Staphylococcus aureus ocular isolates from symptomatic adverse events: antibiotic resistance and similarity of bacteria causing adverse events.

BACKGROUND: Staphylococcus is the leading cause of microbial keratitis. Staphylococcus aureus isolated from ocular infections with resistance to a wide range of antibiotics, including the commonly prescribed fluoroquinolones, is emerging. The aim of this study was to determine the current antibiotic susceptibilities of ocular S. aureus isolates and also determine whether isolates from different adverse events or those with similar antimicrobial susceptibilities are related. METHODS: A collection of 55 S. aureus strains from ocular adverse events were analysed for antibiotic susceptibility using disc diffusion (CDS method) and typed using PCR-ribotyping and pulsed-field gel electrophoresis (PFGE). RESULTS: S. aureus isolated from symptomatic ocular adverse events in the USA exhibited greater resistance to antibiotics than did those isolated from symptomatic ocular adverse events in Australia or India (p<0.05). A larger proportion of ulcerative keratitis isolates was found to be resistant to antibiotics than isolates from conjunctivitis. PFGE analysis separated related isolates determined by ribotype, on the basis of the adverse event caused by the isolate. Isolates were related within geographical regions and adverse event types. CONCLUSIONS: Similar isolates within a geographical location cause adverse events but there is a genetic difference between isolates causing corneal adverse events and those causing conjunctivitis. Isolates from corneal adverse events were more resistant to antibiotics, with those from the USA exhibiting the greatest resistance. This suggests that virulence may correlate with increased resistance to antibiotics.

A Staphylococcus aureus mouse keratitis topical infection model: cytokine balance in different strains of mice.

Staphylococcus is a leading cause of the potentially blinding disease microbial keratitis. Even with the use of antibiotic therapy, the host inflammatory response continues to damage the cornea, which may lead to blindness. Manipulation of the host response may help improve patient outcome from this devastating disease. We aim to understand the contribution of the host response to Staphylococcus aureus infection. A S. aureus keratitis mouse model was developed in both C57BL/6 and BALB/c mice using two different strains of S. aureus (8325-4 and Staph 38). Twenty-four hours postinfection, mice were killed and eyes were harvested for enumeration of bacteria, polymorphonuclear leucocytes, chemokines and cytokines. The laboratory strain 8325-4 was not as virulent as the clinical isolate Staph 38. In vitro data showed a 250-fold increase in invasion of human corneal epithelial cells by Staph 38 compared to 8325-4. BALB/c mice were susceptible to S. aureus infection whereas C57BL/6 mice were resistant. The resistant C57BL/6 mice were polarized towards a Th2 response, which may be protective for these mice. IL-4, IL-10 and IL-6 were elevated significantly in C57BL/6 mice infected with Staph 38 (P < 0.05). Macrophage inflammatory peptide (MIP)-2 was also significantly elevated in C57BL/6 mice (P < 0.001). The susceptible BALB/c mice had a muted cytokine response, which suggests that S. aureus might be 'walled off' during infection and might avoid host defences. IL-4, IL-10 and IL-6 cytokines may be protective during Gram-positive corneal infection and therefore may be useful for adjunct therapies in the treatment of this disease.