A comparison of the early inflammatory effects of an agr-/sar- versus a wild type strain of Staphylococcus aureus in a rat model of endophthalmitis.
OBJECTIVE
We examined the ability of a wild type and an isogenic mutant strain of Staphylococcus aureus, deficient in the production of hemolysins and lipase (agr (-)/sar (-)), to induce endophthalmitis and inflammatory cell infiltration into the eye at 6, 24 and 48 hours after injection in a rat model of endophthalmitis.


METHODS
Rat eyes were injected with 25 microl of viable S. aureus or sterile saline. Eyes were graded for clinical signs of inflammation daily, removed and processed for standard histologic analysis 6, 24 and 48 hours after injections. Comparisons of clinical scores and mean inflammatory cell numbers were made between S. aureus and control injected eyes.


RESULTS
Both experimental groups developed clinical signs of endophthalmitis and demonstrated infiltration of inflammatory cells at 24 and 48 hours. Clinical inflammation in the Mutant I group was less than the wild type group at these times and significantly less at 48 hours (p<0.05). No statistically significant difference in the number of inflammatory cells was detected between the wild type and Mutant I injected eyes at 24 hours. At 48 hours, inflammatory cells increased by 75.0% in the wild type group and decreased by 19.0% in the Mutant I group and a statistically significant difference was seen between these two groups (p<0.05). At all times, the majority of inflammatory cells were neutrophils. By 48 hours, an increase in monocytes-macrophages was noted.


CONCLUSIONS
Both strains of S. aureus induced clinical signs of inflammation and inflammatory cell infiltration. Clinical inflammation and inflammatory cell numbers were less in rats injected with the Mutant I strain. These results suggest that hemolysins and lipase may be important in the early induction phase of the inflammatory response.
Giese
M J
MJ
Jules Stein Eye Institute and Department of Pathology and Laboratory Medicine, UCLA School of Medicine, Los Angeles, CA 90095-7000, USA. mgiese@ucla.edu
Berliner
J A
JA
Riesner
A
A
Wagar
E A
EA
Mondino
B J
BJ
D000818:Animals; D004195:Disease Models, Animal; D009877:Endophthalmitis / Q000382:microbiology* / Q000473:pathology; D015818:Eye Infections, Bacterial / Q000382:microbiology / Q000473:pathology; D005260:Female; D007958:Leukocyte Count; D007962:Leukocytes / Q000473:pathology; D008049:Lipase / Q000096:biosynthesis*; D051381:Rats; D011917:Rats, Inbred Lew; D013203:Staphylococcal Infections / Q000382:microbiology / Q000473:pathology; D013211:Staphylococcus aureus / Q000235:genetics* / Q000378:metabolism / Q000472:pathogenicity; D013301:Streptolysins / Q000096:biosynthesis*; D014774:Virulence; D014822:Vitreous Body / Q000382:microbiology
D013301:Streptolysins; D008049:Lipase