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Published on: March 18, 2014
Experimental infections with protease-deficient mutants of Pseudomonas aeruginosa in mice
Abstract:
The virulence of a protease-producing strain of Psuedomonas aeruginosa was compared with that of mutants that had lost the ability to produce proteases and other extracellular enzymes. Lethal infections were produced by inoculating mice intraperitoneally with bacteria in mucin, or by inoculating mice intraperitoneally or intravenously with bacteria 4 days after treatment with cyclophosphamide, 200 mg per kg body weight. No significant difference in virulence between the wild-type parent strain and some of its protease-deficient mutants was found. Histopatholoical examination of different organs in the cyclophosphamide-treated and infected mice showed striking fatty infiltration and focal necrosis of liver, multiple necrotic foci in the spleen and haemorrhagic cystitis with necorsis. The cystitis was produced by cyclophosphamide alone but was aggravated by the infection. In conclusion, no correlation between the production of protease in broth culture and the ability to produce lethal septicaemia in mice was found, and extracellular proteases probably didnot contribute to the virulence of P. aeruginosa. However, the histopathological changes in the liver suggested a role for exotoxin A insystemic infections.
Insights
Pseudomonas aeruginosa protease production did not correlate with virulence in mice. Extracellular proteases likely do not contribute to P. aeruginosa pathogenicity, though exotoxin A may play a role in systemic infections.
Area of Science:
- Microbiology
- Pathogenesis
- Immunology
Background:
- Pseudomonas aeruginosa is an opportunistic pathogen.
- Extracellular enzymes, including proteases, are virulence factors in many bacteria.
- The role of proteases in P. aeruginosa virulence is not fully understood.
Purpose of the Study:
- To investigate the role of protease production in the virulence of Pseudomonas aeruginosa.
- To compare the virulence of wild-type P. aeruginosa with protease-deficient mutants.
Main Methods:
- Comparison of wild-type P. aeruginosa and protease-deficient mutants in mouse infection models.
- Intraperitoneal inoculation of mice with bacteria in mucin.
- Intraperitoneal or intravenous inoculation of immunosuppressed mice (cyclophosphamide treatment).
- Histopathological examination of infected organs.
Main Results:
- No significant difference in virulence was observed between the wild-type strain and protease-deficient mutants.
- Cyclophosphamide treatment alone caused cystitis, which was aggravated by P. aeruginosa infection.
- Histopathology revealed fatty infiltration and necrosis in the liver, and necrotic foci in the spleen.
Conclusions:
- Extracellular protease production in broth culture does not correlate with P. aeruginosa virulence in mice.
- Extracellular proteases are unlikely to be major contributors to P. aeruginosa pathogenicity.
- Histopathological findings suggest a potential role for exotoxin A in systemic P. aeruginosa infections.
