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Metabolism and Fitness of Urinary Tract Pathogens

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  • Authors: Christopher J. Alteri1, Harry L. T. Mobley2
  • Editors: Tyrrell Conway3, Paul Cohen4
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109; 2: Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109; 3: Oklahoma State University, Stillwater, OK; 4: University of Rhode Island, Kingston, RI
  • Source: microbiolspec June 2015 vol. 3 no. 3 doi:10.1128/microbiolspec.MBP-0016-2015
  • Received 01 May 2015 Accepted 06 May 2015 Published 18 June 2015
  • Harry L.T. Mobley, hmobley@umich.edu
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  • Abstract:

    Among common infections, urinary tract infections (UTI) are the most frequently diagnosed urologic disease. The majority of UTIs are caused by uropathogenic . The primary niche occupied by is the lower intestinal tract of mammals, where it resides as a beneficial component of the commensal microbiota. Although it is well-known that resides in the human intestine as a harmless commensal, specific strains or pathotypes have the potential to cause a wide spectrum of intestinal and diarrheal diseases. In contrast, extraintestinal pathotypes reside harmlessly in the human intestinal microenvironment but, upon access to sites outside of the intestine, become a major cause of human morbidity and mortality as a consequence of invasive UTI (pyelonephritis, bacteremia, or septicemia). Thus, extraintestinal pathotypes like uropathogenic (UPEC) possess an enhanced ability to cause infection outside of the intestinal tract and colonize the urinary tract, the bloodstream, or cerebrospinal fluid of human hosts. Due to the requirement for these to replicate in and colonize both the intestine and extraintestinal environments, we posit that physiology and metabolism of UPEC strains is paramount. Here we discuss that the ability to survive in the urinary tract depends as much on bacterial physiology and metabolism as it does on the well-considered virulence determinants.

  • Citation: Alteri C, Mobley H. 2015. Metabolism and Fitness of Urinary Tract Pathogens. Microbiol Spectrum 3(3):MBP-0016-2015. doi:10.1128/microbiolspec.MBP-0016-2015.

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/content/journal/microbiolspec/10.1128/microbiolspec.MBP-0016-2015
2015-06-18
2018-07-15

Abstract:

Among common infections, urinary tract infections (UTI) are the most frequently diagnosed urologic disease. The majority of UTIs are caused by uropathogenic . The primary niche occupied by is the lower intestinal tract of mammals, where it resides as a beneficial component of the commensal microbiota. Although it is well-known that resides in the human intestine as a harmless commensal, specific strains or pathotypes have the potential to cause a wide spectrum of intestinal and diarrheal diseases. In contrast, extraintestinal pathotypes reside harmlessly in the human intestinal microenvironment but, upon access to sites outside of the intestine, become a major cause of human morbidity and mortality as a consequence of invasive UTI (pyelonephritis, bacteremia, or septicemia). Thus, extraintestinal pathotypes like uropathogenic (UPEC) possess an enhanced ability to cause infection outside of the intestinal tract and colonize the urinary tract, the bloodstream, or cerebrospinal fluid of human hosts. Due to the requirement for these to replicate in and colonize both the intestine and extraintestinal environments, we posit that physiology and metabolism of UPEC strains is paramount. Here we discuss that the ability to survive in the urinary tract depends as much on bacterial physiology and metabolism as it does on the well-considered virulence determinants.

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FIGURE 1

Adaptation of metabolism and basic physiology allows to replicate in diverse host microenvironments. ExPEC that cause urinary tract infection, bacteremia, sepsis, and meningitis, have adapted to grow as a harmless commensal in the nutrient-replete, carbon-rich human intestine but rapidly transition to pathogenic lifestyle in the nutritionally poor, nitrogen-rich urinary tract. In order to establish a commensal association within the human intestine, adaptive factors such as metabolic flexibility allow to successfully compete for carbon and energy sources with a large and diverse bacterial population. acquires nutrients from the intestinal mucus, including N-acetylglucosamine, sialic acid, glucosamine, gluconate, arabinose, fucose and simple sugars released upon breakdown of complex polysaccharides by anaerobic gut residents. When UPEC transition to the urinary tract, the bacteria encounter a drastic reduction in the abundance of nutrients and bacterial competition. Consequently, to replicate in a new host microenvironment, UPEC utilization of metabolic pathways required for growth in the dilute mixture of amino acids and peptides in the bladder signals the bacterium to elaborate virulence properties to successfully cause invasive disease and survive the onslaught of bactericidal host defenses. These adaptations are a unique and essential characteristic of ExPEC that enable a successful transition between disparate microenvironments within the same individual ( 13 ). doi:10.1128/microbiolspec.MBP-0016-2015.f1

Source: microbiolspec June 2015 vol. 3 no. 3 doi:10.1128/microbiolspec.MBP-0016-2015
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FIGURE 2

UPEC acquires amino acids and requires gluconeogenesis and the TCA cycle for fitness . Peptide substrate-binding protein genes and are required to import di- and oligopeptides into the cytoplasm from the periplasm. Short peptides are degraded into amino acids in the cytoplasm and converted into pyruvate and oxaloacetate. Pyruvate is converted into acetyl-CoA and enters the TCA cycle to replenish intermediates and generate oxaloacetate. Oxaloacetate is converted to phosphoenolpyruvate by the gene product during gluconeogenesis. Mutations in the indicated genes , , , , and demonstrated fitness defects . ( 18 ) doi:10.1128/microbiolspec.MBP-0016-2015.f2

Source: microbiolspec June 2015 vol. 3 no. 3 doi:10.1128/microbiolspec.MBP-0016-2015
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FIGURE 3

Diagram of central metabolism and map of the specific pathways disrupted by targeted mutations in uropathogenic . Carbon sources or biochemical intermediates shared between pathways are indicated in capital letters or abbreviated: G6P, glucose-6-phosphate; F6P, fructose-6-phosphate; G3P, glyceraldehyde-3-phosphate; 6PGN, 6-phosphogluconate. Reactions are denoted with arrows. Specific reactions (red arrows) were targeted by deletion or insertion in CFT073. In glycolysis: , glucose-6-phosphate isomerase; , 6-phosphofructokinase transferase; , triosephosphate isomerase; , pyruvate kinase; in pentose phosphate pathway: gnd, 6-phosphogluconate dehydrogenase; , transaldolase; in Entner-Duodoroff pathway: , 6-phosphogluconate dehydratase; in gluconeogenesis: , phosphoenolpyruvate carboxykinase; and in the TCA cycle: , succinate dehydrogenase; , fumarate hydratase; , fumarate reductase. ( 43 ) doi:10.1128/microbiolspec.MBP-0016-2015.f3

Source: microbiolspec June 2015 vol. 3 no. 3 doi:10.1128/microbiolspec.MBP-0016-2015
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FIGURE 4

Model describing the C/N ratio within the urinary tract for . The urinary tract environment has a low C/N ratio due to the dilute mixture of amino acids and peptides as the primary carbon source and the abundance of urea in urine providing a substantial nitrogen contribution. is unable to utilize or sense the nitrogen sequestered in urea because it lacks urease, which liberates ammonia from urea. This results in activation of the glutamine synthetase and glutamate oxo-glutarate aminotransferase system (GS/GOGAT) to assimilate nitrogen. ( 43 ) doi:10.1128/microbiolspec.MBP-0016-2015.f4

Source: microbiolspec June 2015 vol. 3 no. 3 doi:10.1128/microbiolspec.MBP-0016-2015
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