Host response to coagulase-negative staphylococci in abscesses induced within mice Free

Abstract

Summary

A model whereby a known number of coagulase-negative staphylococci were packed into capillary tubes and implanted into the peritoneal cavity of mice proved to be a satisfactory method for generating abscesses that could be easily removed free of extraneous host tissue, and that permitted measurement of the survival of the organisms and accumulation of lipid in the lesion. Strains of and differing in their ability to produce fatty acid modifying enzyme (FAME) and lipase, were packed into either glass or plastic capillary tubes and used to generate abscesses. Abscesses produced by served as comparators. Lipids accumulated within the abscesses caused by in the same manner as previously described for the organism inoculated without tubes. Lipids also accumulated within abscesses produced by all the coagulase-negative staphylococci, but the rate of accumulation was slower and the lipid droplets were smaller than seen with The mobilisation of lipid did not differ in response to cocci in plastic or glass tubes. Strains of and producing FAME and lipase were better able to survive within abscesses than strains unable to produce these enzymes. However, FAME and lipase production did not appear to be the sole determinants of survival within abscesses. Regardless of whether they produced FAME and lipase, the two strains were significantly better able to survive within plastic tubes than in glass tubes. No such difference was seen with between plastic and glass tubes.

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1993-09-01
2024-03-28
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References

  1. Shryock TR, Dye ES, Kapral FA. The accumulation of bactericidal lipids in staphylococcal abscesses. J Med Microbiol 1992; 36:332–336
    [Google Scholar]
  2. Kapral FA. A novel host defense mechanism controlling the survival of Staphylococcus aureus in focal lesions. In: Jeljaszewicz J, Ciborowski S. (eds) The staphylococci New York: Fischer Verlag; 199169–76
    [Google Scholar]
  3. Mortensen JE, Shryock TR, Kapral FA. Modification of bactericidal fatty acids by an enzyme of Staphylococcus aureus. J Med Microbiol 1992; 36:293–298
    [Google Scholar]
  4. Kapral FA, Smith S, Lai D. The esterification of fatty acids by Staphylococcus aureus fatty acid modifying enzyme (FAME) and its inhibition by glycerides. J Med Microbiol 1992; 37:235–237
    [Google Scholar]
  5. Kapral FA. Clumping of Staphylococcus aureus in the peritoneal cavity of mice. J Bacteriol 1966; 92:1188–1195
    [Google Scholar]
  6. Kapral FA, Godwin JR, Dye ES. Formation of intraperitoneal abscesses by Staphylococcus aureus. Infect Immun 1980; 30:204–211
    [Google Scholar]
  7. Lambe DW, Ferguson KP, Gemmell CG, Keplinger JL. Pathogenic studies on five species of coagulase-negative staphylococci: a mouse model with a foreign body implant. In: Wadstrom T et al. (eds) Pathogenesis of wound and biomaterial-associated infections Stuttgart: Springer Verlag; 1990255–263
    [Google Scholar]
  8. Long JP, Hart J, Albers W, Kapral FA. The production of fatty acid modifying enzyme (FAME) and lipase by various staphylococcal species. JMed Microbiol 1992; 37:232–234
    [Google Scholar]
  9. Christensen GD, Simpson WA, Bisno AL, Beachey EH. Adherence of slime-producing strains of Staphylococcus epidermidis to smooth surfaces. Infect Immun 1982; 37:318–326
    [Google Scholar]
  10. Culling CFA. Handbook of histopathological techniques. , 2nd edn.. Washington, DC: Butterworth; 1963
    [Google Scholar]
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