Journal of Postgraduate Medicine
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Year : 1984  |  Volume : 30  |  Issue : 4  |  Page : 229-31  

Experimental foreign body infection in mice by Staphylococcus epidermidis.

SS Gaikwad, LP Deodhar 

Correspondence Address:
S S Gaikwad

How to cite this article:
Gaikwad S S, Deodhar L P. Experimental foreign body infection in mice by Staphylococcus epidermidis. J Postgrad Med 1984;30:229-31

How to cite this URL:
Gaikwad S S, Deodhar L P. Experimental foreign body infection in mice by Staphylococcus epidermidis. J Postgrad Med [serial online] 1984 [cited 2022 Dec 6 ];30:229-31
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In recent years, interest has been evoked in pathogenesis of infections caused by Staphylococcus epidermidis. Various workers[1],[5],[7],[8] have demonstrated the requirement of large bacterial inoculum with unusually virulent strains or the presence of a compromised host for successful establishment of infection by S. epidermidis. Peters et al[6] using scanning electron microscopy showed that the adhesion of staphylococci to catheter surfaces was followed by self proliferation and production of a slimy material covering the bacterial colony. Christensen et al[3] hypothesised that the ability to attach to a foreign body and colonise it, was more important in the pathogenesis of foreign body infection by S. epidermidis. This study was undertaken with a view to test Christensen's hypothesis by a series of animal experiments using a slime producing and five non-slime producing strains of S. epidermidis.


Six strains of Gram positive, catalase positive cocci which attacked glucose fermentatively and classified as S. epidermidis (Baird-Parker)[4] were included in this study. Five of these strains (designated as NE1 to NE5) were non-slime producing and isolated from pus while the sixth (designated as NE6) was slime producing and was isolated from the blood of a septicemic patient. The slime producing bacterium was confirmed as S. epidermidis by the Public Health Service Laboratory, London. The antibiotic disc susceptibility of these strains was determined by the Kirby-Bauer[2] technique. The preparation of inoculum and injection into the animals following insertion of intravenous catheters were done employing techniques described by Christensen et al[3] In brief, the bacterial inoculum was prepared by suspending the washed overnight nutrient broth culture in phosphate buffer saline (PBS) solution; the volume of PBS solution used was as 1/10th of the original volume and yielded 10[11] CFU/ml. Swiss albino mice (20-25 gm) were used and six animals were tested for each strain studied. One cm length polythene intravenous catheters were inserted into both flanks of the animals with strict aseptic precautions. While I.V. catheter was retained in one flank, the same was withdrawn from the other before closing the wound. Three days later, 0.1 ml of the inoculum was injected subcutaneously around the catheter and at the site of the sham procedure in healthy mice. The animals were observed for 10 days and from those showing abscess development, the I.V. catheters were removed and held in the nutrient broth for two days. Subcultures were then made onto blood agar. Antibiotic disc susceptibility of the coagulase negative staphylococci isolated was determined. NE6 strain was inoculated intraperitoneally into 6 mice to rule out capsule production by this strain. The isolated strains were checked for slime production by overnight incubation into trypticase-soy broth and examining the tube for presence of thin lining on the walls of the test tube.


The incidence of abscess formation by Staphylococcus epidermidis in experimental animals is given in the [Table 1]It was seen that Staphylococcus epidermidis infection occurred only in the presence of a foreign body, since abscess did not develop at the site of the sham operation. None of the 6 animals inoculated intraperitoneally with NE6 strain died. While 50% of the mice inoculated with slime producing strains were infected, the animals inoculated with non-slime producing strains were unaffected barring two exceptions (NE2 and NE3) where 16% of the animals were found to be infected. The cultures of the catheters removed from the site of the abscesses yielded coagulase negative staphylococci which had the same antibiotic susceptibility pattern as the parental strain. It was also noticed that the NE6 strain isolated from the infected catheter continued to produce slime.


Our study reveals that the presence of a foreign body is an essential requirement for the establishment of infection by S. epidermidis as no infection occurred in animals in absence of intravenous catheter. Apparently, the foreign body interferes with host's clearance of these normally avirulent organisms. The study also shows that the slime producing organisms produced abscess in 3 of the 6 (50%) animals studied. This corroborates the findings of Christensen et al.[3] However of the 5 non-slime producing strains, 3 strains (6 animals per strain) did not affect the animals and in the other two strains only 1 of the 6 (16%) animals innoculated showed abscess development. This is indicative of a distinct variation in the pathogenicity of non-slime producing strains. The results of this study, while, confirming Christensen's hypothesis of the importance of slime production in the establishment of infections by S. epidermidis also indicates the possibility of a marked variance in the pathogenicity of non-slim producing strains. The findings also have a clinical significance as slime producing S. epidermidis could colonise intravenous catheters in patients, leading to septicemia.


We are thankful to the Dean, L.T.M. Medical College, Sion, Bombay, for granting permission to publish this paper.


1Archer, G. L., Vazquez, G. J. and Johnston, J. L.: Antibiotic prophylaxis of experimental endocarditis due to experimental methicillin-resistant Staphylococcus epidermidis. J. Infect. Dis., 142: 725-731. 1980.
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6Peters, G., Locci, R. and Pulverer, G.: Adherence and growth of coagulase-negative staphylococci on surface of intravenous catheters. .I. Infect. Dis., 146: 479-482, 1982.
7Thorig, L., Thompson, J. and Eulderinle, F.: Effect of warfarin on the induction and course of experimental Staphylococcus epidermidis endocarditis. Infect. Immunol., 17: 504-509, 1977.
8Vazquez, G. J. and Archer, G. L.: Antibiotic therapy of experimental Staphylococcus epidermidis endocarditis. Antimicrob. Agents and Chemother., 17: 280-285, 1980

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