Abstract
Pseudomonas aeruginosa remains a significant pathogen in burn-wound infection, its pathogenicity being associated with the production of a cocktail of virulence determinants which is regulated by a population-density-dependent mechanism termed quorum sensing. Quorum sensing is effected through the production and binding of signalling molecules. Here we present a mathematical model for the early stages of the infection process by P. aeruginosa in burn wounds which accounts for the quorum sensing system and for the diffusion of signalling molecules in the burn-wound environment. The results of the model and the effects of important parameters are discussed in detail. For example, the effect of the degradation rate of signalling molecules and its significance for anti-signalling therapies is discussed.
Similar content being viewed by others
References
Anwar, H., G. H. Shand, K. H. Ward, M. R. W. Brown, K. E. Alpar and J. Gowar (1985). Antibody response to acute Pseudomonas aeruginosa infection in a burn wound. FEMS Microbiol. Lett. 29, 225–230.
Bosworth, C. (Ed.) (1997). Burns Trauma: Management and Nursing Care, Ballière Tindall.
Diller, K. R. and L. J. Hayes (1983). A finite element model of burn injury in blood-perfused skin. J. Biomech. Eng. 105, 300–307.
Dockery, J. D. and J. P. Keener (2001). A mathematical model for quorum sensing in Pseudomonas aeruginosa. Bull. Math. Biol. 63, 95–116.
Felts, A. G., G. Giridhar, D. W. Grainger and J. B. Slunt (1999). Efficacy of locally delivered polyclonal immunoglobulin against Pseudomonas aeruginosa infection in a murine burn wound model. Burns 25, 415–423.
Fuqua, W. C., S. C. Winans and E. P. Greenberg (1996). Census and consensus in bacterial ecosystems: the LuxR-LuxI family of quorum-sensing transcriptional regulators. Ann. Rev. Microbiol. 50, 727–751.
Gang, R. K., R. L. Bang, S. C. Sanyal, E. Mokaddas and A. R. Lari (1999). Pseudomonas aeruginosa septicaemia in burns. Burns 25, 611–616.
Holder, I. A. (1985). The pathogenesis of infections owing to Pseudomonas aeruginosa using the burned mouse model: experimental studies from the Shiners Burns Institute, Cincinnati. Can. J. Mircobiol. 31, 393–402.
Jarrett, A. (Ed.) (1973). The Physiology and Pathophysiology of the Skin, Vol 2: The Nerves and Blood Vessels, Academic Press.
Levin, V. A., C. S. Patlak and H. D. Landahl (1980). Heuristic modelling of drug delivery to malignant brain tumors. J. Pharm. Biopharm. 8, 257–296.
McManus, W. F., C. W. Goodwin, A. D. Mason and B. A. Pruitt (1981). Burn wound infection. J. Trauma 21, 753–756.
Neely, A. N. and I. A. Holder (1999). Antimicrobial resistance. Burns 25, 17–24.
Neu, H. C. (1983). The role of Pseudomonas aeruginosa in infections. J. Antimicrob. Chemother. 11, 1–13.
Revathi, G., J. Puri and B. K. Jain (1998). Bacteriology of burns. Burns 24, 347–349.
Rumbaugh, K. P., J. A. Griswold, B. H. Iglewski and A. N. Hamood (1999). Contribution of quorum sensing to the virulence of Pseudomonas aeruginosa in burn wound infections. Infect. Immun. 67, 5854–5862.
Salmond, G. P. C., B. W. Bycroft, G. S. A. B. Stewart and P. Williams (1995). The bacterial ‘enigma’: cracking the code of cell-cell communication. Mol. Microbiol. 16, 615–624.
Stieritz, D. D., A. Bondi, D. McDermott and E. B. Michaels (1982). A burned mouse model to evaluate anti-pseudomonas activity of topical agents. J. Antimicrob. Chemother. 9, 133–140.
Swift, S., J. P. Throup, P. Williams, G. P. C. Salmond and G. S. A. B. Stewart (1996). Quorum sensing: a population-density component in the determination of bacterial phenotype. Trends Biochem. Sci. 21, 214–219.
Thaler, F., J. E. Rohan and P. Loirat (1998). Brûlés: infection à Pseudomonas aeruginosa. Méd. Mal. Infect. 28, 167–174.
Ward, J. P., J. R. King, A. J. Koerber, P. Williams, J. M. Croft and R. E. Sockett (2001a). Mathematical modelling of quorum sensing in bacteria. IMA J. Math. Appl. Med. Biol. 18, 263–292.
Ward, J. P., J. R. King, A. J. Koerber, J. M. Croft, R. E. Sockett and P. Williams (2001b). Early development and quorum sensing in bacterial biofilms, in preparation.
Winson, M. K. et al. (1995). Multiple N-acyl-L-homoserine lactone signal molecules regulate production of virulence determinants and secondary metabolites in Pseudomonas aeruginosa. Proc. Natl. Acad. Sci. USA 92, 9427–9431.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Koerber, A.J., King, J.R., Ward, J.P. et al. A mathematical model of partial-thickness burn-wound infection by Pseudomonas aeruginosa: Quorum sensing and the build-up to invasion. Bull. Math. Biol. 64, 239–259 (2002). https://doi.org/10.1006/bulm.2001.0272
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1006/bulm.2001.0272