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Pathophysiology of in-vitro induced filaments, spheroplasts and rod-shaped bacteria in neutropenic mice

  1. J. Buijs1,2,
  2. A. S. M. Dofferhoff1,3,
  3. J. W. Mouton1,
  4. J. W. M. Van Der Meer4,5

Article first published online: 31 JUL 2006

DOI: 10.1111/j.1469-0691.2006.01503.x

Issue

Clinical Microbiology and Infection

Clinical Microbiology and Infection

Volume 12, Issue 11, pages 1105–1111, November 2006

Additional Information

How to Cite

Buijs, J., Dofferhoff, A. S. M., Mouton, J. W. and Van Der Meer, J. W. M. (2006), Pathophysiology of in-vitro induced filaments, spheroplasts and rod-shaped bacteria in neutropenic mice. Clinical Microbiology and Infection, 12: 1105–1111. doi: 10.1111/j.1469-0691.2006.01503.x

Author Information

  1. 1

    Department of Medical Microbiology and Infectious Diseases, Canisius-Wilhelmina Hospital, Nijmegen

  2. 2

    Department of Internal Medicine, Atrium Medical Centre, Heerlen

  3. 3

    Department of Internal Medicine, Canisius-Wilhelmina Hospital

  4. 4

    University Centre for Infectious Diseases

  5. 5

    Department of General Internal Medicine, University Medical Centre, Nijmegen, The Netherlands

*Corresponding author and reprint requests: J. Buijs, Department of Internal Medicine, Atrium Medical Centre, H, Dunantstraat 5, 6419 PC Heerlen, PO Box 4446, 6401 CX Heerlen, The Netherlands E-mail: jacqbuijs@hotmail.com

Publication History

  1. Issue published online: 31 JUL 2006
  2. Article first published online: 31 JUL 2006
  3. Original Submission: 4 January 2006; Revised Submission: 16 February 2006; Accepted: 6 March 2006

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Keywords:

  • Endotoxin;
  • Escherichia coli;
  • filaments;
  • mouse model;
  • pathophysiological effects;
  • spheroplasts

Abstract

This study compared the in-vitro properties and in-vivo effects of Escherichia coli filaments, spheroplasts and normal cells in a murine thigh infection model. E. coli was exposed to ceftazidime, meropenem or saline to obtain filaments, spheroplasts or normal bacilli, which were then injected into neutropenic mice. After 24 h, morphology, CFUs, local and circulating endotoxin levels, cytokine levels and mortality were recorded, and correlations between bacterial and host parameters of infection were investigated. Filaments and spheroplasts contained more endotoxin/CFU than controls. Histological studies showed that morphologically altered bacteria changed into rod-shaped cells in the absence of antibiotics. Bacterial spread to the liver was significantly higher in mice challenged with rod-shaped cells, compared with antibiotic-exposed bacteria (p 0.007). Muscle endotoxin levels correlated significantly with circulating interleukin (IL)-6 and tumour necrosis factor (TNF)-α, and both pro-inflammatory cytokines were correlated significantly (p 0.011). Despite a tendency toward higher local and systemic concentrations of endotoxin in the filament group, inflammatory responses and survival did not differ between groups. It was concluded that morphologically altered bacteria contain more endotoxin and can regain a rod shape after withdrawal of antibiotics, while non-antibiotic-exposed bacteria show greater spread to the liver. There was a clear intra-individual relationship between local endotoxin, systemic endotoxin, TNF-α and IL-6 production, but these parameters did not differ among groups.

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