A possible animal model for critical colonisation

J Wound Care. 2010 Jul;19(7):295-300.

Abstract

Objective: To develop a critical colonisation model in rats that will facilitate investigation of its pathophysiology and the development of new and effective diagnosis and treatment protocols.

Method: Three groups of rats were given full-thickness dorsal wounds: a control group received phosphate-buffered saline; an experimental group was inoculated with Pseudomonas aeruginosa; an infection group with streptozotocin-induced diabetes was also inoculated with P. aeruginosa. All groups were assessed on a number of parameters at days 1, 3, 5 and 7 following wounding. Parameters included gross observations, histopathological observations, quantification of redness and swelling, serum C-reactive protein (CRP) measurement and tissue bacterial counts.

Results: Healing was delayed in the experimental group when compared with the control group, with no signs of inflammation. Although the numbers of bacteria were similar in the experimental and infection groups, polymorphonuclear neutrophil (PMN) infiltration was localised to granulation tissue in the experimental group, whereas it extended to muscular tissue in the experimental group. CRP levels remained low in the experimental group.

Conclusion: These findings suggest that the inoculation of bacteria provides a possible model of critical colonisation in rats. We believe this will contribute to a better understanding of critical colonisation.

MeSH terms

  • Analysis of Variance
  • Animals
  • C-Reactive Protein / analysis
  • Colony Count, Microbial
  • Diabetes Mellitus, Experimental / complications*
  • Disease Models, Animal*
  • Granulation Tissue / pathology
  • Granulation Tissue / physiology
  • Male
  • Neutrophil Infiltration / physiology
  • Neutrophils / pathology
  • Neutrophils / physiology
  • Pseudomonas Infections* / etiology
  • Pseudomonas Infections* / pathology
  • Pseudomonas Infections* / physiopathology
  • Rats
  • Rats, Wistar
  • Wound Healing* / physiology
  • Wound Infection* / etiology
  • Wound Infection* / pathology
  • Wound Infection* / physiopathology

Substances

  • C-Reactive Protein