used as an active agent against the effects of P. mirabilis infections (Shwu-Jen Liaw et al 2000). Swarming as well as biofilm formation involve cell to cell signaling in P. mirabilis so more complete understanding of the pathways of cell to cell signaling in P. mirabilis may be helpful to develop the strategies to prevent and minimize the infection (Sturgill at al 2002).

The changing spectrum of microorganisms involved in urinary tract infections and the emerging resistance require continuos monitoring to provide crucial information to guide empirical therapy and encourage prudent use of antibiotics. Recent studies have shown that amoxicilin/clavulanate, cefaclor and ceftazidime have high resistance than nitrofurantoin, trimethoprim, cotrimoxazole and quinolones. Antimicrobial resistance patterns should be assessed periodically and recommendations modified accordingly

Proteus mirabilis is a documented cause of urinary tract infection in the complicated urinary tract. It is also well documented that urease-mediated urea hydrolysis is responsible for both virulence of the organism and the ability to produce urolithiasis. Production of urease appears to be one reason that P. mirabilis infections cause more severe histological damage than E. coli infections (Johnson DE et l, 1993;Mobley HLT 1996 and Salyers AA and Whitt DD 1994). A urease-negative mutant of P. mirabilis is unable to initiate stone formation and colonizes bladder and kidneys at a significantly lower rate (100-fold). Although the role of cellular and humoral responses in resistance to UTI is still on debate, the magnitude of the UTI problem caused by P. mirabilis could justify the work for the development of vaccines. These infections represent an estimated 8 million cases and 1.5 million hospital discharged diagnoses per year in the USA alone and the annual incidence of UTI in young women in the country is 0.5-0.7 % episode per person per year (Hooton TM et al 1996). A vaccine against this organism may be feasible for several reasons. First, the species is quite homogeneous with respect to expression of surface antigens (Merrick MV 1995). Secondly, P. mirabilis is present in the fecal flora of <5% of individuals (Senior BW 1983) and, thus preventing its colonization of the host should not result in disruption of normal bowel flora. Finally, patient populations that would benefit from such a vaccine are well defined and include those with known anatomically or functionally abnormal urinary tracts, possibly women with recurrent UTIs, and those early in the course of long-term catheterization. MR/P fimbria, a surface adhesion of P. mirabilis, looks promising vaccine candidate.

Summary

Most of human urinary tract infections are due to the bacterium, E. coli, but UTI due to P. mirabilis are also well documented. During successful infections stones are precipitated after the action of urease in the form of struvite (magnesium ammonium phosphate and apatite (calcium phosphate). Swarming as well as biofilm formation involve cell to cell signaling in P. mirabilis so more complete understanding of the pathways of cell to cell signaling in P. mirabilis may be helpful to develop the strategies to prevent and minimize the infection (Sturgill et al 2002). P-nitrophenylglycerol (PNPG) is a potent anti-swarming agent that could inhibit swarming pattern. Antimicrobial resistance patterns should be assessed periodically and recommendations modified accordingly. MR/P fimbria, a surface adhesion of P. mirabilis, looks promising vaccine candidate.

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