Establishment and Characterization of UTI and CAUTI in a Mouse Model

Conover, Matt S.; Flores-Mireles, Ana L.; Hibbing, Michael E.; Dodson, Karen W.; Hultgren, Scott J.

doi:10.3791/52892

Cited by 33 publications

(40 citation statements)

References 69 publications

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“…Two overviews of the procedures for induction of urinary tract infection in mice have been published in the Journal of Visualized Experiments (JoVE) (89, 90). Briefly, 6–9 week old mice are anesthetized and the peri-urethra and peri-anal areas are sterilized, generally with 10% povidone iodine.…”

Section: Approaches To Studying Virulencementioning

confidence: 99%

Pathogenesis of Proteus mirabilis Infection

2018

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Proteus mirabilis, a Gram-negative rod-shaped bacterium most noted for its swarming motility and urease activity, frequently causes catheter-associated urinary tract infections (CAUTI) that are often polymicrobial. These infections may be accompanied by urolithiasis, development of bladder or kidney stones due to alkalinization of urine from urease-catalyzed urea hydrolysis. Adherence of the bacterium to epithelial and catheter surfaces is mediated by 17 different fimbriae, most notably MR/P fimbriae. Repressors of motility are often encoded by these fimbrial operons. Motility is mediated by flagella encoded on a single contiguous 54 kb chromosomal sequence. On agar plates, P. mirabilis undergoes a morphological conversion to a filamentous swarmer cell expressing hundreds of flagella. When swarms from different strains meet, a line of demarcation, a “Dienes line”, develops due to the killing action of each strain’s type VI secretion system. During infection, histological damage is caused by cytotoxins including hemolysin and a variety of proteases, some autotransported. The pathogenesis of infection, including assessment of individual genes or global screens for virulence or fitness factors has been assessed in murine models of ascending UTI or CAUTI using both single-species and polymicrobial models. Global gene expression studies carried out in culture and in the murine model have revealed the unique metabolism of this bacterium. Vaccines, using MR/P fimbria and its adhesin, MrpH, have been shown to be efficacious in the murine model. A comprehensive review of factors associated with urinary tract infection is presented, encompassing both historical perspectives and current advances.

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Section: Approaches To Studying Virulencementioning

confidence: 99%

Pathogenesis of Proteus mirabilis Infection

2018

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“…E. faecalis then binds fibrinogen via the pilus tip adhesin EbpA, subsequently forming a biofilm on the catheter [105, 106]. These pathogenic events can be modeled in C57BL/6 mice in which a short length of silicone catheter material is transurethrally deposited in the bladder, followed by introduction of E. faecalis [104, 107]. A structural understanding of bacterial pilus association with catheter material and proteinaceous deposits may enable the design of new strategies to counteract catheter-associated UTI.…”

Section: Emerging Clinically Relevant Models For Utimentioning

confidence: 99%

Urinary Tract Infection: Pathogenesis and Outlook

McLellan

Hunstad

2016

Trends in Molecular Medicine

279

206

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The clinical syndromes comprising urinary tract infection (UTI) continue to exert significant impact on millions of patients worldwide, most of whom are otherwise healthy women. Antibiotic therapy for acute cystitis does not prevent recurrences, which plague up to one fourth of women after an initial UTI. Rising antimicrobial resistance among uropathogenic bacteria further complicates therapeutic decisions, necessitating new approaches based on fundamental biological investigation. In this review, we highlight contemporary advances in the field of UTI pathogenesis and how these might inform both our clinical perspective and future scientific priorities.

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“…In a murine model of catheter-associated UTI (CAUTI) 11 , fibrinogen deposition on catheters is the key pathogenic event leading to colonization by Enterococcus faecalis 12 . In this model, circulating fibrinogen increases in response to tissue damage from catheter placement, enters the bladder and is deposited on catheters in a time-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

Fibrinogen Release and Deposition on Urinary Catheters Placed during Urological Procedures

et al. 2016

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# These authors contributed equally to this work. AbstractPurpose-Catheter-associated urinary tract infections (CAUTI) account for ~40% of all hospitalacquired infections worldwide, with more than one million cases diagnosed annually. Recent data from a CAUTI animal model has shown that inflammation induced by catheterization releases host fibrinogen that accumulates on the catheter. Further, Enterococcus faecalis catheter colonization was found to be dependent on EbpA, a fibrinogen binding adhesin. We sought to evaluate this mechanism in a human model. Materials and methods-Urinary catheters were collected from human subjects hospitalized for surgical or non-surgical urologic procedures. Catheters were subjected to immunofluorescence analyses by incubating them with anti-fibrinogen antibody and then stained for fluorescence. The fluorescence intensity was compared to standard catheters. Catheters were incubated with strains of Enterococcus faecalis, Staphylococcus aureus, or Candida to assess their binding to fibrinogenladen catheters.Results-Fifty catheters were collected after various surgical and urological procedures. In vivo dwell time ranged from 1 hour to 59 days. All catheters had fibrinogen deposition and its accumulation was dependent on dwell time but not on surgical procedure or catheter material. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Conflicts of interest: No author has any conflicts of interest to disclose HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptCatheters were probed ex vivo with E. faecalis, S. aureus, and Candida albicans, which bound to catheters only in those regions where fibrinogen was deposited.Conclusions-Taken together, these data show that urinary catheters act as a binding surface for accumulation of fibrinogen, which is released due to inflammation resulting from a urological procedure or from catheter placement, creating a niche that can be exploited by uropathogens to cause CAUTI.

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Establishment and Characterization of UTI and CAUTI in a Mouse Model

Cited by 33 publications

References 69 publications

Pathogenesis of Proteus mirabilis Infection

Pathogenesis of Proteus mirabilis Infection

Urinary Tract Infection: Pathogenesis and Outlook

Fibrinogen Release and Deposition on Urinary Catheters Placed during Urological Procedures

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