Figure 2. Concepts of Proteus mirabilis Pathogenesis during Urinary Tract Infection (UTI).

Bolded classes of virulence factors have genes that are regulated by MrpJ. For more extensive information on these virulence factors, see references [21,22,99,100]. Adherence: binding catheters, host tissues, and neighboring bacteria may all contribute to disease. Adherence is mediated by chaperone-usher fimbriae and autotransporter adhesins. Urease: involved in stones, crystalline biofilms, and possibly nutrition or host sensing. Motility: P. mirabilis swarms across catheters and may ascend to the kidneys using swimming motility. Both forms of motion are mediated by flagella. Chemotaxis proteins allow the bacteria to follow chemical gradients. Metabolism: likely permits establishment of a nutritional niche, competition with other species, and response to host cues. Metal scavenging: iron and zinc uptake are essential for growth, but are sequestered by the host; therefore, specialized proteins are required for bacteria to scavenge these metals. Toxins: proteins such as HpmA and Pta may aid in nutrient accessibility, immune evasion, or provision of surfaces to colonize. Biofilm formation: Crystalline biofilms readily form on catheters, and bacterial clusters in the bladder may be a biofilm-mediated process. Immune evasion: this can include antibody and antimicrobial peptide degradation, polymyxin resistance, lipopolysaccharide (LPS) variation, and physical obstruction of phagocytosis. Virulence regulation: required to coordinate all steps of infection. MrpJ-controlled systems in this figure are bolded. Type 6 secretion system (T6SS): involved in self-recognition; unknown role during UTI.