title: Immunopathologic features of Staphylococcus aureus endophthalmitis in the rat.
abstract: OBJECTIVE
  To study the clinical, histopathologic, and immunologic responses to Staphylococcus aureus endophthalmitis in rats.
  
  
  METHODS
  Experimental Lewis rats received an intravitreal injection of viable S. aureus (65 organisms), and control rats received sterile saline. The clinical scores, cellular infiltrate, delayed hypersensitivity reaction in skin tests, and serum and vitreous enzyme-linked immunosorbent assay titers of immunoglobulin (Ig) M, IgG, and IgA to ribitol teichoic acid (RTA), the major antigenic determinant of S. aureus cell wall, were measured and compared on days 3, 7, 10, 14, 21, and 30. The differences were statistically assessed using Mann-Whitney nonparametric t-tests and analysis of variance.
  
  
  RESULTS
  The red reflex was abolished in the majority of rats between days 3 and 21. Ocular inflammation resolved by day 30. The vitreous of eyes injected with S. aureus showed bacterial growth on days 3 and 7, followed by a decrease in numbers on days 10 and 14 and disappearance on days 21 and 30. In the vitreous, a peak neutrophil count was observed at day 3 that rapidly declined by day 7. The number of lymphocytes and plasma cells peaked on day 3 but declined more slowly. Plasma cells and Mott cells were seen on days 10 and 14, suggesting intraocular antibody production. IgM titers to RTA increased progressively in serum and vitreous, reached a peak on day 21, and declined on day 30. A weak IgG but absent IgA response to RTA was observed in serum and vitreous. S. aureus endophthalmitis was not associated with delayed hypersensitivity to the bacteria in skin tests.
  
  
  CONCLUSIONS
  S. aureus endophthalmitis is associated with the infiltration of neutrophils, lymphocytes, monocytes, and plasma cells in vitreous. Neutrophils, the predominant infiltrating cells, may be involved in bactericidal activity and opsonophagocytosis. In rat staphylococcal endophthalmitis, IgM rather than IgG may be the protective antibody.
authors.affiliation: Jules Stein Eye Institute, University of California, Los Angeles 90024-1771, USA.
authors.forename: R M
authors.initials: RM
authors.lastname: Ravindranath
authors.forename: B J
authors.initials: BJ
authors.lastname: Mondino
authors.forename: S A
authors.initials: SA
authors.lastname: Adamu
authors.forename: H
authors.initials: H
authors.lastname: Pitchekian-Halabi
authors.forename: S A
authors.initials: SA
authors.lastname: Hasan
authors.forename: B J
authors.initials: BJ
authors.lastname: Glasgow
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000032:analysis; D002634:Chemotaxis, Leukocyte; D015169:Colony Count, Microbial; D009877:Endophthalmitis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D015818:Eye Infections, Bacterial / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D005260:Female; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007962:Leukocytes / Q000276:immunology; D051381:Rats; D011917:Rats, Inbred Lew; D013203:Staphylococcal Infections / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D013211:Staphylococcus aureus / Q000254:growth & development; D013682:Teichoic Acids / Q000276:immunology; D014822:Vitreous Body / Q000276:immunology / Q000382:microbiology / Q000473:pathology
chemical_list: D000907:Antibodies, Bacterial; D013682:Teichoic Acids